CRISPR screen exploring resistance to AKTi (Capivasertib) in ER+ Breast Cancer in MCF7, T47D and CAMA-1 cell lines

ChEBI2026-05-25 更新2026-07-12 收录

CRISPRi功能基因组学

化疗耐药机制

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https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-MTAB-16438 数据链接链接失效反馈

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CRISPR screen exploring resistance to AKTi (Capivasertib) in ER+ Breast Cancer in MCF7, T47D and CAMA-1 cell lines

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2026-05-25

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

化疗耐药机制

表观遗传调控

Purpose: Development of resistance to tamoxifen is an important clinical issue in the treatment of patients with breast cancer. Tamoxifen resistance may be the result of the acquisition of epigenetic

NIAID Data Ecosystem50

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

代谢重编程

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

NIAID Data Ecosystem40

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

化疗耐药机制

ATR抑制剂联合疗法

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

化疗耐药机制

IFN-γ信号通路

"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-?,

NIAID Data Ecosystem40

CRISPR screen exploring resistance to AKTi (Capivasertib) in ER+ Breast Cancer in MCF7, T47D and CAMA-1 cell lines

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