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E3 ubiquitin ligase BTBD3 inhibits tumorigenesis of colorectal cancer by regulating the TYRO3/Wnt/β-catenin signaling axis

Clinical trials and studies have implicated that E3 ubiquitin ligase BTBD3 (BTB Domain Containing 3) is a cancer-associated gene. However, the role and underlying mechanism of BTBD3 in colorectal cancer (CRC) ...

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Exploring the promise of regulator of G Protein Signaling 20: insights into potential mechanisms and prospects across solid cancers and hematological malignancies

RGS (Regulator of G protein signaling) proteins have long captured the fascination of researchers due to their intricate involvement across a wide array of signaling pathways within cellular systems. Their div...

Recent updates on allogeneic CAR-T cells in hematological malignancies

CAR-T cell therapy is known as an effective therapy in patients with hematological malignancies. Since 2017, several autologous CAR-T cell (auto-CAR-T) drugs have been approved by the US Food and Drug Administ...

Curcumin blunts epithelial-mesenchymal transition to alleviate invasion and metastasis of prostate cancer through the JARID1D demethylation

Prostate cancer (PCa) is one of the most common and prevalent cancers in men worldwide. The majority of PCa-related deaths result from metastasis rather than primary tumors. Several studies have focused on the...

Locoregional therapies combined with immune checkpoint inhibitors for liver metastases

Immune checkpoint inhibitors (ICIs) have achieved remarkable success in clinical research and practice. Notably, liver metastasis is not sensitive to ICIs. Liver locoregional therapies can cause irreversible d...

The sEVs miR-487a/Notch2/GATA3 axis promotes osteosarcoma lung metastasis by inducing macrophage polarization toward the M2-subtype

Small extracellular vesicles (sEVs) are important mediators of intercellular communication between tumor cells and their surrounding environment. Furthermore, the mechanisms by which miRNAs carried in tumor sE...

Capsaicin combined with cisplatin inhibits TGF-β1-induced EMT and TSCC cells migration via the Claudin-1/PI3K/AKT/mTOR signaling pathway

Tongue squamous cell carcinoma (TSCC) is one of the most common malignant tumors among oral cancers, and its treatment is based on radio-chemotherapy and surgery, which always produces more serious side effect...

Characterization of the stem cell landscape and identification of a stemness-associated prognostic signature in bladder cancer

It is accepted that cancer stem cells (CSCs) are key to the occurrence, progression, drug resistance, and recurrence of bladder cancer (BLCA). Here, we aimed to characterize the landscapes of CSCs and investig...

Complicated role of ALKBH5 in gastrointestinal cancer: an updated review

Gastrointestinal cancer is the most common malignancy in humans, often accompanied by poor prognosis. N6-methyladenosine (m6A) modification is widely present in eukaryotic cells as the most abundant RNA modifi...

Prognostic and immunological implications of heterogeneous cell death patterns in prostate cancer

Prostate cancer is one of the most common cancers in men with a significant proportion of patients developing biochemical recurrence (BCR) after treatment. Programmed cell death (PCD) mechanisms are known to p...

Extracellular vesicle-bound VEGF in oral squamous cell carcinoma and its role in resistance to Bevacizumab Therapy

Vascular endothelial growth factor (VEGF) is an important proangiogenic factor and has been considered as a key target of antiangiogenetic therapy in oral squamous cell carcinoma (OSCC). However, clinical appl...

Lipid metabolism associated crosstalk: the bidirectional interaction between cancer cells and immune/stromal cells within the tumor microenvironment for prognostic insight

Cancer is closely related to lipid metabolism, with the tumor microenvironment (TME) containing numerous lipid metabolic interactions. Cancer cells can bidirectionally interact with immune and stromal cells, t...

Telomerase related molecular subtype and risk model reveal immune activity and evaluate prognosis and immunotherapy response in prostate cancer

Prostate cancer ranks among the six most lethal malignancies worldwide. Telomerase, a reverse transcriptase enzyme, plays a pivotal role in extending cellular telomeres and is intimately associated with cell p...

Correction: AAA237, an SKP2 inhibitor, suppresses glioblastoma by inducing BNIP3-dependent autophagy through the mTOR pathway

The original article was published in Cancer Cell International 2024 24 :69

Correction: ARAP1-AS1: A novel long non-coding RNA with a vital regulatory role in human cancer development

The original article was published in Cancer Cell International 2024 24 :270

Sensitization of hepatocellular carcinoma cells to HDACi is regulated through hsa-miR-342-5p/CFL1

Increased prevalence of hepatocellular carcinoma (HCC) remains a global health challenge. HCC chemoresistance is a clinical obstacle for its management. Aberrant miRNA expression is a hallmark for both cancer ...

Does rAj-Tspin, a novel peptide from A. japonicus , exert antihepatocellular carcinoma effects via the ITGB1/ZYX/FAK/AKT signaling pathway?

rAj-Tspin, a soluble recombinant peptide from Apostichopus japonicus , can inhibit the integrin β1 (ITGB1)/FAK/AKT signaling pathway in hepatocellular carcinoma (HCC) via cell epithelial–mesenchymal transition (EM...

Retraction Note: Transcription elongation factor A-like 7, regulated by miR-758-3p inhibits the progression of melanoma through decreasing the expression levels of c-Myc and AKT1

Establishment of patient-derived organoids and a characterization based drug discovery platform for treatment of gastric cancer.

Gastric cancer (GC) encompasses many different histological and molecular subtypes. It is a major driver of cancer mortality because of poor survival and limited treatment options. Personalised medicine in the...

Upregulation of MELK promotes chemoresistance and induces macrophage M2 polarization via CSF-1/JAK2/STAT3 pathway in gastric cancer

Gastric cancer (GC) stands out as one of the most prevalent malignancies affecting the digestive system, characterized by a substantial incidence rate and mortality. Maternal embryonic leucine zipper kinase (M...

TTI-101 targets STAT3/c-Myc signaling pathway to suppress cervical cancer progression: an integrated experimental and computational analysis

Cervical cancer (CC) is a significant global health concern, demanding the consideration of novel therapeutic strategies. The signal transducer and activator of transcription 3 (STAT3) pathway has been implica...

Synergistic antitumor effect of liposomal-based formulations of olaparib and topotecan in primary epithelial ovarian cancer cells

Olaparib is a PARP inhibitor inducing synthetic lethality in tumors with deficient homologous recombination (HRD) caused by BRCA1/2 mutations. The FDA has approved monotherapy for first-line platinum-sensitive...

Adipocytes promote metastasis of breast cancer by attenuating the FOXO1 effects and regulating copper homeostasis

Obesity and the forkhead box O1(FOXO1) affect the survival of breast cancer patients, but the underlying mechanism remains unclear. We aimed to investigate the role of FOXO1 in obesity-associated-breast cancer.

AFP-HSP90 mediated MYC/MET activation promotes tumor progression in hepatocellular carcinoma and gastric cancers

Alpha-fetoprotein (AFP) elevation is a well-known biomarker in various diseases, particularly in the diagnosis of hepatocellular carcinoma (HCC). Intracellular AFP has been previously implicated in promoting t...

Enhancing mutation detection in multiple myeloma with an error-corrected ultra-sensitive NGS assay without plasma cell enrichment

Risk stratification in multiple myeloma (MM) patients is crucial, and molecular genetic studies play a significant role in achieving this objective. Enrichment of plasma cells for next-generation sequencing (N...

Retraction Note: Circular RNA hsa_circ_0000517 modulates hepatocellular carcinoma advancement via the miR-326/SMAD6 axis

Identification of pou4f1 as a novel prognostic biomarker and therapeutic target in esophageal squamous cell carcinoma.

Esophageal cancer is a significant global health concern, ranking seventh in incidence and sixth in mortality. It encompasses two pathological types: esophageal squamous cell carcinoma (ESCC) and esophageal ad...

Comprehensive analysis, diagnosis, prognosis, and cordycepin (CD) regulations for GSDME expressions in pan-cancers

The Gasdermin E gene ( GSDME ) plays roles in deafness and cancers. However, the roles and mechanisms in cancers are complex, and the same gene exhibits different mechanisms and actions in different types of cancer...

Harnessing exosomes as cancer biomarkers in clinical oncology

Exosomes are extracellular vesicles well known for facilitating cell-to-cell communication by distributing essential macromolecules like proteins, DNA, mRNA, lipids, and miRNA. These vesicles are abundant in f...

Enhanced anti-tumor effects by combination of tucatinib and radiation in HER2-overexpressing human cancer cell lines

Tucatinib (TUC), a HER2-directed tyrosine kinase inhibitor, is the first targeted drug demonstrating intracranial efficacy and significantly prolonged survival in metastatic HER2-positive breast cancer (BC) pa...

CircUBA2 promotes the cancer stem cell-like properties of gastric cancer through upregulating STC1 via sponging miR-144-5p

Cancer stem cells (CSCs) are critical factors that limit the effectiveness of gastric cancer (GC) therapy. Circular RNAs (circRNAs) are confirmed as important regulators of many cancers. However, their role in...

Multiple mechanisms contribute to acquired TRAIL resistance in multiple myeloma

Multiple Myeloma (MM) prognosis has recently improved thanks to the incorporation of new therapies to the clinic. Nonetheless, it is still a non-curable malignancy. Targeting cancer cells with agents inducing ...

Correction: MicroRNAs targeted mTOR as therapeutic agents to improve radiotherapy outcome

The original article was published in Cancer Cell International 2024 24 :233

MSI2 regulates NLK-mediated EMT and PI3K/AKT/mTOR pathway to promote pancreatic cancer progression

The incidence of pancreatic cancer is increasing by years, and the 5-year survival rate is very low. Our team have revealed that Musashi2 (MSI2) could promote aggressive behaviors in pancreatic cancer by downr...

DDX19A promotes gastric cancer cell proliferation and migration by activating the PI3K/AKT pathway

DEAD-box RNA helicase 19 A (DDX19A) is overexpressed in cervical squamous cell carcinoma. However, its role in gastric cancer remains unclear. The present study aimed to explore the role and underlying mechani...

TERT upstream promoter methylation regulates TERT expression and acts as a therapeutic target in TERT promoter mutation-negative thyroid cancer

DNA hypermethylation and hotspot mutations were frequently observed in the upstream and core promoter of telomerase reverse transcriptase ( TERT ), respectively, and they were associated with increased TERT express...

ARAP1-AS1: a novel long non-coding RNA with a vital regulatory role in human cancer development

Long non-coding RNAs (lncRNAs) have garnered significant attention in biomedical research due to their pivotal roles in gene expression regulation and their association with various human diseases. Among these...

The Correction to this article has been published in Cancer Cell International 2024 24 :292

Oncogenic LINC00698 suppresses apoptosis of melanoma stem cells to promote tumorigenesis via LINC00698-miR-3132-TCF7/hnRNPM axis

Melanoma progression depends on melanoma stem cells (MSCs), which are distinguished by the distinct dysregulated genes. As the key factors in the dysregulation of genes, long non-coding RNAs (lncRNAs) take gre...

