Oncotarget

Cancer cells often survive by disrupting the molecular pathways that normally eliminate damaged or abnormal cells. One of these pathways is apoptosis, a tightly controlled form of programmed cell death. New research suggests that an apoptosis-related receptor called TRAIL-R2 is frequently reduced in breast tumors and that epigenetic changes affecting its gene could contribute to this loss of expression.

A research paper published in Volume 17 of Oncotarget, titled “TRAIL-R2 in the shadows: Epigenetic silencing and clinical implications in breast cancer,” investigated promoter methylation of TRAIL-R2 and its relationship with gene and protein expression in breast cancer.

Why TRAIL-R2 Matters in Cancer

Apoptosis helps the body remove cells that are damaged, abnormal, or no longer needed. Because this process can prevent potentially dangerous cells from surviving, disruption of apoptotic signaling is an important feature of cancer biology.

One pathway involved in apoptosis is controlled by tumor necrosis factor-related apoptosis-inducing ligand, commonly known as TRAIL. TRAIL can interact with several receptors on the cell surface. Two of these, TRAIL-R1 and TRAIL-R2, contain intracellular death domains capable of transmitting signals that lead to apoptosis. TRAIL-R2 is also known as death receptor 5, or DR5.

TRAIL-R2 is particularly complex because its effects are not always exclusively tumor suppressive. Activation of the receptor can promote apoptosis through the extrinsic cell-death pathway, but previous studies discussed by the authors have also linked TRAIL-R2 to non-apoptotic signaling pathways, including NF-κB, MAPK, and PI3K/Akt, that can support tumor survival or metastasis under certain conditions.

This means that TRAIL-R2 activity depends partly on the biological context in which the receptor is expressed and activated.

The researchers focused on another potential regulator of TRAIL-R2: DNA methylation.

DNA methylation is an epigenetic process that can alter gene activity without changing the underlying DNA sequence. When methylation occurs in promoter regions, it can reduce transcription and effectively silence a gene. In cancer, abnormal promoter methylation is one mechanism by which genes involved in growth control or cell death can become less active.

The study therefore asked whether TRAIL-R2 promoter methylation was increased in breast cancer and whether that change was accompanied by lower TRAIL-R2 expression.

Full blog post - https://www.oncotarget.org/2026/10/06/epigenetic-silencing-of-trail-r2-is-linked-to-aggressive-features-in-breast-cancer/

DOI - https://doi.org/10.18632/oncotarget.28891

Correspondence to - Asia Asiaf - [email protected], and Showkat Ahmad Ganie - [email protected]

Abstract video - https://www.youtube.com/watch?v=BvhkOYLTJUY

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Keywords - cancer, TRAIL-R2/DR5, promoter methylation, breast cancer biomarkers, tumor suppressor gene, apoptotic signalling pathways

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BUFFALO, NY – September 28, 2026 – A new #editorial was #published in Volume 17 of Oncotarget on September 23, 2026, titled “Gut feeling: Microbes at the heart of cancer therapy.”

The article examines how the human microbiome may influence cancer development, treatment response and emerging precision-oncology strategies.

The editorial was led by first author Uzma Saqib, with Krishnan Hajela serving as corresponding author. Hajela is affiliated with the School of Life Sciences, Devi Ahilya Vishwavidyalaya, Takshashila Campus, Indore, Madhya Pradesh, India.

The microbiome—the collection of microorganisms living in a particular environment—has increasingly been linked to cancer biology. The gut microbiome can influence inflammation, immune responses and metabolism, while microbial metabolites can affect systemic metabolism, epigenetic processes and immune surveillance. Dysbiosis, or an imbalance in microbial communities, has been associated with several cancers. The authors highlight Fusobacterium nucleatum in colorectal cancer and Helicobacter pylori in gastric cancer as examples of microbes associated with tumor-promoting processes.

