Commentary Calls for Consistent Evaluation of Potential Links Between COVID-19, Vaccination and Cancer

BUFFALO, NY – November 10, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on November 5, 2026, titled “Limitation of the therapeutic potential of DUSP4 through adaptive feedback partially mediated by DUSP5.” The study explores whether targeting a protein called DUSP4 could help control cancer growth. Researchers found that reducing DUSP4 activity slowed tumor growth in experimental models, but an adaptive response involving a related protein, DUSP5, appeared to limit its therapeutic potential. The study was co-first-authored by Barbara Hopfgartner and Monika Kriz, who contributed equally to the research, alongside Donat Alpar, Yvonne Westermaier, Marco H. Hofmann, Ralph A. Neumüller and Sarah Grosche. All authors are affiliated with Boehringer Ingelheim RCV GmbH & Co KG in Vienna, Austria. Neumüller and Grosche are the corresponding authors. Cancer cells depend on molecular signals to grow and divide. One important signaling network, known as the MAPK pathway, is frequently altered in cancer. While many existing treatments aim to block excessive MAPK activity, researchers are also investigating whether increasing this activity beyond tolerable levels could interfere with cancer cell growth. DUSP4 helps regulate the MAPK pathway by limiting the activity of ERK proteins. In cancers carrying the BRAF V600E mutation, DUSP4 may help prevent excessive signaling, making it a potential therapeutic target. To explore this possibility, the researchers used genetic approaches to reduce DUSP4 activity in colorectal cancer and melanoma cell models, including cells resistant to the BRAF inhibitor dabrafenib. They found that DUSP4 reduction increased MAPK signaling and slowed cancer cell proliferation. In colorectal cancer cells, it also caused cell cycle arrest, preventing cells from progressing normally toward division. The team then examined the effects of DUSP4 reduction in mice bearing colorectal tumors. Although tumor growth was significantly inhibited, the tumors remained largely stable rather than shrinking. Signs of regrowth also appeared during the experiment, suggesting that cancer cells could adapt to the disruption. Full press release - https://www.oncotarget.com/news/pr/dusp5-feedback-linked-to-limited-therapeutic-potential-of-dusp4-in-colorectal-cancer/ DOI - https://doi.org/10.18632/oncotarget.28923 Correspondence to - Ralph A. Neumüller - [email protected], and Sarah Grosche - [email protected] Abstract video - https://www.youtube.com/watch?v=0TMvuD5wJvw Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28923 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, signaling, DUSP4, MAPK, biology To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh [email protected]

Ewing sarcoma is an aggressive cancer that primarily affects children, adolescents, and young adults. Although treatment has substantially improved outcomes for localized disease, survival remains much poorer when the cancer has spread or returned. Researchers are therefore continuing to investigate signaling pathways that could provide additional therapeutic targets. A research paper published in Volume 17 of Oncotarget, titled “Delayed growth of SK-ES-1 Ewing sarcoma tumor xenografts is associated with reduced Trk and IGF1R pathway markers,” investigated the effects of the multi-kinase inhibitor K252a in a mouse model of Ewing sarcoma and examined signaling involving Trk receptors, PI3K, and insulin-like growth factor 1 receptor, or IGF1R. The researchers found that K252a temporarily slowed the growth of human Ewing sarcoma tumors implanted into mice while reducing the expression and phosphorylation of several signaling proteins. They also found that combining K252a with an IGF1R inhibitor reduced Ewing sarcoma cell viability more strongly than either treatment alone and identified exploratory associations between NTRK gene expression and patient survival. Full blog post - https://www.oncotarget.org/2026/11/04/multi-kinase-inhibitor-temporarily-delays-ewing-sarcoma-growth-in-preclinical-model/ DOI - https://doi.org/10.18632/oncotarget.28911 Correspondence to - Caroline Brunetto de Farias - [email protected] Abstract video - https://www.youtube.com/watch?v=ZG-vhYfHjuw Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28911 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, Ewing sarcoma, K252a, Trk, NTRK, insulin-like growth factor 1 receptor To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh [email protected]