Uncovering novel mechanisms of chitinase-3-like protein 1 in driving inflammation-associated cancers

Chitinase-3-like protein 1 (CHI3L1) is a secreted glycoprotein that is induced and regulated by multiple factors during inflammation in enteritis, pneumonia, asthma, arthritis, and other diseases. It is associ...

Integrative analysis of aging-related genes reveals CEBPA as a novel therapeutic target in non-small cell lung cancer

To explore the impact of ARGs on the prognosis of NSCLC, and its correlation with clinicopathological parameters and immune microenvironment. Preliminary research on the biological functions of CEBPA in NSCLC.

Unveiling heterogeneity and prognostic markers in ductal breast cancer through single-cell RNA-seq

Breast cancer (BC) is a heterogeneous disease, with the ductal subtype exhibiting significant cellular diversity that influences prognosis and response to treatment. Single-cell RNA sequencing data from the GE...

TGFBI promotes proliferation and epithelial–mesenchymal transition in renal cell carcinoma through PI3K/AKT/mTOR/HIF-1α pathway

Renal cell carcinoma (RCC) is presently recognized as the most prevalent kidney tumor. However, the role and underlying mechanism of action of the conversion factor-inducible protein (TGFBI), an extracellular ...

The systematic role of pancreatic cancer exosomes: distant communication, liquid biopsy and future therapy

Pancreatic cancer remains one of the most lethal diseases worldwide. Cancer-derived exosomes, benefiting from the protective role of the lipid membrane, exhibit remarkable stability in the circulatory system. ...

GluOC promotes proliferation and metastasis of TNBC through the ROCK1 signaling pathway

Triple negative breast cancer (TNBC) is a type of breast cancer that is negative for oestrogen receptor, progesterone receptor and human epidermal growth factor receptor 2, is highly malignant and aggressive, ...

The lncRNA LINC01605 promotes the progression of pancreatic ductal adenocarcinoma by activating the mTOR signaling pathway

This study investigated the molecular mechanism of long intergenic non-protein coding RNA 1605 (LINC01605) in the process of tumor growth and liver metastasis of pancreatic ductal adenocarcinoma (PDAC).

EBP1 promotes the malignant biological behaviors of kidney renal clear cell carcinoma through activation of p38/HIF-1α signaling pathway

Kidney Renal Clear Cell Carcinoma (KIRC) is a common malignant tumor of the urinary system, and its incidence is increasing. ERBB3 binding protein (EBP1) is upregulated in various cancers. However, the connect...

Correction: MALAT1/ mir-1-3p mediated BRF2 expression promotes HCC progression via inhibiting the LKB1/AMPK signaling pathway

The original article was published in Cancer Cell International 2023 23 :188

ALDH5A1/miR-210 axis plays a key role in reprogramming cellular metabolism and has a significant correlation with glioblastoma patient survival

Glioblastoma (GBM) is the most aggressive among the tumors of the central nervous system (CNS), and has a dismal prognosis. Altered metabolism, especially the increased rate of aerobic glycolysis promotes rapi...

Machine learning models for predicting of PD-1 treatment efficacy in Pan-cancer patients based on routine hematologic and biochemical parameters

Immune checkpoint blockade therapy targeting the programmed death-1(PD-1) pathway has shown remarkable efficacy and durable response in patients with various cancer types. Early prediction of therapeutic effic...

Circular RNA circ_ARHGEF28 inhibits MST1/2 dimerization to suppress Hippo pathway to induce cisplatin resistance in ovarian cancer

Cisplatin is integral to ovarian cancer treatment, yet resistance to this drug often results in adverse patient outcomes. The association of circular RNA (circRNA) with cisplatin resistance in ovarian cancer h...

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New approaches and procedures for cancer treatment: Current perspectives

Dejene tolossa debela.

1 Center for Innovative Drug Development and Therapeutic Trials for Africa (CDT-Africa), College of Health Sciences, Addis Ababa University, Addis Ababa, Ethiopia

Seke GY Muzazu

2 Enteric Diseases and Vaccines Research Unit, Centre for Infectious Disease Research in Zambia (CIDRZ), Lusaka, Zambia

Kidist Digamo Heraro

3 Wachemo University, Hossana, Ethiopia

Maureen Tayamika Ndalama

Betelhiem woldemedhin mesele.

4 Kotebe Metropolitan University, Addis Ababa, Ethiopia

Dagimawi Chilot Haile

5 University of Gondar, Gondar, Ethiopia

Sophia Khalayi Kitui

Tsegahun manyazewal.

Cancer is a global health problem responsible for one in six deaths worldwide. Treating cancer has been a highly complex process. Conventional treatment approaches, such as surgery, chemotherapy, and radiotherapy, have been in use, while significant advances are being made in recent times, including stem cell therapy, targeted therapy, ablation therapy, nanoparticles, natural antioxidants, radionics, chemodynamic therapy, sonodynamic therapy, and ferroptosis-based therapy. Current methods in oncology focus on the development of safe and efficient cancer nanomedicines. Stem cell therapy has brought promising efficacy in regenerating and repairing diseased or damaged tissues by targeting both primary and metastatic cancer foci, and nanoparticles brought new diagnostic and therapeutic options. Targeted therapy possessed breakthrough potential inhibiting the growth and spread of specific cancer cells, causing less damage to healthy cells. Ablation therapy has emerged as a minimally invasive procedure that burns or freezes cancers without the need for open surgery. Natural antioxidants demonstrated potential tracking down free radicals and neutralizing their harmful effects thereby treating or preventing cancer. Several new technologies are currently under research in clinical trials, and some of them have already been approved. This review presented an update on recent advances and breakthroughs in cancer therapies.

Introduction

Cancer is a global health problem responsible for one in six deaths worldwide. In 2020, there were an estimated 19.3 million new cancer cases and about 10 million cancer deaths globally. Cancer is a very complicated sequence of disease conditions progressing gradually with a generalized loss of growth control. 1 – 3 There were only a few options of cancer treatment for patients for many decades which include surgery, radiation therapy, and chemotherapy as single treatments or in combination. 4 , 5 But recently, many pathways involved in cancer therapy progression and how they can be targeted has improved dramatically, with combinatorial strategies, involving multiple targeted therapies or “traditional” chemotherapeutics, such as the taxanes and platinum compounds, being found to have a synergistic effect. 6 New approaches, such as drugs, biological molecules, and immune-mediated therapies, are being used for treatment even if the excepted therapy level has not reached that resists the mortality rate and decreases the prolonged survival time for metastatic cancer.

The creation of a new revolution in neoplastic cancer or targeting drugs depends on the pathways and characteristics of different tumor entities. 7 Chemotherapy is considered the most effective and widely used modality in treating cancers as used alone or in combination with radiotherapy. Genotoxicity is how chemotherapy drugs target the tumor cells mainly producing reactive oxygen species that largely destroy tumor cells. 8 Hormonal treatments are also widely used for cancer malignancies and considered as cytostatic because it restricts tumor development by limiting the hormonal growth factors acting through the direction of hypothalamic–pituitary–gonadal axis (HPGA), hormone receptor blockage, and limiting of adrenal steroid synthesis. 9

In this narrative review, a general overview of the most advanced and novel cancer therapies was provided. In addition, also new strategies currently under investigation at the research stage that should overwhelm the drawbacks of standard therapies; different strategies to cancer diagnosis and therapy; and their current status in the clinical context, underlining their impact as innovative anti-cancer approaches.

Cancer treatment modalities

We can see cancer treatment modalities by dividing them into conventional (traditional) and advanced or novel or modern categories. In this era worldwide, over half of all ongoing medical treatment trials are focusing on cancer treatments. 7 Entities, such as the type of cancer, its site, and severity, guide to select treatment options and its progress. The most widely used traditional treatment methods are surgery, chemotherapy, and radiotherapy, while modern modalities include hormone therapy, anti-angiogenic, stem cell therapies, immunotherapy, and dendritic cell-based immunotherapy. 10

Conventional cancer therapies

The most recommended conventional cancer treatment strategies include surgical resection of the tumors followed by radiotherapy with x-rays and/or chemotherapy. 11 Of these modalities, surgery is most effective at an early stage of disease progression. Radiation therapy can damage healthy cells, organs, and tissues. Although chemotherapy has reduced morbidity and mortality, virtually all chemotherapeutic agents damage healthy cells, especially rapidly dividing and growing cells. 12 Drug resistance, a major problem with chemotherapy, is a phenomenon wherein cancer cells that initially were suppressed by an anti-cancer drug develop resistance to the drug. This is caused primarily by reduced drug uptake and increased drug efflux. 13 Limitations of conventional chemotherapeutic modality, such as dosage selection difficulty, lack of specificity, rapid drug metabolism, and mainly harmful side effects. 14

Advanced and innovative cancer therapies

Among the obstacles of cancer, drug resistance and its delivery systems are the most problem in cancer cure and decreasing signs and symptoms; but currently, there are many approved treatment approaches and drugs. The efficiency of conventional cancer is reduced due to tumor pathology and architectural abnormality of tumor tissue blood vessels. 15 The following are the advanced and innovative cancer therapy types with their benefits and challenges.

Stem cells therapy

Stem cells are undifferentiated cells present in the bone marrow (BM) with an ability to differentiate into any type of body cell. Stem cell therapeutic strategy is also one of the treatment options for cancer which are considered to be safe and effective. Application of stem cell is yet in the experimental clinical trial; for example, their use in the regeneration of other damaged tissue is being explored. Mesenchymal stem cells (MSCs) are currently being used in trials that are delivered from the BM, fat tissues, and connective tissues. 16

Pluripotent stem cells

Embryonic stem cells (ESCs) isolated from the uniform inner mass cells of the embryo possess the flexibility to administer rise to any or all kinds of cells except those within the placenta. In 2006, the invention of Yamanaka factors to induce pluripotent stem cells (iPSCs) from physical cells in a culture marked a breakthrough in cell biology. 17 Avoiding ethical issues from embryo destruction, iPSCs and ESCs have the same characteristics. Hematopoietic embryonic stem cells (hESCs) and iPSCs are currently used for the induction of effector T cells and natural killer (NK) cells, 18 and anti-tumor vaccine preparation. 19

Adult stem cells

Adult stem cells (ASCs) groups often used in tumor therapy include hematopoietic stem cells (HSCs), MSCs, and neural stem cells (NSCs). HSCs, located in BM, can form all mature blood cells in the body. Currently, only approved by the Food and Drug Administration (FDA) is the infusion of HSCs derived from cord blood to treat multiple myeloma and leukemia. 20 MSCs are found in many tissues and organs, playing important roles in tissue repair and regeneration into cells, such as osteocytes, adipocytes, and chondrocytes. MSCs have special biological characteristics and are used as complimentary with other approaches in treating tumors. 21 NSCs can self-renew and generate new neurons and glial cells and are used for treating both primary and metastatic breast and other tumors. 22

