Oncotarget [JOURNAL]

UNLABELLED: Copyright: © 2026 Aleid et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reprod... UNLABELLED: Copyright: © 2026 Aleid et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. BACKGROUND/OBJECTIVES: Programmed cell death protein-1 (PD-1) and programmed death ligand-1 (PD-L1) inhibitors are widely used in cancer treatment. Their benefit as adjuvant therapy in solid tumors is still being defined. This systematic review and meta-analysis evaluated the efficacy and safety of PD-1 and PD-L1 inhibitors as adjuvant treatment in patients with solid tumors. METHODS: We conducted a systematic review and meta-analysis of randomized controlled trials in accordance with PRISMA recommendations and PROSPERO registration CRD42024563699. PubMed, Web of Science, Cochrane Library, and Google Scholar were searched for randomized controlled trials published in English that evaluated adjuvant PD-1 or PD-L1 inhibitors in solid cancers. RESULTS: Thirteen randomized controlled trials published between 2021 and 2023 were included. Adjuvant PD-1 and PD-L1 inhibitors improved disease-free survival (hazard ratio 0.75; 95% CI 0.65–0.86) and distant metastasis-free survival (hazard ratio 0.69; 95% CI 0.54–0.87). No clear difference in overall survival was observed. Trial-level subgroup sizes varied across cancer types. CONCLUSIONS: Adjuvant PD-1 and PD-L1 inhibitors improve disease-free and distant metastasis-free survival in selected patients with high-risk solid tumors. The clinical benefit must be balanced against higher toxicity rates. Because the number of studies within each cancer type remains limited, the strength of cancer-specific conclusions is restricted, and further research is required.

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Epigenetic dysregulation and biological function of PDX1 in prostate cancer.

Adeyika TA, Datturgi A, Ettinoffe Y … +3 more , Ghosh S, Albanese C, Kwabi-Addo B

Oncotarget · 2026 Mar · PMID 41955005 · Full text

Copyright: © 2026 Adeyika et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in... Copyright: © 2026 Adeyika et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Aberrant DNA methylation changes lead to abnormal gene expression that contributes to the development and progression of prostate cancer (PCa). Inquiry of genome-wide DNA methylation dataset, we identified the homeodomain pancreatic and duodenal homeobox 1 (PDX1) gene as differentially hypermethylated in PCa compared to normal prostate tissues. Immunohistochemical analysis of matched PCa and normal prostate tissues using tissue microarray showed a significant 2.33-fold (p = 0.0001) higher PDX1 protein expression in the PCa compared to the normal prostate tissues. In PCa cell lines (PC-3 and LNCaP) engineered to stably overexpress or knockdown PDX1, the ectopic PDX1 expression significantly enhanced cell proliferation and migration, whereas PDX1 knockdown suppressed these phenotypic processes. Quantitative RT-PCR and Western blot analysis demonstrated that PDX1 overexpression was associated with increased expression of key metabolic regulators; INSR, IGF1R, CXCR4, CDH2, TWIST1, and SNAI1, whereas there is decreased expression of ESR2, and TNFα. Conversely, PDX1 knockdown led to the opposite effect in expression profiles of these metabolites. Notably, these effects were more pronounced under high-glucose conditions compared to low-glucose environments. Overall, our findings suggest that PDX1 plays a tumor-promoting role in human PCa cells by influencing expression of metabolites in insulin, inflammatory, and epithelial-mesenchymal transition (EMT) signaling pathways. Given its potential role in metabolic regulation, full insights into the function of PDX1 in PCa could contribute to improved treatment and prevention strategies, particularly for men with PCa and comorbidities such as obesity and diabetes.

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Bibliometric mapping of glioma classification research through main path, key route, and K-core analyses.

Ahmed K, N X Fa X F Ez-R X Ed Os JE

Oncotarget · 2026 Mar · PMID 41955004 · Full text

Copyright: © 2026 Ahmed and Núñez-Ríos. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distri... Copyright: © 2026 Ahmed and Núñez-Ríos. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Burgeoning technological and clinical advances have significantly reshaped glioma classification. To assess the evolution of these changes, we analyzed bibliometric data from Web of Science to explore patterns in the socio-clinical domains of glioma classification research. Using network analysis, we built a direct citation network linking articles to authors, focusing on citations. Main Path Analysis provided an overview of research evolution, Key Route Analysis identified influential papers, and K-core analysis revealed densely connected articles. The network comprised 46,204 nodes and 231,432 arcs, highlighting DNA methylation profiling’s role in advancing molecular biomarker-based classification models. KRA emphasized advanced imaging and molecular techniques as key drivers, while K-core analysis identified articles cited at least 19 times. The findings indicate that the subset of articles focusing on glioma classification that incorporate social factors is relatively scarce in the analyzed data, in contrast to the prominence of epigenetic and imaging factors in the literature. Unlike previous studies that focused primarily on metrics such as the h-index, our approach identifies the limited but notable mention of social factors in glioma classification research, thereby highlighting a thematic gap. Through quantitative network analysis complemented by narrative interpretation, we uncovered patterns and substructures that offer deep insights into the evolving research landscape.

