BackgroundAdiponectin protein and some variations in its gene, ADIPOQ have recently been associated with cancer because they regulate glucose and lipid metabolism as well as anti-apoptotic and anti-inflammatory proteins.AimThe aim of this study was to analyse the relationship between selected biochemical markers, anthropometric indices and ADIPOQ rs2241766 and rs1501299 SNPs in ductal infiltrating breast cancer (DIBC) in a Mexican population.MethodsThis cross-sectional study included 64 DIBC patients and 167 healthy women. Polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) analysis was performed to identify the genotypes of the rs2241766 (exon 2) and rs1501299 (intron 2) ADIPOQ polymorphisms. Corporal composition and biochemical markers included body mass index (BMI), waist circumference (WC), hip circumference (HC), waist-hip ratio (WHR), glucose, cholesterol, triglycerides and high- and low-density lipoprotein cholesterol.ResultsPatients with DIBC had higher serum glucose, WC and WHR than controls. Intergroup differences in allele and genotype frequencies were found for both polymorphisms (P < 0.05). Patients carrying the rs2241766 TT and TG genotypes had higher values of WC, HC and WHR, but only TG carriers had higher levels of glucose. For the SNP rs1501299, carriers of the GG genotype in the DIBC group had higher values of glucose, WC, HC and WHR than the respective control group.ConclusionsThese results suggest that WC, HC and WHR are better predictors of DIBC than BMI. The ADIPOQ SNP rs2241766 emerges as a protective factor, whereas rs1501299 is a risk factor for DIBC development in a Mexican population.

Colorectal cancer (CRC) is the third most common cancer and one of the main causes of death around the world. Multiple lines of evidence have suggested the role of the corticotropin-releasing hormone (CRH) family in CRC induction, including the low expression of corticotropin-releasing hormone receptor 2 (CRHR2), which is an angiogenesis inhibitor and inflammatory modulator. Previous research suggests that CRHR2 expression in colonic intestinal cells can regulate migration, proliferation and apoptosis through the modulation of several pathways. The aim of this study was to analyze the association of the rs10250835, rs2267716 and rs2267717 variants of CRHR2 gene with CRC in the Mexican population in order to consider its predictive value in CRC. This cross-sectional study included a group of 187 unrelated patients with sporadic CRC and a control group of 191 healthy blood donors. DNA extraction from peripheral blood was carried out using the Miller method. Identification of the rs10250835 variant was performed using PCR-restriction fragment length polymorphism (RFLP) and the rs2267716 and rs2267717 variants using TaqMan allelic discrimination assay. The minor allele homozygous CC of the rs2267716 variant of CRHR2 showed significant difference between CRC and control group (p=0.025), as well as the GCA haplotype (p=0.007), corresponding to the rs10250835, rs2267716 and rs2267717 variants, respectively. Our results suggest that the rs2267716 variant and GCA haplotype of CRHR2 represent a risk factor for CRC development in Mexican patients.

Introducción: El cáncer colorrectal (CCR) es una enfermedad compleja debido al gran número de factores que influyen en su desarrollo, incluyendo variantes en genes supresores de tumores. Objetivo: Estimar las frecuencias alélicas y genotípicas de las variantes c.3915G>A y c.5371G>A del gen TSC2 en una población mexicana con CCR, así como analizar la asociación con el desarrollo de CCR. Métodos: Se incluyeron 126 muestras de sangre periférica de pacientes con diagnóstico de CCR esporádico y 134 de individuos sanos, considerados como grupo de control. La identificación de los genotipos se llevó a cabo mediante PCR tradicional y digestión enzimática. Todos los individuos firmaron una carta de consentimiento informado. Resultados: El alelo A de la variante c.3915G>A (RM = 0.31, IC 95 % = 0.15-0.69, p = 0.004), así como el haplotipo A/G de las variantes c.3915G>A y c.5371G>A (RM = 0.28, IC 95 % = 0.12-0.68, p = 0.005) mostraron un posible efecto protector contra CCR esporádico. El análisis in silico indicó que ambas variantes generan modificaciones en el proceso de corte y empalme. Conclusión: La presencia de la variante c.3915G>A del gen TSC2 sugiere un posible efecto protector contra CCR esporádico en población mexicana; sin embargo, no se observó esta asociación con la variante c.5371G>A.