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Genetic changes in familial prostate cancer by comparative genomic hybridization
The Prostate, 2001-02, Vol.46 (3), p.233-239
Rökman, Annika
Koivisto, Pasi A.
Matikainen, Mika P.
Kuukasjärvi, Tuula
Poutiainen, Marita
Helin, Heikki J.
Karhu, Ritva
Kallioniemi, Olli-P.
Schleutker, Johanna
2001
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Rökman, Annika
Koivisto, Pasi A.
Matikainen, Mika P.
Kuukasjärvi, Tuula
Poutiainen, Marita
Helin, Heikki J.
Karhu, Ritva
Kallioniemi, Olli-P.
Schleutker, Johanna
Titel
Genetic changes in familial prostate cancer by comparative genomic hybridization
Ist Teil von
The Prostate, 2001-02, Vol.46 (3), p.233-239
Ort / Verlag
New York: John Wiley & Sons, Inc
Erscheinungsjahr
2001
Quelle
Access via Wiley Online Library
Beschreibungen/Notizen
Background Germline mutations in recessive cancer predisposition genes are uncovered by somatic genetic deletions during tumor development. Analysis of genetic changes in tumor tissues from patients with an inherited predisposition may therefore highlight regions of the genome containing susceptibility or modifier genes. Our aim was to characterize genetic changes in familial prostate cancer Methods Twenty‐one primary prostate cancers from 19 Finnish prostate cancer families were analyzed for somatic genetic changes by comparative genomic hybridization (CGH). Results The average number of genetic alterations per tumor was 4.0 ± 1.9, distributed equally among losses and gains. The most common losses were found at chromosomal regions 13q14–q22 (29%), 8p12‐pter (24%), and 6q13–q16 (14%), and the most common gains at 19p (25%), 19q (14%) and 7q (14%). Conclusions These results suggest that prostate cancers in genetically predisposed individuals arise for the most part through similar somatic genetic progression pathways as sporadic prostate cancers. This also implies that the biological properties of tumors from the two groups may not be different from one another. Prostate 46:233–239, 2001. © 2001 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0270-4137
eISSN: 1097-0045
DOI: 10.1002/1097-0045(20010215)46:3<233::AID-PROS1028>3.0.CO;2-W
Titel-ID: cdi_proquest_miscellaneous_70632269
Format
–
Schlagworte
Aged
,
Aged, 80 and over
,
Biological and medical sciences
,
cancer predisposition
,
Carcinoma - genetics
,
Chromosome Aberrations
,
deletion
,
Genetic Predisposition to Disease - genetics
,
hereditary prostate cancer
,
Humans
,
Karyotyping
,
Male
,
Medical sciences
,
Middle Aged
,
molecular cytogenetics
,
Nephrology. Urinary tract diseases
,
Nucleic Acid Hybridization
,
Prostatic Neoplasms - genetics
,
Tumors of the urinary system
,
Urinary tract. Prostate gland
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