Gene Polymorphism Modifies the Effect of Common Gene Variants on Severe Toxicity in Patients with Gastrointestinal Tumors Treated with Fluoropyrimidine-Based Anticancer Therapy.

To reduce severe fluoropyrimidine-related toxicity, pharmacogenetic guidelines recommend a dose reduction for carriers of four high-risk variants in the gene (*2A, *13, c.2846A>T, HapB3). The polymorphism in the gene has been shown to enhance the predictive value of these variants.

virulence: a current view.

is an opportunistic pathogen intrinsically resistant to multiple and broad-spectrum antibiotics. Although the bacterium is considered a low-virulence pathogen, it can cause various severe diseases and contributes significantly to the pathogenesis of multibacterial infections. During the COVID-19 pandemic, has been recognized as one of the most common causative agents of respiratory co-infections and bacteremia in critically ill COVID-19 patients.

3'-UTR Polymorphism: A Novel Association with FOLFIRINOX-Induced Neurotoxicity in Pancreatic Cancer Patients.

Pancreatic ductal adenocarcinoma (PDAC) is a highly fatal malignancy that has the worst 5-year survival rate of all of the common malignant tumors. Surgery, chemotherapy, and/or chemoradiation remain the main tactics for PDAC treatment. The efficacy of chemotherapy is often compromised because of the substantial risk of severe toxicities.

Exogenous contaminating DNA in Taq polymerases: A method to avoid false-positive results when detecting the bla gene.

In the course of developing an assay to identify genes responsible for antibiotic resistance in gram-negative bacteria, it has been found that standard (not DNA-free) Taq DNA polymerases were contaminated with bla gene fragments that varied in length and quantities. The complete bla gene sequence was either absent or was detected in infinitesimal amounts. We developed an approach to avoid false-positive findings caused by contaminating bla gene sequences in conventional polymerases.

Hydrogel microarray for detection of polymorphisms in the UGT1A1, DPYD, GSTP1 and ABCB1 genes.

Background: Improving the efficacy of anticancer therapy remains an urgent and very important task. Screening of the individual genetic metabolism of cancer patients allows for prescribing adequate medication in the correct dose as well as for decreasing side effects associated with drug toxicity.

Objective: Estimation of a microarray-based method for genotyping of the UGT1A1, DPYD, GSTP1, and ABCB1 metabolic regulation genes to evaluate for an increased risk of toxicity of anticancer drugs.