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[Genetic, epidemiologic and clinical study of familial prostate cancer].
Bull Acad Natl Med. 2002; 186(4):779-88; discussion 788-91.BA

Abstract

Prostate cancer (CaP) is the most frequent cancer among men over 50 and its frequency increases with age. It has become a significant public health problem due to the ageing population. Epidemiologists report familial aggregation in 15 to 25% of cases and inherited susceptibility with autosomal dominant or X-linked model in 5 to 10% of cases. Clinical and biological features of familial CaP remain controversial.

OBJECTIVES

To perform: (1) Genetic study of familial Cap (mapping of susceptibility genes), (2) epidemiologic study (prevalence, associated cancers in the genealogy, model of transmission), and clinical study of familial CaP.

METHODOLOGY AND RESULTS

(I) conducting a nationwide family collection (ProGène study) with 2+ CaP we have performed a genomewide linkage analysis and identified a predisposing locus on 1q42.2-43 named PCaP (Predisposing to Cancer of the Prostate); (II) conducting a systematic genealogic analysis of 691 CaP followed up in 3 University departments of urology (Hospitals of Brest, Paris St Louis and Nancy) we have observed: (1) 14.2% of familial and 3.6% of hereditary CaP, (2) a higher risk of breast cancer in first degree relatives of probands (CaP+) in familial CaP than in sporadic CaP and in early onset CaP (< 55 years) when compared with late onset CaP ([dG]75 years), (3) an autosomal dominant model with brother-brother dependance), (4) the lack of specific clinical or biological feature (except for early onset) in hereditary CaP when compared with sporadic CaP.

CONCLUSION

(1) The mapping of a susceptibility locus will permit the cloning of a predisposing gene on 1q42.2-43, offer the possibility of genetic screening in families at risk and permit genotype/phenotype correlation studies; (2) the transmission model will improve parameteric linkage studies; (3) the lack of distinct specific clinical patterns suggest diagnostic and follow up modalities for familial and hereditary CaP similar to sporadic cancer while encouraging early screening of families at risk, given the earlier onset (5 to 10 years earlier) observed.

Authors+Show Affiliations

Service Urologie, Hôpital de la Cavale Blanche-29609 Brest.

Pub Type(s)

English Abstract
Journal Article
Research Support, Non-U.S. Gov't

Language

fre

PubMed ID

12412374

Citation

Valéri, Antoine. "[Genetic, Epidemiologic and Clinical Study of Familial Prostate Cancer]." Bulletin De l'Academie Nationale De Medecine, vol. 186, no. 4, 2002, pp. 779-88; discussion 788-91.
Valéri A. [Genetic, epidemiologic and clinical study of familial prostate cancer]. Bull Acad Natl Med. 2002;186(4):779-88; discussion 788-91.
Valéri, A. (2002). [Genetic, epidemiologic and clinical study of familial prostate cancer]. Bulletin De l'Academie Nationale De Medecine, 186(4), 779-88; discussion 788-91.
Valéri A. [Genetic, Epidemiologic and Clinical Study of Familial Prostate Cancer]. Bull Acad Natl Med. 2002;186(4):779-88; discussion 788-91. PubMed PMID: 12412374.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Genetic, epidemiologic and clinical study of familial prostate cancer]. A1 - Valéri,Antoine, PY - 2002/11/5/pubmed PY - 2002/11/26/medline PY - 2002/11/5/entrez SP - 779-88; discussion 788-91 JF - Bulletin de l'Academie nationale de medecine JO - Bull. Acad. Natl. Med. VL - 186 IS - 4 N2 - UNLABELLED: Prostate cancer (CaP) is the most frequent cancer among men over 50 and its frequency increases with age. It has become a significant public health problem due to the ageing population. Epidemiologists report familial aggregation in 15 to 25% of cases and inherited susceptibility with autosomal dominant or X-linked model in 5 to 10% of cases. Clinical and biological features of familial CaP remain controversial. OBJECTIVES: To perform: (1) Genetic study of familial Cap (mapping of susceptibility genes), (2) epidemiologic study (prevalence, associated cancers in the genealogy, model of transmission), and clinical study of familial CaP. METHODOLOGY AND RESULTS: (I) conducting a nationwide family collection (ProGène study) with 2+ CaP we have performed a genomewide linkage analysis and identified a predisposing locus on 1q42.2-43 named PCaP (Predisposing to Cancer of the Prostate); (II) conducting a systematic genealogic analysis of 691 CaP followed up in 3 University departments of urology (Hospitals of Brest, Paris St Louis and Nancy) we have observed: (1) 14.2% of familial and 3.6% of hereditary CaP, (2) a higher risk of breast cancer in first degree relatives of probands (CaP+) in familial CaP than in sporadic CaP and in early onset CaP (< 55 years) when compared with late onset CaP ([dG]75 years), (3) an autosomal dominant model with brother-brother dependance), (4) the lack of specific clinical or biological feature (except for early onset) in hereditary CaP when compared with sporadic CaP. CONCLUSION: (1) The mapping of a susceptibility locus will permit the cloning of a predisposing gene on 1q42.2-43, offer the possibility of genetic screening in families at risk and permit genotype/phenotype correlation studies; (2) the transmission model will improve parameteric linkage studies; (3) the lack of distinct specific clinical patterns suggest diagnostic and follow up modalities for familial and hereditary CaP similar to sporadic cancer while encouraging early screening of families at risk, given the earlier onset (5 to 10 years earlier) observed. SN - 0001-4079 UR - https://www.unboundmedicine.com/medline/citation/12412374/[Genetic_epidemiologic_and_clinical_study_of_familial_prostate_cancer]_ L2 - http://www.diseaseinfosearch.org/result/2768 DB - PRIME DP - Unbound Medicine ER -