Oncotarget [JOURNAL]
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Xiao Y, Yurievich UA, Yosypovych SV
Oncotarget
· 2026 Jan · PMID 42370829
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Khursheed N, Andrabi SI, Thakur N
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, Qadir Q, Ashraf S, Farooq A, Rashid S, Jabeen F, Khan WY, Khursheed AU, Zargar MA, Asiaf A, Ganie SA
Oncotarget
· 2026 Jun · PMID 42370800
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Copyright: © 2026 Khursheed 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 Khursheed 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. Breast cancer is considered to be one of the most widespread malignancies, however, its molecular processes are not fully comprehended. Another important epigenetic process that regulates the expression of genes in cancer is promoter methylation. TRAIL-R2 is also a key mediator of apoptosis but its clinical implications and epigenetic regulation in breast cancer are not clearly understood. In this research, the level of the promoter of the gene TRAIL-R2 in the matched tumor and normal breast tissues was analyzed using methylation-specific PCR and the level of the mRNA and protein products in the matched tumor and normal breast tissues were measured using quantitative real-time PCR and western blotting. Methylation of TRAIL-R2 promoter was significantly enhanced in tumor tissues and was negatively correlated with the levels of mRNA and protein. We found that hypermethylation was much more common in invasive ductal carcinoma patients and in patients with a history of use of oral contraceptives. A decreased expression of mRNA of TRAIL-R2 was significantly related to advanced TNM stage (III–IV) and the absence of progesterone receptor, and low protein expression was significantly related to postmenopausal status. These results suggest that aggressive clinicopathological phenotypes are associated with TRAIL-R2 silencing via promoter hypermethylation that may be relevant as a prognostic biomarker and therapeutic target in breast cancer.
Huo Y, Li Q, Wang X
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, Jiao X, Zheng J, Li Z, Pan X
Oncotarget
· 2026 Jan · PMID 42308376
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Shalabaev B, Kurash S, Nurzhanov A
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, Serikbaiuly D, Kochiev B, Manatova A, Burkitbayev Z, Kuanysh Z
Oncotarget
· 2026 May · PMID 42262152
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UNLABELLED: Copyright: © 2026 Shalabaev 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 re...UNLABELLED: Copyright: © 2026 Shalabaev 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: Laryngeal leiomyosarcoma (LLMS) is an exceptionally rare malignant tumor, accounting for less than 1 % of all laryngeal cancers, which are predominantly epithelial in origin. Since the first description in 1939, fewer than 70 cases have been reported worldwide. In the largest pooled analysis reported a 5-year overall survival rate of 64%, with distant metastasis identified as the main adverse prognostic factor. CASE PRESENTATION: We report a 64-year-old male who presented with progressive dyspnea and hoarseness caused by a supraglottic mass. Preoperative biopsy revealed spindle-cell proliferation consistent with leiomyosarcoma (SMA +, Vimentin +, Ki-67 60 %). Comprehensive staging with CT, MRI, and ultrasound excluded regional and distant metastases. The patient underwent extended laryngectomy with R0 margins and left neck dissection (levels II–IV). Based on multidisciplinary tumor-board discussion, four cycles of adjuvant doxorubicin and ifosfamide were administered according to national sarcoma guidelines. At 12-month follow-up, the patient remains alive and free of disease. CONCLUSIONS: This report, representing the first documented case of LLMS from Central Asia, contributes to the limited global experience with this rare tumor. Our review identified four additional LLMS cases published between 2021 and 2024, totaling five recent reports including the present case. Collectively, these demonstrate persistent male predominance, glottic and supraglottic predilection, and survival outcomes consistent with previous observations. Complete surgical excision remains the cornerstone of therapy, while multidisciplinary-guided adjuvant treatment may benefit selected high-grade or high-risk patients. Continued accumulation and molecular characterization of cases are needed to refine prognostic assessment and optimize management strategies.
Fazioli F, Colella G, Miceli R
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, Salvatore MGD, Gallo M, Boccella S, Chiara A, Ruosi C, Nigris F
Oncotarget
· 2026 Jan · PMID 42262148
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Sharma C, Hwang S, Liu Q
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, Hemler ME
Oncotarget
· 2026 Jun · PMID 42258147
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Copyright: © 2026 Sharma 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 a...
