Results 191 to 200 of about 308,092 (299)

Calcium Channel Blockers Inhibit Pancreatic Neuroendocrine Neoplasms Progression via Cav1.2‐Epigenetic Circuit

open access: yesAdvanced Science, EarlyView.
Our study reveals a novel mechanism of a positive regulatory circuit between Cav1.2 and H3K27ac for pancreatic neuroendocrine neoplasms (pNENs) progression. Cav1.2 is identified as a crucial target for promoting disease progression and correlates with malignant behaviors, which are remarkably inhibited by the administration of calcium channel blockers (
Yangyinhui Yu   +12 more
wiley   +1 more source

Mapping Genetic Regulation of Transcription to Identify Functional Variants and Genes Associated with Pancreatic Cancer Risk

open access: yesAdvanced Science, EarlyView.
Integration of a pancreatic eQTL map with a GWAS meta‐analysis identifies 82 putative functional variants and 15 genes. The association between rs11102484 and pancreatic cancer risk is observed in a total of 5699 cases and 8467 controls. The G allele of rs11102484 weakens ZNF263 binding and the silencer‐promoter interaction, thereby increasing ST7L ...
Xiaoyang Wang   +14 more
wiley   +1 more source

GPCRs in CAR‐T Cell Immunotherapy: Expanding the Target Landscape and Enhancing Therapeutic Efficacy

open access: yesAdvanced Science, EarlyView.
Chimeric antigen receptor T cell therapy faces dual challenges of target scarcity and an immunosuppressive microenvironment in solid tumors. This review highlights how G protein‐coupled receptors can serve as both novel targets to expand the therapeutic scope and functional modules to enhance CAR‐T cell efficacy.
Zhuoqun Liu   +11 more
wiley   +1 more source

BCR::ABL1‐Induced Enhancer Reprogramming Uncovers Hypersensitivity of Ph+B‐ALL Cells to Enhancer‐Targeting Drugs

open access: yesAdvanced Science, EarlyView.
Ng et al. show that the BCR::ABL1 kinase that drives the lymphoid leukemia Ph+B‐ALL modulates enhancer function by coopting signaling‐inducible transcription factors such as MYC, STAT5, and ETV5. BCR::ABL1 thereby promotes the transcriptional program driving and defining this leukemia and renders Ph+B‐ALL cells hypersensitive to enhancer‐inhibiting ...
Han Leng Ng   +19 more
wiley   +1 more source

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