The Age Incidence of Childhood B-cell Precursor Acute Lymphoblastic Leukemia in Mexico City

Bernáldez-Rı́os, Roberto; Ortega-Álvarez, Manuel; Pérez-Saldivar, María Luisa; Alatoma-Medina, Norma E.; Campo-Martínez, María de los Ángeles del; Rodrı́guez-Zepeda, Maria del Carmen; Montero-Ponce, Inés; Franco-Ornelas, Sergio; Fernández-Castillo, Gabriela Jazmin; Núñez-Villegas, Nora Nancy; Taboada-Flores, Miguel A.; Flores-Lujano, Janet; Argüelles-Sanchez, Muriel E.; Juárez-Ocaña, Servando; Fajardo-Gutiérrez, Arturo; Mejı́a-Aranguré, Juan Manuel

doi:10.1097/mph.0b013e318162bcdc

Cited by 17 publications

(24 citation statements)

References 17 publications

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“…However, it is consistent with the report by Roman et al (2007) that the infection during the first year of life was a risk factor for ALL at ages 2 -5 years, particularly when the infection occurred during the first month of life. It may be relevant that a study in Mexico City reported a double incidence peak for AL, at 2 -3 and 6 -9 years of age (Bernaldez-Rios et al, 2008). If infections during the first year of life are a genuine factor, our findings may imply that in Mexico City these peaks have different etiologies with infection being more important for the 6 -9 years age group.…”

Section: Discussionmentioning

confidence: 57%

Breastfeeding and early infection in the aetiology of childhood leukaemia in Down syndrome

et al. 2009

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BACKGROUND: For a child to develop acute leukaemia (AL), environmental exposure may not be sufficient: interaction with a susceptibility factor to the disease, such as Down syndrome (DS), may also be necessary. We assessed whether breastfeeding and early infection were associated with the risk of developing AL in children with DS. METHODS: Children with DS in Mexico City, and either with or without AL, were the cases (N ¼ 57) and controls (N ¼ 218), respectively. Population was divided in children with AL and with acute lymphoblastic leukaemia (ALL) and also in children p6 and 46 years old. RESULTS: Breastfeeding and early infections showed moderate (but not significant) association for AL, whereas hospitalisation by infection during the first year of life increased the risk: odds ratios (confidence interval 95%) were 0.84 (0.43 -1.61), 1.70 (0.82 -3.52); and 3.57 (1.59 -8.05), respectively. A similar result was obtained when only ALL was analysed. CONCLUSION: We found that breastfeeding was a protective factor for developing AL and ALL, and during the first year of life, infections requiring hospitalisation were related to a risk for developing the disease in those children with DS 46 years of age. These data do not support the Greaves's hypothesis of early infection being protective for developing ALL.

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Section: Discussionmentioning

confidence: 57%

Breastfeeding and early infection in the aetiology of childhood leukaemia in Down syndrome

et al. 2009

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“…The pre-B ALL and the immature T-cell precursor are generally associated with a poorer prognosis (30). Two studies have shown that the Hispanic population has a high frequency of B-cell precursor immunophenotype (31,32). Our findings are consistent with these studies; we found that the 68.18% of cases with relapse On separate analyses of the -A317G and C829T polymorphisms in the DHFR gene, analyses of the G/G and T/T genotypes alone appear to be worse prognostic markers than leukocytes at diagnosis and age (OR=8.55, 95% CI 1.84-39.70; OR=14.00, 95% CI 1.13-172.63; OR=7.64, 95% CI 1.90-30.73; OR=4.54, 95% CI 1.14-18.09, respectively).…”

Section: Discussionmentioning

confidence: 99%

Survival and risk of relapse of acute lymphoblastic leukemia in a Mexican population is affected by dihydrofolate reductase gene polymorphisms

