Physiologic Hypoxia Promotes Maintenance of CML Stem Cells Despite Effective BCRM-bM-^HM-^RABL1 Inhibition

ChEBI2014-06-03 更新2026-07-21 收录

白血病微环境

化疗耐药机制

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https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-48294 数据链接链接失效反馈

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Physiologic Hypoxia Promotes Maintenance of CML Stem Cells Despite Effective BCRM-bM-^HM-^RABL1 Inhibition

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2014-06-03

Gene expression profile of patient-derived head and neck squamous carcinoma cells subjected to different treatments.. Gene expression profile of patient-derived head and neck squamous carcinoma cells subjected to different treatments.

头颈部鳞状细胞癌基因

化疗耐药机制

In order to investigate the mechanisms underlying response and resistance towards treatment in HNSCC, we used low passage in vitro HNSCC cultures from two patients, namely SJG26 and SJG17. Both cultur

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Integrative Analyses of Gene Expression and DNA Methylation Profiles in a Breast Cancer Cell Line Model of Tamoxifen-Resistance Indicate a Crucial Role of Cells with Stem-like Properties. Homo sapiens

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Loss of IFN-g signaling in tumor cells associates with primary resistance to anti-CTLA-4 therapy

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"Antibody blockade of the inhibitory CTLA-4 pathway has led to clinical benefit in a subset of patients with metastatic melanoma. Anti-CTLA-4 enhances T cell responses, including production of IFN-?,

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ZEB1 inhibition sensitizes cells to the ATR inhibitor VE-821 by abrogating epithelial–mesenchymal transition and enhancing DNA damage

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The ataxia-telangiectasia-mutated (ATM) and rad3-related (ATR) checkpoint pathway plays an essential role in modulating cellular responses to replication stress and DNA damage to maintain genomic stab

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MRTF/SRF link the cytoskeleton and hedgehog pathway in drug-resistant basal cell carcinomas

化疗耐药机制

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We use multi-dimensional genomic analysis using mouse resistant BCCs to identify a non-canonical hedgehog activation pathway driven by the transcription factor, serum response factor (SRF). RNA and wh

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Physiologic Hypoxia Promotes Maintenance of CML Stem Cells Despite Effective BCRM-bM-^HM-^RABL1 Inhibition

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