The microbiome may also affect how patients respond to cancer therapy. The editorial discusses evidence linking favorable gut microbial profiles with responses to immune checkpoint inhibitors such as anti-PD-1 and anti-CTLA-4 therapies. Certain microbial communities may support dendritic-cell maturation, T-cell priming and antitumor immunity, whereas dysbiosis has been associated with treatment resistance. Microbial metabolism can also influence chemotherapy efficacy and gastrointestinal toxicity.

These findings have encouraged investigation of the microbiome as both a therapeutic target and a biomarker. Microbial signatures may potentially help predict responses to immunotherapy, while probiotics, prebiotics and fecal microbiota transplantation are being explored as ways of modifying treatment response. The authors highlight Akkermansia muciniphila, which has enhanced anti-PD-1 efficacy in preclinical models. These approaches remain investigational and are not established replacements for standard cancer treatments.

Full press release - https://www.oncotarget.com/news/pr/gut-microbiome-emerges-as-a-potential-partner-in-precision-cancer-therapy/

DOI - https://doi.org/10.18632/oncotarget.28919

Correspondence to - Krishnan Hajela - [email protected] (ORCID: https://orcid.org/0000-0002-4742-9643)

Abstract video - https://www.youtube.com/watch?v=IDY6pK5yo-A

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Keywords - cancer, gut microbiome, immunomodulation, precision therapeutics, tumor

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Cancer cells do not grow in isolation. Their ability to survive and form tumors depends partly on how they interact with immune cells in the surrounding tumor microenvironment. Melanoma is particularly responsive to immune-based mechanisms, making it important to understand the molecular processes that allow melanoma cells to limit or escape antitumor immune responses.

A research paper published in Volume 17 of Oncotarget, titled “DHHC3 interferes with antitumor immunity in melanoma cells,” investigated the role of the protein acyltransferase DHHC3 in melanoma growth, oxidative stress, cellular senescence, and antitumor immunity.

Why Study DHHC3 in Melanoma?

DHHC3 is one of 23 members of the DHHC family of protein acyltransferases. These enzymes modify proteins through a process known as palmitoylation, which can influence where proteins are located within cells and how they function.

Previous research from the investigators showed that DHHC3 palmitoylates numerous antioxidant and redox-regulatory proteins, providing a mechanism through which it helps control intracellular oxidative stress. Higher DHHC3 expression has also been associated with poorer survival across several cancer types, while DHHC3 ablation has previously been shown to reduce breast tumor growth.

However, an important question remained unresolved: does eliminating DHHC3 suppress tumors because of changes occurring directly within cancer cells, or because those changes allow the immune system to attack the tumor more effectively?

Full blog post - https://www.oncotarget.org/2026/09/23/dhhc3-helps-melanoma-tumors-evade-antitumor-immunity/

DOI - https://doi.org/10.18632/oncotarget.28880

Correspondence to - Martin E. Hemler - [email protected], and Chandan Sharma - [email protected]

Abstract video - https://www.youtube.com/watch?v=QQhP2VhzKSE

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Keywords - cancer, oxidative stress, DHHC3, anti-cancer immunity, palmitoylation, melanoma

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BUFFALO, NY – September 17, 2026 – A new #commentary was #published in Volume 17 of Oncotarget on September 11, 2026, titled “Are both COVID-19 and COVID-19 vaccines associated with cancer?”

The paper was authored by Raphael Lataster, an independent researcher at the University of Sydney, and responds to a recent Oncotarget review by Charlotte Kuperwasser and Wafik S. El-Deiry examining published reports concerning cancer following COVID-19 vaccination or infection.

Lataster highlights research concerning potential associations between COVID-19 and cancer and discusses mechanisms proposed in the literature. He argues that similar mechanisms reported in connection with COVID-19 vaccination warrant consideration and further study.

The commentary also highlights differences in how evidence concerning COVID-19 vaccines and cancer has been evaluated in the scientific literature. He calls for the same evidentiary standards to be applied when considering potential links between COVID-19 infection, vaccination, and cancer.

