Phase II trial evaluating addition of fulvestrant to erlotinib in patients with stage IIIb/IV non-small cell lung cancer (NSCLC) who are stable on erlotinib and exhibit immunohistochemical (IHC) or PCR positivity for estrogen or progesterone receptor (PR).

Bazhenova, Lyudmila; Quintana, R.; Hastings, Randolph H.; Messer, K.

doi:10.1200/jco.2010.28.15_suppl.tps294

Cited by 2 publications

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“…In fact, ERs are expressed independently of gender and histology [118] and oestrogens stimulate growth of NSCLC cells and tumour xenografts [118,119]. EGFR and ER pathways share signalling molecules; thus, activation of EGFR results in activation of ERs.…”

Section: Controlling Oestrogensmentioning

confidence: 99%

“…EGFR and ER pathways share signalling molecules; thus, activation of EGFR results in activation of ERs. Studies in cell cultures and xenographic models have shown that the combination of the ER antagonist, fulvestrant and gefitinib resulted in an additional inhibition of growth [118,120]. In an analysis of 317 NSCLC tumours it has been shown that oestrogen receptor a and b expression distinguishes a subset of NSCLC that has defined clinicopathologic and genetic features.…”

Section: Controlling Oestrogensmentioning

confidence: 99%

“…These findings suggest the possibility of treating this population by targeting both hormonal factors and genetic abnormalities [122]. Several Phase II trials are evaluating the hypothesis that the combination of fulvestrant and an EGFR inhibitor, such as erlotinib [118,119] or gefitinib [117] will provide improved efficacy over the EGFR inhibitor alone in NSCLC patients.…”

Section: Controlling Oestrogensmentioning

confidence: 99%

See 2 more Smart Citations

Novel therapeutic strategies for patients with NSCLC that do not respond to treatment with EGFR inhibitors

Rolfo

Giovannetti

Hong

et al. 2014

Cancer Treatment Reviews

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a b s t r a c tIntroduction: Treatment with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) yields tumour responses in non-small cell lung cancer (NSCLC) patients harbouring activating EGFR mutations. However, even in long-lasting responses, resistance to EGFR TKIs invariably occurs. Areas covered: This review examines resistance mechanisms to EGFR TKI treatment, which mainly arise from secondary EGFR mutations. Other resistance-inducing processes include mesenchymal-epithelial transition factor (MET) amplification, epithelial-mesenchymal transformation, phenotypic change from NSCLC to small-cell lung carcinoma, and modifications in parallel signalling pathways. Current therapeutic strategies to overcome these EGFR TKI resistance mechanisms focus on the inhibition or blocking of multiple members of the ErbB family. Several molecules which target multiple ErbB receptors are being investigated in NSCLC and other indications including afatinib, an ErbB Family Blocker, as well as dacomitinib and lapatinib. Novel, non-quinazoline, EGFR inhibitors, that also target EGFR activating and resistance (T790M) mutations, are currently under clinical development. Other therapeutic strategies include inhibition of parallel and downstream pathways, using agents which target heat shock protein (HSP)90 or http://dx.doi.org/10.1016/j.ctrv.2014.05.009 0305-7372/Ó 2014 Elsevier Ltd. All rights reserved.Abbreviations: AEG-1, astrocyte elevated gene-1; ALK, anaplastic lymphoma kinase; ATP, adenosine triphosphate; BARD1, BRCA1-associated protein 1; BIM, B-cell lymphoma 2 interacting mediator of cell death; BRAF, v-raf murine sarcoma viral oncogene homolog B1; BRCA1, breast cancer 1, early onset; CNS, central nervous system; CRKL, crk-like protein; DCR, disease control rate; EGFR, epidermal growth factor receptor; EMT, epithelial-mesenchymal transformation; EphB4, ephrin type-B receptor 4; ER, oestrogen receptor; ERK, extracellular-signal-regulated kinases; HER, human epidermal growth factor receptor; HGF, hepatocyte growth factor; HSP90, heat shock protein 90; IGF-1R, insulin-like growth factor 1 receptor; KRAS, Kirsten rat sarcoma viral oncogene homologue; MBP-QP, mutation-biased PCR quenching probe; MEK, mitogen-activated protein kinase; MET, mesenchymal-epithelial transition factor; mRNA, messenger RNA; mTOR, mammalian target of rapamycin; NF-jB, nuclear factor kappa-light-chainenhancer of activated B cells; NSCLC, non-small-cell lung cancer; ORR, overall response rate; OS, overall survival; PARP, poly (ADP-ribose) polymerase; PCR, polymerase chain reaction; PFS, progression free survival; PI3K, phosphoinositide-3-kinase; PIK3CA, phosphoinositide-3-kinase, catalytic, alpha polypeptide; PTEN, phosphatase and tensin homologue; RECIST, Response Evaluation Criteria in Solid Tumours; RR, response rate; SCLC, small-cell lung cancer; TGF, transforming growth factor; TKI, tyrosine kinase inhibitors; VEGF, vascular endothelial growth factor; VEGFR, VEGF receptor. E-mail address: christian.rolfo@uza.be (C. Rolfo).Can...

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Section: Controlling Oestrogensmentioning

confidence: 99%

Section: Controlling Oestrogensmentioning

confidence: 99%