BUFFALO, NY - November 4, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on November 2, 2026, titled “Survival factors in lung cancer patients with mutations in the PROS1, SERPINC1, F2, and F5 genes.” The study identified associations between genes involved in blood coagulation and survival outcomes in patients with lung cancer. Analyzing genetic and clinical data from 1,419 patients, the researchers found that the prognostic significance of four coagulation-related genes varied according to mutation status, tumor location and other clinical characteristics. The findings suggest that these genes may provide additional information for understanding lung cancer prognosis, although their clinical usefulness remains to be established. The research was led by first and corresponding author Ryan Brownlee, affiliated with the Medical College of Georgia at Augusta University. Lung cancer remains a leading cause of cancer-related death worldwide. Although advances in targeted therapies, immunotherapy and molecular diagnostics have improved outcomes for some patients, survival varies considerably depending on disease stage, tumor characteristics and treatment response. Identifying additional biological factors associated with prognosis could help researchers better understand these differences. One area of growing interest is the relationship between cancer and blood coagulation. Patients with malignancies are at increased risk of abnormal blood clots, known as cancer-associated thrombosis. Beyond causing potentially serious complications, coagulation-related proteins can influence inflammation, tumor growth and interactions between malignant cells and their surrounding tissues. The researchers focused on four genes associated with thrombophilia, an increased tendency to develop blood clots: PROS1, SERPINC1, F2 and F5. These genes encode proteins involved in regulating the coagulation cascade, and alterations in their function have been linked to thrombotic disorders. Full press release - https://www.oncotarget.com/news/pr/coagulation-related-genes-and-tumor-location-linked-to-lung-cancer-survival/ DOI - https://doi.org/10.18632/oncotarget.28914 Correspondence to - Ryan Brownlee - [email protected] Abstract video - https://www.youtube.com/watch?v=3leoNrmo3Ag Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28914 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, F5, PROS1, SERPINC1, lung cancer, thrombophilia To learn more about the journal, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh [email protected]

BUFFALO, NY - October 26, 2026 – A new #casereport was #published in Volume 17 of Oncotarget on October 16, 2026, titled “WIN-MTB-2024002 – WIN International Molecular Tumor Board: A 52-year-old female with unmeasurable Stage IIIc colon cancer.” The report describes a 52-year-old woman with stage IIIc colon cancer whose disease remained difficult to monitor despite extensive treatment. Although conventional imaging showed no measurable cancer, repeated blood tests detected circulating tumor DNA (ctDNA), raising concern about possible residual disease. The case highlights how comprehensive molecular profiling and international collaboration may help guide treatment decisions when imaging and molecular findings provide different information. The report was led by first and corresponding author Oncotarget Editor-in-Chief Dr. Wafik S. El-Deiry, affiliated with the Worldwide Innovative Network (WIN) Consortium and the Legorreta Cancer Center at Brown University. Equal-contributing author Razelle Kurzrock is affiliated with the WIN Consortium and the Medical College of Wisconsin. Colorectal cancer is a leading cause of cancer-related deaths worldwide. Stage IIIc colon cancer involves extensive regional lymph node involvement and carries a substantial risk of recurrence even after surgery and chemotherapy. Monitoring for residual disease can be challenging when suspicious lymph nodes are too small or show limited activity on conventional imaging. Molecular profiling can help identify genetic alterations that influence cancer growth and treatment response. Liquid biopsy testing offers additional information by detecting ctDNA released by cancer cells into the bloodstream, potentially identifying molecular evidence of residual disease even when imaging shows no measurable tumor. The patient initially experienced weight loss, paleness and reduced appetite in June 2021. In February 2022, severe anemia prompted hospitalization and further investigation. Colonoscopy revealed an obstructing mass, and she underwent a right hemicolectomy. Pathological examination confirmed moderately differentiated adenocarcinoma with mucinous features, classified as stage IIIc (pT4bN2bM0). Ten of 25 examined lymph nodes contained cancer. Full press release - https://www.oncotarget.com/news/pr/international-tumor-board-explores-personalized-treatment-strategies-for-colon-cancer-without-measurable-disease/ DOI - https://doi.org/10.18632/oncotarget.28921 Correspondence to - Wafik S. El-Deiry - [email protected] Abstract video - https://www.youtube.com/watch?v=GzT1QhYiexg Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28921 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, precision oncology, molecular tumor board, colon cancer To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh [email protected]

BUFFALO, NY – October 22, 2026 – A new #case report was #published in Volume 17 of Oncotarget on October 16, 2026, titled “Case Report WIN-MTB-2024001 – WIN International Molecular Tumor Board: A 55-year-old male with glioblastoma exhibiting amplifications in MDM2 and EGFR.” The report describes the clinical journey of a 55-year-old man diagnosed with glioblastoma (GBM), an aggressive brain cancer, whose tumor carried amplifications of the MDM2 and EGFR genes alongside other molecular alterations. Through comprehensive genomic profiling and an international molecular tumor board, the case highlights how precision oncology may identify potential treatment strategies when standard therapies offer limited long-term control. The report was led by first and corresponding author Oncotarget Editor-in-Chief Dr. Wafik S. El-Deiry, affiliated with the Worldwide Innovative Network (WIN) Consortium and the Legorreta Cancer Center at Brown University. Equal-contributing author Razelle Kurzrock is affiliated with the WIN Consortium and the Medical College of Wisconsin. Glioblastoma is among the most aggressive primary brain tumors in adults, characterized by rapid growth, extensive infiltration into surrounding tissue and frequent recurrence. Standard treatment generally combines maximal safe surgical resection, radiotherapy and temozolomide chemotherapy. However, median survival remains approximately 15 months, underscoring the need for additional therapeutic approaches. One major challenge is molecular heterogeneity, meaning that tumors can contain genetic alterations that influence growth, treatment response and resistance. Next-generation sequencing (NGS) can help identify these abnormalities and reveal potential targets for individualized treatment. The patient initially experienced dizziness and a generalized seizure in February 2023, followed by impaired speech. Brain imaging revealed a small mass in the left temporal lobe. Following another seizure in June 2023, imaging showed tumor growth, prompting an anterior temporal lobectomy and amygdalohippocampectomy. Histopathological examination confirmed glioblastoma. Full press release - https://www.oncotarget.com/news/pr/international-tumor-board-explores-personalized-treatment-options-for-glioblastoma-with-mdm2-and-egfr-amplifications/ DOI - https://doi.org/10.18632/oncotarget.28920 Correspondence to - Wafik S. El-Deiry - [email protected] Abstract video - https://www.youtube.com/watch?v=s8L4gukgKWU Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28920 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, precision oncology, molecular tumor board, glioblastoma To learn more about the journal, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh [email protected]

