ArticleCancer biology & medicine2012
Molecular mechanisms contributing to resistance to tyrosine kinase-targeted therapy for non-small cell lung cancer.
Article in Cancer biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Postpartum breast cancer progression is driven by semaphorin 7a-mediated invasion and survival.Oncogene · 2020Article
- GPR119 agonist enhances gefitinib responsiveness through lactate-mediated inhibition of autophagy.Journal of experimental & clinical cancer research : CR · 2018Article
- Evaluation of therapeutic effectiveness of (131)I-antiEGFR-BSA-PCL in a mouse model of colorectal cancer.World journal of gastroenterology · 2016Article
- Pulmonary adenocarcinoma: implications of the recent advances in molecular biology, treatment and the IASLC/ATS/ERS classification.Journal of thoracic disease · 2014Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the most important pathways in non-small cell lung cancer (NSCLC) is the epidermal growth factor receptor (EGFR) pathway. This pathway affects several crucial processes in tumor development and progression, including tumor cell proliferation, apoptosis regulation, angiogenesis, and metastatic invasion. Targeting EGFR is currently being intensely explored. We are witnessing the development of a number of potential molecular-inhibiting treatments for application in clinical oncology. In the last decade, the tyrosine kinase (TK) domain of the EGFR was identified in NSCLC patients, and it has responded very well with a dramatic clinical improvement to TK inhibitors such are gefitinib and erlotinib. Unfortunately, there were primary and/or secondary resistance to these treatments, as shown by clinical trials. Subsequent molecular biology studies provided some explanations for the drug resistance phenomenon. The molecular mechanisms of resistance need to be clarified. An in-depth understanding of these targeted-therapy resistance may help us explore new strategies for overcoming or reversing the resistance to these inhibitors for the future of NSCLC treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.