scholarly journals Association between family history and lung cancer risk among Chinese women in Singapore

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xin Yin ◽  
Cheryl Pui Yi Chan ◽  
Adeline Seow ◽  
Wai-Ping Yau ◽  
Wei Jie Seow

AbstractRisk factors of lung cancer unrelated to smoking are not well-studied, especially among women. Family history has been shown to play a role in predisposing individuals to lung cancer, but this relationship has not been investigated in the Southeast Asian population. A total of 1159 women were recruited in a case–control study conducted in public hospitals in Singapore from 2005 to 2008. After excluding participants with incomplete family history information, 374 cases and 785 controls remained in the final analysis. Adjusted odds ratios (aORs) and 95% confidence intervals (CIs) were calculated using logistic regression, adjusting for potential confounders. Overall, family history of lung cancer was associated with a higher risk for lung cancer (aOR 2.08, 95% CI 1.25–3.47). When stratified by smoking status, a significant association was observed among never-smokers (aOR 2.78, 95% CI 1.57–4.90). Further stratification by fruit consumption identified a significant association between family history of lung cancer and higher risk of lung cancer among never-smokers who had low fruit consumption (aOR 3.09, 95% CI 1.37–7.01). Our findings suggest that family history of lung cancer is a significant risk factor for lung cancer in Singaporean Chinese women, especially among never-smokers.

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Xifeng Wu ◽  
Chi Pang Wen ◽  
Yuanqing Ye ◽  
MinKwang Tsai ◽  
Christopher Wen ◽  
...  

Abstract The objective of this study was to develop markedly improved risk prediction models for lung cancer using a prospective cohort of 395,875 participants in Taiwan. Discriminatory accuracy was measured by generation of receiver operator curves and estimation of area under the curve (AUC). In multivariate Cox regression analysis, age, gender, smoking pack-years, family history of lung cancer, personal cancer history, BMI, lung function test, and serum biomarkers such as carcinoembryonic antigen (CEA), bilirubin, alpha fetoprotein (AFP), and c-reactive protein (CRP) were identified and included in an integrative risk prediction model. The AUC in overall population was 0.851 (95% CI = 0.840–0.862), with never smokers 0.806 (95% CI = 0.790–0.819), light smokers 0.847 (95% CI = 0.824–0.871), and heavy smokers 0.732 (95% CI = 0.708–0.752). By integrating risk factors such as family history of lung cancer, CEA and AFP for light smokers, and lung function test (Maximum Mid-Expiratory Flow, MMEF25–75%), AFP and CEA for never smokers, light and never smokers with cancer risks as high as those within heavy smokers could be identified. The risk model for heavy smokers can allow us to stratify heavy smokers into subgroups with distinct risks, which, if applied to low-dose computed tomography (LDCT) screening, may greatly reduce false positives.


2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 7579-7579
Author(s):  
Elizabeth Mary Gaughan ◽  
Sarah K Cryer ◽  
Beow Yong Yeap ◽  
David Michael Jackman ◽  
Daniel Botelho Costa

7579 Background: Inherited susceptibility to lung cancer is an understudied subject, however it has been described among never smokers (<100 cigarettes/lifetime). Never smokers with NSCLC comprise an important subgroup of patients enriched for tumors harboring oncogene aberrations in the EGFR and ALK genes. We aimed to better characterize the incidence of family history of lung cancer in the setting of routine tumor genotyping among never smokers with NSCLC. Methods: Clinicopathologic data plus tumor genotype (EGFR, KRAS, ALK) from 230 consecutive never smokers seen at Beth Israel Deaconess Medical Center and Dana-Farber Cancer Institute was compiled. We retrospectively analyzed the incidence of a family history of any cancer and lung cancer in these patients. Results: In our cohort, the average age was 56 years, 67% of the patients were women, 75% were white, 41% had advanced NSCLC and 87% had adenocarcinoma histology. In these tumors, 98/230 (43%) had an EGFR mutation, 16/155 (10%) had KRAS mutations and 27/127 (17%) had an ALK translocation. Family history of any cancer was common (57%) and specific family history of lung cancer was present in 42/230 cases (18%). Out of thecases with a family history of any cancer, 22/53 (41.5%) EGFR-mutated, 1/6 (17%) KRAS-mutated and 3/20 (15%) ALK-translocated cohorts had a family history of lung cancer. The rate of family history of lung cancer to family history of cancer was significantly higher in the EGFR-mutated cohort when compared to the ALK translocated plus KRAS-mutated cohorts (p=0.023). Conclusions: Family history of lung cancer is common in never smokers with NSCLC, and there seems to be a particular link in families in which the proband has an EGFR-mutated tumor. Further study of families with EGFR-mutated NSCLC may yield insights into the pathogenesis of this tumor type.