When one person develops several cancers over the course of many years, treatment decisions can become increasingly difficult. Each tumor may have a different biological origin, yet some may share genetic alterations that suggest a common ancestry or point toward the same therapeutic target. A recent case report shows how detailed molecular profiling and an international molecular tumor board can help disentangle these questions and identify possible strategies when standard treatment pathways become complicated. A precision oncology paper published in Volume 17 of Oncotarget, titled “WIN-MTB-2024017 – WIN International Molecular Tumor Board: A 48-year-old female with multiple primary cancers,” describes the clinical history and molecular evaluation of a woman carrying a pathogenic germline BRCA1 mutation who developed breast, skin, ovarian, colon, and later small bowel cancer. Full blog post - https://www.oncotarget.org/2026/10/20/molecular-tumor-board-maps-precision-treatment-options-for-a-woman-with-multiple-primary-cancers/ DOI - https://doi.org/10.18632/oncotarget.28899 Correspondence to - Wafik S. El-Deiry - [email protected] Abstract video - https://www.youtube.com/watch?v=4KIDbmq6ui8 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28899 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, precision oncology, molecular tumor board To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh [email protected]

BUFFALO, NY – October 14, 2026 – A new #research paper was #published in Volume 17 of #Oncotarget on October 12, 2026, titled “Integrative pan-cancer analysis of AKT1 and structure-based drug design by buckwheat derived compounds.” The study examined the role of AKT1 across 33 cancer types and identified fagopyrine, a naturally occurring compound found in buckwheat, as a potential starting point for developing new AKT1-targeting drugs. By combining large-scale cancer datasets with computational drug-design techniques, the researchers identified cancer-specific patterns of AKT1 expression and predicted that fagopyrine could bind strongly to the AKT1 protein. However, its ability to inhibit AKT1 or produce anticancer effects has not yet been experimentally demonstrated. The research was led by first and corresponding author Ramjan Sheikh, affiliated with the Plasma Cell Research Center and the Hajee Mohammad Danesh Science and Technology University. AKT1 is a protein kinase involved in regulating cell growth, survival, metabolism and resistance to treatment. It functions within the PI3K/AKT/mTOR signaling pathway, a major network that controls how cells respond to growth signals and changing metabolic conditions. When this pathway becomes abnormally activated, it can contribute to uncontrolled cell proliferation and cancer progression. Understanding how AKT1 behaves across different tumors may therefore help identify potential biomarkers and therapeutic targets. The researchers analyzed data from The Cancer Genome Atlas (TCGA) covering 33 cancer types, integrating information from multiple databases on gene expression, genetic alterations, DNA methylation, patient survival, immune-cell infiltration and drug sensitivity. This approach allowed them to investigate both the shared functions of AKT1 and the differences in its biological significance across malignancies. Full press release - https://www.oncotarget.com/news/pr/pan-cancer-analysis-identifies-buckwheat-derived-compound-as-potential-akt1-drug-design-candidate/ DOI - https://doi.org/10.18632/oncotarget.28922 Correspondence to - Ramjan Sheikh - [email protected] (ORCID: https://orcid.org/0009-0007-8248-7869) Abstract video - https://www.youtube.com/watch?v=XNoPbxo8YJQ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28922 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, AKT1, pan-cancer, buckwheat, fagopyrine, molecular docking To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh [email protected]

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 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28891 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, TRAIL-R2/DR5, promoter methylation, breast cancer biomarkers, tumor suppressor gene, apoptotic signalling pathways To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh [email protected]

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 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28919 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, gut microbiome, immunomodulation, precision therapeutics, tumor To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh [email protected]

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 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28880 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, oxidative stress, DHHC3, anti-cancer immunity, palmitoylation, melanoma To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh [email protected]