Evidence for Disease Control with Erlotinib after Gefitinib Failure in Typical Gefitinib-Sensitive Asian Patients with Non-small Cell Lung Cancer

Wong, Alvin Seng Cheong; Soong, Richie; Seah, S.K.W.; Lim, Siew-Woon; Chuah, K.L.; Nga, Min‐En; Chin, Tan-Min; Soo, Ross A.

doi:10.1097/jto.0b013e318168c801

Cited by 54 publications

(52 citation statements)

References 27 publications

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“…Certain clinical characteristics, including response or time to progression (TTP) to previous EGFR-TKI, chemotherapy between EGFR-TKIs, and EGFR-TKI free interval have been examined as predictive markers for the success of EGFR-TKI re-challenge (16)(17)(18)(19)(20)(21). The association between the occurrence of disease control (PR or SD), previous EGFR-TKI and to EGFR-TKI re-challenge has been described frequently, but other markers are controversial.…”

Section: Discussionmentioning

confidence: 99%

“…When evaluation of the efficacy of EGFR-TKI re-challenge was limited to patients who achieved good control of disease with the first line of EGFR-TKI, disease control rate and PFS were 56-73% and 3.4-5.6 months, respectively (16)(17)(18)(19)(20)(21). On the other hand, patients whose disease was not be controlled with the first line of EGFR-TKI tended to exhibit poor efficacy with re-challenge (19,20,(22)(23)(24). From these results, the effect of first EGFR-TKI may be considered a predictive marker of efficacy of re-challenge, but specific molecular markers associated with mechanisms of acquired resistance have not been identified.…”

Section: Introductionmentioning

confidence: 99%

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Plasma T790M and HGF as potential predictive markers for EGFR-TKI re-challenge

et al. 2017

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Abstract. Re-challenge with epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) has been suggested to potentially improve survival in certain populations of patients with advanced lung cancer, but predictive markers for the success of EGFR-TKI re-challenge have not been identified. The present study analyzed 16 re-challenges with EGFR-TKI undertaken in 12 patients with lung adenocarcinoma by investigating T790M and hepatocyte growth factor (HGF) in plasma coupled with clinical characteristics. EGFR mutations in plasma DNA were detected using the wild inhibiting PCR and quenched probe system for exon 19 deletions, and T790M and L858R were detected using the mutation-biased PCR and quenched probe system. HGF levels in the plasma were measured by enzyme-linked immunosorbent assay, and the ratio of HGF levels prior to re-challenge to those prior to the previous EGFR-TKI treatment was calculated. Two re-challenges demonstrated partial response, six remained as stable disease and eight had progressive disease (PD). A total of 4 of the 5 patients with a history of T790M positivity based on plasma DNA levels had PD. A total of 7 of the 8 patients who had ≥1.5-fold elevation of HGF prior to re-challenge with EGFR-TKI suffered PD. Elevation of the HGF ratio to ≥1.5 was significantly associated with poor response to EGFR-TKI re-challenge. Having no history of T790M and an HGF ratio <1.5 was significantly associated with a positive response to EGFR-TKI re-challenge. A combination of T790M detection and HGF quantification using plasma is a potentially useful assay system for predicting the effect of EGFR-TKI re-challenge. Future prospective studies are required to confirm the predictive validity of these markers. IntroductionEpidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) have produced dramatic anti-cancer effects in patients with non-small cell lung cancer (NSCLC) carrying EGFR activating mutations (1-3). The first generation of EGFR-TKIs, including gefitinib and elrotinib, conferred significantly prolonged progression-free survival (PFS) in these patients. The second generation of these drugs, afatinib, brought a remarkable prolongation of overall survival, up to 33 months, in particular in patients with exon 19 deletions (4). In spite of the effectiveness of EGFR-TKIs, patients eventually acquire resistance. Several treatment strategies have been evaluated in clinical trials and practice following the onset of acquired resistance. First, agents targeted at molecules contributing to acquired resistance have been considered. Based on mechanisms including the secondary EGFR mutation, T790M, MET proto-oncogene, receptor tyrosine kinase (MET) amplification, and hepatocyte growth factor (HGF) overexpression, second and third generation EGFR-TKIs and MET inhibitors have been developed (5-9). Afatinib confers a potent anti-cancer effect against lung cancer cells harboring T790M, but a phase 2b/3 randomized trial revealed that the overall response rate and PFS of patients with lung cancer ...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Plasma T790M and HGF as potential predictive markers for EGFR-TKI re-challenge

