Incidence Rates¹ and Rate Ratios (RR) of HCC in Latinos from US SEER, Texas and South Texas, 1995-2010.

<p>Incidence Rates^{<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0099365#nt101" target="_blank">1</a>} and Rate Ratios (RR) of HCC in Latinos from US SEER, Texas and South Texas, 1995-2010.</p

Annual Age-adjusted incidence rates of hepatocellular carcinoma by ethnicity, 1995–2010.

<p>Annual age-adjusted incidence of HCC increased over the study period and was highest among South Texas Latinos. HCC incidence for the three Latino populations was consistently higher than for non-Hispanic whites (NHW).</p

Annual percent change (APC) of HCC incidence¹ from 1995 to 2010 by age for US SEER, Texas and South Texas.

<p>Annual percent change (APC) of HCC incidence^{<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0099365#nt103" target="_blank">1</a>} from 1995 to 2010 by age for US SEER, Texas and South Texas.</p

Age-specific incidence trends of hepatocellular carcinoma.

<p>Age-specific incidence of HCC was consistently higher among Latinos than among non-Hispanic whites (NHW). Each point was estimated as a 3-yr moving average.</p

Incidence Rates¹ and Rate Ratios (RR) of HCC in Latinos from US SEER, Texas and South Texas, 1995–2006.

1<p>Rates per 100,000 and age-adjusted to the 2000 US Standard Population (19 age groups).</p>2<p>Data for non-Latino whites (NLW) is included for general comparison.</p

HCC risk factor prevalence among U.S., Texas and South Texas Latinos, 1995–1997 and 2004–2006.

<p>A) Obesity prevalence increased among all three populations of Latinos and was highest among Latinos in South Texas. B) Diabetes prevalence significantly increased among U.S. Latinos. There were also non-significant increases among Texas and South Texas Latinos. Latino women in South Texas had significantly higher diabetes prevalence than U.S. Latino women. C) Heavy alcohol use did not change significantly over time among any Latino group, though there were non-significant increases in South Texas. D) Cigarette smoking significantly declined only among U.S. Latinos. During 2004–2006, there were no significant differences among the three Latino groups.</p

Annual Age-adjusted incidence rates of hepatocellular carcinoma by ethnicity, 1995–2006.

<p>Annual age-adjusted incidence of HCC increased over the study period and was highest among South Texas Latinos. Data for non-Latino whites (NLW) is included for general comparison purposes.</p

Annual percent change (APC) of HCC incidence¹ from 1995 to 2006 by age for US SEER, Texas and South Texas.

1<p>Incidence rates are age-adjusted for all ages and unadjusted for specific age groups.</p>2<p>Data for non-Latino whites (NLW) is included for general comparison.</p>*<p>Significantly increasing trend (p<.05).</p><p>APC = Annual Percent Change.</p><p>CI = Confidence Interval.</p>∧<p>Less than 6 cases for one or more years.</p

Baseline characteristics for the two study groups.

<p>Data is presented of the Dutch study group (n = 110) and the Texan study group (n = 119). Values are presented as * mean (SD) or ^† median (IQR). Chi-square, t- and Mann-Whitney U tests were used to test differences between NTD and control children.</p

Epigenetic Profiles in Children with a Neural Tube Defect; A Case-Control Study in Two Populations

<div><p>Folate deficiency is implicated in the causation of neural tube defects (NTDs). The preventive effect of periconceptional folic acid supplement use is partially explained by the treatment of a deranged folate-dependent one carbon metabolism, which provides methyl groups for DNA-methylation as an epigenetic mechanism. Here, we hypothesize that variations in DNA-methylation of genes implicated in the development of NTDs and embryonic growth are part of the underlying mechanism. In 48 children with a neural tube defect and 62 controls from a Dutch case-control study and 34 children with a neural tube defect and 78 controls from a Texan case-control study, we measured the DNA-methylation levels of imprinted candidate genes (<i>IGF2</i>-DMR, <i>H19, KCNQ1OT1)</i> and non-imprinted genes (the <i>LEKR/CCNL</i> gene region associated with birth weight, and <i>MTHFR</i> and <i>VANGL1</i> associated with NTD). We used the MassARRAY EpiTYPER assay from Sequenom for the assessment of DNA-methylation. Linear mixed model analysis was used to estimate associations between DNA-methylation levels of the genes and a neural tube defect. In the Dutch study group, but not in the Texan study group we found a significant association between the risk of having an NTD and DNA methylation levels of <i>MTHFR</i> (absolute decrease in methylation of −0.33% in cases, P-value = 0.001), and <i>LEKR/CCNL</i> (absolute increase in methylation: 1.36% in cases, P-value = 0.048), and a borderline significant association for <i>VANGL</i> (absolute increase in methylation: 0.17% in cases, P-value = 0.063). Only the association between <i>MTHFR</i> and NTD-risk remained significant after multiple testing correction. The associations in the Dutch study were not replicated in the Texan study. We conclude that the associations between NTDs and the methylation of the <i>MTHFR</i> gene, and maybe <i>VANGL</i> and <i>LEKKR/CNNL</i>, are in line with previous studies showing polymorphisms in the same genes in association with NTDs and embryonic development, respectively.</p></div