scholarly journals Association between lung cancer somatic mutations and occupational exposure in never-smokers

2017 ◽  
Vol 50 (4) ◽  
pp. 1700716 ◽  
Author(s):  
Christophe Paris ◽  
Pascal Do ◽  
Bénédicte Mastroianni ◽  
Adrien Dixmier ◽  
Patrick Dumont ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Risk Factor ◽  
Occupational Exposure ◽  
Lung Cancers ◽  
Molecular Alterations ◽  
Molecular Pattern ◽  
Exhaust Fumes ◽  
Polycyclic Aromatic ◽  
Never Smokers ◽  
Molecular Patterns

Occupational exposure constitutes a common risk factor for lung cancer. We observed molecular alterations in 73% of never-smokers, 35% of men and 8% of women were exposed to at least one occupational carcinogen. We report herein associations between molecular patterns and occupational exposure.BioCAST was a cohort study of lung cancer in never-smokers that reported risk factor exposure and molecular patterns. Occupational exposure was assessed via a validated 71-item questionnaire. Patients were categorised into groups that were unexposed and exposed to polycyclic aromatic hydrocarbons (PAH), asbestos, silica, diesel exhaust fumes (DEF), chrome and paints. Test results were recorded for EGFR, KRAS, HER2, BRAF and PIK3 mutations, and ALK alterations.Overall, 313 out of 384 patients included in BioCAST were analysed. Asbestos-exposed patients displayed a significantly lower rate of EGFR mutations (20% versus 44%, p=0.033), and a higher rate of HER2 mutations (18% versus 4%, p=0.084). ALK alterations were not associated with any occupational carcinogens. The DEF-exposed patients were diagnosed with a BRAF mutation in 25% of all cases. Chrome-exposed patients exhibited enhanced HER2 and PIK3 mutation frequency.Given its minimal effects in the subgroups, we conclude that occupational exposure slightly affects the molecular pattern of lung cancers in never-smokers. In particular, asbestos-exposed patients have a lower chance of EGFR mutations.

Exposure to Polycyclic Aromatic Hydrocarbons - Risk Factor for Lung Cancer

Epidemiology ◽  
2006 ◽  
Vol 17 (Suppl) ◽  
pp. S318
Author(s):  
D Surcel ◽  
A Mocan ◽  
S Beldeanu ◽  
A David ◽  
M Botoc ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Risk Factor ◽  
Polycyclic Aromatic Hydrocarbons ◽  
Aromatic Hydrocarbons ◽  
Polycyclic Aromatic

scholarly journals Dual TMPRSS2:ERG Fusion in a Patient with Lung and Prostate Cancers

Diagnostics ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 1109
Author(s):  
Francesca Giunchi ◽  
Francesco Massari ◽  
Annalisa Altimari ◽  
Elisa Gruppioni ◽  
Elisabetta Nobili ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Objective Response ◽  
Lung Nodule ◽  
Thoracic Wall ◽  
Lung Cancers ◽  
Molecular Alterations ◽  
First Case ◽  
Prostate Cancers ◽  
Cancer Of The Prostate ◽  
Antiandrogen Therapy

The TMPRSS2:ERG fusion is considered prostate specific and has been rarely described in other tumors. We describe the case of a patient who developed lung and prostate cancers, both harboring the TMPRSS2:ERG fusion. The patient developed a cancer of the prostate with lymph node metastases and after two years a nodule of the thoracic wall. The histology and immunohistochemical profile of the two tumors were typical of prostate and lung cancers. The presence of the TMPRSS2:ERG fusion was demonstrated by next-generation sequencing on both malignancies, leading to the assumption that the lung nodule was a metastasis from the prostate cancer. The patient failed to respond to antiandrogen therapy, while chemotherapy for lung cancer led to a significant objective response. To our knowledge, this is the first case of a lung cancer harboring the TMPRSS2:ERG fusion, widening the spectrum of lung cancer-associated molecular alterations.

scholarly journals Lung cancer screening with low-dose computed tomography at a tertiary hospital in Anhui, China and secondary analysis of trial data

