Cigarette smoking, dietary habits and genetic polymorphisms inGSTT1,GSTM1andCYP1A1metabolic genes: A case-control study in oncohematological diseases

Abstract

AIMTo analyze the association between oncohematological diseases and GSTT1/GSTM1/CYP1A1 polymorphisms, dietary habits and smoking, in an argentine hospital-based case-control study.METHODSThis hospital-based case-control study involved 125 patients with oncohematological diseases and 310 control subjects. A questionnaire was used to obtain sociodemographic data and information about habits. Blood samples were collected, and DNA was extracted using salting out methods. Deletions in GSTT1 and GSTM1 (null genotypes) were addressed by PCR. CYP1A1 MspI polymorphism was detected by PCR-RFLP. Odds ratio (OR) and 95%CI were calculated to estimate the association between each variable studied and oncohematological disease.RESULTSWomen showed lower risk of disease compared to men (OR 0.52, 95%CI: 0.34-0.82, P = 0.003). Higher levels of education (> 12 years) were significantly associated with an increased risk, compared to complete primary school or less (OR 3.68, 95%CI: 1.82-7.40, P < 0.001 adjusted for age and sex). With respect to tobacco, none of the smoking categories showed association with oncohematological diseases. Regarding dietary habits, consumption of grilled/barbecued meat 3 or more times per month showed significant association with an increased risk of disease (OR 1.72, 95%CI: 1.08-2.75, P = 0.02). Daily consumption of coffee also was associated with an increased risk (OR 1.77, 95%CI: 1.03-3.03, P = 0.03). Results for GSTT1, GSTM1 and CYP1A1 polymorphisms showed no significant association with oncohematological diseases. When analyzing the interaction between polymorphisms and tobacco smoking or dietary habits, no statistically significant associations that modify disease risk were found.CONCLUSIONWe reported an increased risk of oncohematological diseases associated with meat and coffee intake. We did not find significant associations between genetic polymorphisms and blood cancer.

Increased Risk of Acute Lymphoblastic Leukemia in Adult Patients with GSTM1 Null Genetic Polymorphism

“…Additionally, cell signaling, post-translational modifications, cell proliferation, differentiation, cellular apoptosis, anti-inflammatory, proinflammatory, prevention of DNA damages, and resistance to chemotherapeutic drugs are other non–enzymatic function of GTs. 12 , 32 GSTT1 and GSTM1 genetic polymorphisms are associated with loss–of–function mutations that leads to the complete loss of activities of these enzymes. 16 In the present study, GSTT1 and GSTM1 genetic polymorphisms were investigated in newly diagnosed adult patients with ALL in Sudanese population.…”

“…4 , 8–12 Furthermore, administration of chemotherapeutic drugs in patients with malignancies could also develop secondary neoplasia due to the impaired detoxification process of GTs. 12 , 13…”

Association of CYP1A1, GSTM1 and GSTT1 gene polymorphisms with risk of prostate cancer in Algerian population

“…Xenobiotic-metabolizing enzymes (XME), coded by a family of xenobiotic-metabolizing genes (XMG), have a major role in elimination of many xenobiotics or environmental chemical compounds from the body. This mechanism of detoxification occurs in two phases [7]. In phase I, cytochrome P450 enzymes play an important role in the metabolism of estrogen and polycyclic aromatic hydrocarbons (PAHs).…”

relationship between GSH enzyme with risk of childhood acute lymphoblastic leukemia ALL

“…Glutathione S-transferases are pivotal in maintaining cellular homeostasis by providing cytoprotection from environmental carcinogens, toxins, byproducts of oxidative stress and drugs. Additionally, cell signaling, post-translational modifications, cell proliferation, differentiation, cellular apoptosis, antiinflammatory, proinflammatory, prevention of DNA damages, and resistance to chemotherapeutic drugs are other non-enzymatic function of GTs (Cerliani et al ., 2016;Singh et al ., 2021). GSTT1 and GSTM1 genetic polymorphisms are associated with loss-of-function mutations that leads to the complete loss of activities of these enzymes (Baba et al, 2021).…”