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      The epidemiology of Her-2/ neu and P53 in breast cancer Translated title: Epidemiología de los genes Her2/neu y P53 en relación al cáncer mamario

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          Abstract

          Breast cancer is an etiologically heterogeneous disease with marked geographical variations. Joint consideration of the relationship between specific molecular alterations and known or suspected epidemiologic risk factors for this disease should help distinguish subgroups of women that are at elevated risk of developing breast cancer. In this article, we present a comprehensive literature review of the etiologic and prognostic roles of Her-2/neu and P53 among women. In addition, we discuss the advantages and limitations of using biomarkers in epidemiological studies. We conclude that more research is needed to understand the complex relationships between genetic alterations and etiologic risk factors for breast cancer.

          Translated abstract

          El cáncer mamario es una enfermedad con gran variabilidad geográfica y cuya etiología es heterogénea. La evaluación conjunta de los factores de riesgo que se conocen por estudios epidemiológicos y de las alteraciones específicas a nivel molecular, podría ser útil para identificar subgrupos de mujeres con alto riesgo de padecer dicho tumor maligno. En este artículo presentamos una revisión de la literatura acerca del papel que el Her-2/neu y el P53 tienen en la etiología y el pronóstico del cáncer mamario en mujeres. Además, discutimos las ventajas y limitaciones de utilizar biomarcadores en los estudios epidemiológicos. Concluimos que se requieren nuevas investigaciones orientadas a dilucidar las complejas relaciones que existen entre las alteraciones genéticas y los factores de riesgo para el cáncer mamario.

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          Most cited references110

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          Mutations in the p53 tumor suppressor gene: clues to cancer etiology and molecular pathogenesis.

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            The p53 proto-oncogene can act as a suppressor of transformation.

            DNA clones of the wild-type p53 proto-oncogene inhibit the ability of E1A plus ras or mutant p53 plus ras-activated oncogenes to transform primary rat embryo fibroblasts. The rare clones of transformed foci that result from E1A plus ras plus wild-type p53 triple transfections all contain the p53 DNA in their genome, but the great majority fail to express the p53 protein. The three cell lines derived from such foci that express p53 all produce mutant p53 proteins with properties similar or identical to transformation-activated p53 proteins. The p53 mutants selected in this fashion (transformation in vitro) resemble the p53 mutants selected in tumors (in vivo). These results suggest that the p53 proto-oncogene can act negatively to block transformation.
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              Systematic population-based assessment of cancer risk in first-degree relatives of cancer probands.

              Cancer has long been recognized to have a familial component. Elevated risks for cancers at the same site for relatives of cancer probands have been reported for both common cancers and a number of the rarer cancer sites. For a particular cancer site, however, the estimated risks to relatives have varied considerably depending on criteria for selection of probands, how cancers were determined in relatives, and overall study design. Not surprisingly, the estimated risks of other cancers in relatives of probands with cancer at a given site have been subject to even more variation. The aim of this study was to use the Utah Population Database resource to systematically study familial clustering of 28 distinct cancer site definitions among first-degree relatives (parents, siblings, and off-spring) of cancer probands. We estimated familial relative risks from the Utah Population Database by identifying all cases of cancer in these first-degree relatives. These observed values were compared with those expected based on cohort-specific internal rates calculated from 399,786 relatives of all individuals in the Utah Population Database known to have died in Utah. All sites showed an excess of cancers of the same site among relatives, with thyroid and colon cancers and lymphocytic leukemia showing the highest familial risks. When the analyses were restricted to cases with early ages at diagnosis, increased familial components for most cancer sites became evident. A significant difference in familial relative risk (FRR) between male (FRR = 4.04; 95% confidence interval [CI] = 3.13-5.07) and female (FRR = 2.24; 95% CI = 1.54-3.08) probands was found for colon cancer. Highly significant familial associations (one-sided; P < .001) were found among breast, colon, and prostate cancers and between breast and thyroid cancers. Statistically significant (one-sided, P < .01) associations were also found between tobacco-associated sites (lung, larynx, lip, and cervix). This study represents a unique comprehensive population-based study of familial cancer. The familial associations reported here will be useful in generating hypotheses about specific genetic and environmental factors that can be tested in genetic linkage and case-control studies.
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                Author and article information

                Journal
                spm
                Salud Pública de México
                Salud pública Méx
                Instituto Nacional de Salud Pública (Cuernavaca, Morelos, Mexico )
                0036-3634
                November 1999
                : 41
                : suppl 2
                : S114-S121
                Affiliations
                [01] New York New York orgnameMount Sinai School of Medicine United States of America
                [02] orgnameInstituto Nacional de Salud Pública orgdiv1 Centro de Investigación de Salud Poblacional México
                Article
                S0036-36341999000800008 S0036-3634(99)04100008
                10.1590/s0036-36341999000800008
                b5e77c3a-ed2c-4b3a-987b-5b4a1b082bfa

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.

                History
                : 03 June 1998
                : 07 April 1999
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 125, Pages: 0
                Product

                SciELO Public Health

                Self URI: Full text available only in PDF format (EN)
                Categories
                Articles

                genes,biological markers,factores de riesgo,razas,marcadores biológicos,risk factors,breast neoplasms,racial stocks,neoplasmas de la mama

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