“Such inquiries should proceed without preconceptions, applying the same evidentiary standards regardless of whether findings implicate infection, vaccination, or both.”

The commentary does not establish a causal relationship between COVID-19 vaccination and cancer. Rather, it calls for potential associations and biological mechanisms to be investigated without predetermined conclusions and with appropriate consideration of alternative explanations and the limitations of observational evidence.

DOI - https://doi.org/10.18632/oncotarget.28918

Correspondence to - Raphael Lataster - [email protected] (ORCID: https://orcid.org/0000-0002-6670-1702)

Preview video - https://www.youtube.com/watch?v=uSbIKNe3Hho

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Keywords - cancer, COVID-19, COVID-19 vaccines, double standards

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BUFFALO, NY – September 9, 2026 – A new #review was #published in Volume 17 of Oncotarget on September 8, 2026, titled “Re-expression of MHC-I to treat CNS cancers.”

The review examines emerging strategies to restore major histocompatibility complex class I (MHC-I) expression in cancers of the central nervous system (CNS), with the goal of making these tumors more visible and vulnerable to immune attack.

The review was authored by Arseniy E. Yuzhalin from the Sirius University of Science and Technology in Sochi, Russia.

Malignant central nervous system (CNS) tumors such as glioblastoma and brain metastases are often immunologically “cold,” with limited T-cell infiltration and poor responses to immune checkpoint therapy. One important mechanism of immune escape is the reduction or loss of major histocompatibility complex class I (MHC-I), which normally displays tumor-associated antigens to cytotoxic CD8+ T cells. When MHC-I expression falls, cancer cells become less visible to immune surveillance.

The review examines several strategies for restoring MHC-I expression. Epigenetic therapies, including histone deacetylase and DNA methyltransferase inhibitors, could potentially reverse epigenetic silencing of MHC-I genes, although blood-brain barrier penetration remains a major limitation in CNS cancers. A more direct approach could use adeno-associated virus (AAV) vectors to deliver patient-specific HLA-A, HLA-B, or HLA-C genes or transcription factors such as NLRC5 that promote MHC-I expression. However, efficient tumor targeting, gene delivery, and control of the immunosuppressive tumor microenvironment remain unresolved challenges.

The review also highlights PCSK9 inhibition as a clinically relevant strategy. PCSK9 can promote MHC-I degradation, and a recent surgical-window trial tested the cholesterol-lowering drug evolocumab in patients with newly diagnosed or recurrent glioma. A single preoperative dose showed measurable blood-brain barrier penetration, and tumors with higher drug concentrations displayed increased surface MHC-I expression, greater CD8+ T-cell infiltration, and enhanced cytotoxic activity. These findings provide proof-of-mechanism, although drug delivery into the brain remains a limiting factor.

Full press release - https://www.oncotarget.com/news/pr/restoring-mhc-i-expression-could-strengthen-immune-responses-against-cns-cancers/

DOI - https://doi.org/10.18632/oncotarget.28917

Correspondence to - Arseniy E. Yuzhalin - [email protected]

Abstract video - https://www.youtube.com/watch?v=NDvQ7QS3DFg

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Keywords - cancer, brain tumor, CNS cancer, glioblastoma, brain metastasis; MHC-I

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Head and neck squamous cell carcinoma (HNSCC) can return even after patients complete surgery, radiation, chemotherapy, or combinations of these treatments. Preventing recurrence therefore remains an important challenge in head and neck cancer care. Human papillomavirus (HPV), particularly HPV type 16, is also an established cause of a subset of these cancers, especially oropharyngeal squamous cell carcinoma.

A research paper published in Volume 17 of Oncotarget, titled “A randomized double-blind placebo-controlled phase I/II clinical trial of a human papillomavirus therapeutic vaccine, PepCan, for reducing head and neck squamous cell carcinoma recurrence,” investigated whether an experimental therapeutic HPV vaccine could safely reduce the risk of HNSCC recurrence after standard treatment.