Cancer stem cells

Cancer stem cells (CSCs) are generated in normal stem cells or precursor/progenitor cells by the epigenetic mutations process. Their role in tumor treatment includes cancer growth, metastasis, and recurrence, so that it could give promise in the treatment of solid tumors. 23 Stem cells have several action mechanisms in treating the tumor. The homing process is one mechanism which is a rapid migration of HSCs into defined stem cell niches in BM after that the transplants undergo the engraftment process before giving rise to specialized blood cells. This mechanism is dependent on the active interaction between stem cell CXCR4 receptors and requires their interaction with endothelial cells through LFA-1, VLA-4/5, CD44, and the secretion of matrix degradable enzyme MMP-2/9. 22 The second mechanism is the tumor-tropic effect in which the migration of MSCs toward tumor microenvironment (TM) after attraction by CXCL16, SDF-1, CCL-25, and IL-6 secreted by tumor cells and differentiation of MSCs within the tumor cells which contributes to tumor stromal development. 24 Stem cells also act by paracrine factor secretion, including extracellular vesicles (EVs) and soluble materials, 25 and their differentiation capacity, such as transplanted HSCs, can give rise to all blood cell types. 26

Generally, cancer treatment using stem cell therapy by various strategies, including transplantation of HSC, 27 MSC infusion, 28 therapeutic carriers, 29 generation of immune effector cells, 30 and vaccine production. 31 The stem cell cancer therapy approach confronted the following side effects: (1) tumorigenesis, (2) adverse events in allogeneic HSC transplantation, (3) drug toxicity and drug resistance, (4) increased immune responses and autoimmunity, and (5) viral infection. 22 Despite several successes, there are challenges, such as therapeutic dose control, low cell targeting, and retention in tumor sites, that should be investigated and overcome in the future. In addition, existing results from stem cell technologies are highly encouraging for tumor treatment but it still needs further efforts to improve the safety and efficacy before they could enter clinical trials. Table 1 summarized the licensed list of stem cell therapies.

Licensed stem cell therapies.

AML: acute myelogenous leukemia; FDA: The US Food and Drug Administration; iPSC: induced pluripotent stem cell; MSC-INβ: mesenchymal stem cells with interferon beta.

Targeted drug therapy

Targeted cancer therapies are drugs or other substances which are sometimes interchangeably used as “molecularly targeted drugs,” “molecularly targeted therapies,” and “precision medicines.” Those drugs’ mechanism of action is by interfering with growth molecules which leads to blocking the growth and spreading of cancer. 34 Tumor initiation and progression are determined by the TM of an atypical tumor which comprises endothelial cells, pericytes, smooth muscle cells, fibroblasts, various inflammatory cells, dendritic cells, and CSCs. There are various signaling mechanisms and pathways that TM-forming cells dynamically interact with the cancerous cells which are suitable for sustaining a reasonably high cellular proliferation. So, it is the area of research interest using TM conditions to mediate effective targeting measures for cancer therapy. 35

Selectively treating cancer cells with conventional chemotherapy is difficult since it is similar to normal cells. So those problems are intervened by cellular mechanisms, such as cell cycle arrest, apoptosis induction, proliferation prevention, and interfering with metabolic reprogramming by targeted drug therapy agents. 36 Modifying TM and targeting TM for drug delivery for effective treatment are two strategies that can be used for the treatment of cancer. 37 Targeted therapy drugs do work in different ways from standard chemotherapy drugs treatment like attacking cancer cells while doing less damage to normal cells which is a programming that sets them apart from normal, healthy cells. 38

Using targeted therapy markedly increased the survival rate for some diseases, for example, from 17% to 24% in patients with advanced pancreatic cancer, the addition of erlotinib to standard chemotherapy. Imatinib has had a dramatic effect on chronic myeloid leukemia, and rituximab, sunitinib, and trastuzumab have revolutionized the treatment of renal cell carcinoma and breast cancer, respectively. 39

We can classify the targeted cell agents based on the mechanism of their work or their target site. Some enzymes serve as signals for cancer cells to grow. Some targeted therapies inhibit enzymes that are signals for cancer cells to grow. These drugs are called enzyme inhibitors. Blocking these cell signals can inhibit cancer from getting bigger and spreading. 40

Some targeted therapies are called apoptosis-inducing drugs because they are aimed right at the parts of the cell that control whether cells live or die. The examples are serine/threonine kinase, protein kinase B (PKB/Akt), which promotes cell survival, and inhibitors of this protein are in the preclinical phase. 41

These agents stop the tumors from making new blood vessels which helps cut off the tumors’ blood supply so that tumors cannot grow. In addition, they arrest tumor growth that involves by curtailing blood supply to the tumor by inhibiting angiogenic factors, such as vascular endothelial growth factor (VEGF) or its receptors. The study showed the survival of patients with advanced colorectal carcinoma extended by months after the use of Avastin (bevacizumab) in combination with 5-fluorouracil-based chemotherapy. 42

Types of target agents

Monoclonal antibodies.

Antibody drugs are man-made versions of immune system proteins administered intravenously to attack certain targets on cancer cells. They contain a more proportion of human components than murine components. 43 Their attack mechanisms of action are recruiting host immune functions to attack the target cell, binding to ligands or receptors thereby interrupting essential cancer cell processes, and carrying a lethal payload, such as radioisotope or toxin, to the target cell. 44 Gemtuzumab is an example of a CD-33-specific monoclonal antibody currently used for AML treatment by conjugating with calicheamicin. 45 In addition, ibritumomab tiuxetan is an anti-CD20, a 90Y metal isotope-based is developed in clinical therapy. 46 Delivery of active therapeutics, prodrug activation enzymes, and chemotherapy toxins are also another use of target agents of monoclonal antibodies. 47

Small molecule inhibitors

These are smaller protein in size (⩽500 Da) than monoclonal antibodies, so that they can simply translocate through plasma membranes and can be taken orally. Their main function is interrupting cellular processes by interfering with the intracellular signaling of tyrosine kinases which leads to the inhibition of tyrosine kinase signaling and initiates a molecular cascade that can lead to the inhibition of cell growth, proliferation, migration, and angiogenesis in malignant tissues. 48 Examples of small molecule inhibitors are gefitinib and erlotinib which inhibit epidermal growth factor receptor (EGFR) kinase and EGFR in non-small cell lung cancer (NSCLC) patients, respectively. There are also lapatinib and sorafenib which act on the inhibition of EGFR/Erb-B2 Receptor Tyrosine Kinase 2 (ERBB2) for ERBB2-positive breast cancer and VEGFR kinase, in renal cancer. 49

Ablation cancer therapy

Ablation is a treatment technique that destroys tumors without removing them mostly indicated for small-size tumors of less than 3 cm and the surgical option is contraindicated. Ablation is also used with embolization for larger tumors. However, this technique might not be indicated for treating tumors near major blood vessels, the diaphragm, or major bile ducts due to destroying some of the normal tissue around the tumor. 50

Thermal ablation

This technique uses extreme hyperthermia or hypothermia to destruct tumor tissue concentrating on a focal zone in and around the tumor. Similar to surgery, thermal ablation removes the tumor and a 5–10 mm thick margin of seemingly normal tissue but the tissue is killed in situ and then absorbed by the body later. The procedure is similar to surgery using an open, laparoscopic, or endoscopic approach but is commonly applied using a percutaneous or non-invasive approach. The type of tumor, site, physician’s choice, and health status determine the approach. 51

Radiofrequency ablation (RFA), microwave ablation, high-intensity focused ultrasound, and cryoablation are currently being used in the clinical setting. Cryoablation uses a hypothermic modality to induce tissue damage by a freeze-thaw process against others. All these treatments operate on the principle of hyperthermia except cryoablation. Of all the ablation techniques, cryoablation demonstrated the highest potential to elicit a post-ablative immunogenic response. 52

Recent studies showed additional to tissue disruption RFA and cryoablation can modulate the immune system that they were applied as therapy on TM and in the systematic circulation. Evidence has shown that ablation procedures affect carcinogenesis due to its local inflammatory response leading to an immunogenic gene signature. 53

The advantage of this procedure over surgery is that it provides a minimal (e.g. percutaneously or laparoscopically) or non-invasive approach to cancer therapy and gets attention as an alternative to standard surgical therapies. 54

Cryoablation

Cryoablation is one of the ablation techniques which ablates the extensive tissue by freezing to lethal temperatures followed by liquid formation, causing extensive tissue. Benign and malignant primary tumors are mostly treated by this therapy. 55 James Arnott reported that the freezing temperatures can impair cancer cell viability after he attempted the usage of cold temperatures by salt and ice solutions for the generation of local numbness before surgical operations in the nineteenth century. He suggested cryoablation as an attractive therapeutic option and increased a patient’s survival. 56

Cryoablation techniques are based on the principle of the Joule–Thomson effect which was studied in the 1930s by many researchers and concluded using liquid CO 2 under high pressure, liquid air, and liquid oxygen to achieve the cooling effect and the subsequent formation of ice crystals so employed to treat lesions, warts, and keratosis. However, after 1950, Allington replaced liquid N 2 for the treatment of various skin lesion disorders. 47

RFA therapy

RFA is a minimally invasive procedure and an image-guided technique using hyperthermic (high-frequency electrical currents) conditions to destroy cancer cells. Imaging techniques, such as ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI), guide needle electrodes into a tumor cell. Generally, RFA is the most effective approach for treating small-size tumors of less than 3 cm in diameter. RFA can be used in combination with other conventional cancer treatment options. 57 After starting the use of deployable devices or multiple-electrode systems, RFA can treat medium tumors (up to 5 cm diameter). 58

Gene therapy

Gene therapy is the insertion of a normal copy of a defective gene in the genome to cure a specific disorder. The first application dates back to 1990 when a retroviral vector was exploited to deliver the adenosine deaminase (ADA) gene to T cells in patients with severe combined immunodeficiency (SCID). Approximately, about 2900 gene therapy clinical trials are currently ongoing, two-third of which are related to cancer. Strategies, such as expression of proapoptotic and chemosensitizing genes, expression of wild-type tumor suppressor genes, expression of genes able to solicit specific anti-tumor immune responses, and targeted silencing of oncogenes, are under evaluation for cancer gene therapy. 47

Thymidine kinase (TK) gene delivery is effective for the administration of prodrug ganciclovir to activate its expression and induce specific cytotoxicity. 59 The p53 tumor suppressor gene which is vectors carrying has been assessed for the clinical purpose very recently. ONYX-015 has been tested in NSCLC patients and gave a high response rate when given alone or combined with chemotherapy. 60 Gendicine, a recombinant adenovirus carrying wild-type p53-induced complete disease regression in head and neck squamous cell cancer had similar success when combined with radiotherapy. 61

