Prevalence of EGFR mutations in newly diagnosed locally advanced or metastatic non-small cell lung cancer Spanish patients and its association with histological subtypes and clinical features: The Spanish REASON study

Esteban, Emilio; Majem, Margarita; Aguillo, Maite Martinez; Banaclocha, N. Martínez; Dómine, Manuel; Aldaravi, L. Gómez; Juan, Óscar; Cajal, R.; Arenas, Meritxell; Provencio, Mariano

doi:10.1016/j.canep.2015.02.003

Cited by 37 publications

(26 citation statements)

References 30 publications

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“…We did not find differences among histotypes with regard EGFR status, while Kras mutations were found only among adenocarcinomas. Consistently with literature, EGFR mutations were more frequent in never smokers, while Kras mutations were present only in smokers [7,36,38].…”

Section: Discussionsupporting

confidence: 91%

“…Published data show a large variation of mutations in tumor samples, ranging between 7% and 45% for EGFR [26,35,36] and between 7% and 23% for Kras [25,26]. In Western countries, a higher percentage of Kras mutations (30-50%) was found in adenocarcinomas with respect to the other histotypes, while the mutation rate of EGFR tended to be low (3% to 12%) [37,38]. We did not find differences among histotypes with regard EGFR status, while Kras mutations were found only among adenocarcinomas.…”

Section: Discussionmentioning

confidence: 99%

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Outcome of EGFR inhibitors treatment in advanced NSCLC patients, not enrolled in clinical trials

Filiberti

Taveggia²,

Bruzzone³

et al. 2017

neo

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Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have become a treatment after first-line chemotherapy in patients with advanced NSCLC. We assessed the predictive and prognostic role of EGFR and Kras mutations in NSCLC patients treated with TKIs after progression, not included in clinical trials. Gefitinib 250 mg or Erlotinib 150 mg per os were administered to 70 patients. Radiological assessment was performed every six weeks. EGFR and Kras mutations were found in 21.4% and 24.3% of patients, respectively. At multivariate analysis, Kras mutation was positively associated with progression-free survival (PFS; HR=0.71, 95% CI: 0.53-0.96; p=0.027) and, less clearly, with response (OR=1.84, 95% CI: 0.98-3.45; p=0.057) and survival (HR=0.74, 95% CI:0.54-1.02; p=0.066). EGFR mutation influenced positively PFS (HR=0.69, 95% CI: 0.47-1.02; p=0.06), but not survival. In conclusion, in our unselected patients mutation of Kras correlated with a better outcome. The small number of patients may explain some discrepancies with data in literature.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Outcome of EGFR inhibitors treatment in advanced NSCLC patients, not enrolled in clinical trials

Filiberti

Taveggia²,

Bruzzone³

et al. 2017

neo

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show abstract

“…A woman with an affected parent has a higher risk than a man of developing lung cancer, and the molecular profile and prognosis of the disease in women differs from that in men [23]. A key driver of lung adenocarcinoma tumorigenesis especially in never-smoker women is somatic mutation of EGFR [24,25].…”

Section: Introductionmentioning

confidence: 99%

Germline mutations in young non-smoking women with lung adenocarcinoma

et al. 2018

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Potentially pathogenic variants were found in eight Cancer Gene Census germline genes: BRCA1, BRCA2, ERCC4, EXT1, HNF1 A, PTCH1, SMARCB1 and TP53. The variants in TP53, BRCA1, and BRCA2 are likely to have contributed to the early onset lung cancer in the respective patients (3/21 or 14%). This supports the notion that lung adenocarcinoma can be a component of certain cancer predisposition syndromes. Fifteen genes displayed potentially pathogenic mutations in at least two patients: ABCC10, ATP7B, CACNA1S, CFTR, CLIP4, COL6A1, COL6A6, GCN1, GJB6, RYR1, SCN7A, SEC24A, SP100, TTN and USH2A. Four patients showed a mutation in COL6A1, three in CLIP4 and two in the rest of the genes. Some of these candidate genes may explain a subset of female lung adenocarcinoma.

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“…2 Genes implicated in CPAM, PPB and BAC [14,30,31,32,33,34,35,127,137,138,139,140,141,142,143]. TTF1 = Thyroid transcription factor 1; PDGF-B = platelet-derived growth factor B; FABP-7 = fatty acid-binding protein 7; GDNF = glial cell-derived neurotrophic factor; Shh = sonic hedgehog; FGFR2b = FGF receptor-2b; FHIT = fragile histidine triad; Rb = retinoblastoma protein; EGFR = epidermal growth factor receptor. …”

Section: Managementmentioning

confidence: 99%

Prenatal and Postnatal Management of Congenital Pulmonary Airway Malformation

2016

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Congenital pulmonary airway malformation (CPAM) is one of the most common lung lesions detected prenatally. Despite the research efforts made in the past few years, controversy and lack of clarity in the literature still exist regarding nomenclature, classification, pathogenesis and the management of CPAM. Therefore, it is of greatest importance to delineate the natural history of CPAMs and to create a consensus to guide the management and follow-up of these lesions. This review will focus on classification systems, highlighting the most recent advancements in pathogenesis, and current practice in the prenatal diagnosis of CPAM. Strategies of prenatal management and postnatal management will be reviewed. Long-term follow-up, including lung cancer risk, is discussed and an outcome perspective is presented.

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Prevalence of EGFR mutations in newly diagnosed locally advanced or metastatic non-small cell lung cancer Spanish patients and its association with histological subtypes and clinical features: The Spanish REASON study

Cited by 37 publications

References 30 publications

Outcome of EGFR inhibitors treatment in advanced NSCLC patients, not enrolled in clinical trials

Outcome of EGFR inhibitors treatment in advanced NSCLC patients, not enrolled in clinical trials

Germline mutations in young non-smoking women with lung adenocarcinoma

Prenatal and Postnatal Management of Congenital Pulmonary Airway Malformation

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