Full blog post - https://www.oncotarget.org/2026/09/08/therapeutic-hpv-vaccine-pepcan-tested-for-preventing-head-and-neck-cancer-recurrence/

DOI - https://doi.org/10.18632/oncotarget.28892

Correspondence to - Mayumi Nakagawa - [email protected]

Abstract video - https://www.youtube.com/watch?v=oh0MNrrPGhw

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Keywords - cancer, human papillomavirus, head and neck cancer, therapeutic vaccine, adjuvant, clinical trial

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BUFFALO, NY - September 8, 2026 – Oncotarget is proud to support the WIN 2026 Symposium, organized by the Worldwide Innovative Networking (WIN) Consortium, taking place October 2–3, 2026, at the Rhode Island Convention Center in Providence.

The two-day symposium, themed “Precision Oncology: Innovation and Equity Across the Globe,” will bring together researchers, clinicians, healthcare professionals, industry leaders, and other experts from around the world to explore advances in precision oncology and strategies for improving personalized cancer care.

The WIN Consortium is chaired by Wafik S. El-Deiry, MD, PhD, FACP, who also serves as Editor-in-Chief of Oncotarget. Dr. El-Deiry is also the Associate Dean for Oncologic Sciences at the Warren Alpert Medical School, Director of the Legorreta Cancer Center at Brown University, and Director of the Joint Program in Cancer Biology at Brown University and affiliated hospitals.

As a peer-reviewed oncology journal dedicated to publishing impactful cancer research, Oncotarget is pleased to support initiatives that encourage international collaboration and advance innovative approaches to cancer prevention, diagnosis, and treatment.

Full press release - https://www.oncotarget.com/news/pr/oncotarget-supports-win-2026-symposium-advancing-precision-oncology/

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BUFFALO, NY – September 1, 2026 – A new #review was published in Volume 17 of Oncotarget on August 28, 2026, titled “Emerging biomedical imaging applications of tumor-derived extracellular vesicles for premetastatic niche detection: Biological rationale, engineering strategies, and translational challenges.”

The review was led by first author Omkar Dhaygude, who is affiliated with Johns Hopkins University. Corresponding authors Franck Housseau and John Michel are affiliated with Johns Hopkins University, with Housseau also affiliated with the Cancer Research Center of Lille in France.

Extracellular vesicles (EVs) are membrane-enclosed particles released by cells that transport proteins, lipids, nucleic acids, metabolites, and other molecular cargo. In cancer, tumor-derived extracellular vesicles (TEVs) can influence the tumor microenvironment and distant tissues by promoting processes such as angiogenesis, extracellular matrix remodeling, inflammatory signaling, immune evasion, and stromal reprogramming.

Of particular interest is the role of TEVs in establishing premetastatic niches—biological environments in distant organs that become permissive to metastatic cells before overt tumors are detectable. TEVs can carry organ-specific molecular signals, and their surface molecules may influence which tissues they reach. For example, previous experimental research has linked the integrins α6β4 and α6β1 with lung tropism, providing a biological rationale for using TEVs to direct imaging probes toward metastasis-prone organs.

This possibility could address an important limitation of conventional cancer imaging. Computed tomography and other anatomical methods are designed primarily to detect established structural lesions, whereas premetastatic niches are characterized by earlier molecular and microenvironmental alterations. The authors therefore examine whether TEV-associated imaging could provide information about metastatic conditioning before conventional imaging can identify overt metastatic lesions.