Some challenges that have been faced with gene therapy are the selection of the right conditions and the choice of the best delivery mechanism. Identified drawbacks of this therapy are genome integration, limited efficacy in specific subsets of patients, and high chances of being neutralized by the immune system. Basic research and medical translation used RNA interference (RNAi) as an efficient technology that able to produce targeted gene silencing. 62 RNA-induced silencing complex (RISC) mediates the targeted gene silencing process by cleaving the messenger RNA (mRNA) and interference with protein synthesis. 63 A siRNAs can be designed to block desired targets, involving cell proliferation and metastatic invasion; hence, precise molecular mechanisms are a triggering factor for tumor formation. This method relies on siRNA-mediated gene silencing of anti-apoptotic proteins, transcription factors (i.e. c-myc gene), 64 , 65 or cancer mutated genes (i.e. K-RAS). 66

Advantages of siRNA-based drugs are safety, high efficacy, specificity, few side effects, and low costs of production. 67 However, occasionally, they can induce off-target effects or elicit innate immune responses, followed by specific inflammation. 68 Delivery methods currently under study are chemical modification (insertion of a phosphorothioate at 3’ end, introduction of a 2’ O-methyl group, and modification by 2,4-dinitrophenol) and lipid encapsulation, or conjugation with organic molecules (polymers, peptides, lipids, antibodies, small molecules) efficiently target to spontaneously cross cell membranes of naked siRNAs. 69 Interaction of cationic liposomes with negatively charged nucleic acids facilitates easy transfection by simple electrostatic interactions. 70 They can be constituted by 1,2-dioleoyl-3-trimethylammonium propane (DOTAP) and N-[1-(2,3-dioleoyloxy) propyl]-N, Ntrimethylammonium methyl sulfate (DOTMA). 71 Currently, a Phase I clinical trial is recruiting patients for evaluating the safety of Eph receptor A2 (EphA2) targeting 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC) encapsulated siRNA (siRNA-EphA2- DOPC) in patients with advanced and recurrent cancer. 72 siRNAs can be concentrated in cationic polymers, such as chitosan, cyclodextrin, and polyethyleneimine (PEI). 73 CALAA-01 is one of the cyclodextrin polymers conjugated with human transferrin is being entered a Phase I clinical trial. PEI has been used as an anti-cancer by forming small cationic nanoparticles and loading with human epidermal growth factor receptor 2 (HER-2 receptor)-specific siRNA. 74 Phase II clinical trial has been started to evaluate Local Drug EluteR (siG12D LODER) directed to mutated Kirsten rat sarcoma (K-RAS) oncogene for the treatment of advanced pancreatic cancer. Conjugating to peptides, antibodies, and aptamers improves stability during circulation and enhances cellular uptake of siRNAs. 75 The introduction of nanocarriers has largely improved siRNAs stability, pharmacokinetics and biodistribution properties, and targeting specificity. Polyallylamine phosphate nanocarriers have been developed to release siRNAs in the cytoplasm after disassembly at low endosomal pH. 76

Dose correction and variabilities between individuals and different stages of disease are challenging issues on clinical translation of the siRNA-based approach. In the future, the needed research is on setting up the best-personalized therapy and toward controlled release to reach only specific targets on treating the tumor. Table 2 summarizes the gene therapy drugs based on their mechanism of action and induction.

Summary of gene therapy approaches.

Natural antioxidants

Day to day, the anatomy undergoes many exogenous insults, such as ultraviolet (UV) rays, pollution, and tobacco smoke, that end in the assembly of reactive species, particularly oxidants and free radicals, liable for the onset of many diseases, together with cancer. These molecules can even be made as a consequence of clinical administration of medication; however, they are additionally naturally created within our cells and tissues by mitochondria and peroxisomes, and from macrophages metabolism, throughout traditional physiological aerobic processes. 47

Oxidative stress and radical oxygen species can significantly change the regulation of transcription factors by damaging the DNA and other bio-macromolecule. 77

Vitamins, polyphenols, and plant-derived bioactive compounds are natural antioxidants used as preventive and therapeutic drugs against these molecules that damage the body due to their anti-inflammatory and antioxidant properties. 78 Studies added to cancer therapy after appreciating their anti-proliferative and proapoptotic properties. Compounds, such as vitamins, alkaloids, flavonoids, carotenoids, curcumin, berberine, quercetin, and others, are examples of natural antioxidants screened in vitro and in vivo. 79

Limited bioavailability and/ or toxicity is one of the challenges of natural drugs while their translation into clinical practice. 47 Curcumin has cytotoxic effects in different kinds of tumors, such as the brain, lung, leukemia, pancreatic, and hepatocellular carcinoma, 80 while sparing normal cells at effective therapeutic doses. The curcumin’s biological properties, treatment duration and efficient therapeutic doses are under study. 80 This day, about 27 clinical trials are done, while 40 are under study on curcumin.

Berberine is an alkaloid compound that has been studied to be effective against different cancers as a chemopreventive agent, modulating many signaling pathways. Different nanotechnological strategies have been developed to facilitate its delivery across cell membranes due to their poorly soluble in water. 81 Six clinical trials are under study and two have been completed.

Quercetin is another natural plant origin agent that is effective alone and also in combination with chemotherapeutic agents in treating many cancers, such as lung, prostate, liver, colon, and breast cancers. 82 Quercetin’s mechanism of action is by binding to cellular receptors and the interference of several signaling pathways. 83 Currently, six clinical trials are under study and seven studies have been completed.

Current clinical trials

In recent years, analysis of cancer medication has taken outstanding steps toward more practical, precise, and fewer invasive cancer treatments in the research of clinical trials ( Figure 1 ).

Current status of clinical trials of innovative and novel strategies of cancer therapy.

Currently, the most frequent entries focusing on cancer therapies in the database of clinical trials ( www.clinicalTrials.gov ) include the terminologies stem cell, targeted therapy, immunotherapy, and gene therapy because they are very promising and effective. Table 3 summarizes the potential advantages and disadvantages of the new treatment approaches.

Comparison of advantageous and disadvantageous of new cancer therapies.

MRI: magnetic resonance imaging.

Table 4 summarizes the approaches to advanced cancer therapies and their respective delivery systems with examples.

Advanced therapy approaches and delivery systems.

Current methods in oncology focus on the development of safe and efficient cancer nanomedicines. Targeted medical care helped rising the biodistribution of recent or already tested chemotherapeutical agents around the specific tissue to be treated; different methods, such as sequence medical care, siRNAs delivery, therapy, and inhibitor molecules, supply new potentialities to cancer patients. Gene therapy acts by direct in situ insertion of exogenous genes into benign tumors. Noticeably, stem cells can be used as regenerative medicine, therapeutic carriers, drug targeting, and generation of immune cells because of having unique biological actions on other cells. 22 On the opposite hand, thermal ablation and magnetic hyperthermia are promising alternatives to the growth surgical process. Finally, radionics and pathomics approaches facilitate the management of huge knowledge sets from cancer patients to enhance prognosis and outcomes. Much progress has been made, but many others are likely to come soon, producing more and more ad hoc personalized therapies. Further development and refinement of drug delivery systems are essential for improving therapeutic outcomes.

Acknowledgments

The authors thank the Center for Innovative Drug Development and Therapeutic Trials for Africa (CDT-Africa), Addis Ababa University, for the support rendered.

Author contributions: D.T.D. is a major contributor in writing the manuscript. All others reviewed and approved the manuscript.

Declaration of conflicting interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding: The author(s) received no financial support for the research, authorship, and/or publication of this article.

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Collection  10 March 2022

Top 100 in Cancer

This collection highlights our most downloaded* cancer papers published in 2021. Featuring authors from aroud the world, these papers showcase valuable research from an international community.

*Data obtained from SN Insights which is based on Digital Science's Dimensions.

Radiotherapy for brain metastasis and long-term survival

• Kawngwoo Park
• Gi Hwan Bae
• Jaehun Jung

The Angelina Jolie effect: Contralateral risk-reducing mastectomy trends in patients at increased risk of breast cancer

• Narendra Nath Basu
• James Hodson
• D. Gareth Evans

Deep learning classification of lung cancer histology using CT images

• Tafadzwa L. Chaunzwa
• Ahmed Hosny
• Hugo J. W. L. Aerts

Pancancer survival analysis of cancer hallmark genes

• Gyöngyi Munkácsy
• Balázs Győrffy

Anti-estrogenic and anti-aromatase activities of citrus peels major compounds in breast cancer

• Dina M. El-Kersh
• Shahira M. Ezzat
• Mohey M. Elmazar

Arsenic exposure in Indo Gangetic plains of Bihar causing increased cancer risk

• Mohammad Ali
• Ashok Kumar Ghosh

CIBERSORT analysis of TCGA and METABRIC identifies subgroups with better outcomes in triple negative breast cancer

• Kelly E. Craven
• Yesim Gökmen-Polar
• Sunil S. Badve

The incidence and clinical analysis of non-melanoma skin cancer

• Magdalena Ciążyńska
• Grażyna Kamińska-Winciorek
• Aleksandra Lesiak

Real-world outcomes versus clinical trial results of immunotherapy in stage IV non-small cell lung cancer (NSCLC) in the Netherlands

• Christine M. Cramer-van der Welle
• Marjon V. Verschueren
• The Santeon NSCLC Study Group

Anti-tumour activity of deer growing antlers and its potential applications in the treatment of malignant gliomas

• Louis Chonco
• Tomás Landete-Castillejos
• Tomás Segura

Risk of cancer development in patients with keloids

• Hung-Pin Tu
• Chih-Hung Lee

Neutrophil to lymphocyte ratio influences impact of steroids on efficacy of immune checkpoint inhibitors in lung cancer brain metastases

• Bicky Thapa
• Manmeet S. Ahluwalia

Prediction of survival in patients with advanced, refractory colorectal cancer in treatment with trifluridine/tipiracil: real-world vs clinical trial data

• Ana Fernández Montes
• Alberto Carmona-Bayonas
• Teresa Garcia García

Hyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia and induction of tumor apoptosis in A549-cell-transferred lung cancer

• Shao-Yuan Chen
• Koichi Tsuneyama
• Shih-Ming Huang

Histopathological analysis of mucinous breast cancer subtypes and comparison with invasive carcinoma of no special type

• Michał Piotr Budzik
• Marta Magdalena Fudalej
• Anna Maria Badowska-Kozakiewicz

Copper-67 radioimmunotheranostics for simultaneous immunotherapy and immuno-SPECT

• Guiyang Hao
• Tara Mastren
• Xiankai Sun

Associations between the gut microbiome and fatigue in cancer patients

• Joud Hajjar
• Tito Mendoza

cGAS–STING cytosolic DNA sensing pathway is suppressed by JAK2-STAT3 in tumor cells

• Manuel Adrian Suter
• Nikki Y. Tan
• Y. L. Zhang

Iodine containing porous organosilica nanoparticles trigger tumor spheroids destruction upon monochromatic X-ray irradiation: DNA breaks and K-edge energy X-ray

• Yuya Higashi
• Kotaro Matsumoto
• Fuyuhiko Tamanoi

COVID-19 engages clinical markers for the management of cancer and cancer-relevant regulators of cell proliferation, death, migration, and immune response

