Evidence for diverse mutagens in breast cancer

Blaszyk, Hagen; Hartmann, Arndt; Dz, Liao; Js, Kovach; Ss, Sommer

doi:10.1016/s0140-6736(05)65106-9

Cited by 5 publications

(2 citation statements)

References 4 publications

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“…Another example of a mutagen fingerprint is a G>T transversion at arginine 249 that occurs in approximately one-half of all hepatocellular carcinomas from areas of South Africa or Southern China where aflatoxin exposure is high (Bressac et al, 1991;Hsu et al, 1991). In addition, patterns of as few as 13 to 18 p53 mutations in human breast cancers differ significantly among populations, suggesting possible diverse environmental etiologies (Blaszyk et al, 1996). In contrast, endogenous processes (e.g., errors in DNA replication/repair, mutation due to free radicals, depurination, recombination, and transposition), in the absence of significant genetic differences are expected to produce a similar pattern of mutation in populations despite different diets and environmental exposures.…”

Section: Introductionmentioning

confidence: 99%

Factor IX mutations in South Africans and African Americans are compatible with primarily endogenous influences upon recent germline mutations

Drost

Roberts

et al. 2000

Hum. Mutat.

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Similar patterns of germline mutations in the factor IX gene (F9) have been observed in certain geographically and racially diverse populations. Germline mutation data have not been available from any region of Africa or from the Black race. Analysis of mutation data for Blacks is of interest, since this race has a high frequency of polymorphism compared to other races. This high frequency has been interpreted as evidence for the “out of Africa” hypothesis for the origin of humans, but it is possible that Blacks have a higher mutation rate due to genetic differences or environmental exposures. We report 26 independent mutations that were detected in patients of mixed races with hemophilia B from South Africa. The pattern of mutation in patients from this African country was similar to that of U.S. Caucasians. In addition, 22 independent mutation were detected in African American patients. The patterns of independent germline mutation in 22 African Americans (and in a combination 34 North American and African Blacks) is similar to that of U.S. Caucasians. Neither genetic differences between the Black and Caucasian races nor environmental and cultural differences between South Africa and the U.S. alter the germline pattern of mutation observed in F9. Hum Mutat 16:372, 2000. © 2000 Wiley‐Liss, Inc.

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Section: Introductionmentioning

confidence: 99%

Factor IX mutations in South Africans and African Americans are compatible with primarily endogenous influences upon recent germline mutations

Drost

Roberts

et al. 2000

Hum. Mutat.

View full text Add to dashboard Cite

show abstract

“…This variation contrasts with the constancy of the mutational pattern in most other situations, e.g., ethnically and geographically diverse populations have similar patterns of germline and p53 mutations in lung cancer associated with smoking. These results led to the hypothesis that the unique biology of breast tissue (i.e., islands of cancer-prone mammary epithelial cells surrounded by nondividing, nontransformable adipose tissue) predisposes mammary epithelial cells to transformation secondary to the diversity of lipophilic mutagens present in the diet [Blaszyk et al, 1996]. This hypothesis predicts that the source of fat in the diet often will affect the pattern of mutation in those tissues with the highest exposure to lipophilic mutagens: the liver, which receives intestinally absorbed dietary fat and transfers it to apolipoprotein carriers, adipose tissue, which is the major reservoir, and mammary gland tissue, which is intimately exposed to adipose tissue.…”

Section: ϫ6mentioning

confidence: 99%