2020 ◽  
pp. 20200438
Author(s):  
Wulin Shan ◽  
Zhaowu Chen ◽  
Donghua Wei ◽  
Ming Li ◽  
Liting Qian
Keyword(s):  
Lung Cancer ◽  
Cancer Screening ◽  
Screening Program ◽  
Early Stage ◽  
Lung Cancer Screening ◽  
Cancer History ◽  
Lung Cancers ◽  
Family Cancer History ◽  
Never Smokers ◽  
Low Dose Computed Tomography

Objective: Lung cancer screening with low-dose computed tomography (LDCT) partly reduces cancer-specific mortality. However, few data have described this specific population for screening in mainland China. Here, we conducted a population-based screening program in Anhui, China. Methods: 9084 individuals were participating in the screening program for lung cancer in Anhui province from 1 June 2014 to 31 May 2017. LDCT was offered to all participants who joined the program. Results: Of 9084 individuals undergoing LDCT, we detected 54 lung cancers (0.594%). The age with the highest rate was 61–65 years (up to 1.016%), followed by 56–60 (0.784%). Most patients (98.1%, 53/54) were in stage I–II (early stage), and only one was in stage III (advanced stage). Adenocarcinoma, squamous cell carcinoma and small cell lung cancer accounted for 57.4% (31/54), 37% (20/54) and 5.6% (3/54) of the individuals, respectively. Notably, There were 4,102 never smokers in our study. The median age was 63 years. Males and females accounted for 53.4 and 46.6%, respectively. Among the 4102 never smokers, 96 participants had a positive family cancer history. Additionally, we detected 20 lung cancers (0.488%), slightly lower than the whole rate 0.594%. Finally, our data showed that age, smoking, family cancer history and features of nodules were risk factors for lung cancer. Conclusion: Our study qualified the efficiency of LDCT to detect early-stage lung cancers in Anhui, China. Further establishment of appropriate lung cancer screening methods specifically for individuals in China is warranted. Advances in knowledge: We evaluated the performance of lung cancer screening for asymptomatic populations using LDCT in Anhui, an eastern inland province of China. Our study qualified the efficiency of LDCT to detect early-stage lung cancers in Anhui, China.

scholarly journals MET Exon 14 Mutations in Non–Small-Cell Lung Cancer Are Associated With Advanced Age and Stage-Dependent MET Genomic Amplification and c-Met Overexpression

2016 ◽  
Vol 34 (7) ◽  
pp. 721-730 ◽  
Author(s):  
Mark M. Awad ◽  
Geoffrey R. Oxnard ◽  
David M. Jackman ◽  
Daniel O. Savukoski ◽  
Dimity Hall ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Molecular Subtype ◽  
Stage Iv ◽  
Small Cell ◽  
Chromosome 7 ◽  
Small Cell Lung ◽  
Genomic Amplification ◽  
Lung Cancers ◽  
Never Smokers ◽  
Egfr Mutant

Purpose Non–small-cell lung cancers (NSCLCs) harboring mutations in MET exon 14 and its flanking introns may respond to c-Met inhibitors. We sought to describe the clinical, pathologic, and genomic characteristics of patients with cancer with MET exon 14 mutations. Patients and Methods We interrogated next-generation sequencing results from 6,376 cancers to identify those harboring MET exon 14 mutations. Clinical characteristics of MET exon 14 mutated NSCLCs were compared with those of NSCLCs with activating mutations in KRAS and EGFR. Co-occurring genomic mutations and copy number alterations were identified. c-Met immunohistochemistry and real-time polymerase chain reaction to detect exon 14 skipping were performed where sufficient tissue was available. Results MET exon 14 mutations were identified in 28 of 933 nonsquamous NSCLCs (3.0%) and were not seen in other cancer types in this study. Patients with MET exon 14–mutated NSCLC were significantly older (median age, 72.5 years) than patients with EGFR-mutant (median age, 61 years; P < .001) or KRAS-mutant NSCLC (median age, 65 years; P < .001). Among patients with MET exon 14 mutations, 68% were women, and 36% were never-smokers. Stage IV MET exon 14–mutated NSCLCs were significantly more likely to have concurrent MET genomic amplification (mean ratio of MET to chromosome 7, 4.3) and strong c-Met immunohistochemical expression (mean H score, 253) than stage IA to IIIB MET exon 14–mutated NSCLCs (mean ratio of MET to chromosome 7, 1.4; P = .007; mean H score, 155; P = .002) and stage IV MET exon 14–wild-type NSCLCs (mean ratio of MET to chromosome 7, 1.2; P < .001; mean H score, 142; P < .001). A patient whose lung cancer harbored a MET exon 14 mutation with concurrent genomic amplification of the mutated MET allele experienced a major partial response to the c-Met inhibitor crizotinib. Conclusion MET exon 14 mutations represent a clinically unique molecular subtype of NSCLC. Prospective clinical trials with c-Met inhibitors will be necessary to validate MET exon 14 mutations as an important therapeutic target in NSCLC.

