Treating &lt;em&gt;EGFR &lt;/em&gt;mutation resistance in non-small cell lung cancer &amp;ndash;&amp;nbsp;role of osimertinib

Mazza, Valentina; Cappuzzo, Federico

doi:10.2147/tacg.s103471

Cited by 26 publications

(26 citation statements)

References 51 publications

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“…Mazza and Cappuzzo observation of T790M, PIK3CA mutation, and EGFR, MET gene amplification in cases of non-small-cell lung cancer was closely associated with its profound resistance to EGFR inhibitors. [1] A similar observation was made by Bissada et al, K-RAS codon 12 mutations were linked to treatment resistance in head and neck squamous cell carcinoma. [2] Condorelli et al noted that the mutations in retinoblastoma 1 gene were linked to the development of resistance to cyclin-dependent kinases 4/6 inhibitor in breast cancer.…”

supporting

confidence: 65%

Efficacy of ozone therapy on Porphyromonas gingivalis count in chronic periodontitis: An in vivo study

Londhe¹,

Bagul²,

Gupta³

et al. 2018

jodm

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supporting

confidence: 65%

Efficacy of ozone therapy on Porphyromonas gingivalis count in chronic periodontitis: An in vivo study

Londhe¹,

Bagul²,

Gupta³

et al. 2018

jodm

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“…Unfortunately, acquired drug resistance affects a patient's treatment and prognosis. More recently, a combination therapy enhanced the success rate of treatments for NSCLC . In our study, combinations of BetA with an EGFR TKI were applied to EGFR TKI‐resistant cell line H1975.…”

Section: Discussionmentioning

confidence: 97%

Effects and mechanisms of betulinic acid on improving EGFR TKI‐resistance of lung cancer cells

Lin

Chen

et al. 2018

Environmental Toxicology

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Epidermal growth factor receptor (EGFR) mutations have been identified in approximately 55% of lung cancer patients in Taiwan. Gefitinib (Iressa) and Erlotinib (Tarceva) are the first-generation targeting drugs to patients with EGFR gene mutants a work by inhibiting tyrosine kinase activity. However, resistance in EGFR-mutated patients to first-generation tyrosine kinase inhibitor (TKI) therapy after 8-11 months of treatment has occurred. Betulinic acid (BetA) is a pentacyclic triterpenoid natural product derived from widespread plants. BetA has been reported to have a cytotoxic effect in several cancers. The purpose of this study is to investigate the effects and mechanisms of BetA on dampening EGFR TKI-resistance of lung cancer cells. Our study has demonstrated by MTT assay that combining BetA and an EGFR TKI increased the cytotoxicity against EGFR TKI-resistance lung cancer cells. Based on flow cytometry, combination treatments of BetA with an EGFR TKI enhanced Sub-G1 accumulation, induced apoptosis and induced mitochondrial membrane potential loss. Using western blotting, BetA and EGFR TKI combined treatments inhibited cell cycle related protein and triggered apoptosis- and autophagy- related protein expression. Taken together, our data suggests that a target therapy combining BetA with an EGFR TKI improves drug efficacy in EGFR TKI-resistant lung cancer cells.

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“…Therefore the dose-limiting toxicities from wild-type EGFR inhibition prevent the administration of doses that are sufficient to fully suppress T790M. The third generation of EGFR-TKIs, such as osimertinib, were developed to overcome these limitations [ 63 ].…”

Section: Vegfr-tkis and Other Signalling Pathwaysmentioning

confidence: 99%

Crosstalk between VEGFR and other receptor tyrosine kinases for TKI therapy of metastatic renal cell carcinoma

et al. 2018

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Clear cell renal cell carcinoma (ccRCC) is the most common subtype of renal cell carcinoma (RCC), and is frequently accompanied by the genetic features of von Hippel–Lindau (VHL) loss. VHL loss increases the expression of hypoxia-inducible factors (HIFs) and their targets, including epidermal growth factor (EGF), vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF). The primary treatment for metastatic RCC (mRCC) is molecular-targeted therapy, especially anti-angiogenic therapy. VEGF monoclonal antibodies and VEGF receptor (VEGFR) tyrosine kinase inhibitors (TKIs) are the main drugs used in anti-angiogenic therapy. However, crosstalk between VEGFR and other tyrosine kinase or downstream pathways produce resistance to TKI treatment, and the multi-target inhibitors, HIF inhibitors or combination strategies are promising strategies for mRCC. HIFs are upstream of the crosstalk between the growth factors, and these factors may regulate the expression of VEGR, EGF, PDGF and other growth factors. The frequent VHL loss in ccRCC increases HIF expression, and HIFs may be an ideal candidate to overcome the TKI resistance. The combination of HIF inhibitors and immune checkpoint inhibitors is also anticipated. Various clinical trials of programmed cell death protein 1 inhibitors are planned. The present study reviews the effects of current and potential TKIs on mRCC, with a focus on VEGF/VEGFR and other targets for mRCC therapy.

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Treating <em>EGFR </em>mutation resistance in non-small cell lung cancer – role of osimertinib

Cited by 26 publications

References 51 publications

Efficacy of ozone therapy on Porphyromonas gingivalis count in chronic periodontitis: An in vivo study

Efficacy of ozone therapy on Porphyromonas gingivalis count in chronic periodontitis: An in vivo study

Effects and mechanisms of betulinic acid on improving EGFR TKI‐resistance of lung cancer cells

Crosstalk between VEGFR and other receptor tyrosine kinases for TKI therapy of metastatic renal cell carcinoma

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