Gómez‐Gómez

Organista‐Nava

Saavedra‐Herrera

et al. 2012

Experimental and Therapeutic Medicine

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Abstract. Dihydrofolate reductase (DHFR) is the major target of methotrexate, a key component in childhood acute lymphoblastic leukemia (ALL) treatment. Polymorphisms in the gene coding for DHFR have been associated with adverse event treatment. This study evaluated the effect of the -A317G and C829T polymorphisms in the DHFR gene on survival and risk of relapse of ALL. Seventy patients with ALL and 100 healthy individuals were genotyped by the polymerase chain reactionrestriction fragment length polymorphism method. An association between the polymorphisms and the risk of relapse was found (p<0.05); patients with the -317G/G genotype were found to have an 8.55 (95% CI 1.84-39.70) higher chance of relapse and carriers of the 829T/T genotype had a 14.0 (95% CI 1.13-172.63) higher chance of relapse. Other variables, such as age and leukocyte count, were associated (p<0.05) with the risk of relapse of the disease. Individuals with the G/G and T/T genotype of the -A317G and C829T polymorphisms had poorer survival compared to other genotype groups (log-rank test; p<0.05). Although preliminary, these data seem to suggest a role for the DHFR polymorphisms in the risk of relapse of ALL and the mortality risk in these patients. IntroductionIn Mexico, acute leukemia is considered a public health issue; it represents the fourth leading cause of mortality of all neoplastic malignancies in children under 15 years of age (1). The mortality rate from 1996 to 2000 was 63.7 per 1 million children, one of the highest rates reported in the world (2). In 2005, leukemia was the second cause of mortality in the State of Guerrero in children less than 15 years of age, according to the National Institute of Statistics, Geography and Computing (INEGI) (3).Methotrexate (MTX) is an antineoplastic agent used in the treatment of patients with acute lymphoblastic leukemia (ALL) and was introduced five decades ago to clinical oncology. It is presently used in the treatment of other neoplastic diseases, including osteosarcoma, breast cancer, head and neck cancer, and non-Hodgkin's lymphoma (4,5). MTX is a folic acid antagonist, and its efficacy as an antineoplastic treatment is largely attributed to its high affinity for dihydrofolate reductase (DHFR) (EC 1.5.1.3), the enzyme which is responsible to catalyze the reduction of dihydrofolate (DHF) to tetrahydrofolate (THF) (6). The major mechanism of MTX action involves competitive inhibition of DHFR, leading to the impaired regeneration of THF from DHF; essential for the biosynthesis of purines and thymidylate, thus it also blocks the novo synthesis of DNA (7,8). A subset of patients develop adverse events of resistance to MTX; however, approximately 80% of ALL children experience good clinical response (5,9,10).The mechanisms that lead to clinical failure to MTX are DHFR overexpression, impaired intracellular transport and decreased levels of reduced folate carrier at the cell membrane (11,12). Changes in the levels of DHFR expression and consequently in the sensitivity to MTX can also be due t...

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“…The aforementioned peak at 2-5 years of age is reduced, or even absent, for Black Africans and for other developing communities (Court & Doll, 1961;Hewitt, 1955;Ramot & Magrath, 1982, as cited in Chan et al, 2002). In Mexico, for example, two peaks have been reported; the first occurring at 2-3 years of age and the second at 6-9 (Bernaldez- Rios et al, 2008). A recent epidemiological study done in Mexico City showed that severe infections, occurring in the first year of life and requiring hospitalization, were associated with a higher risk of developing leukemia for children with Down syndrome (Flores-Lujano et al, 2009).…”

Section: Greaves' Hypothesismentioning

confidence: 99%

Childhood Acute Leukemias in Hispanic Population: Differences by Age Peak and Immunophenotype

Mejı́a-Aranguré¹,

Pérez-Saldivar²,

Pelayo-Camacho³

et al. 2011

Novel Aspects in Acute Lymphoblastic Leukemia

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The Age Incidence of Childhood B-cell Precursor Acute Lymphoblastic Leukemia in Mexico City

Cited by 17 publications

References 17 publications

Breastfeeding and early infection in the aetiology of childhood leukaemia in Down syndrome

Breastfeeding and early infection in the aetiology of childhood leukaemia in Down syndrome

Survival and risk of relapse of acute lymphoblastic leukemia in a Mexican population is affected by dihydrofolate reductase gene polymorphisms

Childhood Acute Leukemias in Hispanic Population: Differences by Age Peak and Immunophenotype

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