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Site‐specific familial aggregation of prostate cancer
Over the last decade, epidemiologic evidence has accumulated in favor of a significant but heterogeneous hereditary component in prostate cancer (PC) susceptibility. In order to map and clone PC susceptibility genes, stratification of PC families into genetically homogeneous groups appears to be a k...
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Published in: | International journal of cancer 2004-04, Vol.109 (4), p.611-617 |
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container_title | International journal of cancer |
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description | Over the last decade, epidemiologic evidence has accumulated in favor of a significant but heterogeneous hereditary component in prostate cancer (PC) susceptibility. In order to map and clone PC susceptibility genes, stratification of PC families into genetically homogeneous groups appears to be a key issue. Subset definition based on age at diagnosis, presumed mode of inheritance, number of affecteds per family and coaggregation of PC with other cancers has already proven successful in some studies. Previously, the finding of the coaggregation of malignancies of the central nervous system within PC families helped to link a prostate‐brain cancer susceptibility gene (CAPB) to chromosome 1p36. In this study, we evaluate the risk of PC and malignancies at other sites among first‐degree relatives of a large population‐based group of Dutch PC patients. A population‐based family case‐control study was initiated that included Caucasian PC patients newly diagnosed between July 1996 and December 1999. Information on 12,575 first‐degree relatives of 704 PC patients and 1,371 controls was collected through postal questionnaires and telephone interviews. All reported PC in first‐degree relatives was verified through medical records. In our population, PC has a strong familial component that is reflected by a 2.9‐fold increased risk (95% CI = 2.2–3.9) of PC for first‐degree relatives of PC patients. This familial risk was somewhat higher among brothers (hazard ratio = 3.9; 95% CI = 2.4–6.4) compared to fathers (hazard ratio = 2.5; 95% CI = 1.7–3.6). Cancers at other sites did not coaggregate with PC. Our data suggest that familial PC, at least in this Western European population, is site‐specific, not part of an inherited cancer syndrome. © 2004 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/ijc.20015 |
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Alfred ; Straatman, Huub ; Schalken, Jack A. ; Kiemeney, Lambertus A.L.M.</creator><creatorcontrib>Verhage, Bas A.J. ; Aben, Katja K.H. ; Witjes, J. Alfred ; Straatman, Huub ; Schalken, Jack A. ; Kiemeney, Lambertus A.L.M.</creatorcontrib><description>Over the last decade, epidemiologic evidence has accumulated in favor of a significant but heterogeneous hereditary component in prostate cancer (PC) susceptibility. In order to map and clone PC susceptibility genes, stratification of PC families into genetically homogeneous groups appears to be a key issue. Subset definition based on age at diagnosis, presumed mode of inheritance, number of affecteds per family and coaggregation of PC with other cancers has already proven successful in some studies. Previously, the finding of the coaggregation of malignancies of the central nervous system within PC families helped to link a prostate‐brain cancer susceptibility gene (CAPB) to chromosome 1p36. In this study, we evaluate the risk of PC and malignancies at other sites among first‐degree relatives of a large population‐based group of Dutch PC patients. A population‐based family case‐control study was initiated that included Caucasian PC patients newly diagnosed between July 1996 and December 1999. Information on 12,575 first‐degree relatives of 704 PC patients and 1,371 controls was collected through postal questionnaires and telephone interviews. All reported PC in first‐degree relatives was verified through medical records. In our population, PC has a strong familial component that is reflected by a 2.9‐fold increased risk (95% CI = 2.2–3.9) of PC for first‐degree relatives of PC patients. This familial risk was somewhat higher among brothers (hazard ratio = 3.9; 95% CI = 2.4–6.4) compared to fathers (hazard ratio = 2.5; 95% CI = 1.7–3.6). Cancers at other sites did not coaggregate with PC. Our data suggest that familial PC, at least in this Western European population, is site‐specific, not part of an inherited cancer syndrome. © 2004 Wiley‐Liss, Inc.