Many studies demonstrate that cancer incidence and mortality patterns among Asian Americans are heterogeneous, but national statistics on cancer for Asian ethnic groups are not routinely available. This article summarizes data on cancer incidence, mortality, risk factors, and screening for 5 of the largest Asian American ethnic groups in California. California has the largest Asian American population of any state and makes special efforts to collect health information for ethnic minority populations. We restricted our analysis to the 4 most common cancers (prostate, breast, lung, colon/rectum) and for the 3 sites known to be more common in Asian Americans (stomach, liver, cervix). Cancer incidence and mortality were summarized for 5 Asian American ethnic groups in California in order of population size (Chinese, Filipino, Vietnamese, Korean, and Japanese). Chinese Americans had among the lowest incidence and death rate from all cancer combined; however, Chinese women had the highest lung cancer death rate. Filipinos had the highest incidence and death rate from prostate cancer and the highest death rate from female breast cancer. Vietnamese had among the highest incidence and death rates from liver, lung, and cervical cancer. Korean men and women had by far the highest incidence and mortality rates from stomach cancer. Japanese experienced the highest incidence and death rates from colorectal cancer and among the highest death rates from breast and prostate cancer. Variations in cancer risk factors were also observed and were for the most part consistent with variations in cancer incidence and mortality. Differences in cancer burden among Asian American ethnic groups should be considered in the clinical setting and in cancer control planning.

Objective. Based on a small clinical series and previously published case reports, concordance for systemic lupus erythematosus (SLE) among monozygous (MZ) twins has been reported to be as high as 69%. Using a larger and less biased sample, we provide another estimate of this percentage.Methods. We established a registry of twins with SLE, based upon self-reports and information provided by the patients' physicians. We used DNA fingerprinting to validate the reported zygosity in a sample of these twins.Results. firmed by DNA fingerprinting in a subsample of 15 self-described MZ twins and 7 self-described DZ twins. All individuals had correctly predicted their zygosity.Conclusion. MZ concordance for SLE is similar to that for other autoimmune diseases and is much lower than previously believed.Concordance for disease in pairs of twins provides evidence of the relative etiologic contributions of genetic and environmental factors, as well as the timing of these effects. Low rates of concordance for disease over a lifetime, especially among monozygotic (MZ) twins, suggests a greater influence of environment; a large difference in concordance between MZ and dizygotic (DZ) twins suggests a greater influence of genetic determinants. However, for most diseases, there are no population-based twin concordancy data.Although the estimated annual incidence rate for systemic lupus erythematosus (SLE) is 5CL75 per million (1,2), no population-based studies of concordance rates in twins have been published. One case series reported that 69% of the MZ twin pairs were concordant (3), and anecdotal reports describe a similar proportion of concordance among MZ twin pairs. These reports also suggest that a much lower proportion of DZ twin pairs are concordant. In the study presented here, we used a larger sample size and an ascertainment mechanism that is less overtly biased in an effort to derive more meaningful data concerning the etiology of SLE.

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Although well studied in families at high-risk, the roles of mutations in the BRCA1 and BRCA2 genes are poorly understood in breast cancers in the general population, particularly in Black women and in age groups outside of the very young. We examined the prevalence and predictors of BRCA1 and BRCA2 mutations in 1,628 women with breast cancer and 674 women without breast cancer who participated in a multicenter population-based case-control study of Black and White women, 35 to 64 years of age. Among cases, 2.4% and 2.3% carried deleterious mutations in BRCA1 and BRCA2, respectively. BRCA1 mutations were significantly more common in White (2.9%) versus Black (1.4%) cases and in Jewish (10.2%) versus non-Jewish (2.0%) cases; BRCA2 mutations were slightly more frequent in Black (2.6%) versus White (2.1%) cases. Numerous familial and demographic factors were significantly associated with BRCA1 and, to a lesser extent, BRCA2 carrier status, when examined individually. In models considering all predictors together, early onset ages in cases and in relatives, family history of ovarian cancer, and Jewish ancestry remained strongly and significantly predictive of BRCA1 carrier status, whereas BRCA2 predictors were fewer and more modest in magnitude. Both the combinations of predictors and effect sizes varied across racial/ethnic and age groups. These results provide first-time prevalence estimates for BRCA1/BRCA2 in breast cancer cases among understudied racial and age groups and show key predictors of mutation carrier status for both White and Black women and women of a wide age spectrum with breast cancer in the general population.

PURPOSE Genetic testing for cancer risk has expanded rapidly. We examined clinical genetic testing and results among population-based patients with breast and ovarian cancer. METHODS The study included all women 20 years of age or older diagnosed with breast or ovarian cancer in California and Georgia between 2013 and 2014 and reported to the SEER registries covering the entire state populations. SEER data were linked to results from four laboratories that performed nearly all germline cancer genetic testing. Testing use and results were analyzed at the gene level. RESULTS There were 77,085 patients with breast cancer and 6,001 with ovarian cancer. Nearly one quarter of those with breast cancer (24.1%) and one third of those with ovarian cancer (30.9%) had genetic test results. Among patients with ovarian cancer, testing was lower in blacks (21.6%; 95% CI, 18.1% to 25.4%; v whites, 33.8%; 95% CI, 32.3% to 35.3%) and uninsured patients (20.8%; 95% CI, 15.5% to 26.9%; v insured patients, 35.3%; 95% CI, 33.8% to 36.9%). Prevalent pathogenic variants in patients with breast cancer were BRCA1 (3.2%), BRCA2 (3.1%), CHEK 2 (1.6%), PALB2 (1.0%), ATM (0.7%), and NBN (0.4%); in patients with ovarian cancer, prevalent pathogenic variants were BRCA1 (8.7%), BRCA2 (5.8%), CHEK2 (1.4%), BRIP1 (0.9%), MSH2 (0.8%), and ATM (0.6%). Racial/ethnic differences in pathogenic variants included BRCA1 (ovarian cancer: whites, 7.2%; 95% CI, 5.9% to 8.8%; v Hispanics, 16.1%; 95% CI, 11.8% to 21.2%) and CHEK2 (breast cancer: whites, 2.3%; 95% CI, 1.8% to 2.8%; v blacks, 0.1%; 95% CI, 0% to 0.8%). When tested for all genes that current guidelines designate as associated with their cancer type, 7.8% of patients with breast cancer and 14.5% of patients with ovarian cancer had pathogenic variants. CONCLUSION Clinically-tested patients with breast and ovarian cancer in two large, diverse states had 8% to 15% prevalence of actionable pathogenic variants. Substantial testing gaps and disparities among patients with ovarian cancer are targets for improvement.