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Transcription profiling of human diploid and tetraploid HCT116 cells treated with cisplatin and/or a Chk1 inhibitor to investigate resistance to genotoxic stress

ChEBI2008-06-09 更新2026-07-21 收录

化疗耐药机制

热激应激转录组

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-TABM-172 数据链接链接失效反馈

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Transcription profiling of human diploid and tetraploid HCT116 cells treated with cisplatin and/or a Chk1 inhibitor to investigate resistance to genotoxic stress

应用场景：

创建时间：

2008-06-09

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化疗耐药机制

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化疗耐药机制

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化疗耐药机制

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DataSheet2_Exogenous proline enhances susceptibility of NSCLC to cisplatin via metabolic reprogramming and PLK1-mediated cell cycle arrest.xlsx

化疗耐药机制

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The occurrence of cisplatin resistance is still the main factor limiting the therapeutic effect of non-small cell lung cancer (NSCLC). It is urgent to elucidate the resistance mechanism and develop no

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A feedforward loop between STAT1 and YAP1 stimulates lipid biosynthesis, accelerates tumor growth, and promotes chemotherapy resistance in mutant KRAS colorectal cancer.

结直肠癌脂质代谢

化疗耐药机制

In tumorous conditions, the transcription factor STAT1, traditionally recognized for its anti-tumor role in immunology, exhibits pro-survival characteristics, though the underlying mechanisms remain u

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Transcription profiling of human diploid and tetraploid HCT116 cells treated with cisplatin and/or a Chk1 inhibitor to investigate resistance to genotoxic stress

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