</description><identifier>ISSN: 0020-7136</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/ijc.20015</identifier><identifier>PMID: 14991584</identifier><identifier>CODEN: IJCNAW</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Aged ; Biological and medical sciences ; cancer ; Case-Control Studies ; clustering ; Cohort Studies ; European Continental Ancestry Group ; familial aggregation ; Family Health ; Humans ; Interviews as Topic ; Male ; Medical sciences ; Middle Aged ; Neoplasms - diagnosis ; Neoplasms - epidemiology ; Neoplasms - genetics ; Neoplastic Syndromes, Hereditary - diagnosis ; Neoplastic Syndromes, Hereditary - epidemiology ; Neoplastic Syndromes, Hereditary - genetics ; Nephrology. Urinary tract diseases ; prostate cancer ; Prostatic Neoplasms - diagnosis ; Prostatic Neoplasms - epidemiology ; Prostatic Neoplasms - genetics ; risk factor ; Risk Factors ; Surveys and Questionnaires ; Tumors of the urinary system ; Urinary tract. 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Alfred</creatorcontrib><creatorcontrib>Straatman, Huub</creatorcontrib><creatorcontrib>Schalken, Jack A.</creatorcontrib><creatorcontrib>Kiemeney, Lambertus A.L.M.</creatorcontrib><title>Site‐specific familial aggregation of prostate cancer</title><title>International journal of cancer</title><addtitle>Int J Cancer</addtitle><description>Over the last decade, epidemiologic evidence has accumulated in favor of a significant but heterogeneous hereditary component in prostate cancer (PC) susceptibility. In order to map and clone PC susceptibility genes, stratification of PC families into genetically homogeneous groups appears to be a key issue. Subset definition based on age at diagnosis, presumed mode of inheritance, number of affecteds per family and coaggregation of PC with other cancers has already proven successful in some studies. Previously, the finding of the coaggregation of malignancies of the central nervous system within PC families helped to link a prostate‐brain cancer susceptibility gene (CAPB) to chromosome 1p36. In this study, we evaluate the risk of PC and malignancies at other sites among first‐degree relatives of a large population‐based group of Dutch PC patients. A population‐based family case‐control study was initiated that included Caucasian PC patients newly diagnosed between July 1996 and December 1999. Information on 12,575 first‐degree relatives of 704 PC patients and 1,371 controls was collected through postal questionnaires and telephone interviews. All reported PC in first‐degree relatives was verified through medical records. In our population, PC has a strong familial component that is reflected by a 2.9‐fold increased risk (95% CI = 2.2–3.9) of PC for first‐degree relatives of PC patients. This familial risk was somewhat higher among brothers (hazard ratio = 3.9; 95% CI = 2.4–6.4) compared to fathers (hazard ratio = 2.5; 95% CI = 1.7–3.6). Cancers at other sites did not coaggregate with PC. Our data suggest that familial PC, at least in this Western European population, is site‐specific, not part of an inherited cancer syndrome. © 2004 Wiley‐Liss, Inc.</description><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>cancer</subject><subject>Case-Control Studies</subject><subject>clustering</subject><subject>Cohort Studies</subject><subject>European Continental Ancestry Group</subject><subject>familial aggregation</subject><subject>Family Health</subject><subject>Humans</subject><subject>Interviews as Topic</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neoplasms - diagnosis</subject><subject>Neoplasms - epidemiology</subject><subject>Neoplasms - genetics</subject><subject>Neoplastic Syndromes, Hereditary - diagnosis</subject><subject>Neoplastic Syndromes, Hereditary - epidemiology</subject><subject>Neoplastic Syndromes, Hereditary - genetics</subject><subject>Nephrology. Urinary tract diseases</subject><subject>prostate cancer</subject><subject>Prostatic Neoplasms - diagnosis</subject><subject>Prostatic Neoplasms - epidemiology</subject><subject>Prostatic Neoplasms - genetics</subject><subject>risk factor</subject><subject>Risk Factors</subject><subject>Surveys and Questionnaires</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. Prostate gland</subject><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNqF0LtOwzAUBmALgWgpDLwAygISQ1ofx9cRVVyKKjEAc-S4duUqaUqcCnXjEXhGngSXRGJCTB7Op_Mf_widAx4DxmTiV2ZMMAZ2gIaAlUgxAXaIhnGGUwEZH6CTEFZRAMP0GA2AKgVM0iESz761Xx-fYWONd94kTle-9LpM9HLZ2KVufb1Oapdsmjq0urWJ0Wtjm1N05HQZ7Fn_jtDr3e3L9CGdP93Ppjfz1FAQLCWWCcHBaqwkByYkk8oI4ZymlmSiKLJMOLKQmSqE41gqSjTFFsMiExQ4z0boqtsb89-2NrR55YOxZanXtt6GXACXkmLxLwRFGOVURXjdQRN_FBrr8k3jK93scsD5vs481pn_1BntRb90W1R28Sv7_iK47IEORpeuieX48OsYU5SS_XWTzr370u7-Tsxnj9Mu-htveonR</recordid><startdate>20040420</startdate><enddate>20040420</enddate><creator>Verhage, Bas A.J.</creator><creator>Aben, Katja K.H.</creator><creator>Witjes, J. Alfred</creator><creator>Straatman, Huub</creator><creator>Schalken, Jack A.</creator><creator>Kiemeney, Lambertus A.L.M.