Copyright: © 2026 Sharma 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. The protein-acyltransferase DHHC3 supports a few different tumor malignancies, but mechanisms have been unclear. Here we report that DHHC3-null B16F10 melanoma cells showed markedly elevated oxidative stress and senescence, accompanied by diminished tumor growth within immunocompetent C57/BL6 mice, but not in immunodeficient NOD-SCID mice. These results suggest that absence of DHHC3 enhances innate and/or adaptive anti-melanoma immunity. Consistent with this, DHHC3-null melanomas contained elevated numbers of anti-tumor cells (M1 macrophages, NK, CD4+T, CD8+T), whereas pro-tumor cells (M2 macrophages, MDSCs) were diminished. Unexpectedly, DHHC3 ablation minimally affected experimental metastasis of cells injected into either immunocompetent C57/BL6 or immunodeficient NOD-SCID mice. We conclude that DHHC3 ablation does not fundamentally alter melanoma cell growth and invasion/metastasis (independent of the immune system) despite its effects on oxidative stress and senescence. However, DHHC3 does control primary melanoma growth by supporting anti-melanoma immunity.
Bhartendra S, Sukhbir K, Vikas S
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, Sanjay S
Oncotarget
· 2026 Jan · PMID 42258146
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Bivens E, Atiq O, Evans T
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, Bimali M, Brown G, Crane J, Darwish N, Faulkner JL, Govindarajan R, Johnson A, Kurilung A, Lazarenko O, Lu YW, Marsh K, Moreno M, Nookaew I, Robeson M, Sunde J, Ussery D, Vural E, Wilman M, Nakagawa M
Oncotarget
· 2026 Jun · PMID 42249801
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UNLABELLED: Copyright: © 2026 Bivens 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 repro...UNLABELLED: Copyright: © 2026 Bivens 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. OBJECTIVES: The main goals were to assess safety and efficacy (i.e., recurrence reduction). RESULTS: Seventeen patients were enrolled. The most common adverse events were grades 1 and 2 injection site reactions, and they occurred more frequently in the PepCan group (p < 0.0001). Two patients had allergic reactions (grade 2 and grade 3), at the 6th vaccination, which were considered to be a dose-limiting toxicity. No serious adverse events were reported. In the intention-to-treat analyses, 45% (5/11) had non-recurrence in the PepCan group while 80% (4/5) had non-recurrence in the placebo group (p = not significant). Those who received PepCan and experienced non-recurrence showed a trend of having higher new peripheral T cell immune responses to human papillomavirus type 16 E6 (p = 0.05). Pre-vaccination T helper type 1 cells were higher in the PepCan non-recurrence group compared to the PepCan recurrence group (p = 0.01). METHODS: PepCan consists of four human papillomavirus type16 E6 peptides and a Candida skin testing reagent. Patients with head and neck squamous cell carcinoma who had no evidence of disease after standard of care treatments were randomized at 3:1 to PepCan versus placebo (saline). Seven intradermal injections were given followed with two observational visits. Safety was assessed using CTCAE version 5, and efficacy was assessed based on not having recurrence within 2 years. In addition, immune responses and oral and gut microbiome were assessed. CONCLUSIONS: PepCan was well tolerated. PepCan does not seem to be effective in reducing recurrence; however, the results are inconclusive given the small patient numbers.
Zhang XJ, Yu HY, Cai YJ
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, Ke M
Oncotarget
· 2026 Jan · PMID 42234597
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Ofosu-Asante K, Lazarte JMS, Burra AG
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, Lamango NS
Oncotarget
· 2026 Jun · PMID 42233520
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Copyright: © 2026 Ofosu-Asante 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 reproductio...
Copyright: © 2026 Ofosu-Asante 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. There remains an unmet need for effective drugs targeting KRAS-driven cancers. Polyisoprenylated cysteinyl amide inhibitors (PCAIs) were designed to disrupt hyperactive mutant KRAS in cancer. Here, we determined the effects of PCAIs on the viability and downstream mediators of KRAS on pancreatic cancer-derived PANC-1 and MIAPaCa-2 cells. NSL-YHJ-2-45 and NSL-YHJ-2-27 were the most potent of the analogs with EC50 values of 3.6 and 3.8 μM, respectively. NSL-YHJ-2-27 treatment of PANC-1 cells stimulated BRAF, MEK 1/2, ERK 1/2 and p90RSK phosphorylation levels by 64 to 150% while CRAF phosphorylation significantly decreased by 27%. Furthermore, 5 μM NSL-YHJ-2-27 depleted 20 to 61% of the monomeric G-proteins, CDC42, RHOA and RAC 1/2/3 while increasing pAKT (Ser 473) and pAKT (Thr 308) phosphorylation by 72 and 190%, respectively. Reactive oxygen species production significantly increased at 3 μM NSL-YHJ-27 in PANC-1 and MIA PaCa-2 by 2- and 9-fold, respectively. Bulk RNA sequencing analysis revealed that treatment of MIA PaCa-2 cells with 3 μM NSL-YHJ-27 resulted in significant differential expression of 88 genes. NSLYHJ-2-27 at 1 μM inhibited over 90% of pancreatic cancer cell migration. The PCAIs induced apoptosis in both PANC-1 and MIA PaCa-2 3D spheroids while doubling caspase 3/7 activity in PANC-1 cells. Taken together, these data obtained using pancreatic cancer cells with KRAS mutations suggest the ability of the PCAIs to prevent metastasis and tumor growth, strongly indicating their potential to serve as effective targeted therapies for treating cancer types driven by the multiple mutant forms of KRAS.
