TY - JOUR
T1 - CYP1A1 and GSTM1 genes associated with the risk of developing colorectal cancer
T2 - a case-control study in the Lima region of Peru
AU - Alvarado, Angel T.
AU - Saravia-Bartra, María
AU - Malpartida-Palomino, Robert
AU - Cárdenas-Guerrero, Cynthya Carolin
AU - García, Jorge A.
AU - Bendezú, María R.
AU - Chávez, Haydee
AU - Laos-Anchante, Doris
AU - Palomino-Jhong, Juan J.
AU - Molina-Cabrera, Aura
AU - Cuba-Garcia, Pompeyo
AU - Melgar-Merino, Elizabeth J.
AU - Vega-Ramos, Nelly
AU - Surco-Laos, Felipe
AU - Yarasca-Carlos, Paulina Eliades
AU - Varela, Nelson
AU - Quiñones, Luis Abel
AU - Cáceres-Lillo, Dante Daniel
AU - Zavaleta, Amparo Iris
AU - Pineda-Pérez, Mario
N1 - Publisher Copyright:
Alvarado AT et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC-BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2025
Y1 - 2025
N2 - The presence of CYP1A1 allelic variants and deletion of the glutathione S-transferase GSTM1 gene, and their imbalance, have been suggested as risk factors for inducing colorectal cancer (CRCa). The objective was to identify CYP1A1 and GSTM1 and evaluate the association with the risk of developing colorectal cancer in a sample of cases and controls from Lima, Peru. This was a case-control study of CYP1A1 and GSTM1 genes in 50 samples from patients diagnosed with colorectal cancer and 50 samples from controls without cancer, using the PCR -based restriction fragment length polymorphism method. A significant risk of developing CRCa was found in the following groups: GSTM1*0 carriers with no history of smoking or family history of cancer (OR = 3.56, 95% CI 1.43–8.88, p = 0.0060); GSTM1*0 with family history of cancer without smoking (OR = 2.81, 95% CI 0.35–22.49, p = 0.3280); GSTM1*0 exacerbated by smoking (OR = 1.41, 95% CI 0.11–17.11, p = 0.7880); CYP1A1*2A/*2A carriers with family history and smoking (OR = 1.50, 95% CI 0.13–16.54, p = 0.7410). An association of wild genotypes exacerbated by non-genetic factors with risk of developing CRCa was also found: CYP1A1*1A/*1A with family history of cancer but no history of smoking (OR = 2.94, 95% CI 0.11–35.80, p = 0.6380); GSTM1 (+) with history of smoking but no family history of cancer (OR = 5.63, 95% CI 0.46–68.46, p = 0.1750); GSTM1 (+) associated with family history and smoking (OR = 9.86, 95% CI 1.77–54.89, p = 0.0090). According to univariate statistical analysis, carriers of CYP1A1*2A and GSTM1*0 without association with family history of cancer and smoking would not be related to the risk of CRCa. An association was established between GSTM1*0 and CYPA1*2A/*2A with colorectal cancer exacerbated by family history and smoking. The risk is higher with wild-type genotypes of CYP1A1*1A/*1A and GSTM1 (+) induced by family history and smoking, respectively.
AB - The presence of CYP1A1 allelic variants and deletion of the glutathione S-transferase GSTM1 gene, and their imbalance, have been suggested as risk factors for inducing colorectal cancer (CRCa). The objective was to identify CYP1A1 and GSTM1 and evaluate the association with the risk of developing colorectal cancer in a sample of cases and controls from Lima, Peru. This was a case-control study of CYP1A1 and GSTM1 genes in 50 samples from patients diagnosed with colorectal cancer and 50 samples from controls without cancer, using the PCR -based restriction fragment length polymorphism method. A significant risk of developing CRCa was found in the following groups: GSTM1*0 carriers with no history of smoking or family history of cancer (OR = 3.56, 95% CI 1.43–8.88, p = 0.0060); GSTM1*0 with family history of cancer without smoking (OR = 2.81, 95% CI 0.35–22.49, p = 0.3280); GSTM1*0 exacerbated by smoking (OR = 1.41, 95% CI 0.11–17.11, p = 0.7880); CYP1A1*2A/*2A carriers with family history and smoking (OR = 1.50, 95% CI 0.13–16.54, p = 0.7410). An association of wild genotypes exacerbated by non-genetic factors with risk of developing CRCa was also found: CYP1A1*1A/*1A with family history of cancer but no history of smoking (OR = 2.94, 95% CI 0.11–35.80, p = 0.6380); GSTM1 (+) with history of smoking but no family history of cancer (OR = 5.63, 95% CI 0.46–68.46, p = 0.1750); GSTM1 (+) associated with family history and smoking (OR = 9.86, 95% CI 1.77–54.89, p = 0.0090). According to univariate statistical analysis, carriers of CYP1A1*2A and GSTM1*0 without association with family history of cancer and smoking would not be related to the risk of CRCa. An association was established between GSTM1*0 and CYPA1*2A/*2A with colorectal cancer exacerbated by family history and smoking. The risk is higher with wild-type genotypes of CYP1A1*1A/*1A and GSTM1 (+) induced by family history and smoking, respectively.
KW - CYP1A1
KW - GSTM1
KW - colorectal cancer
KW - family history
KW - smoking
UR - https://www.scopus.com/pages/publications/105011643801
U2 - 10.3897/pharmacia.72.e156391
DO - 10.3897/pharmacia.72.e156391
M3 - Artículo
AN - SCOPUS:105011643801
SN - 0428-0296
VL - 72
JO - Pharmacia
JF - Pharmacia
M1 - e156391
ER -
SDG 3 Good Health and Well-being