Aflatoxin levels and prevalence of TP53 aflatoxin-mutations in hepatocellular carcinomas in Mexico.

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Bibliographic Details
Title:	Aflatoxin levels and prevalence of TP53 aflatoxin-mutations in hepatocellular carcinomas in Mexico.
Authors:	Lino-Silva, Leonardo S.¹, Lajous, Martín^2,3, Brochier, Marion², Santiago-Ruiz, Luis², Melchor-Ruan, Javier⁴, Yi Xie⁵, Mingyi Wang⁶, Dongjing Wu⁶, Higson, Herbert⁶, Jones, Kristine⁶, Romero-Martínez, Martin⁷, Villalpando, Salvador⁸, Mohar, Alejandro⁹, Smith, Joshua W.¹⁰, Alvarez, Christian S.⁵, McGlynn, Katherine A.⁵, Dean, Michael⁵, Groopman, John¹⁰ mlajous@insp.mx
Source:	Salud Pública de México. Jan/Feb2022, Vol. 64 Issue 1, p35-40. 6p.
Subjects:	AFLATOXINS, HEPATOCELLULAR carcinoma, NUTRITION surveys, CANCER patients, GENETIC mutation, HEALTH surveys
Geographic Terms:	MEXICO, CHIAPAS (Mexico)
Abstract (English):	Objective. To determine the exposure to aflatoxin B1 (AFB1) in southern Mexico and the presence of the aflatoxin signature mutation in hepatocellular carcinoma (HCC) tissue from patients from a cancer referral center. Materials and methods. We estimated the prevalence and distribution of AFB1 in a representative sample of 100 women and men from Chiapas using the National Health and Nutrition Survey 2018-19. We also examined the presence of the aflatoxin signature mutation in codon 249 (R249S), and other relevant mutations of the TP53 gene in HCC tissue blocks from 24 women and 26 men treated in a national cancer referral center. Results. The prevalence of AFB1 in serum samples was 85.5% (95%CI 72.1-93.1) and the median AFB1 was 0.117 pg/μL (IQR, 0.050-0.350). We detected TP53 R249S in three of the 50 HCCs (6.0%) and observed four other G>T transversions potentially induced by AFB1. Conclusion. Our analysis provides evidence that AFB1 may have a relevant role on HCC etiology in Mexico. [ABSTRACT FROM AUTHOR]
Abstract (Spanish):	Objetivo. Determinar la exposición a aflatoxina_B1 (AFB1) en el sur de México y la presencia de la mutación característica de AFB1 en tejido de carcinoma hepatocelular (CHC) de pacientes de un centro oncológico. Material y métodos. Se estimó la prevalencia y distribución de AFB1 en una muestra representativa de 100 mujeres y hombres de Chiapas a partir de la Encuesta Nacional de Salud y Nutrición 2018-19. También se observó la presencia de la mutación característica de AFB1 en el codón 249 (R249S), y otras mutaciones relevantes del gen TP53 en bloques de tejido de CHC de 24 mujeres y 26 hombres estudiados en un centro de referencia nacional de oncología. Resultados. La prevalencia de AFB1 en las muestras de suero fue de 85.5% (IC95% 72.1-93.1) y la mediana de la concentración 0.117 pg/μL (IQR, 0.050-0.350). Se detectó TP53 R249S en tres de 50 casos de CHC (6.0%) y se observaron cuatro transversiones G>T potencialmente inducidas por AFB1. Conclusión. El presente análisis proporciona evidencia de que la AFB1 puede tener un papel relevante en la etiología del CHC en México. [ABSTRACT FROM AUTHOR]
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Database:	MedicLatina

Description
Abstract:	Objective. To determine the exposure to aflatoxin B1 (AFB1) in southern Mexico and the presence of the aflatoxin signature mutation in hepatocellular carcinoma (HCC) tissue from patients from a cancer referral center. Materials and methods. We estimated the prevalence and distribution of AFB1 in a representative sample of 100 women and men from Chiapas using the National Health and Nutrition Survey 2018-19. We also examined the presence of the aflatoxin signature mutation in codon 249 (R249S), and other relevant mutations of the TP53 gene in HCC tissue blocks from 24 women and 26 men treated in a national cancer referral center. Results. The prevalence of AFB1 in serum samples was 85.5% (95%CI 72.1-93.1) and the median AFB1 was 0.117 pg/μL (IQR, 0.050-0.350). We detected TP53 R249S in three of the 50 HCCs (6.0%) and observed four other G>T transversions potentially induced by AFB1. Conclusion. Our analysis provides evidence that AFB1 may have a relevant role on HCC etiology in Mexico. [ABSTRACT FROM AUTHOR]
ISSN:	00363634
DOI:	10.21149/13189