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Correction: LKB1 promotes cell survival by modulating TIF-IA-mediated pre-ribosomal RNA synthesis under uridine downregulated conditions.

Liu F, Jin R, Liu X … +8 more , Huang H, Wilkinson SC, Zhong D, Khuri FR, Fu H, Marcus A, He Y, Zhou W

Oncotarget · 2026 Jan · PMID 41955003 · Full text

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Retraction: Efficacy and safety of traditional chemotherapies for patients with ovarian neoplasm: a network meta-analysis.

Yang L, Guo G, Sun L … +2 more , Li C, Zhang H

Oncotarget · 2026 Jan · PMID 41955002 · Full text

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Correction: Enhancement of the anti-tumor activity of FGFR1 inhibition in squamous cell lung cancer by targeting downstream signaling involved in glucose metabolism.

Fumarola C, Cretella D, Monica S … +14 more , Bonelli MA, Alfieri R, Caffarra C, Quaini F, Madeddu D, Falco A, Cavazzoni A, Digiacomo G, Mazzaschi G, Vivo V, Barocelli E, Tiseo M, Petronini PG, Ardizzoni A

Oncotarget · 2026 Jan · PMID 41954999 · Full text

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Correction: Bisphenol A induces cell cycle arrest in primary and prostate cancer cells through EGFR/ERK/p53 signaling pathway activation.

Bilancio A, Bontempo P, Donato MD … +5 more , Conte M, Giovannelli P, Altucci L, Migliaccio A, Castoria G

Oncotarget · 2026 Jan · PMID 41954998 · Full text

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Cancer without borders: Policy frameworks for oncology care in humanitarian and conflict settings.

Parmar P, Rathod G

Oncotarget · 2026 Mar · PMID 41954997 · Full text

Copyright: © 2026 Parmar and Rathod. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction... Copyright: © 2026 Parmar and Rathod. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Cancer is an escalating yet neglected health crisis among refugees, migrants, and populations affected by conflict. Despite increasing global focus on non-communicable diseases (NCDs), oncology remains largely absent from humanitarian health agendas. This narrative review synthesizes evidence from peer-reviewed literature, humanitarian agency reports, and case studies from Gaza, Sudan, and Ukraine to examine the policy, ethical, and clinical dimensions of oncology care in crisis settings. Findings reveal systemic neglect of cancer services due to disrupted infrastructure, legal barriers, and fragmented policy frameworks. Vulnerable groups - women, children, and the elderly - experience the greatest inequities. Ethical dilemmas in triage, limited palliative care, and inadequate digital connectivity further hinder equitable access. Emerging solutions include bilateral treatment agreements, WHO-led humanitarian oncology corridors, and tele-oncology or mobile unit models that sustain care across borders. Addressing cancer in humanitarian contexts is not merely a technical challenge but a moral imperative. Integrating oncology into emergency response protocols and global health governance is essential to ensure continuity, dignity, and justice in care for displaced and conflict-affected populations.

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CREB5 regulates stem cell-like transcriptional programs to enhance tumor progression in prostate cancer.

Makovec A, Phoenix JT, Bergom HE … +21 more , Boytim E, Gustafson AP, Deacon A, Tape S, Ali A, Ludwig M, Pitzen SP, Moline D, Richter C, Longie H, Su MC, Jena S, Likasitwatanakul P, Drake JM, Huang RS, Hahn WC, Rennhack JP, Dehm SM, Kregel S, Antonarakis ES, Hwang J

