Acquired resistance to TKIs in solid tumours: learning from lung cancer
By D. Camidge, William Pao, L. Sequist. Nature Reviews Clinical Oncology, 2014
819 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/3665e608e6bd29a3694665a5264ff67a1bac345b
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Citations in the corpus
- Autophagy and multidrug resistance in cancer (2017, background): “the main transporters [30]; (2) reducing drug uptake by influx transporters, such as solute carriers [31]; (3) boosting drug metabolism, including elimination by glutathione S-transferase and cytochrome P450 enzymes [32, 33]; (4) blocking apoptotic signaling pathways due to change in the expression ”
- Alectinib in Crizotinib-Refractory ALK-Rearranged Non-Small-Cell Lung Cancer: A Phase II Global Study. (2016, neutral): “Any cause, in $ 10% Patients Constipation 39 (28) 6 (4) 0 0 45 (33) Fatigue 26 (19) 8 (6) 2 (1) 0 36 (26) Peripheral edema 27 (20) 6 (4) 1 (1) 0 34 (25) Myalgia 25 (18) 5 (4) 1 (1) 0 31 (23) Asthenia 16 (12) 8 (6) 1 (1) 0 25 (18) Headache 16 (12) 4 (3) 2 (1) 0 22 (16) Cough 15 (11) 4 (3) 0 0 19 (14)”
- Kinase-targeted cancer therapies: progress, challenges and future directions (2018, background): “Despite several challenges that need to be overcome, reviewed in [171, 172], precision medicine has yielded important dividends for patients with advanced cancers [173].”
- Overcoming Endocrine Resistance in Breast Cancer (2020, neutral): “These include 1) secondary mutations in the drug target that block drug-mediated target inhibition (ie, ESR1, EGFR, ALK, NTRK, ERBB2, etc) (Camidge et al., 2014; Hanker et al., 2017; Lin et al., 2017; Pao et al., 2005; Russo et al., 2016), 2) target-independent activation of downstream or bypass sig”
- Tumor cells can follow distinct evolutionary paths to become resistant to epidermal growth factor receptor inhibition (2016, neutral): “The gene targets covered by this assay are as follows (exons): AKT1 (3), ALK (22, 23, 25), APC (16), BRAF (11, 15), CDH1 (1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11,12, 13, 14, 15, 16), CDKN2A (1, 2, 3), CTNNB1 (3), DDR2 (12, 13, 14, 15, 16, 17, 18), EGFR (7, 15, 18, 19, 20, 21), ERBB2 (10, 20), ESR1 (8), FB”
- Current Challenges in Cancer Treatment. (2016, background): “Actually, the genetic basis and some clinically relevant mechanisms of acquired resistance in EGFR- or ALK-mutant lung cancers have been characterized, enabling the development of selective drugs to overcome resistant clones.(53) This has been done either by studying clinical samples (re-biopsies ta”