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U1</scope><scope>7U2</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>20040420</creationdate><title>Site‐specific familial aggregation of prostate cancer</title><author>Verhage, Bas A.J. ; Aben, Katja K.H. ; Witjes, J. Alfred ; Straatman, Huub ; Schalken, Jack A. ; Kiemeney, Lambertus A.L.M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4175-2e57761ea09861578589c77ffa4e237bb337f2d839b7f608942a40e01d3741663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>cancer</topic><topic>Case-Control Studies</topic><topic>clustering</topic><topic>Cohort Studies</topic><topic>European Continental Ancestry Group</topic><topic>familial aggregation</topic><topic>Family Health</topic><topic>Humans</topic><topic>Interviews as Topic</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neoplasms - diagnosis</topic><topic>Neoplasms - epidemiology</topic><topic>Neoplasms - genetics</topic><topic>Neoplastic Syndromes, Hereditary - diagnosis</topic><topic>Neoplastic Syndromes, Hereditary - epidemiology</topic><topic>Neoplastic Syndromes, Hereditary - genetics</topic><topic>Nephrology. Urinary tract diseases</topic><topic>prostate cancer</topic><topic>Prostatic Neoplasms - diagnosis</topic><topic>Prostatic Neoplasms - epidemiology</topic><topic>Prostatic Neoplasms - genetics</topic><topic>risk factor</topic><topic>Risk Factors</topic><topic>Surveys and Questionnaires</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Verhage, Bas A.J.</creatorcontrib><creatorcontrib>Aben, Katja K.H.</creatorcontrib><creatorcontrib>Witjes, J. Alfred</creatorcontrib><creatorcontrib>Straatman, Huub</creatorcontrib><creatorcontrib>Schalken, Jack A.</creatorcontrib><creatorcontrib>Kiemeney, Lambertus A.L.M.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Risk Abstracts</collection><collection>Safety Science and Risk</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Verhage, Bas A.J.</au><au>Aben, Katja K.H.</au><au>Witjes, J. Alfred</au><au>Straatman, Huub</au><au>Schalken, Jack A.</au><au>Kiemeney, Lambertus A.L.M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Site‐specific familial aggregation of prostate cancer</atitle><jtitle>International journal of cancer</jtitle><addtitle>Int J Cancer</addtitle><date>2004-04-20</date><risdate>2004</risdate><volume>109</volume><issue>4</issue><spage>611</spage><epage>617</epage><pages>611-617</pages><issn>0020-7136</issn><eissn>1097-0215</eissn><coden>IJCNAW</coden><abstract>Over the last decade, epidemiologic evidence has accumulated in favor of a significant but heterogeneous hereditary component in prostate cancer (PC) susceptibility. In order to map and clone PC susceptibility genes, stratification of PC families into genetically homogeneous groups appears to be a key issue. Subset definition based on age at diagnosis, presumed mode of inheritance, number of affecteds per family and coaggregation of PC with other cancers has already proven successful in some studies. Previously, the finding of the coaggregation of malignancies of the central nervous system within PC families helped to link a prostate‐brain cancer susceptibility gene (CAPB) to chromosome 1p36. In this study, we evaluate the risk of PC and malignancies at other sites among first‐degree relatives of a large population‐based group of Dutch PC patients. A population‐based family case‐control study was initiated that included Caucasian PC patients newly diagnosed between July 1996 and December 1999. Information on 12,575 first‐degree relatives of 704 PC patients and 1,371 controls was collected through postal questionnaires and telephone interviews. All reported PC in first‐degree relatives was verified through medical records. In our population, PC has a strong familial component that is reflected by a 2.9‐fold increased risk (95% CI = 2.2–3.9) of PC for first‐degree relatives of PC patients. This familial risk was somewhat higher among brothers (hazard ratio = 3.9; 95% CI = 2.4–6.4) compared to fathers (hazard ratio = 2.5; 95% CI = 1.7–3.6). Cancers at other sites did not coaggregate with PC. Our data suggest that familial PC, at least in this Western European population, is site‐specific, not part of an inherited cancer syndrome. © 2004 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>14991584</pmid><doi>10.1002/ijc.20015</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aged Biological and medical sciences cancer Case-Control Studies clustering Cohort Studies European Continental Ancestry Group familial aggregation Family Health Humans Interviews as Topic Male Medical sciences Middle Aged Neoplasms - diagnosis Neoplasms - epidemiology Neoplasms - genetics Neoplastic Syndromes, Hereditary - diagnosis Neoplastic Syndromes, Hereditary - epidemiology Neoplastic Syndromes, Hereditary - genetics Nephrology. Urinary tract diseases prostate cancer Prostatic Neoplasms - diagnosis Prostatic Neoplasms - epidemiology Prostatic Neoplasms - genetics risk factor Risk Factors Surveys and Questionnaires Tumors of the urinary system Urinary tract. Prostate gland |
title | Site‐specific familial aggregation of prostate cancer |
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