Pepsinogen I, pepsinogen II, gastrin-17, and serological biomarkers in the diagnosis of precursor lesions of gastric cancer.

Introduction: Atrophic gastritis and intestinal metaplasia are precursor lesions of gastric cancer. The aim of this study was to determine the usefulness of the biomarkers pepsinogen I(PgI), pepsinogen II (PgII), gastrin-17, and antibodies in the identification of precursor lesions.

Methods: We studied 129 patients with gastric symptoms.

Association of gene variants with metabolic and renal function parameters in Mexican patients living with type 2 diabetes.

Objective: Type 2 diabetes (T2D) and high blood pressure are the main causes of chronic kidney disease (CKD) in adulthood. Both metabolic and oxidative stresses driven by hyperglycemia as well as genetic factors have been suggested as pathogenic causes of renal failure. Some single nucleotide variants (SNVs) on gene coding KLOTHO () have been implicated in several clinical scenarios including hypertension, diabetes, and cardiovascular disease.

Foetal haemoglobin elevation, unfavourable prognosis, and protective role of genetic variants rs7482144, rs9399137 and rs4671393 in children with ALL.

In acute lymphoblastic leukaemia (ALL), elevated foetal haemoglobin (HbF) levels have been associated with the prognosis of patients. Genetic variants in HbF regulatory genes: BAF chromatin remodelling complex subunit (), HBS1L-MYB transcriptional GTPase intergenic region (), Krüppel-like factor 1 (), haemoglobin gamma subunit 2 (), haemoglobin gamma subunit 1 (HBG1), and haemoglobin subunit beta pseudogene 1 () are often associatedwith elevatedHbF concentration. This study investigated the association of genetic variants in HbF regulatory genes with HbF concentration, unfavourable prognosis, and outcome in children with ALL.

Genetic analysis of TMPRSS6 catalytic domain variants in Mexican patients with iron treatment refractoriness.

Objective: To identify the TMPRSS6 gene variants in Mexican patients with iron treatment refractoriness, to describe hematological and iron profile parameters, and to use bioinformatic prediction and protein modeling tools to assess a possible biological impact for the detected missense variants.

Methods: Nineteen patients referred with iron treatment refractoriness were studied. Peripheral blood was collected to determine hematic cytometry, iron profile, hemoglobin electrophoresis, and quantification.

Association of Serum Fibroblast Growth Factor 23 and FGF23 Gene Variants with Chronic Kidney Disease in Patients with Type 2 Diabetes and Essential Hypertension.

Introduction: Fibroblast growth factor 23 (FGF23) gene variants could influence the production of FGF23 in subjects at risk for chronic kidney disease (CKD). Our purpose was to analyze the association of serum levels of FGF23 and two FGF23 gene variants with metabolic and renal function parameters in Mexican patients with Type 2 Diabetes (T2D) and/or essential hypertension (HTN).

Materials/methods: The study included 632 individuals diagnosed with T2D and/or HTN, of which 269 (43%) were diagnosed with CKD.

The Genetic Variant (rs361525) Is Associated with Increased Susceptibility to Developing Dengue Symptoms.

Dengue virus (DENV) is the causal agent of dengue fever. The symptoms and signs of dengue vary from febrile illness to hemorrhagic syndrome. and are genes of the innate immune system.

Role of the BMP6 protein in breast cancer and other types of cancer.

The BMP6 protein (Bone Morphogenetic Protein 6) is part of the superfamily of transforming growth factor-beta (TGF-β) ligands, participates in iron homeostasis, inhibits invasion by increasing adhesions and cell-cell type interactions and induces angiogenesis directly on vascular endothelial cells. BMP6 is coded by a tumor suppressor gene whose subexpression is related to the development and cancer progression; during neoplastic processes, methylation is the main mechanism by which gene silencing occurs. This work presents a review on the role of BMP6 protein in breast cancer (BC) and other types of cancer.

Molecular and Hematological Analysis of Alpha- and Beta-Thalassemia in a Cohort of Mexican Patients.

Alpha- and beta-thalassemia are caused by reduced or absent synthesis of hemoglobin (Hb) subunits α and/or β. , , and mutations are the main cause of thalassemias. The aim of this article is to analyze molecular and hematological features of α- and β-thal in a cohort of Mexican patients.

Three Mexican Families with β thalassemia intermedia with different molecular basis.

Beta thalassemia (β-thal) is a frequent monogenic disease, is clinically and molecularly heterogeneous. This study described molecular and laboratory findings for three Mexican patients with β-thal intermedia phenotype and their relatives. Three Mexican families were studied for presenting β-thal intermedia, ARMS-PCR and Gap-PCR were performed to screen for common mutations, Sanger sequencing for rare or new alleles, and MLPA for identifying deletions and or duplications.