This is an archive of papers published by the staff and faculty of Fox Chase Cancer Center. For questions about content, please contact Talbot Research Library
Last updated on
Pakkanen S , Baffoe-Bonnie AB , Matikainen MP , Koivisto PA , Tammela TLJ , Deshmukh S , Ou L , Bailey-Wilson JE , Schleutker J
Segregation analysis of 1,546 prostate cancer families in Finland shows recessive inheritance
Human Genetics. 2007 Apr;121(2) :257-267
AbstractProstate cancer (PCa) is the most frequently diagnosed cancer in men worldwide and is likely to be caused by a number of genes with different modes of inheritance, population frequencies and penetrance. The objective of this study was to assess the familial aggregation of PCa in a sample of 1,546 nuclear families ascertained through an affected father and diagnosed during 1988-1993, from the unique, founder population-based resource of the Finnish Cancer Registry. Segregation analysis was performed for two cohorts of 557 early-onset and 989 late-onset families evaluating residual paternal effects and assuming that age at diagnosis followed a logistic distribution after log-transformation. The results did not support an autosomal dominant inheritance as has been reported in many of the hospital-based prostatectomy series. Instead, it confirmed the existence of hereditary PCa in the Finnish population under a complex model that included a major susceptibility locus with Mendelian recessive inheritance and a significant paternal regressive coefficient that is indicative of a polygenic/multifactorial component. The strengths of our study are the homogenous Finnish population, large epidemiological population-based data, histologically confirmed cancer diagnosis done before the PSA-era in Finland and registry based approach. Our results support the evidence that the inheritance of PCa is controlled by major genes and are in line with the previous linkage studies. Moreover, this is the first time a recessive inheritance is suggested to fit PCa in all data even when divided to early and late-onset cohorts.
NotesISI Document Delivery No.: 145TT Times Cited: 0 Cited Reference Count: 46 Cited References: *FINN CANC REG, 2006, CANC INC FINL 1995 2 *WHO, 2003, GLOB CANC RAT COULD AKAIKE H, 1974, IEEE T AUTOMATIC CON, V19, P716 BAFFOEBONNIE AB, 2002, GENET EPIDEMIOL, V23, P349 BAFFOEBONNIE AB, 2005, HUM GENET, V117, P307 BONNEY GE, 1986, BIOMETRICS, V42, P611 CANNINGS C, 1977, CLIN GENET, V12, P208 CANNINGS C, 1978, ADV APPL PROBAB, V10, P26 CARPTEN J, 2002, NAT GENET, V30, P181 CARTER BS, 1992, P NATL ACAD SCI USA, V89, P3367 CONLON EM, 2003, INT J CANCER, V105, P630 CUI JS, 2001, AM J HUM GENET, V68, P1207 DELACHAPELLE A, 1993, J MED GENET, V30, P857 ELSTON RC, 1971, HUM HERED, V21, P523 ELSTON RC, 1975, AM J HUM GENET, V27, P31 ELSTON RC, 1979, AM J HUM GENET, V31, P62 ELSTON RC, 1981, ADV HUM GENET, V11, P63 ELSTON RC, 1989, GENET EPIDEMIOL, V6, P217 GIANFERRARI L, 1956, ACTA GENTICAE MED GE, V5, P224 GONG G, 2002, CANCER CAUSE CONTROL, V13, P471 GRONBERG H, 1997, AM J EPIDEMIOL, V146, P552 LICHTENSTEIN P, 2000, NEW ENGL J MED, V343, P78 MAKINEN T, 2002, J CLIN ONCOL, V20, P2658 MAKINEN T, 2003, CLIN CANCER RES, V9, P2435 MATIKAINEN MP, 2001, CANCER CAUSE CONTROL, V12, P223 MONROE KR, 1995, NAT MED, V1, P827 NAROD SA, 1995, NAT MED, V1, P99 PELTONEN L, 1997, ANN MED, V29, P553 REBBECK TR, 2000, AM J HUM GENET, V67, P1014 ROKMAN A, 2001, CANCER RES, V61, P6038 ROKMAN A, 2002, AM J HUM GENET, V70, P1299 SAGE MR, 1997, INT J NEURORADIOL, V3, P1 SCHAID DJ, 1998, AM J HUM GENET, V62, P1425 SCHAID DJ, 2004, HUM MOL GENET, V13, P103 SCHLEUTKER J, 2000, CLIN CANCER RES, V6, P4810 SCHLEUTKER J, 2003, PROSTATE, V57, P280 SEPPALA EH, 2003, BRIT J CANCER, V89, P1966 SEPPALA EH, 2003, CLIN CANCER RES, V9, P5252 SMITH JR, 1996, SCIENCE, V274, P1371 TEPPO L, 1994, ACTA ONCOL, V33, P365 TZVTIGIAN SV, 2001, NAT GENET, V27, P172 VALERI A, 2003, ANN HUM GENET 2, V67, P125 VERHAGE BAJ, 2001, UROLOGY, V57, P97 XU JF, 1998, NAT GENET, V20, P175 XU JF, 2002, NAT GENET, V32, P321 XU JF, 2005, AM J HUM GENET, V77, P219