Margheri F, Luciani C, Taddei ML
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, Giannoni E, Laurenzana A, Biagioni A, Chill xE A, Chiarugi P, Fibbi G, Rosso MD
Oncotarget
· 2026 Jan · PMID 42191350
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Duval H, Toomey B, Karam M
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, Braun T, Fournier D, Grant C, Fairfield H, Chepurko V, Chepurko E, Schimelman A, Nestor B, Ryzhov S, Lindner V, Reagan MR
Oncotarget
· 2026 May · PMID 42191349
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Copyright: © 2026 Duval 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 Duval 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. Collagen triple helix repeat containing 1 (CTHRC1) is a secreted protein that has previously been explored for its role in tissue remodeling and cancer. However, its function in the tumor microenvironment (TME) remains poorly understood, despite its known expression in tumor-associated stroma. Colorectal cancer (CRC), a malignancy characterized by extensive stromal involvement, poses an excellent opportunity to investigate this gap. Here, we provide the first evidence that host-derived CTHRC1 drives colon cancer progression, with this effect consistently observed across three independent cohorts. Specifically, when injected with CRC cells, Cthrc1 null (global knockout, KO) mice develop significantly smaller and less dense tumors compared to wild-type (WT) mice. Additionally, median survival increased approximately 2.5-fold in Cthrc1 KO mice, from 28 days post-inoculation in WT (n = 10) to 69 days in CTHRC1-deficient mice (n = 10), suggesting CTHRC1 promotes tumor growth within the TME. Immune cell profiling revealed differences in the composition of tumors and spleens of these mice; specifically, Cthrc1 KO mice exhibited an increased percentage of CD3+ T cells in both tumors and spleens and decreased Gr-1+ myeloid cells in the spleen, compared to WT, indicating an immunoregulatory role for CTHRC1 in CRC. These results identify CTHRC1 as a key driver of CRC that may suppress the immune system, allowing for easier immune evasion by tumor cells, highlighting CTHRC1 as a potential new target for therapy.
Shao Y, Li P, Zhu ST
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, Yue JP, Ji XJ, Ma D, Wang L, Wang YJ, Zong Y, Wu YD, Zhang ST
Oncotarget
· 2026 Jan · PMID 42191215
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Zhou XM, Sun R, Luo DH
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, Sun J, Zhang MY, Wang MH, Yang Y, Wang HY, Mai SJ
Oncotarget
· 2026 Jan · PMID 42191130
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Zhang Y, Liu Y, Zou J
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, Yan L, Du W, Zhang Y, Sun H, Lu P, Geng S, Gu R, Zhang H, Bi Z
Oncotarget
· 2026 Jan · PMID 42191122
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Zeng H, Zhang JM, Du Y
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, Wang J, Ren Y, Li M, Li H, Cai Z, Chu Q, Yang C
Oncotarget
· 2026 Jan · PMID 42190741
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Pan B, Feng B, Chen Y
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, Huang G, Wang R, Chen L, Song H
Oncotarget
· 2026 Jan · PMID 42190736
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Gu Y, Xiao X, Yang S
Oncotarget
· 2026 Jan · PMID 42190263
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Zhou W, Zou B, Liu L
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, Cui K, Gao J, Yuan S, Cong N
Oncotarget
· 2026 Jan · PMID 42190130
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Zhang L, Wang JH, Liang RX
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, Huang ST, Xu J, Yuan LJ, Huang L, Zhou Y, Yu XJ, Wu SY, Luo RZ, Yun JP, Jia WH, Zheng M
Oncotarget
· 2026 Jan · PMID 42127300
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