Vulnerability of drug-resistant EML4-ALK rearranged lung cancer to transcriptional inhibition

ChEBI2019-12-22 更新2026-07-12 收录

肿瘤耐药机制

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Vulnerability of drug-resistant EML4-ALK rearranged lung cancer to transcriptional inhibition

创建时间：

2019-12-22

AZ1366: An inhibitor of tankyrase and the canonical Wnt pathway that limits the persistence of non-small cell lung cancer cells following EGFR inhibition. Homo sapiens

肿瘤耐药机制

组合治疗

EGFR-mut NSCLC lines show differential suceptibility to inhibition of tankyrase in the presence of EGFR inhibitors Overall design: NSCLC cells were treated in quadruplicate with gefitinib, AZ1366 (tan

NIAID Data Ecosystem80

Additional file 1 of Cancer of unknown primary with EGFR mutation successfully treated with targeted therapy directed by clinical next-generation sequencing: a case report

癌症基因组数据

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Additional file 1: Supplementary Table 1. Target genes of the comprehensive genomic analysis.

NIAID Data Ecosystem50

Reversing Melanoma Cross-Resistance to BRAF and MEK Inhibitors by Co-Targeting the AKT/mTOR Pathway

肿瘤耐药机制

信号通路靶向治疗

BackgroundThe sustained clinical activity of the BRAF inhibitor vemurafenib (PLX4032/RG7204) in patients with BRAFV600 mutant melanoma is limited primarily by the development of acquired resistance le

Figshare2016-01-18 更新50

The evolution of MET and NRAS gene amplification as sequential acquired resistance mechanisms in a patient with EGFR mutation positive non-small cell lung cancer

化疗耐药机制

靶向治疗

EGFR mutant non-small cell lung cancer patients disease demonstrates remarkable responses to EGFR targeted therapy, but inevitably they succumb to acquired resistance, which can be complex and difficu

NIAID Data Ecosystem70

Inactivation of p21-Activated Kinase 2 (Pak2) Inhibits the Development of Nf2-Deficient Tumors by Restricting Downstream Hedgehog and Wnt Signaling

肿瘤分子机制

靶向治疗

Since loss of the NF2 tumor suppressor gene results in p21-activated kinase (Pak) activation, PAK inhibitors hold promise for the treatment of NF2-deficient tumors. To test this possibility, we asked

NIAID Data Ecosystem50

Vulnerability of drug-resistant EML4-ALK rearranged lung cancer to transcriptional inhibition

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