• Serhiy Souchelnytskyi
• Andriy Nera
• Nazariy Souchelnytskyi

High-dose methotrexate-based regimens and post-remission consolidation for treatment of newly diagnosed primary CNS lymphoma: meta-analysis of clinical trials

• Haowen Xiao

Sensitivity, specificity, and accuracy of a liquid biopsy approach utilizing molecular amplification pools

• Jessica Garcia
• Nick Kamps-Hughes
• Cristian Ionescu-Zanetti

A survival analysis of surgically treated incidental low-grade glioma patients

• Lingcheng Zeng

Integrated multi-omics analysis of ovarian cancer using variational autoencoders

• Muta Tah Hira
• M. A. Razzaque
• Mosharraf Sarker

Cell-free DNA concentration and fragment size as a biomarker for prostate cancer

• Emmalyn Chen
• Clinton L. Cario
• John S. Witte

Real-world outcomes of first-line pembrolizumab plus pemetrexed-carboplatin for metastatic nonsquamous NSCLC at US oncology practices

• Vamsidhar Velcheti
• Thomas Burke

Graphene oxide loaded with tumor-targeted peptide and anti-cancer drugs for cancer target therapy

Comprehensive analysis of metastatic gastric cancer tumour cells using single-cell RNA-seq

• Yingyi Zhang
• Xianbao Zhan

Ex vivo culture of intact human patient derived pancreatic tumour tissue

• John Kokkinos
• George Sharbeen
• Phoebe A. Phillips

A phase 2a clinical study on the safety and efficacy of individualized dosed mebendazole in patients with advanced gastrointestinal cancer

• S. Mansoori

Palliative radiation therapy for symptomatic advance breast cancer

• Galia Jacobson
• Orit Kaidar-Person
• Merav Akiva Ben-David

Deep learning identifies morphological features in breast cancer predictive of cancer ERBB2 status and trastuzumab treatment efficacy

• Dmitrii Bychkov
• Nina Linder
• Johan Lundin

A prostate-specific membrane antigen (PSMA)-targeted prodrug with a favorable in vivo toxicity profile

• Srikanth Boinapally
• Hye-Hyun Ahn
• Martin G. Pomper

Comparison of microsatellite instability detection by immunohistochemistry and molecular techniques in colorectal and endometrial cancer

• Franceska Dedeurwaerdere
• Kathleen BM Claes
• Geert Martens

Valerian and valeric acid inhibit growth of breast cancer cells possibly by mediating epigenetic modifications

• Fengqin Shi

Efficacy and safety of new anti-CD20 monoclonal antibodies versus rituximab for induction therapy of CD20 + B-cell non-Hodgkin lymphomas: a systematic review and meta-analysis

• Chengxin Luo

Morphofunctional analysis of human pancreatic cancer cell lines in 2- and 3-dimensional cultures

• Fuuka Minami
• Norihiko Sasaki
• Toshiyuki Ishiwata

Potentiality of multiple modalities for single-cell analyses to evaluate the tumor microenvironment in clinical specimens

• Yukie Kashima
• Yosuke Togashi
• Toshihiko Doi

Polysaccharide hydrogel based 3D printed tumor models for chemotherapeutic drug screening

• Aragaw Gebeyehu
• Sunil Kumar Surapaneni
• Mandip Singh

PTEN loss promotes oncogenic function of STMN1 via PI3K/AKT pathway in lung cancer

• Guangsu Xun

Co-culture model of B-cell acute lymphoblastic leukemia recapitulates a transcription signature of chemotherapy-refractory minimal residual disease

• Stephanie L. Rellick
• Gangqing Hu
• Laura F. Gibson

Effect of SSRI exposure on the proliferation rate and glucose uptake in breast and ovary cancer cell lines

• Britta Stapel
• Catharina Melzer

Impact of tumor-parenchyma biomechanics on liver metastatic progression: a multi-model approach

• Erik Brodin
• Paul Macklin

Pembrolizumab in vaginal and vulvar squamous cell carcinoma: a case series from a phase II basket trial

• Jeffrey A. How
• Amir A. Jazaeri

Relationship of breast volume, obesity and central obesity with different prognostic factors of breast cancer

• Daniel María Lubián López
• Carmen Aisha Butrón Hinojo
• Ernesto González Mesa

Meta-analysis of host transcriptional responses to SARS-CoV-2 infection reveals their manifestation in human tumors

• Fengju Chen
• Yiqun Zhang
• Chad J. Creighton

Selection and characterisation of Affimers specific for CEA recognition

• Shazana Hilda Shamsuddin
• David G. Jayne
• Paul A. Millner

Epidemiology and prognosis in young lung cancer patients aged under 45 years old in northern China

Real-world data of fulvestrant as first-line treatment of postmenopausal women with estrogen receptor-positive metastatic breast cancer

• M. Ruiz-Borrego

Classification of paediatric brain tumours by diffusion weighted imaging and machine learning

• Niloufar Zarinabad
• Andrew Peet

Metagenomic analysis of formalin-fixed paraffin-embedded tumor and normal mucosa reveals differences in the microbiome of colorectal cancer patients

• Gabriela Debesa-Tur
• Vicente Pérez-Brocal
• Andrés Moya

A novel proteomics approach to epigenetic profiling of circulating nucleosomes

• Priscilla Van den Ackerveken
• Alison Lobbens
• Marielle Herzog

A review and comparison of breast tumor cell nuclei segmentation performances using deep convolutional neural networks

• Andrew Lagree
• Majidreza Mohebpour
• William T. Tran

Comparative analysis of machine learning approaches to classify tumor mutation burden in lung adenocarcinoma using histopathology images

• Apaar Sadhwani
• Huang-Wei Chang
• Peter Cimermancic

Alteration of DNA mismatch repair capacity underlying the co-occurrence of non-small-cell lung cancer and nonmedullary thyroid cancer

• Shiro Fujita
• Katsuhiro Masago

Anticancer potential of rhizome extract and a labdane diterpenoid from Curcuma mutabilis plant endemic to Western Ghats of India

• T. Lakshmipriya
• P. R. Manish Kumar

Serum-derived exosomal PD-L1 expression to predict anti-PD-1 response and in patients with non-small cell lung cancer

• Yoshihisa Shimada
• Jun Matsubayashi
• Norihiko Ikeda

Transcript levels of keratin 1/5/6/14/15/16/17 as potential prognostic indicators in melanoma patients

• Guo-Liang Shen

Enhancing the landscape of colorectal cancer using targeted deep sequencing

• Chul Seung Lee
• In Hye Song
• Sung Hak Lee

PGMD/curcumin nanoparticles for the treatment of breast cancer

• Mankamna Kumari
• Nikita Sharma
• Surendra Nimesh

GATA3 somatic mutations are associated with clinicopathological features and expression profile in TCGA breast cancer patients

• Fahimeh Afzaljavan
• Ayeh Sadat Sadr
• Alireza Pasdar

Explainable drug sensitivity prediction through cancer pathway enrichment

• Yi-Ching Tang
• Assaf Gottlieb

A novel biosensor for the ultrasensitive detection of the lncRNA biomarker MALAT1 in non-small cell lung cancer

• Dongming Wu

Neuroendocrine prostate cancer has distinctive, non-prostatic HOX code that is represented by the loss of HOXB13 expression

• Siyuan Cheng

New combination chemotherapy of cisplatin with an electron-donating compound for treatment of multiple cancers

• Qinrong Zhang
• Qing-Bin Lu

Lung adenocarcinoma and lung squamous cell carcinoma cancer classification, biomarker identification, and gene expression analysis using overlapping feature selection methods

• Joe W. Chen
• Joseph Dhahbi

Similarities between pandemics and cancer in growth and risk models

• Lode K. J. Vandamme
• Ignace H. J. T. de Hingh
• Paulo R. F. Rocha

Flavonoids increase melanin production and reduce proliferation, migration and invasion of melanoma cells by blocking endolysosomal/melanosomal TPC2

• Ponsawan Netcharoensirisuk
• Carla Abrahamian
• Christian Grimm

Convolutional autoencoder based model HistoCAE for segmentation of viable tumor regions in liver whole-slide images

• Mousumi Roy
• Vandana Mukherjee

Low temperature plasma irradiation products of sodium lactate solution that induce cell death on U251SP glioblastoma cells were identified

• Hiromasa Tanaka
• Masaru Hori

CAD systems for colorectal cancer from WSI are still not ready for clinical acceptance

• Sara P. Oliveira
• Pedro C. Neto
• Jaime S. Cardoso

Applicability of pan-TRK immunohistochemistry for identification of NTRK fusions in lung carcinoma

• Simon Strohmeier

Sulforaphane induces S-phase arrest and apoptosis via p53-dependent manner in gastric cancer cells

• Huazhang Wu

Repositioning metformin and propranolol for colorectal and triple negative breast cancers treatment

• L. E. Anselmino
• M. V. Baglioni
• M. Menacho Márquez

Evaluation of wavelength ranges and tissue depth probed by diffuse reflectance spectroscopy for colorectal cancer detection

• Marcelo Saito Nogueira
• Siddra Maryam
• Stefan Andersson-Engels

C. elegans -based chemosensation strategy for the early detection of cancer metabolites in urine samples

• Enrico Lanza
• Martina Di Rocco
• Viola Folli

Detection of colorectal cancer in urine using DNA methylation analysis

• R. D. M. Steenbergen

Learning deep features for dead and living breast cancer cell classification without staining

• Gisela Pattarone
• Laura Acion
• Emmanuel Iarussi

Epidemiological overview of multidimensional chromosomal and genome toxicity of cannabis exposure in congenital anomalies and cancer development

• Albert Stuart Reece
• Gary Kenneth Hulse

Adipose-derived mesenchymal stem cells differentiate into heterogeneous cancer-associated fibroblasts in a stroma-rich xenograft model

• Yoshihiro Miyazaki
• Tatsuya Oda
• Yasuyuki S. Kida

Loss of Parkinson’s susceptibility gene LRRK2 promotes carcinogen-induced lung tumorigenesis

• Chandra Lebovitz
• Nicole Wretham
• Sharon M. Gorski

Enhanced anti-cancer activity of andrographis with oligomeric proanthocyanidins through activation of metabolic and ferroptosis pathways in colorectal cancer

• Tadanobu Shimura
• Priyanka Sharma

Differential expression of PD-L1 between primary and metastatic epithelial ovarian cancer and its clinico-pathological correlation

• Sandeep Kumar Parvathareddy
• Abdul K. Siraj
• Khawla S. Al-Kuraya

Fibroblast activation protein targeted near infrared photoimmunotherapy (NIR PIT) overcomes therapeutic resistance in human esophageal cancer

• Ryoichi Katsube
• Kazuhiro Noma
• Toshiyoshi Fujiwara

Prognostic gene expression signatures of breast cancer are lacking a sensible biological meaning

• Kalifa Manjang
• Shailesh Tripathi
• Frank Emmert-Streib

Activity of docetaxel, carboplatin, and doxorubicin in patient-derived triple-negative breast cancer xenografts

