Zhang, Zuo‐Feng

Abstract Background: Although colorectal cancer survival rates are improving, the risk of incident type 2 diabetes mellitus (T2D) among Asian, Native Hawaiian, and Pacific Islander (ANHPI) ethnic groups is poorly understood. This study aims to identify high-risk groups and quantify the risk across different periods. Methods: Using the SEER–Medicare database, colorectal cancer survivors who were ANHPI were matched to non-Hispanic White (NHW) survivors at a ratio of 1:3. Multivariable Cox regression models computed HRs and 95% confidence intervals (CI) for incident T2D. Results: The study included 6,463 NHW and 2,901 ANHPI colorectal cancer survivors diagnosed between 2000 and 2017. Among them, 715 NHW and 484 ANHPI developed T2D during 39,097 and 10,769 person-years of follow-up, respectively. ANHPI colorectal cancer survivors had an elevated T2D risk compared with NHW across all follow-up periods (HRoverall: 1.84, 95% CI, 1.51–2.25; HR1–5 years: 1.83, 95% CI, 1.45–2.30). Southeast and East Asians demonstrated the highest T2D risks. Colon cancer was linked to early postdiagnosis T2D risk, whereas rectal cancer was associated with later risk. No significant association was observed for Native Hawaiians and Pacific Islanders. Conclusions: ANHPI colorectal cancer survivors face a greater risk of T2D, particularly among Southeast and East Asians. These findings highlight the need for evidence-based survivorship strategies to prevent T2D and reduce ethnic disparities. Impact: This is the first study to examine T2D risk among ANHPI colorectal cancer survivors, providing critical insights to inform tailored diabetes prevention and survivorship care.

Abstract The aim of this study was to estimate the effect of exposure to secondhand tobacco smoke on the incidence of lung adenocarcinoma in situ/minimally invasive adenocarcinoma (AIS/MIA). Data from seven case–control studies participating in the International Lung Cancer Consortium (ILCCO) were pooled, resulting in 625 cases of AIS/MIA and 7,403 controls, of whom 170 cases and 3,035 controls were never smokers. Unconditional logistic regression was used to estimate adjusted ORs (ORadj) and 95% confidence intervals (CI), controlling for age, sex, race, smoking status (ever/never), and pack-years of smoking. Study center was included in the models as a random-effects intercept term. Ever versus never exposure to secondhand tobacco smoke was positively associated with AIS/MIA incidence in all subjects (ORadj = 1.48; 95% CI, 1.14–1.93) and in never smokers (ORadj = 1.45; 95% CI, 1.00–2.12). There was, however, appreciable heterogeneity of ORadj across studies (P = 0.01), and the pooled estimates were largely influenced by one large study (40% of all cases and 30% of all controls). These findings provide weak evidence for an effect of secondhand tobacco smoke exposure on AIS/MIA incidence. Further studies are needed to assess the impact of secondhand tobacco smoke exposure using the newly recommended classification of subtypes of lung adenocarcinoma. Cancer Epidemiol Biomarkers Prev; 24(12); 1902–6. ©2015 AACR.

Abstract Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-186.

Abstract To clarify the role of previous lung diseases (PLDs) (chronic bronchitis, emphysema, pneumonia, tuberculosis, asbestosis and silicosis) in the development of lung cancer we conducted a pooled analysis in the International Lung Cancer Consortium (ILCCO). Data from 16 studies (9 population based case-control, 4 hospital based case-control, 2 mixed case-control and 1 cohort - 10 from North America, 5 from Europe and 1 from Asia) were pooled, including 24044 cases and 81256 controls. Study-specific effect estimates were derived using logistic regression models for case-control studies and Cox proportional hazards models for cohort studies adjusted for age, sex, education and pack-years of smoking. Effect estimates were then pooled using random effects models where summary effects for each of the PLDs were evaluated separately. Stratified analyses were conducted based on smoking status, histology and study design or control source. Heterogeneity was evaluated using the Cochrane Q statistic and Galbraith plots, and publication bias was evaluated using funnel plots as well as the Begg test. A previous history of emphysema conferred a relative risk (RR) of 2.17, 95% confidence interval (CI): 1.67-2.82 (from 15 studies, p-het<.001). A previous history of chronic bronchitis conferred a RR of 1.49, 95% CI: 1.33-1.60 (from 12 studies, p-het.=0.434). Tuberculosis was associated with a RR of 1.54, 95% CI: 1.19-1.99 (from 15 studies, p-het.=0.001). Both asbestosis (RR 2.51, 95% CI: 1.53-4.12 (from 7 studies, p-het=0.379)) and silicosis (RR 1.70, 95% CI: 1.15-2.54, (from 3 studies, p-het. p=0.476)) were also associated with lung cancer risk. When the outlying studies were removed, effect estimates changed minimally and heterogeneity was reduced. Findings were consistent in subgroup analyses by smoking status and histology (adenocarcinoma, squamous cell carcinoma and small cell lung cancer). Effect estimates among never smokers were for emphysema a RR of 2.21, 95% CI: 0.99-4.90 (from 8 studies), for chronic bronchitis 1.12, 95% CI: 0.78-1.62 (from 9 studies), for pneumonia 1.37, 95% CI: 1.10-1.70 (from 10 studies) and for tuberculosis 1.54, 95% CI: 0.99-2.39 (from 9 studies). In this analysis of data from multiple continents, PLDs were associated with an increased risk of lung cancer. The evidence among never smokers supports a direct relationship between previous lung diseases and lung cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4826.

Abstract Background: The International Lung Cancer Consortium was established in 2004. To clarify the role of DNA repair genes in lung cancer susceptibility, we conducted a pooled analysis of genetic variants in DNA repair pathways, whose associations have been investigated by at least 3 individual studies. Methods: Data from 14 studies were pooled for 18 sequence variants in 12 DNA repair genes, including APEX1, OGG1, XRCC1, XRCC2, XRCC3, ERCC1, XPD, XPF, XPG, XPA, MGMT, and TP53. The total number of subjects included in the analysis for each variant ranged from 2,073 to 13,955 subjects. Results: Four of the variants were found to be weakly associated with lung cancer risk with borderline significance: these were XRCC3 T241M [heterozygote odds ratio (OR), 0.89; 95% confidence interval (95% CI), 0.79-0.99 and homozygote OR, 0.84; 95% CI, 0.71-1.00] based on 3,467 cases and 5,021 controls from 8 studies, XPD K751Q (heterozygote OR, 0.99; 95% CI, 0.89-1.10 and homozygote OR, 1.19; 95% CI, 1.02-1.39) based on 6,463 cases and 6,603 controls from 9 studies, and TP53 R72P (heterozygote OR, 1.14; 95% CI, 1.00-1.29 and homozygote OR, 1.20; 95% CI, 1.02-1.42) based on 3,610 cases and 5,293 controls from 6 studies. OGG1 S326C homozygote was suggested to be associated with lung cancer risk in Caucasians (homozygote OR, 1.34; 95% CI, 1.01-1.79) based on 2,569 cases and 4,178 controls from 4 studies but not in Asians. The other 14 variants did not exhibit main effects on lung cancer risk. Discussion: In addition to data pooling, future priorities of International Lung Cancer Consortium include coordinated genotyping and multistage validation for ongoing genome-wide association studies. (Cancer Epidemiol Biomarkers Prev 2008;17(11):3081–9)