Oncotarget · 2026 Mar · PMID 41954995 · Full text

Copyright: © 2026 Makovec et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in... Copyright: © 2026 Makovec et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Prostate gland cells can be transcriptionally and morphologically characterized as basal and luminal. About 30–40% of advanced prostate cancers (PC) harbor basal-like transcription programs. In castration-resistant PC (CRPC), studies indicate that basal and stem cell-like (SCL) tumors are major resistance mechanisms to androgen receptor (AR)-targeted therapies. SCL tumors have reduced AR activity and increased stem-cell activity that promotes tumor formation, which contributes to poor clinical outcomes. We determined that CREB5 is a key regulator of basal and SCL transcriptional programs and tumor-forming phenotypes in PC. Through in silico modeling of PC transcriptomes and several pre-defined PC signaling programs, CREB5 expression was best associated with basal-like gene signatures and SCL-associated genes in primary PC and CRPCs (n = 493 and 208). This included associations with FOSL1 and other AP-1 transcription factors. We further found that CREB5 interacted with AP-1 proteins and bound to the regulatory elements of AP-1 genes, suggesting a mechanistic role in regulating the activity of AP-1 genes. In AR-positive cells, CREB5 overexpression promoted cell colony growth with tumorigenic properties and increased tumor size in vivo. These findings implicate CREB5 as a driver of the transcriptional programs underlying AR-independent basal and SCL CRPC subtypes, and this activity is detectable in primary PC.

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The SCD1 inhibitor aramchol interacts with regorafenib and metformin to kill tumor cells.

Booth MR, Booth L, Roberts JL … +2 more , Kirkwood JM, Dent P

Oncotarget · 2026 Mar · PMID 41954991 · Full text

Copyright: © 2026 Booth et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in an... Copyright: © 2026 Booth et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Mechanisms by which the Stearoyl-CoA desaturase (SCD1) inhibitor aramchol kills tumor cells have recently been described, demonstrating that enhanced signaling through the AMPK played a key role in the processes regulating cell death. Metformin is an anti-hyperglycemic drug which utilizes AMPK signaling to reduce plasma glucose levels. The primary site of metastatic spread of uveal melanoma (UM) is the liver and aramchol concentrates in the liver compared to plasma and other tissues. Aramchol and metformin interacted to modestly enhance cell death in PDX UM cells, though this was less than that caused by the combination of aramchol and the multi-kinase inhibitor regorafenib. Metformin significantly enhanced killing by aramchol plus regorafenib. Metformin significantly enhanced autophagosome formation and autophagic flux caused by aramchol plus regorafenib. Knock down of Beclin1, ATG5 or LAMP2 reduced autophagosome and autolysosome formation, and tumor cell killing. Knock down of BID further enhanced the protective effect of Beclin1 knock down. Knock down of SCD1 enhanced the percentage of dead cells in vehicle control treated cells but did not alter the abilities of drugs to kill tumor cells. Our data demonstrates that UM cells are killed by treatment with aramchol plus regorafenib plus metformin via enhanced autophagic flux and that this combination may have the potential to control UM tumors that have metastasized to the liver.

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Correction: The effectiveness of nano chemotherapeutic particles combined with mifepristone depends on the PR isoform ratio in preclinical models of breast cancer.

Sequeira G, Vanzulli SI, Rojas P … +5 more , Lamb C, Colombo L, May MXEA, Molinolo A, Lanari C

Oncotarget · 2026 Jan · PMID 41954990 · Full text

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Exploring the potential link between mRNA COVID-19 vaccinations and cancer: A case report with a review of haematopoietic malignancies with insights into pathogenic mechanisms.

Gentilini P, Lindsay JC, Konishi N … +2 more , Fukushima M, Polykretis P

Oncotarget · 2026 Feb · PMID 41954969 · Full text

Copyright: © 2026 Gentilini et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction i... Copyright: © 2026 Gentilini et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. This article investigates the potential association between modified mRNA (modRNA) COVID-19 vaccinations and the development of haematopoietic cancers. We present a case involving a healthy, young, athletic woman who developed acute lymphoblastic leukaemia (ALL) and lymphoblastic lymphoma (LBL) following her second dose of the Pfizer/BioNTech COVID-19 vaccine (Comirnaty®). This case is part of an expanding body of literature documenting similar occurrences after modRNA vaccinations, which we critically examine. Emerging evidence suggests that the biodistribution and persistence of modRNA, facilitated by lipid nanoparticles, can affect various tissues and organs, including the bone marrow and other blood-forming organs. Notably, modRNA vaccines exhibit a particular affinity for the bone marrow, potentially influencing the immune system at multiple levels and triggering both autoimmune disorders and neoplastic processes. In this article, we assess the risk of developing haematopoietic cancers post-modRNA vaccination based on current scientific literature and explore the reported potential genetic and molecular mechanisms involved in disease pathogenesis. By integrating clinical observations and current research, we aim to provide valuable insights into the potential carcinogenic outcomes associated with modRNA vaccination.

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