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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, 
    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, 
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Bge43-008

Host brain infection induces RNAi epimutation in Mucor circinelloides and enhances blood-brain barrier invasion

Quote: This model revealed that bepA mutation enhances fungal migration across brain endothelial monolayers without detectable changes in electrical barrier resistance. These findings identify brain-induced RNAi epimutation as a mechanism of organ-specific fungal adaptation and reveal reversible silencing of a MAPK-like kinase as a route to enhanced central nervous system invasion.
Article: https://www.biorxiv.org/content/10.64898/2026.10.23.761329v1
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Search Authors: Mara Isabel Navarro-Mendoza Carlos Prez-Arques Yeseul Choi Emma Cao Zanetta Chang Ziyan Xu Yong-Sun Bahn E. Ashley Moseman Joseph Heitman, 
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Bim43-016

Neonatal T cell maternal microchimerism is common and associates with early pregnancy SARS2 vaccination

Article: https://www.biorxiv.org/content/10.64898/2026.10.23.761412v1
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Search Authors: Jacquelyn Weaver John Houck Yonghou Jiang Cara Tobey Jia Wong Swati Shree Whitney E Harrington, 
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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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Sd432-006

Scientists Solve a 30-year Mystery Behind Inflammatory Bowel Disease

Quote: The findings indicate that IBD is not simply one disease. Instead, it appears to include several biologically distinct conditions that develop through different processes in the body. Identifying these differences could make it possible to provide treatments tailored to the specific cause of each patients illness. In a study published in the New England Journal of Medicine, researchers examined more than 4,900 people with IBD and identified two important findings. First, some patients produce antibodies that interfere with interleukin-10 (IL-10), an essential protein that helps prevent excessive inflammation. Second, this autoimmune reaction explains how one of the strongest known genetic risk factors for IBD contributes to the disease.
Article: https://www.sciencedaily.com//releases/2026/10/261025073053.htm https://www.sciencedaily.com//releases/2026/10/261025073053.htm/releases/2026/10/261025073053.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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