Research
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Scanned: 3718
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Bcb43-002

Tumor SETDB1 expression predicts worse overall survival for bladder cancer patients

Quote: Exploratory analyses identified transcriptional differences associated with SETDB1 expression, providing rationale for further exploration of the mechanisms by which SETDB1 may promote bladder cancer.
Article: https://www.biorxiv.org/content/10.64898/2026.10.23.761403v1
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Search Authors: Sarah R Athans Meegan Young Han Yu Bhavisha Doshi Ellen Karasik Shuhei Ueshima Jia Fang Anna Woloszynska-Read, 
    CANCER    IMMUNE   

Bcb43-004

Targeting alpha-ketoglutarate starvation within the tumor-immune microenvironment rescues T cell effector function in cancer immunotherapy

Quote: In vivo, dietary supplementation with commercially available calcium-aKG (Ca-aKG) supplements led to an elevation of serum and intratumoral aKG levels associated with a significant increase of immunotherapy effectiveness in mouse models of NSCLC. Clinical samples from patients with NSCLC contained significantly decreased serum aKG levels in older NSCLC patients (65 years of age). Analysis identified a novel association between serum aKG levels and poor immunotherapy response. Thus, our work demonstrates that intratumoral metabolite starvation can be therapeutically exploited to improve immunotherapy outcomes in non-small cell lung cancer (NSCLC).
Article: https://www.biorxiv.org/content/10.64898/2026.10.24.761570v1
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Search Authors: Katarina Benejova Kristina Travis Deepti Mathur No joon Song Zihai Li Mitch A. Phelps Elaine Mardis Liza Makowski David P. Carbone Dwight H. Owen Martin Benej, 
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Bcb43-005

CBX3 Deletion Overcomes Ferroptosis Resistance in Colorectal Cancer by Targeting IFN/SLC7A11/SLC3A2 Axis

Quote: Mechanistically, CBX3 binds directly to the promoter of Slc7a11 or Slc3a2 to sustain their expression and redox balance to resist ferroptosis in CRC. Knockout of CBX3 in CRC cells significantly impaired RNA polymerase II recruitment to the promoter of SLC7A11 or SLC3A2 and reduced SLC7A11 and SLC3A2 expression, an effect that was further exacerbated under IFN#947; stimulation but restored by STAT1 deletion. Overall, CBX3 protects CRC from oxidative stress by maintaining the functional integrity of IFN#947;/STAT1/SLC7A11/SLC3A2 axis, positioning CBX3 as a potential therapeutic target for enhancing ferroptosis therapies in CRC.
Article: https://www.biorxiv.org/content/10.64898/2026.10.23.761323v1
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Search Authors: Yao Xiang Yuanji Fu Christophe Desterke Eric Batsche Abdelali Jalil Rima Elhage Clemence Duruel Jean-Christophe Beche Eric Frapy David Skurnik Caroline Reisacher Sedlik Christine Eliane Piaggio Laurence Arbibe Ahmed Hamai Yunhua CHANG, 
    BRAIN    CANCER    IMMUNE   

Bcb43-008

Aquaporin-4 Regulates Edema, Sustains Astrocyte Differentiation, and Constrains Immunosuppressive Remodeling in Glioblastoma

Quote: Treatment with anti-VEGFA antibody, an established anti-edema therapy, increased expression of Aqp4 and reduced vessel leakage, underscoring the role of AQP4 in the therapeutic modulation of brain water balance. Overall, this study highlights the important role of AQP4 in resolving edema and its critical function in maintaining astrocyte identity and shaping the immune landscape of GBM.
Article: https://www.biorxiv.org/content/10.64898/2026.10.23.761345v1
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Search Authors: Tanvi Joshi Kaisha Garvin Matthew J Flick Montserrat Puigdelloses Vallcorba Mehek Dedhia Zhihong Chen Raina Roche Emir Radkevich Susana Isabel Ramos Nadejda M Tsankova Nhan L Tran Leland S Hu Katherine B Peters Alex J Smith Dieter Henrik Heiland Dolores Hambardzumyan, 
    CANCER    GENETICS   

Bcb43-021

Transient Splicing-Associated Isoform Remodeling Defines Early MAPKi Resistance Adaptation in Melanoma

Quote: Notably, most genes undergoing differential transcript usage showed no corresponding change in total gene expression, and genes with isoform-level changes more strongly highlighted MAPKi resistance-associated pathways, including PI3K/AKT/mTOR and receptor tyrosine kinase signaling. Further, classifiers trained on cell-line transcript-usage features identified the adaptive state more accurately than gene-expression-based models in independent PDX and patient datasets. Interestingly, MAPKi-associated isoform changes recapitulated melanoblast-associated developmental splicing programs and were linked to a few key splicing regulators. Together, these findings identify an underappreciated regulatory layer connecting drug tolerance, developmental plasticity, and acquired resistance.
Article: https://www.biorxiv.org/content/10.64898/2026.10.26.761932v1
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Search Authors: Sumit Mukherjee Arashdeep Singh Sumeet Patiyal Hyunjeong Joo Hyungsoo Kim Lipika R. Pal Kun Wang Chi-Ping Day Zeev A Ronai Eytan Ruppin Sridhar Hannenhalli, 
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Bcb43-022

Response to SMAC mimetics in patient-derived models of triple-negative breast cancer relies on RIPK1 activation

Quote: Together, these findings identify impaired RIPK1 autophosphorylation as a mechanism of birinapant resistance in TNBC and suggest that RIPK1 activation state may distinguish SMAC mimetic-sensitive and -resistant tumors. Targeting HOIP may provide a strategy to overcome resistance in selected tumors.
Article: https://www.biorxiv.org/content/10.64898/2026.10.26.761582v1
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Search Authors: Elisabeth Brown Paige Jensen Chieh-Hsiang Yang Emilio Cortes Sanchez Zhengtao Chu Huiyi Yang Yi Qiao Martin Golkowski Apurva Srivastava Bryan Welm Jaime Fornetti Alana L Welm, 
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Bim43-020

Cancer cells hijack mitochondria from Bhlhe40 T cells for immune evasion

Article: https://www.biorxiv.org/content/10.64898/2026.10.23.761277v1
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Search Authors: Hailong Hu Yuhao Tan Irina Shkundina Richard Madnick Jing Hu Hongyi Zhang Ziqi Yang Tong Wang Xuexin Yu Julia Fleming Mingyao Pan Yizhou Wang Yuanyuan Pang Drew Weissman Bo Li, 
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Sd432-013

Scientists Discover How Pancreatic Cancer Rewrites Its DNA to Escape Treatment

Quote: The researchers discovered that pancreatic tumors contain a variety of distinct cell populations known as clones. Each clone consists of cancer cells with similar genetic characteristics, but their behavior can differ dramatically. Some clones develop changes that help them withstand cancer treatments, while others become better equipped to invade surrounding tissues and spread to other parts of the body. These findings suggest that the cancers ability to continually reorganize its genetic material plays a central role in both treatment resistance and metastasis.
Article: https://www.sciencedaily.com//releases/2026/10/261024221849.htm
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Sd432-037

AI Detects invisible Signs of Pancreatic Cancer Years Before Diagnosis

Quote: A powerful new AI system could help doctors detect pancreatic cancer years before it becomes visible on conventional scans. The technology, called REDMOD, identified hidden warning signs an average of 475 days before diagnosis and was nearly twice as sensitive as experienced radiologists.
Article: https://www.sciencedaily.com//releases/2026/10/261024222031.htm
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  Javilk's Research Links Newsletter for Week 43
Updated 10/31/2026-02:16:20 AM
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