• Miguel Martin
• Rocio Ramos-Medina
• Sara Lopez-Tarruella

Evidence for improved prognosis of colorectal cancer diagnosed following the detection of iron deficiency anaemia

• Orouba Almilaji
• Sally D. Parry
• Jonathon Snook

CDC2-like (CLK) protein kinase inhibition as a novel targeted therapeutic strategy in prostate cancer

• Sean R. Porazinski
• Michael R. Ladomery

Prognostic value of prostate volume in non-muscle invasive bladder cancer

• Won Sik Ham
• Jee Soo Park
• Jongchan Kim

Histamine H1 receptor antagonists selectively kill cisplatin-resistant human cancer cells

• Nobuki Matsumoto
• Miku Ebihara
• Toru Imamura

A prognostic model for colorectal cancer based on CEA and a 48-multiplex serum biomarker panel

• Kajsa Björkman
• Sirpa Jalkanen
• Caj Haglund

Breath biopsy of breast cancer using sensor array signals and machine learning analysis

• Hsiao-Yu Yang
• Yi-Chia Wang
• Chi-Hsiang Huang

Targeting the DNA replication stress phenotype of KRAS mutant cancer cells

• Tara Al Zubaidi
• O. H. Fiete Gehrisch
• Henning Willers

CD73 facilitates EMT progression and promotes lung metastases in triple-negative breast cancer

• Nataliia Petruk
• Sanni Tuominen
• Katri S. Selander

Targeting galectin-3 with a high-affinity antibody for inhibition of high-grade serous ovarian cancer and other MUC16/CA-125-expressing malignancies

• Marina Stasenko
• David R. Spriggs

The clinical significance of microvascular invasion in the surgical planning and postoperative sequential treatment in hepatocellular carcinoma

• Wentao Wang

Elevated levels of mitochondrial CoQ 10 induce ROS-mediated apoptosis in pancreatic cancer

• Tulin Dadali
• Anne R. Diers
• Rangaprasad Sarangarajan

Evaluation of dose-volume histogram prediction for organ-at risk and planning target volume based on machine learning

• Sheng xiu Jiao
• Ming li Wang
• Xiao-wei Liu

Parvimonas micra , Peptostreptococcus stomatis, Fusobacterium nucleatum and Akkermansia muciniphila as a four-bacteria biomarker panel of colorectal cancer

• Muhammad Afiq Osman
• Hui-min Neoh
• Rahman Jamal

Abiraterone acetate versus bicalutamide in combination with gonadotropin releasing hormone antagonist therapy for high risk metastatic hormone sensitive prostate cancer

• Takashi Ueda
• Takumi Shiraishi
• Osamu Ukimura

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September 3, 2024

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Preventing cell damage: Working principle of proton-activated chloride channels revealed

by DGIST (Daegu Gyeongbuk Institute of Science and Technology)

A research team led by Prof. Seo Byeong-Chang of the Department of Brain Sciences at DGIST has made the world's first discovery of how proton-activated chloride (PAC) channels—which play an important role in protecting cells in our bodies—work. PAC channels are important mediators of cell damage caused by tissue acidification, and by unraveling the mystery of how they are activated, the research team has opened up a new road for treating cancer and brain diseases.

The study is published in the journal Nature Communications .

Our bodies become acidic when we exercise for long periods of time or when we are sick. This can damage cells. In particular, when the balance of intracellular chloride ions (Cl - ) is disturbed, edema, or swelling of cells, occurs, which can damage cells and tissues. To prevent cell damage, Prof. Seo's research team has studied how PAC channels work and is now one step closer to developing new treatments.

PAC channels are activated in response to an acidic extracellular environment, that is, a high concentration of protons (H + ). Until now, however, researchers did not have a good understanding of how the activation of PAC channels is regulated in cells. An in-depth study was needed to solve this problem.

Prof. Seo's research team discovered that the activation of PAC channels requires a substance called PI (4, 5) P 2 on the inside of the cell membrane. Without this substance, PAC channels barely function, and the movement of chloride ions is reduced, thereby preventing cell damage. By unraveling this process, the research team has revealed the principle governing the working of PAC channels.

This study is significant because it has unlocked the secret of how exactly PAC channels work. This discovery is expected to help develop new treatments to inhibit cell damage in diseases such as cancer and brain diseases.

"We have identified the regulatory mechanism of PAC channels, which has received relatively little attention," said Prof. Seo. "It is expected that the working principle of PAC channels that we have discovered through this study will be very helpful in preventing cell damage in diseases such as cancer and stroke."

The first author of this study is Dr. Go Woori from the Department of Brain Sciences, DGIST, and the co-authors are Lee Eun-ah, a Ph.D. student, and Dr. Lim Hyun-ho from the Korea Brain Research Institute.

Journal information: Nature Communications

Provided by DGIST (Daegu Gyeongbuk Institute of Science and Technology)

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Can Chemo Help KRAS Inhibitors Work Better Against Pancreatic Cancer?

August 20, 2024 , by Sharon Reynolds

Results from two studies suggest that giving chemotherapy along with KRAS inhibitors may make these targeted therapies much more effective in people with pancreatic cancer.

A newer class of drugs that target pancreatic cancer may get a helping hand from an old treatment workhorse: chemotherapy. Two new studies in mice show that adding chemotherapy to an experimental KRAS inhibitor called MRTX1133 greatly reduced tumor growth and spread compared with either treatment alone.

This potent effect, both studies found, appears to come about because chemotherapy and KRAS inhibitors each shut down a different set of cellular instructions that can drive cancer cell growth in pancreatic tumors.  

Results from both studies were published June 28 in Cancer Discovery .

More than 90% of pancreatic tumors carry a cancer-fueling change in the KRAS gene . Early clinical trials testing drugs targeting a specific change in KRAS , like adagrasib (Krazati) and sotorasib (Lumakras) , alone in pancreatic cancer showed promising results. However, these drugs given alone do not work in all patients. And even though tumors shrink in some people, invariably they start growing again, within months after starting treatment.

“We’ve seen several different genetic alterations emerge that cause tumors to become resistant” to KRAS inhibitors, said Andrew Aguirre, M.D., Ph.D., of Dana-Farber Cancer Institute, who led one of the studies. “So, the question comes up: Could you give something in combination that would prevent resistance from emerging?” 

Surprisingly, Dr. Aguirre continued, both studies strongly suggest that chemotherapy may be one way to do that.

The chemotherapy regimens used to treat pancreatic cancer significantly shrink tumors in less than a third of patients and can cause serious side effects, so researchers have hoped to replace them with newer, less toxic therapies, explained Christine Alewine, M.D., Ph.D., of NCI’s Center for Cancer Research , who was not involved with the new studies.

Although that may eventually happen, Dr. Alewine said, “for now, it looks like adding on to standard chemotherapy, rather than eliminating it, may turn into our best weapon against pancreatic cancer.” 

It's not yet known how much chemotherapy is needed to prevent pancreatic tumors from escaping the effects of KRAS inhibition, Dr. Alewine added. “If we can give lower doses of chemotherapy [with a KRAS inhibitor] than we do now [on its own], we may be able to both improve effectiveness and reduce toxicity,” she said.

Same pancreatic cancer cells, different programs

Within a tumor, cells that look alike can actually function very differently, Dr. Alewine explained. This difference is driven not by differences in their genes , but by how those genes are expressed—that is, what proteins they make and how those proteins behave. 

“All of our cells have the same [genetic] instruction program, but only some of those instructions are used in different cell types,” she said. 

Drug Targets Common Mutation in Pancreatic Cancer

In mice, experimental drug MRTX1133 shrank pancreatic tumors with KRAS G12D mutations.

These instructions cause cells to act differently in response to other cells, infectious agents, or molecules in their surrounding environment—and in response to cancer treatments.

Based on these behavioral patterns, researchers have grouped pancreatic tumor cells into different “states,” including classical, basal, and mesenchymal. Studies have shown that the latter two seem to be very sensitive to KRAS inhibitors, at least initially.

Both research teams set out with the same goal: To better understand what happens to pancreatic cancer cells being treated with KRAS inhibitors, including whether there are changes in their cell state. 

How tumors use cell states to escape treatment

For their study, Dr. Aguirre and his team conducted in-depth analyses of circulating tumor DNA in blood samples taken from people with pancreatic cancer before and after treatment with a KRAS-targeted drug. They also tested KRAS inhibitors in different laboratory models of pancreatic cancer.

The team found a wide range of genetic mutations and other changes that potentially contribute to the rapid resistance to these drugs. But they also observed a more global phenomenon . Before treatment, tumors contained a mix of cell states. After KRAS inhibition, classical-state cells came to dominate the tumor.

The other research team, led by Tuomas Tammela, M.D., Ph.D., of Memorial Sloan Kettering Cancer Center, observed a similar phenomenon.

For example, in mice engineered to develop pancreatic tumors in much the same way that pancreatic cancer develops in humans, treatment with a KRAS inhibitor led to a sharp decrease in the number of basal-like cells and their subsequent replacement with classical cells. These classical cells appeared to rely much less on KRAS to survive . That finding, they concluded, identifies these type of pancreatic cells as key culprits in tumor resistance to KRAS-targeted therapies.

“Both of these studies seem to be saying that, while there are some genetic changes that can occur in cells that make up pancreatic tumors, this underlying ability to change their cell state appears to be a main thing driving resistance,” Dr. Alewine said.

Targeting cellular plasticity

But could this escape route by pancreatic cancer cells also be a vulnerability? Classical-state pancreatic cancer cells are known to be more sensitive to treatment with chemotherapy than other cell states.

To investigate, both teams tested the combination of the KRAS inhibitor MRTX1133 plus a standard chemotherapy regimen used to treat pancreatic cancer, gemcitabine and nab-paclitaxel, in mice implanted with pancreatic tumors. 

A Potential New Immunotherapy Approach for KRAS-Mutant Cancers

KRAS-targeted drugs may also alert the immune system to attack these cancers.

In experiments done by Dr. Aguirre and his team, mice given the combination lived substantially longer without their tumors growing than mice given either chemotherapy or the KRAS inhibitor alone.

In another mouse model of metastatic pancreatic cancer, treatment with chemotherapy or the KRAS inhibitor alone reduced the number of lung metastases but didn’t prevent metastasis entirely. The combination of both therapies did prevent spread to the lungs.

Dr. Tammela’s team saw similar results in their animal experiments. In mice with pancreatic tumors, the combination of chemotherapy and KRAS inhibition led to an average reduction in tumor size of about 60% compared with the reduction seen with a KRAS inhibitor alone.

More work is needed to better understand how to use these two therapies together, Dr. Aguirre said. “What combination or sequence of treatments should we use to get the most benefit? Should we give them both upfront together? Or would you get more benefit from giving one [first], then the other? The jury’s still out on all of that,” he said.

His team and others are now planning clinical trials to test some such combinations.

“We know how to give chemotherapy—it’s a tried and true standard of care ,” he added. “So there’s a lot of optimism that we’ll be able to combine these effectively.”