scholarly journals No impact of passive smoke on the somatic profile of lung cancers in never-smokers

2015 ◽  
Vol 45 (5) ◽  
pp. 1415-1425 ◽  
Author(s):  
Sébastien Couraud ◽  
Didier Debieuvre ◽  
Lionel Moreau ◽  
Patrick Dumont ◽  
Jacques Margery ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Passive Smoking ◽  
Smoke Exposure ◽  
Nonsignificant Trend ◽  
Lung Cancers ◽  
Significant Difference ◽  
Passive Smoke ◽  
Cumulative Duration ◽  
Never Smokers ◽  
Never Smoker

EGFR and HER2 mutations and ALK rearrangement are known to be related to lung cancer in never-smokers, while KRAS, BRAF and PIK3CA mutations are typically observed among smokers. There is still debate surrounding whether never-smokers exposed to passive smoke exhibit a “smoker-like” somatic profile compared with unexposed never-smokers.Passive smoke exposure was assessed in the French BioCAST/IFCT-1002 never-smoker lung cancer cohort and routine molecular profiles analyses were compiled.Of the 384 patients recruited into BioCAST, 319 were tested for at least one biomarker and provided data relating to passive smoking. Overall, 219 (66%) reported having been exposed to passive smoking. No significant difference was observed between mutation frequency and passive smoke exposure (EGFR mutation: 46% in never exposed versus 41% in ever exposed; KRAS: 7% versus 7%; ALK: 13% versus 11%; HER2: 4% versus 5%; BRAF: 6% versus 5%; PIK3CA: 4% versus 2%). We observed a nonsignificant trend for a negative association between EGFR mutation and cumulative duration of passive smoke exposure. No association was found for other biomarkers.There is no clear association between passive smoke exposure and somatic profile in lifelong, never-smoker lung cancer.

EXPOSURE TO POLYCYCLIC AROMATIC HIDROCARBONS - RISK FACTOR FOR LUNG CANCER

Epidemiology ◽  
2004 ◽  
Vol 15 (4) ◽  
pp. S164
Author(s):  
Didi Surcel ◽  
Beldean Simion ◽  
Aurel Mocan
Keyword(s):  
Lung Cancer ◽  
Risk Factor ◽  
Polycyclic Aromatic

Smoking and estrogen plus progestin (E+P) and lung cancer incidence and mortality.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 1524-1524
Author(s):  
Rowan T. Chlebowski ◽  
Heather A. Wakelee ◽  
Thomas E Rohan ◽  
Jingmin Liu ◽  
Michael S. Simon ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Clinical Trial ◽  
Cancer Incidence ◽  
Smoking Status ◽  
Controlled Clinical Trial ◽  
Lung Cancer Incidence ◽  
Lung Cancers ◽  
Risk Of Death ◽  
Incidence And Mortality ◽  
Never Smokers

1524 Background: In the Women’s Health Initiative (WHI) randomized, placebo-controlled clinical trial, E+P increased deaths from lung cancer (those cancer-attributed) and after lung cancer (regardless of cause) (Lancet 2009:374:1243). To examine smoking status influence on this process, a cohort combining WHI clinical trial (CT) and observational study (OS) participants, the latter meeting criteria as in the CT, was identified to examine E+P associations with lung cancer incidence and outcome. Methods: 31,966 postmenopausal women (12,299 CT, 19,668 OS) with no prior hysterectomy and no prior hormone therapy use were classified at baseline as not hormone users or E+P users and as current or never smokers. Lung cancers were verified by medical record review. Multi-variant adjusted Cox proportional hazards regression, including pack-year use, calculated hazard ratios (HRs, 95% confidence intervals [CI]) for groups defined by smoking status and E+P use for lung cancer incidence, deaths from lung cancer and deaths after lung cancer. Results: After 12 years mean follow-up, 664 lung cancers were diagnosed with 444 deaths from lung cancer and 513 deaths after lung cancer. Analyzed from cohort entry; see Table. In nonusers of E+P, lung cancer incidence, deaths from lung cancer, and deaths after lung cancer were significantly and substantially greater in current smokers vs never smokers (p< .0001 for all comparisons). In current smokers, lung cancer incidence, deaths from lung cancer and deaths after lung cancer were significantly and substantially greater in E+P users vs non-users (p=.0021, .0005 and .0002, respectively). Conclusions: E+P use in current smokers nearly doubles their already high risk of death from and after lung cancer. Based on this risk, current smokers should not use E+P. [Table: see text]