Full press release - https://www.oncotarget.com/news/pr/tumor-derived-extracellular-vesicles-show-promise-for-earlier-detection-of-metastatic-risk/

DOI - https://doi.org/10.18632/oncotarget.28916

Correspondence to - Franck Housseau - [email protected], and John Michel - [email protected]

Abstract video - https://www.youtube.com/watch?v=0zygNvj4_YY

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Keywords - cancer, lung metastases, cancer imaging, theranostic, premetastatic niches, extra-cellular vesicles

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BUFFALO, NY – August 31, 2026 – A new #editorial was published in Volume 17 of Oncotarget on June 8, 2026, titled “Tumor infiltrating lymphocyte (TIL) therapy for treating the solid tumors: Challenges and future perspectives.”

The editorial was led by first and corresponding author Bhartendra Sharma from Mahatma Gandhi University of Medical Sciences and Technology, Jaipur, Rajasthan, India, along with co-authors Sukhbir Kaur, Vikas Sharma and Sanjay Soni.

Tumor-infiltrating lymphocyte (TIL) therapy is a form of adoptive cellular therapy that uses immune cells naturally present within tumors to attack cancer. Unlike chimeric antigen receptor (CAR) T-cell therapy, which genetically modifies a patient’s T cells to recognize specific tumor antigens and has achieved its greatest success in hematological malignancies, TIL therapy has shown potential in several types of solid tumors.

The approach has a history spanning more than four decades. Steven Rosenberg first isolated TILs from a mouse tumor in 1982, and subsequent experiments demonstrated antitumor effects when TILs were combined with cyclophosphamide and interleukin-2 (IL-2). In 1988, Rosenberg and colleagues reported favorable clinical outcomes after administering TIL therapy to patients with metastatic melanoma.

Full press release - https://www.oncotarget.com/news/pr/tumor-infiltrating-lymphocyte-therapy-offers-a-promising-approach-for-treating-solid-tumors/

DOI - https://doi.org/10.18632/oncotarget.28883

Correspondence to - Bhartendra Sharma - [email protected]

Intro video - https://www.youtube.com/watch?v=QAr_R4WCJfk

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Keywords - cancer, tumor infiltrating lymphocytes, solid tumors, adoptive cellular therapy, immunotherapy

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BUFFALO, NY – August 28, 2026 – A new #research paper was published in Volume 17 of Oncotarget on August 19, 2026, titled “Incidence of KRAS G12C mutations in genitourinary malignancies; emerging target in precision medicine.”

The study was led by first author Kelly Crane from the Department of Urology at SUNY Upstate Medical University. The corresponding author is K. R. Seetharam Bhat, who is affiliated with the Department of Urology at SUNY Upstate Medical University and Upstate Urology at MVHS.

KRAS is one of the most extensively studied oncogenes in cancer, and the G12C variant has become clinically important following the development of mutation-specific inhibitors. Although KRAS G12C-targeted therapy is established in other malignancies, its frequency and genomic characteristics in genitourinary cancers have remained less well defined.

To address this gap, the researchers performed comprehensive genomic profiling of 13,654 tumor specimens from patients with metastatic disease, including 1,453 renal clear cell carcinomas, 3,879 urothelial bladder carcinomas, and 8,322 prostate acinar adenocarcinomas. Tumor mutational burden, microsatellite instability, and PD-L1 expression were also evaluated.

Across the full cohort, KRAS alterations were detected in 367 tumors, or 2.7%, while KRAS G12C was identified in only 25 tumors, representing approximately 0.2% of all specimens. No G12C variants were found among the renal clear cell carcinomas. In urothelial bladder carcinoma, 24 of 202 KRAS-altered tumors, or 12%, carried G12C, while only one of 158 KRAS-altered prostate tumors contained the variant.

Full press release - https://www.oncotarget.com/news/pr/kras-g12c-mutation-identified-as-a-rare-potential-target-in-genitourinary-cancers/

DOI - https://doi.org/10.18632/oncotarget.28912

Correspondence to - K. R. Seetharam Bhat - [email protected]

Abstract video - https://www.youtube.com/watch?v=me9HXtnDmp4

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Keywords - cancer, KRAS mutation, genitourinary malignancy, precision medicine, emerging target

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