et al. 2017

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“…Tarceva is the only one that possesses a survival advantage in treating lung cancer (21,22). It is a new targeted therapy drug which can be selected after failed first-or second-line chemotherapy in patients with progressive and metastatic NSCLC (Tarceva received a certification license in the US in 2004 and in the European Union in 2005, respectively).…”

Section: Introductionmentioning

confidence: 99%

“…In 2004, Lynch et al (24) and Paez et al (25) reported that EGFR mutations in lung cancer cells were a prerequisite for targeted drugs. That EGFR mutations are closely related to targeted therapy in NSCLC is widely recognized (13,18,(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28).…”

Section: Introductionmentioning

confidence: 99%

EGFR mutations predict a favorable outcome for malignant pleural effusion of lung adenocarcinoma with Tarceva therapy

Guo

Wan²,

Tian³

et al. 2011

Oncol Rep

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Abstract. The aim of the present study was to evaluate the therapeutic effects and adverse reactions of Tarceva treatment for malignant pleural effusion (MPE) caused by metastatic lung adenocarcinomas. One hundred and twenty-eight patients who failed first-line chemotherapy drug treatment were divided into a mutation and a non-mutation group according to the presence or absence of epidermal growth factor receptor (EGFR) mutations. Each patient received closed drainage combined with simple negative pressure suction after thoracoscopic talc poudrage pleurodesis and oral Tarceva treatment. Short-term and long-term clinical therapeutic effects of Tarceva were evaluated. The EGFR mutation rate in pleural metastatic tissues of lung adenocarcinoma acquired through video-assisted thoracoscopic surgery was higher compared to that in surgical resection specimens, plasma specimens and pleural effusion specimens compared to previously reported results. There were significant statistical differences in the average extubation time (p<0.01), drainage volume of pleural effusion (p<0.05), Karnofsky score and formation of encapsulated pleural effusion 4 weeks after surgery (p<0.05) between these two groups. The number of patients with mild pleural hypertrophy in the mutation group was significantly higher compared to the non-mutation group (p<0.01), while the number of patients with severe pleural hypertrophy was significantly reduced (p<0.05). There was significant statistical discrepancy between these two groups in terms of improvement of peripheral blood carcinoembryonic antigen and tissue polypeptide antigen after 4 weeks of therapy. The complete remission rate and the efficacy rate were higher in the mutation group compared to that in the non-mutation group (p<0.05). There was a longer overall survival time after Tarceva treatment in patients with EGFR mutations than those without EGFR mutation. EGFR mutations predict a favorable outcome for malignant pleural effusion of lung adenocarcinoma with Tarceva therapy. Detection of EGFR mutations may determine the responsiveness of malignant pleural effusion to Tarceva treatment.

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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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Evidence for Disease Control with Erlotinib after Gefitinib Failure in Typical Gefitinib-Sensitive Asian Patients with Non-small Cell Lung Cancer

Abstract: A significant proportion of typical gefitinib-sensitive Asian NSCLC patients can have disease control with erlotinib after gefitinib failure. The role of subsequent administration of a second EGFR TKI after failure of the first TKI in advanced NSCLC should be further pursued.

Cited by 54 publications

References 27 publications

Plasma T790M and HGF as potential predictive markers for EGFR-TKI re-challenge

Plasma T790M and HGF as potential predictive markers for EGFR-TKI re-challenge

EGFR mutations predict a favorable outcome for malignant pleural effusion of lung adenocarcinoma with Tarceva therapy

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

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