Identification of AEG-1 and BARD1 as predictors of erlotinib outcome in EGFR-mutant non-small cell lung cancer (NSCLC) by NanoString multiple target profiling.

Tarón, Miquel; Benlloch, Susana; Rosell, R.; Sánchez, José Javier; Costa, Carlota; Capitan, Ana Gimenez; Mayo, Carlos A.; Bertrán-Alamillo, Jordi; Molina, Matias; Massutí, B.; Camps, Carlos; Majem, Margarita; Isla, D.; Santarpia, M.; Viteri, Santiago; Gasco, Amaya; Morán, Teresa; Carcereny, Enric; Queralt, Cristina; Aguirre, Itziar de

doi:10.1200/jco.2011.29.15_suppl.7589

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“…Aside from BRCA1, other genes potentially involved in erlotinib resistance have been explored using NanoString Ò [62]. This tool utilises digital technology based on a direct multiplexed measurement of targeted gene expression, allowing the expression analysis of 48 genes in a single reaction.…”

Section: New Polymerase Chain Reaction Techniquesmentioning

confidence: 99%

“…This tool utilises digital technology based on a direct multiplexed measurement of targeted gene expression, allowing the expression analysis of 48 genes in a single reaction. Using NanoString Ò , both BRCA1-associated protein 1 (BARD1) and astrocyte elevated gene-1 (AEG-1) were found to predict PFS in erlotinib-treated EGFRmutant NSCLC [62]. Hence, wider adoption of NanoString Ò may have important implications for optimal NSCLC management.…”

Section: New Polymerase Chain Reaction Techniquesmentioning

confidence: 99%

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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: New Polymerase Chain Reaction Techniquesmentioning

confidence: 99%

Section: New Polymerase Chain Reaction Techniquesmentioning

confidence: 99%