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Deadly liver cancer rewires cell metabolism to grow, study finds

by Krishna Ramanujan, Cornell University

A deadly liver cancer that mainly affects children and young adults rewires its cellular metabolism in order to thrive, according to a new study that opens the door to exploring new targets for therapies.

Fibrolamellar carcinoma, which does not respond to conventional treatments, accounts for only 1–2% of all liver cancers, but is without standard of care and has often metastasized by the time it is detected, leaving patients with approximately a year to live on average.

While many cancers prefer glucose to promote their survival, some show dependence on other nutrients. Fibrolamellar carcinoma depends on glutamine for energy production , and also seems to place a strong emphasis on serine utilization for this purpose as well, according to the study.

"There appears to be with this cancer an impairment in metabolizing sugar and it actually seems to be very keen on amino acids , which is something that deviates from the norm in terms of what the general public typically think about cancer," said Donald Long Jr., the study's lead author, Howard Hughes Medical Institute Gilliam Fellow, and a doctoral candidate in the lab of senior author Praveen Sethupathy '03, professor of physiological genomics and chair of the Department of Biomedical Sciences in the College of Veterinary Medicine.

The paper, "Proteo-metabolomics and Patient Tumor Slice Experiments Point to Amino Acid Centrality for Rewired Mitochondria in Fibrolamellar Carcinoma," published Aug. 28 in the journal Cell Reports Medicine .

"Our findings point to specific features of the cancer that represent therapeutic vulnerabilities, and could be very useful for testing specific drug combinations," Sethupathy said.

In the study, the researchers used proteomics (to determine the spectrum of proteins in the cancer cells ) and metabolomics (the spectrum of metabolites) and identified more than 8,000 proteins and 135 metabolites. They obtained frozen patient tissue samples from the Fibrolamellar Cancer Foundation Biobank and developed a predictive model based on the omics data that was generated in collaboration with co-author Lukas Orre, an associate professor at the Karolinska Institute in Sweden.

Several key aspects of the model were experimentally validated via functional studies using fresh tumor tissue slices directly from patients, in collaboration with co-author Taranjit Gujral, an associate professor at the Fred Hutchinson Cancer Center.

Under normal circumstances, the glycolytic pathway breaks down glucose to form a metabolite called pyruvate, which then enters the mitochondria (the cell's powerhouse) and is used to produce ATP, a small molecule that stores chemical energy used to power the cell's biochemical reactions.

"We saw from our analysis of the proteomic and metabolomic data, and additional experiments in a cell model of fibrolamellar carcinoma, that this pathway was impaired," Long said.

The researchers then identified a liver-specific protein, called serine dehydratase, as the 10th-most upregulated protein in the proteomics dataset. This enzyme can convert the amino acid serine into pyruvate. The pyruvate then follows the usual path into the mitochondria to produce ATP.

In tests using the fresh patient cancer tissue slices, the researchers inhibited serine dehydratase and found the cancer tissues became much less viable. A drug that blocks pyruvate entry into the mitochondria also dramatically affected the survival of the fibrolamellar cancer tissues.

The researchers also predict another use of pyruvate, where the metabolite is also employed in the production of proline. Proline is a non-essential amino acid that is integral to making collagen, the primary building block of connective tissue.

One of the hallmarks of fibrolamellar carcinoma is that its tumors have fibrous bands of collagen running through them.

"It looks like, potentially, the mitochondria is being rewired to produce copious amounts of proline, presumably to integrate into this collagen matrix that promotes the tumor's growth," Long said.

Co-authors also included Rosanna Ma and Adam Francisco in the Sethupathy lab; Nathaniel Vacanti, assistant professor, Joeva Barrow, assistant professor, and Pei-Yin Tsai, a doctoral student, all in the Division of Nutritional Sciences in the College of Human Ecology; and researchers from UCLA, the Johns Hopkins University School of Medicine and Rutgers University.

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Lab-grown stem cells could be a 'breakthrough' for cancer treatment

Stem cells made in the lab may one day aid cancer treatment by reducing our reliance on donors

By James Woodford

2 September 2024

Stem cells are produced by bone marrow and can turn into different types of blood cells

KATERYNA KON / SPL/ Alamy

Human blood stem cells have been made in a laboratory for the first time, which could significantly improve how we treat certain types of cancer .

The lab-grown cells have so far only been tested in mice, but when infused into the animals, the cells became functional bone marrow at similar levels to those seen after umbilical cord blood cell transplants.

A new understanding of how your blood type influences your health

Treating cancers such as leukaemia and lymphoma via radiation and chemotherapy can destroy the blood-forming cells in bone marrow. A stem cell transplant means that new, healthy bone marrow and blood cells can grow. Umbilical cords are a particularly rich source of stem cells, but donations are limited and the transplant can be rejected by the body.

The new method would allow researchers to produce stem cells from the actual patient, eliminating the supply issue and reducing the risk that their body would reject them.

First, human blood or skin cells were turned into so-called pluripotent stem cells through a process called reprogramming. “This involves temporarily turning on four genes, with the result that the patient cells revert to an early stage of development when they can become any cell in the body,” says Andrew Elefanty at the Murdoch Children’s Research Institute in Melbourne.

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The second stage involved turning the pluripotent cells into blood stem cells. “We first make thousands of small floating balls of cells, a few hundred cells in each ball, and direct them to change from being stem cells to sequentially become blood vessels and then blood cells,” says Elefanty. This process, called differentiation, takes about two weeks and makes millions of blood cells, he says.

These cells were then infused into mice that lacked an immune system and became functional bone marrow in up to 50 per cent of cases. This means it made the same cells that carry oxygen and fight infections as healthy human bone marrow does, says Elefanty. “It is this unique ability to make all the blood cell types for a prolonged period of time that defines the cells as blood stem cells,” he says.

We are finally improving prostate cancer diagnoses – here's how

Cases of prostate cancer are surging alarmingly around the world. Thankfully, we are developing more accurate tests that can catch the condition early

Abbas Shafiee at the University of Queensland in Brisbane says the work is a “magnificent breakthrough” towards new therapies for blood cancers. “It has not been done before and it has a lot of potential for the future.” But even once animal testing is complete, a lot of research in humans needs to be done before the approach can be used in clinics, he says.

Simon Conn at Flinders University in Adelaide, Australia, says a key advantage of the team’s approach is that it could be scaled up to produce “an essentially never-ending supply” of blood stem cells. But he adds that the rate of success and the diversity of the blood cells varied. “This suggests the treatment, even at the preclinical stage in mice, is not consistent, which will need to be addressed prior to any clinical trials in human patients,” he says.

Journal reference:

Nature Biotechnology DOI: 10.1038/s41587-024-02360-7

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The Latest Research on Why So Many Young Adults Are Getting Cancer

By Bill Piersol Tuesday, September 3, 2024

Charisma McDuffie, diagnosed with breast cancer at age 28, was treated by MSK's Dr. Shari Goldfarb in a program specifically tailored for young women with breast cancer.

It’s a disturbing mystery that has drawn the attention of investigators from across Memorial Sloan Kettering Cancer Center (MSK).

Why are a growing number of young people under 50 being diagnosed with over a dozen forms of cancer around the world?

Types of Cancers Becoming More Common in Young People

Men and women in the prime of their lives are increasingly being diagnosed with serious cancers, including  colorectal ,  breast ,  prostate ,  uterine ,  stomach (gastric) ,  pancreatic , and more. One  forecast predicts cancer for this age group will increase by 30% globally from 2019 to 2030.

“This is serious and worrisome,” says  Shari Goldfarb, MD, breast oncologist and Director of MSK’s  Young Women With Breast Cancer program.   

MSK breast oncologist Dr. Shari Goldfarb

“This is not a blip,” explains  Andrea Cercek, MD, gastrointestinal oncologist and Co-Director of  The Center for Young Onset Colorectal and Gastrointestinal Cancer . “The more data we gather, the clearer this becomes.”

MSK is a pioneer in caring for the specific needs of people facing what are often called early-onset cancers, who confront very different challenges than older adults. The coming surge in cases is a key reason MSK is building a new state-of-the-art hospital, called the MSK Pavilion.

Just as importantly, MSK experts are leading the investigation into why this is happening.

Is Obesity Causing More Young People to Get Cancer?

An obvious focus for rising cancer rates is the vicious circle of  obesity, highly processed foods, and sed­entary lifestyles , which are an epidemic in America and growing in many countries.

“We know obesity causes inflamma­tion, which can lead to cancer,” explains Dr. Goldfarb. “We believe that plays a role and needs to be addressed. But it doesn’t fully explain the growing rates of young women with breast cancer.”

MSK gastroenterologist Dr. Robin Mendelsohn

Nor does it explain the increase in cases seen by MSK’s Center for Young Onset Colorectal and Gastrointestinal Cancer, which is co-directed by  gastroenterologist Robin Mendelsohn, MD . The center has tracked more than 4,000 younger adults. “They are actually less likely to be obese than the general popu­lation,” says Dr. Mendelsohn. “They are also less likely to use tobacco or have other known risk factors.”

Promising Leads for the Mystery of Increasing Rates of Cancer in Young Adults

MSK experts agree there is not a single smoking gun. “If there was, researchers would have found it,” says Dr. Mendelsohn. “Instead, there are likely several causes.”

Dr. Cercek explains, “The working hypothesis is that there is an environmen­tal exposure — or multiple exposures — that people born starting in the 1950s came in contact with.” It’s possible, she says, that the “exposures began in the 1960s or ’70s and have been continuously present since then.”

While MSK researchers don’t yet know what that exposure might be, they have discovered promising leads.

How Microbiome Diversity Effects Cancer Rates

In May, Dr. Mendelsohn presented prelim­inary data at a medical conference about the microbiome of people with early-onset colorectal cancer. The microbiome, also known as the invisible organ, is the enormous community of bacteria and other microbes that live in our gut, which help regulate our digestive system.

“We found that younger people with colorectal cancer had less diversity in their microbiome than older patients,” says Dr. Mendelsohn. “And the makeup of the two groups’ microbiome is different too.” That’s important because more diversity generally means better health.

By scouring the vast amount of life­style data younger patients at MSK have provided, she says, MSK is “investigating factors we know affect the microbiome, including dietary changes, medications such as antibiotics, and even factors from childhood, such as breastfeeding and C-section patterns, age of parents at birth, and more.”

The goal, says Dr. Mendelsohn, is to “look for a possible trigger that would explain why the microbiomes of these patients are different.” 

MSK gastroenterologist Dr. Monika Laszkowska

Stomach cancer research by  gastro­enterologist Monika Laszkowska, MD, MS , focuses on another angle: how to identify younger people at high risk so they can be screened.

“We know that certain groups, such as people of East Asian ancestry, are at higher risk of stomach cancer, which is often trig­gered by a microbe called Helicobacter pylori ,” she explains. “Our research involv­ing patients at MSK also found other groups, such as younger Hispanic women, are more likely to develop early-onset stomach cancer.” That insight could lead to more awareness among Hispanic and Latina women and their doctors.