Comparison of the characteristics and clinical course of 677 patients with metastatic lung cancers with mutations in KRAS codons 12 and 13.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 8025-8025 ◽  
Author(s):  
Helena Alexandra Yu ◽  
Camelia S. Sima ◽  
Ronglai Shen ◽  
Samantha Lindsay Kass ◽  
Mark G. Kris ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Overall Survival ◽  
Amino Acid ◽  
Smoking Status ◽  
Specific Amino Acid ◽  
Lung Cancers ◽  
Specific Amino Acid Substitution ◽  
Metastatic Lung ◽  
Never Smokers ◽  
Kras Codon

8025 Background: Patients (pts) with KRAS mutant lung cancers have a shorter survival compared to pts with KRAS/EGFR wild type tumors (Johnson et al, Cancer 2012). Whether outcomes for patients with KRAS mutant metastatic lung cancers differ by smoking status or specific amino acid substitution is unknown. In order to understand the impact of KRAS mutation subtype in the metastatic setting, we analyzed a large cohort of patients with KRAS mutant metastatic lung cancer. Methods: We identified all pts with KRAS mutant metastatic or recurrent lung cancers from Feb 2005 to Aug 2011. KRAS mutation type, clinical characteristics, and outcomes from diagnosis were obtained from the medical record. A multivariate cox proportion hazard model was used to identify factors associated with overall survival. Results: KRAS mutations were identified in 677 pts (53 at codon 13, 624 at codon 12). Median age: 66 (range 31-89), women: 62%, never smokers: 7%. Pts with transition mutations (n=157) were more likely to be never-smokers (p<0.0001). There was no difference in outcome for pts with KRAS transition versus transversion mutations (p=1) or when comparing current/former smokers to never smokers (p=0.33). There was no difference in overall survival (OS) when comparing specific amino acid substitutions (G12C=366, G12V=141, G12D=114, G12A=68, G13C=27, G13D=23, G12S=19, G12F=11)(p=0.20). Pts with KRAS codon 13 mutant tumors had inferior OS compared to pts with codon 12 mutant tumors, median 13 months (mo) (95% CI 13-17 mo) and 16 mo (95% CI 9-16 mo), respectively (p=0.009). There was no difference in frequency of receiving platinum-based chemotherapy or chemotherapy of any kind between pts with codon 12 and 13 mutant tumors. In a multivariate Cox model which included age, gender and smoking status, KRAS codon 13 mutation was associated with worse overall survival than KRAS codon 12 mutation (HR 1.52 95% CI 1.11-2.08 p=0.008). Conclusions: Among pts with KRAS mutant metastatic lung cancers, smoking history, and specific amino acid substitution do not affect outcome. Patients with KRAS codon 13 mutant metastatic lung cancer have shorter survival compared to pts with KRAS codon 12 mutant lung cancer.

scholarly journals Whole-Genome Sequencing of Asian Lung Cancers: Second-Hand Smoke Unlikely to Be Responsible for Higher Incidence of Lung Cancer among Asian Never-Smokers

2014 ◽  
Vol 74 (21) ◽  
pp. 6071-6081 ◽  
Author(s):  
Vidhya G. Krishnan ◽  
Philip J. Ebert ◽  
Jason C. Ting ◽  
Elaine Lim ◽  
Swee-Seong Wong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Whole Genome Sequencing ◽  
Genome Sequencing ◽  
Second Hand Smoke ◽  
Whole Genome ◽  
Lung Cancers ◽  
Never Smokers
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