Lung Cancer ◽  
2013 ◽  
Vol 79 (3) ◽  
pp. 193-197 ◽  
Author(s):  
Elizabeth M. Gaughan ◽  
Sarah K. Cryer ◽  
Beow Y. Yeap ◽  
David M. Jackman ◽  
Daniel B. Costa

2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S150-S150
Author(s):  
H Li ◽  
M Arslan ◽  
Z Fu ◽  
H Lee ◽  
M Mikula

Abstract Introduction/Objective A subset of patients with an established diagnosis of UC develops signs of CD (de novo CD) following IPAA. While the etiology and risk factors of de novo CD remain largely unknown, preliminary studies have shown controversial results regarding family history of inflammatory bowel disease (IBD) and smoking history. Methods Patients that underwent IPAA for UC, with at least 1 year of follow-up, were identified (n=161; 1996 to 2018). We retrospectively reviewed the electronic medical records. Patients that were diagnosed with de novo CD during the follow-up period were further identified. Smoking history and family history of IBD were evaluated. Chi square test was performed to compare the frequencies. Odds ratio (OR) and 95% confidence intervals (CIs) were estimated by logistic regression model. P&lt;0.05 was considered statistically significant. Results 29 de novo CD were identified. At the time of proctocolectomy, the family history of IBD and smoking history was documented in 152 UC patients including 27 that subsequently developed de novo CD. 23 of 152 had a family history of IBD (12 UC, 9 CD and 2 IBD, NOS). 19/129 (14.7%) UC patients without a family history of any type of IBD, 4/9 (44.4%) with a family history of CD, and 4/12 (33.3%) with a family history of UC developed de novo CD. Patients with a family history of CD were more likely to develop de novo CD post IPAA than those without a family history of any type of IBD (OR 4.63, 95% CI 1.14-18.82, p=0.03). Family history of UC did not correlate with development of de novo CD (OR 2.90; 95% CI 0.79-10.57, p=0.108). At the time of proctocoletomy, 11 were current smokers, 25 were former smokers, and 116 never smoked. In de novo CD group, there were 4/27 (14.8 %) former smokers and 23/27 (85.2 %) never smokers. No de novo CD patient was current smoker. In the UC group that remained as UC following IPAA, 11/125 (8.8%) were current smokers, 21/125 (16.8 %) former smokers, and 93/125 (74.4 %) were never smokers. Current smoking status was not associated with development of de novo CD (p = 0.214). Conclusion Family history of CD may be a risk factor for developing de novo CD following IPAA for UC. Current smoking status was not associated with development of de novo CD following IPAA for UC.


2012 ◽  
Vol 13 (1) ◽  
pp. 75-79 ◽  
Author(s):  
Yu Kurahara ◽  
Tomoya Kawaguchi ◽  
Kazunobu Tachibana ◽  
Shinji Atagi ◽  
Seiji Hayashi ◽  
...  

2007 ◽  
Vol 16 (11) ◽  
pp. 2432-2435 ◽  
Author(s):  
Y. Zhang ◽  
X.-O. Shu ◽  
Y.-T. Gao ◽  
B.-T. Ji ◽  
G. Yang ◽  
...  

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 1570-1570
Author(s):  
Vijaya Raj Bhatt ◽  
Fausto R. Loberiza ◽  
Apar Kishor Ganti

1570 Background: Although a well-established risk factor for lung cancer, the impact of smoking on the survival of non-small cell lung cancer (NSCLC) is not well-known. This study evaluated the effects of tobacco exposure on outcomes from NSCLC. Methods: We performed a retrospective analysis of Veteran’s Affairs Comprehensive Cancer Registry of NSCLC patients diagnosed between 1995 and 2009. Data abstracted included age, gender, family history, stage at diagnosis, histology, tumor grade, smoking history, other exposures, treatment received and overall survival (OS). Smoking status was categorized as never-smoker, past-smoker and current-smoker based on the self-reported history at diagnosis. Multivariate analysis was performed using SAS version 10.2. Results: The study population (n=61,440) comprised predominantly of males (98%), of which Caucasians (81%) formed the majority. The median age at diagnosis within this cohort was 68 years (range: 22-108 years) and median follow-up was 6 months (range: <1 – 161 months). Squamous cell carcinoma (35%) and adenocarcinoma (30%) were the most common histologies. The majority (71%) presented with stage III or IV disease. Positive family history was identified in one-third. Current smokers were diagnosed with NSCLC at a younger age (65 yrs) compared to never-smokers (71 yrs) and past-smokers (72 yrs) (p<0.001). After adjusting for age at diagnosis, grade, histology, family history and treatment, current-smokers (n=34613) [Hazard ratio (HR) 1.059; 95% CI, 1.012-1.108], but not past-smokers (n=23864) (HR 1.008; 95% CI, 0.962-1.056), had worse OS for Stage III and IV NSCLC, compared to never-smokers (n=2963). Smoking status was not prognostic in stage I and II NSCLC. Conclusions: Current smokers were 6 years younger than never-smokers at diagnosis of NSCLC. Although current smoking was associated with worse prognosis, especially in stages III and IV, the impact of smoking status on OS was modest, at least in males. Therefore, primary prevention of smoking cessation is more likely to be meaningful than efforts on smoking cessation after the diagnosis of NSCLC.


Lung Cancer ◽  
2015 ◽  
Vol 89 (2) ◽  
pp. 94-98 ◽  
Author(s):  
Huan Lin ◽  
Yi-Sheng Huang ◽  
Hong-hong Yan ◽  
Xue-Ning Yang ◽  
Wen-Zhao Zhong ◽  
...  

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