Genetic Analysis of Hereditary Prostate Cancer

NCT ID: NCT00001469

Last Updated: 2020-03-16

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Total Enrollment

7776 participants

Study Classification

OBSERVATIONAL

Study Start Date

1995-01-01

Study Completion Date

2009-07-17

Brief Summary

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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.

Detailed Description

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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-onset and/or less strong family history of PRCA or in case-control data.

Conditions

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Prostate Cancer

Study Design

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Observational Model Type

COHORT

Study Time Perspective

OTHER

Study Groups

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Specimens

Specimens

No interventions assigned to this group

Eligibility Criteria

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Inclusion Criteria

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:

1. A cluster of 3 or more first degree relatives, such as a father and 2 sons or 3 brothers
2. The occurrence of prostate cancer in each of 3 generations in either the proband's paternal or maternal lineages
3. Two first or second-degree relatives affected at an early age (age 55 years or younger).
Minimum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

No

Sponsors

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National Human Genome Research Institute (NHGRI)

NIH

Sponsor Role lead

Responsible Party

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Responsibility Role SPONSOR

Principal Investigators

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Joan Bailey-Wilson, Ph.D.

Role: PRINCIPAL_INVESTIGATOR

National Human Genome Research Institute (NHGRI)

Locations

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Translational Genomics Research Institute

Phoenix, Arizona, United States

Site Status

Howard University Hospital

Washington D.C., District of Columbia, United States

Site Status

Louisiana State University

New Orleans, Louisiana, United States

Site Status

Johns Hopkins University

Baltimore, Maryland, United States

Site Status

National Institutes of Health Clinical Center, 9000 Rockville Pike

Bethesda, Maryland, United States

Site Status

Albert Einstein College of Medicine

The Bronx, New York, United States

Site Status

Wake Forest University

Winston-Salem, North Carolina, United States

Site Status

Tampere University

Tampere, , Finland

Site Status

Countries

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United States Finland

References

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Ichikawa T, Ichikawa Y, Dong J, Hawkins AL, Griffin CA, Isaacs WB, Oshimura M, Barrett JC, Isaacs JT. Localization of metastasis suppressor gene(s) for prostatic cancer to the short arm of human chromosome 11. Cancer Res. 1992 Jun 15;52(12):3486-90.

Reference Type BACKGROUND
PMID: 1596907 (View on PubMed)

Bishop JM. The molecular genetics of cancer. Science. 1987 Jan 16;235(4786):305-11. doi: 10.1126/science.3541204.

Reference Type BACKGROUND
PMID: 3541204 (View on PubMed)

Knudson AG Jr. Hereditary cancer, oncogenes, and antioncogenes. Cancer Res. 1985 Apr;45(4):1437-43. No abstract available.

Reference Type BACKGROUND
PMID: 2983882 (View on PubMed)

Related Links

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Other Identifiers

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95-HG-0158

Identifier Type: -

Identifier Source: secondary_id

950158

Identifier Type: -

Identifier Source: org_study_id

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