Pooled analysis of the reports of erlotinib after failure of gefitinib for non-small cell lung cancer

Kaira, Kyoichi; Naito, Tateaki; Takahashi, Toshiaki; Ayabe, Eriko; Shimoyama, Rai; Kaira, Rieko; Ono, Akira; Igawa, Satoshi; Shukuya, Takehito; Murakami, Haruyasu; Tsuya, Asuka; Nakamura, Yukiko; Endo, Masahiro; Yamamoto, Nobuyuki

doi:10.1016/j.lungcan.2009.05.006

Cited by 48 publications

(46 citation statements)

References 33 publications

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“…Since EGFR was initially signalled as an attractive target for cancer chemotherapy [24], reports have shown a relationship between the presence of EGFR mutations and a better response to TK inhibitors in patients with lung adenocarcinoma and unspecified NSCLC [1][2][3][4][5][6][7][8][9][10][11][12]. Since the 2006, some reports have focused on proving that it is feasible to detect EGFR mutations in nonsurgical specimens, a particularly relevant approach considering that most patients with lung cancer have a disseminated stage of the disease at diagnosis.…”

Section: Discussionmentioning

confidence: 99%

“…n nonsmall cell lung cancer (NSCLC), the presence of somatic mutations in the part of the gene encoding the tyrosine kinase (TK) domain of the epidermal growth factor receptor (EGFR) correlates with a good response to TK inhibitors, such as gefitinib [1][2][3][4][5][6][7][8][9] or erlotinib [9][10][11][12]. These mutations consist of small in-frame deletions or substitutions clustered around the adenosinetriphosphate-binding site in exons 18, 19 and 21 of the EGFR gene.…”

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confidence: 99%

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Endobronchial ultrasound-guided transbronchial needle aspiration for identifying EGFR mutations

García-Olivé¹,

Monsó²,

Andreo³

et al. 2009

Eur Respir J

121

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The presence of somatic mutations of the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) gene in patients with advanced nonsmall cell lung cancer (NSCLC) correlates with a good response to tyrosine kinase inhibitors. The usefulness of endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) for the detection of EGFR mutations in cells recovered from malignant mediastinal nodes in patients with NSCLC was assessed.All patients with lung adenocarcinoma or unspecified NSCLC referred for staging with EBUS-TBNA were included. Nodes with a short-axis diameter of .5 mm were sampled, and genomic DNA from metastatic tumour cells was obtained for analysis of exons 19 and 21. The impact of sampling on management was assessed.EGFR gene analysis of the EBUS-TBNA sample was feasible in 26 (72.2%) out of the 36 patients with lymph node metastasis. Somatic mutations of the EGFR gene were detected in tissue obtained through EBUS-TBNA in two (10%) out of 20 patients with metastasic lung adenocarcinoma.Malignant tissue samples obtained by EBUS-TBNA from patients with nodal metastasis of NSCLC are suitable for the detection of EGFR mutations in most cases, and this technique demonstrates mutated neoplastic cells in a tenth of patients with adenocarcinoma.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Endobronchial ultrasound-guided transbronchial needle aspiration for identifying EGFR mutations

García-Olivé¹,

Monsó²,

Andreo³

et al. 2009

Eur Respir J

121

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“…In a retrospective study of patients with stage IV NSCLC who progressed after previously achieving long term disease control on EGFR TKI treatment, subsequent treatment with standard chemotherapy and, at renewed progression, retreatment with erlotinib (alone or in combination with cetuximab) was considered a viable option [132]. Several evidences support the retreatment with the same [133][134][135][136][137], or different [138][139][140][141][142][143] EGFR-TKI in patients who showed SD during 1st TKI treatment, while lower activity is reported for those patients who had PD to 1st TKI [144]. The highly heterogeneous nature of NSCLC tumours with respect to the mutations causing both the initial tumour and treatment response, which can also change in response to treatment, can create an apparent paradox whereby failure of a treatment at one stage of the disease does not mean that the same treatment might not be beneficial at a later stage.…”

Section: Re-treatment With Egfr Tkis After Having Completed Treatmentmentioning

confidence: 99%

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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“…Following gefitinib failure, most patients receive chemotherapy. However, it was recently suggested that rechallenging with an EGFR TKI after gefitinib may be effective [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

“…According to previous reports of salvage erlotinib following gefitinib failure, the PFS of erlotinib was 1.7 to 4.0 months [5,6], and the disease control rate (DCR) was 29.2% [8]. However, most reports examined a relatively small number of patients, case reports or pooled analyses of previous data [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Clinical efficacy of erlotinib, a salvage treatment for non-small cell lung cancer patients following gefitinib failure

Cho

Keam

Kim

et al. 2016

Korean J Intern Med

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Background/Aims: The purpose of this study was to identify predictive factors for erlotinib treatment in non-small cell lung cancer (NSCLC) patients following gefitinib failure. Methods: Forty-five patients with NSCLC who were treated with erlotinib following gefitinib failure at Seoul National University Hospital between August 2005 and November 2011 were enrolled. Epidermal growth factor receptor (EGFR) mutation status, pathologic findings and other clinical factors, including response to tyrosine kinase inhibitors (TKIs) and progression-free survival (PFS), were evaluated. Results: Of the 45 patients, 40 patients (88.8%) had adenocarcinoma. The following EGFR mutations were observed: five patients with a deletion of exon 19, six patients with an L858R mutation, three patients with wild-type EGFR, and 31 patients with unknown mutations. The response rate of erlotinib was 4.4%, and stable disease was 42.2%. The median PFS for erlotinib was 2.6 months (95% confidence interval, 1.4 to 3.7). Patients with a PFS ≥ 4 months during previous gefitinib treatment had a significantly longer PFS with erlotinib (3.3 months vs. 1.6 months, respectively; p < 0.01) than patients with PFS < 4 months with gefitinib. According to multivariate analyses, PFS ≥ 4 months for previous gefitinib treatment was significantly associated with prolonged PFS with erlotinib (p = 0.04). However, the response rate of gefitinib and treatment sequence were not associated with prolonged PFS with erlotinib (p = 0.28 and p = 0.67, respectively). Conclusions: Following rechallenge with the EGFR TKI erlotinib following gefitinib failure, patients who showed prolonged PFS with gefitinib benefit from erlotinib. However, further prospective studies are needed to confirm these findings.

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Pooled analysis of the reports of erlotinib after failure of gefitinib for non-small cell lung cancer

Cited by 48 publications

References 33 publications

Endobronchial ultrasound-guided transbronchial needle aspiration for identifying EGFR mutations

Endobronchial ultrasound-guided transbronchial needle aspiration for identifying EGFR mutations

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

Clinical efficacy of erlotinib, a salvage treatment for non-small cell lung cancer patients following gefitinib failure

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