Dr. Laszkowska’s research also raises new questions. “Stomach cancer is slow-moving. So why is it developing more quickly in younger people?” she asks. “Could the malignancy be growing through a different pathway? Or could it be spurred by another condition, such as an autoimmune disease?”

Is Early-Onset Cancer Biologically Different?

These questions led to another: Is early-onset cancer biologically different and more aggressive than cancer in older people?

MSK gastrointestinal oncologist Dr. Andrea Cercek

A  study led by Dr. Cercek discovered an intriguing dynamic involving colorectal cancer. Her research found that colorectal patients treated at MSK responded the same way to chemotherapy “whether they were 17 or 70,” she says. “Those in the younger group were more likely to have rectal cancer. But the biology of the disease looked the same as in older patients.

More Dangerous Breast Cancer Subtypes Appearing in Younger Women

However, cancer is not a single disease. Instead, it is over 400 different diseases.

Dr. Goldfarb points out, “Breast cancer subtypes called  triple-negative and  HER2-positive are more common among young women — and have a worse prognosis.”

She explains that “some of the risk factors for breast cancer are increasingly found in younger women.” She adds, “For example, they are exposed to more years of unopposed reproductive hormones because they are experiencing menstru­ation earlier and having children later.”

However, she stresses that this — along with the rise of obesity — does not fully explain why more women under 50 are developing particularly aggressive forms of breast cancer.

MSK’s investigation into why includes every tool at researchers’ disposal, from surveys that reveal all aspects of lifestyle and personal history to next-generation genomic testing to determine what’s happening on the genetic level.

Dr. Goldfarb points to research by  breast oncologist Pedram Razavi, MD, PhD , to uncover minimal residual disease in patients. She also uses blood tests that look for mutations in tumors to help guide treatment decisions by predicting which treatments will be most effective.

Comprehensive Cancer Care for the Needs of Younger People

As the investigations continue, MSK specialists support the unique needs of younger adults. “Our program helps with the specific concerns of this stage of life, including  fertility preservation , talking with children , parents and colleagues about a cancer diagnosis, discussing impact on work , dating ,  sexual health and much more” says Dr. Goldfarb.

“When a person is diagnosed with cancer, it turns their world upside down. We’re there to help not just with their physical health, but their entire social and emotional well-being.”

Change lives with us.

Mobile phones are not linked to brain cancer, according to a major review of 28 years of research

Director Radiation Research and Advice (ARPANSA), and Adjunct Associate Professor (UOW), University of Wollongong

Assistant Director, Health Impact Assessment, ARPANSA and Adjunct Associate Professor (Practice), School of Public Health and Preventive Medicine, Monash University

Disclosure statement

Sarah Loughran receives funding from The National Health and Medical Research Council of Australia (NHMRC). She is the Director of Radiation Research and Advice at the Australian Radiation Protection and Nuclear Safety Agency (ARPANSA), a member of the Scientific Expert Group at the International Commission on Non-Ionizing Radiation Protection (ICNIRP), and a member of the World Health Organisation Task Group on Radiofrequency Fields and Health Risks.

Ken Karipidis is the Assistant Director of Health Impact Assessment at the Australian Radiation Protection and Nuclear Safety Agency and he is also the Vice Chair of the International Commission of Non-Ionizing Radiation Protection.

Monash University provides funding as a founding partner of The Conversation AU.

University of Wollongong provides funding as a member of The Conversation AU.

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A systematic review into the potential health effects from radio wave exposure has shown mobile phones are not linked to brain cancer. The review was commissioned by the World Health Organization and is published today in the journal Environment International .

Mobile phones are often held against the head during use. And they emit radio waves, a type of non-ionising radiation . These two factors are largely why the idea mobile phones might cause brain cancer emerged in the first place.

The possibility that mobile phones might cause cancer has been a long-standing concern. Mobile phones – and wireless tech more broadly – are a major part of our daily lives. So it’s been vital for science to address the safety of radio wave exposure from these devices.

Over the years, the scientific consensus has remained strong – there’s no association between mobile phone radio waves and brain cancer, or health more generally.

Radiation as a possible carcinogen

Despite the consensus, occasional research studies have been published that suggested the possibility of harm.

In 2011, the International Agency for Research on Cancer (IARC) classified radio wave exposure as a possible carcinogen to humans . The meaning of this classification was largely misunderstood and led to some increase in concern.

IARC is part of the World Health Organization. Its classification of radio waves as a possible carcinogen was largely based on limited evidence from human observational studies. Also known as epidemiological studies, they observe the rate of disease and how it may be caused in human populations.

Observational studies are the best tool researchers have to investigate long-term health effects in humans, but the results can often be biased.

The IARC classification relied on previous observational studies where people with brain cancer reported they used a mobile phone more than they actually did. One example of this is known as the INTERPHONE study .

This new systematic review of human observational studies is based on a much larger data set compared to what the IARC examined in 2011.

It includes more recent and more comprehensive studies. This means we can now be more confident that exposure to radio waves from mobile phones or wireless technologies is not associated with an increased risk of brain cancer.

No association

The new review forms part of a series of systematic reviews commissioned by the World Health Organization to look more closely at possible health effects associated with exposure to radio waves.

This systematic review provides the strongest evidence to date that radio waves from wireless technologies are not a hazard to human health.

It is the most comprehensive review on this topic – it considered more than 5,000 studies, of which 63, published between 1994 and 2022, were included in the final analysis. The main reason studies were excluded was that they were not actually relevant; this is very normal with search results from systematic reviews.

No association between mobile phone use and brain cancer, or any other head or neck cancer, was found.

There was also no association with cancer if a person used a mobile phone for ten or more years (prolonged use). How often they used it – either based on the number of calls or the time spent on the phone – also didn’t make a difference.

Importantly, these findings align with previous research . It shows that, although the use of wireless technologies has massively increased in the past few decades, there has been no rise in the incidence of brain cancers.

A good thing

Overall, the results are very reassuring. They mean that our national and international safety limits are protective. Mobile phones emit low-level radio waves below these safety limits, and there is no evidence exposure to these has an impact on human health.

Despite this, it is important that research continues. Technology is developing at a rapid pace. With this development comes the use of radio waves in different ways using different frequencies. It is therefore essential that science continues to ensure radio wave exposure from these technologies remains safe.

The challenge we now face is making sure this new research counteracts the persistent misconceptions and misinformation out there regarding mobile phones and brain cancer.

There remains no evidence of any established health effects from exposures related to mobile phones, and that is a good thing.

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Mobile phone use doesn't increase brain cancer risk, says research review

The authors also found no increased risk of leukaemia or brain cancers in children from radio or TV transmitters or mobile phone base stations.

Tuesday 3 September 2024 16:29, UK

A review of 63 studies has found no link between mobile phone use and an increased risk of brain cancer.

Commissioned by the World Health Organization (WHO), it found no rise in cases despite a huge increase in wireless technology over the last 20 years.

The review was headed by experts from the Australian Radiation Protection and Nuclear Safety Agency, and included investigators from 10 countries.

It looked at research on radio frequencies in the wavelengths of 300 Hz to 300 GHz - used for mobile phones, wi-fi, radar, baby monitors and other applications.

Co-author of the review Professor Mark Elwood, an honorary professor of cancer epidemiology at University of Auckland, said the team looked at cancers of the brain, pituitary gland, salivary glands, and leukaemias.

"None of the major questions studied showed increased risks," he said.

"For the main issue, mobile phones and brain cancers, we found no increased risk, even with 10+ years exposure and the maximum categories of call time or number of calls."

During the pandemic, 5G mobile phone masts were attacked in the UK and elsewhere in the baseless belief they were contributing to the virus.

The research review looked at 63 relevant articles, published between 1994 and 2022, from 22 countries.

"For mobile phones and brain cancers, there were studies with 10 or more years' use, and quite extensive use," said Professor Elwood.

"Most phone use in these studies was from past years and 1G -2G networks; the newer 3G-4G networks have substantially lower RF emissions.

"There were several studies that reported some increased risks, but these were outweighed in considering all the available evidence."

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When it comes to 5G mobile networks, Professor Elwood said there were no major studies so far, but that studies of radar - which has similar high frequencies - did not show an increased brain cancer risk.

The review is published in the Environment International journal and took four years to complete.

The risk in relation to other cancer types is due to be reported separately.

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Professor Alberto Najera, a physicist and expert on radio frequencies and health at the University of Castilla-La Mancha in Spain, praised the "exhaustive systematic review".

He said the conclusions were "robust" and "supported by quality studies".

"The main implications of this study are that, according to the best available evidence to date, exposure to radiofrequency electromagnetic fields, such as those produced by mobile phones or telephone antennas, does not appear to significantly increase the risk of developing cancer," said Professor Najera.

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Chemical Science

Comparative study of the antiproliferative activity of heterometallic carbene gold( i )–platinum( ii ) and gold( i )–palladium( ii ) complexes in cancer cell lines †.

* Corresponding authors

a Organisch-Chemisches Institut, Heidelberg University, Im Neuenheimer Feld 270, 69120 Heidelberg, Germany E-mail: [email protected]

b Pathology Unit, Centro di Riferimento Oncologico di Aviano (C.R.O.) IRCCS via Franco Gallini 2, Aviano, Italy

c Dipartimento di Scienze Molecolari e Nanosistemi, Università Ca’ Foscari, Campus Scientifico Via Torino 155, 30174 Venezia-Mestre, Italy

d Chemistry Department, Faculty of Science, King Abdulaziz University, Jeddah 21589, Saudi Arabia

e Dipartimento di Scienze Molecolari e Nanosistemi, Università Ca’ Foscari, Campus Scientifico Via Torino 155, 30174 Venezia-Mestre, Italy

f Instituto Federal de Educação, Ciência e Tecnologia Sul-rio-grandense (IFSul), Av. Leonel de Moura Brizola, 2501, Bagé, RS, Brazil

g Dipartimento di Scienze Chimiche, Università degli Studi di Padova, via Marzolo 1, 35131 Padova, Italy E-mail: [email protected]

The stepwise, one-pot synthesis of heterobimetallic carbene gold( I ) platinum( II ) complexes from readily available starting materials is presented. The protecting group free methodology is based on the graduated nucleophilicities of aliphatic and aromatic amines as linkers between both metal centers. This enables the selective, sequential installation of the metal fragments. In addition, the obtained complexes were tested as potential anticancer agents and directly compared to their gold( I ) palladium( II ) counterparts.

Supplementary files

• Supplementary information PDF (11742K)
• Crystal structure data CIF (1744K)

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Comparative study of the antiproliferative activity of heterometallic carbene gold( I )–platinum( II ) and gold( I )–palladium( II ) complexes in cancer cell lines

M. C. Dietl, M. Maag, S. Ber, F. Rominger, M. Rudolph, I. Caligiuri, P. K. Andele, I. A. I. Mkhalid, F. Rizzolio, P. A. Nogara, L. Orian, T. Scattolin and A. S. K. Hashmi, Chem. Sci. , 2024, Advance Article , DOI: 10.1039/D4SC04585H

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