Cancer patterns in Hmong in Minnesota, 2000 to 2012.

BACKGROUND: Minnesota has the second largest Hmong population in the United States. The objective of the current study was to estimate the cancer incidence among Hmong individuals in Minnesota between 2000 and 2012 to determine targets for screening and interventions. METHODS: Cancer cases in Minnesota between 2000 and 2012 were obtained from the Minnesota Cancer Surveillance System, and proportional incidence ratios (PIRs) were calculated. The 2000 and 2010 US Census reports were used to obtain total population estimates. Age-adjusted cancer incidence rates (AAR) and 95% confidence intervals (95% CIs) were calculated for Hmong individuals, Asian/Pacific Islander individuals, and all Minnesotans using direct method and Poisson regression. RESULTS: Compared with all Minnesotans, the Hmong had elevated PIRs and AARs for malignancies related to infections, including nasopharyngeal, stomach, liver, and cervical cancers. The AAR ratios in Hmong versus all Minnesotans were found to be significantly increased for nasopharyngeal (AAR, 15.90; 95% CI, 9.48-26.68), stomach (AAR, 2.99; 95% CI, 2.06-4.33), liver (AAR, 1.77; 95% CI, 1.04-3.02), and cervical (AAR, 3.88; 95% CI, 2.61-5.77) cancers. The AARs in Hmong versus all Minnesotans were significantly lower for all-cause cancer (AAR, 0.39; 95% CI, 0.35-0.44); cancers of the breast, lung, and colorectum; melanoma; and non-Hodgkin lymphoma. Compared with Asian/Pacific Islander individuals, the rates in Hmong were significantly higher for melanoma and cervical cancer, with AAR ratios of 2.23 (95% CI, 1.09-4.56) and 1.59 (95% CI, 1.01-2.49), respectively. CONCLUSIONS: Compared with all Minnesotans, the Hmong have an increased incidence of cancers related to infectious agents. These findings indicate a need for cancer prevention and screening programs in this population.

The role of CSM3, MRC1, and TOF1 in minisatellite stability and large loop DNA repair during meiosis in yeast.

Double-stranded break (DSB) repair during meiotic recombination in yeast Saccharomyces cerevisiae leads to the formation of heteroduplex DNA, a hybrid DNA molecule composed of single strands from two homologous chromosomes. Differences in sequence between the strands within heteroduplex DNA generate mismatches or large unpaired loops that are substrates for repair. At least two pathways function to repair large loops that form within heteroduplex DNA: the RAD1-dependent large loop repair (LLR) pathway and another as yet uncharacterized RAD1-independent LLR pathway. Repair of large loops during meiotic recombination is especially important for the genomic stability of the repetitive DNA sequences known as minisatellites. Minisatellite DNA tracts are generally stable during mitotic cell divisions but frequently alter in length during meiosis. Using a yeast minisatellite system in which the human minisatellite associated with the HRAS1 proto-oncogene has been inserted into the recombination hotspot region upstream of HIS4 in S. cerevisiae, our lab previously showed that the RAD1-dependent LLR pathway controls minisatellite length expansions, but not contractions. Here we show that minisatellite length expansions are controlled by the products of the CSM3 and TOF1 genes, while contractions are controlled by MRC1. By examining meiotic segregation patterns in yeast strains heterozygous for the 26bp his4-lopd insert, we found that deleting CSM3 caused a loss of LLR activity similar to that seen in a RAD1 mutant. Double mutant analysis revealed that failure to repair loops is exacerbated upon deleting both RAD1 and CSM3 - specifically the type of repair that fills in loops, which would generate minisatellite length expansions. A model for minisatellite length alteration based on these results is presented.