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Sponsored by: |
National Human Genome Research Institute (NHGRI) |
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Information provided by: | National Institutes of Health Clinical Center (CC) |
ClinicalTrials.gov Identifier: | NCT00001469 |
Molecular approaches to the understanding of human neoplastic disease have revealed that multiple genetic alterations are an essential component of tumorigenesis (1,2). Both germline and somatic genetic alterations can be involved in the malignant transformation of normal cells. Identification of the genes involved in neoplastic transformation has been approached through the molecular analysis of sporadic cancers and the genetic study of families with an inherited predisposition for cancer. The interplay of these two approaches has led to the characterization of genes such as the retinoblastoma (Rb) gene, the p53 gene and the adenomatous polyposis coli (APC) gene that are all involved in the development of both hereditary and non-hereditary forms of cancer. Inherited mutations in such genes predispose affected families to hereditary cancer syndromes, affording an opportunity to identify genetic lesions that also cause the more common sporadic cancers.
Prostate cancer (PRCA) is the most common cancer diagnosed (1999 estimate 179,300 cases) and the second leading cause of cancer mortality (1999 estimate 37,000 deaths) in men in the United States. Family history is the single strongest risk factor currently known for prostate cancer. This raises the possibility that heritable genetic factors may be involved in the development of this disease in a subset of men. The genetic contribution to diseases of complex origin such as cancer is often most salient in families of early onset cases. Therefore, prostate cancer inheritance following a simple Mendelian pattern, may be identified in the families of probands with early-onset cases. Common susceptibility alleles of small effect may be detectable in families with later-onsent and/or less strong family history of PRCA or in case-control data.
Condition |
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Hereditary Neoplastic Syndrome Prostatic Neoplasm |
Study Type: | Observational |
Official Title: | Genetic Analysis of Hereditary Prostate Cancer |
Estimated Enrollment: | 20000 |
Study Start Date: | July 1995 |
Molecular approaches to the understanding of human neoplastic disease have revealed that multiple genetic alterations are an essential component of tumorigenesis. Both germline and somatic genetic alterations can be involved in the malignant transformation of normal cells. Identification of the genes involved in neoplastic transformation has been approached through the molecular analysis of sporadic cancers and the genetic study of families with an inherited predisposition for cancer. The interplay of these two approaches has led to the characterization of genes such as the retinoblastoma (Rb) gene, the p53 gene and the adenomatous polyposis coli (APC) gene that are all involved in the development of both hereditary and non-hereditary forms of cancer. Inherited mutations in such genes predispose affected families to hereditary cancer syndromes, affording an opportunity to identify genetic lesions that also cause the more common sporadic cancers.
Prostate cancer (PRCA) is the most common cancer diagnosed (1999 estimate 179,300 cases) and the second leading cause of cancer mortality (1999 estimate 37,000 deaths) in men in the United States. Family history is the single strongest risk factor currently known for prostate cancer. This raises the possibility that heritable genetic factors may be involved in the development of this disease in a subset of men. The genetic contribution to diseases of complex origin such as cancer is often most salient in families of early onset cases. Therefore, prostate cancer inheritance following a simple Mendelian pattern, may be identified in the families of probands with early-onset cases. Common susceptibility alleles of small effect may be detectable in families with later-onsent and/or less strong family history of PRCA or in case-control data.
Ages Eligible for Study: | 18 Years and older |
Genders Eligible for Study: | Both |
Accepts Healthy Volunteers: | No |
Enrollment in this study includes case-control data from men with prostate cancer and matched controls who are free from the disease, plus affected and unaffected individuals from families who meet the following criteria for Hereditary Prostate Cancer:
Contact: Patient Recruitment and Public Liaison Office | (800) 411-1222 | prpl@mail.cc.nih.gov |
Contact: TTY | 1-866-411-1010 |
United States, Arizona | |
Translational Genomics Research Institute | Recruiting |
Phoenix, Arizona, United States | |
United States, District of Columbia | |
Howard University Hospital | Recruiting |
Washington, District of Columbia, United States, 20060 | |
United States, Louisiana | |
Louisiana State University | Recruiting |
New Orleans, Louisiana, United States, 70112-2282 | |
United States, Maryland | |
Johns Hopkins University | Recruiting |
Baltimore, Maryland, United States, 21205 | |
National Institutes of Health Clinical Center, 9000 Rockville Pike | Recruiting |
Bethesda, Maryland, United States, 20892 | |
United States, New York | |
Albert Einstein College of Medicine | Recruiting |
Bronx, New York, United States, 10461 | |
United States, North Carolina | |
Wake Forest University | Recruiting |
Winston-Salem, North Carolina, United States, 27103 | |
Finland | |
Tampere University | Recruiting |
Tampere, Finland |
Study ID Numbers: | 950158, 95-HG-0158 |
Study First Received: | November 3, 1999 |
Last Updated: | September 13, 2008 |
ClinicalTrials.gov Identifier: | NCT00001469 |
Health Authority: | United States: Federal Government |
Genotyping Linkage Analysis Adenocarcinoma |
Micro Satellite Hereditary Prostate Cancer (hereditary) |
Neoplastic Syndromes, Hereditary Prostatic Diseases Genital Neoplasms, Male Genetic Diseases, Inborn Urogenital Neoplasms |
Genital Diseases, Male Adenocarcinoma Prostatic Neoplasms Prostate cancer, familial |
Neoplasms Pathologic Processes Disease Neoplasms by Site Syndrome |