Pancreatic cancer genetic epidemiology consortium

Gloria M. Petersen, Mariza De Andrade, Michael Goggins, Ralph H. Hruban, Melissa Bondy, Jeannette F. Korczak, Steven Gallinger, Henry T. Lynch, Sapna Syngal, Kari G. Rabe, Daniela Seminara, Alison P. Klein

Research output: Contribution to journalArticle

95 Citations (Scopus)

Abstract

We have organized the Pancreatic Cancer Genetic Epidemiology (PACGENE) Consortium to identify susceptibility genes in familial pancreatic cancer (FPC). The Consortium comprises seven data collection centers, a statistical genetics core, and a pathology/archival genotyping core. We recruit kindreds containing two or more affected blood relatives ascertained through incident pancreatic adenocarcinoma cases, physician referrals, and/or through Internet recruitment. Accrual to a database containing core clinical, demographic, lifestyle, and family history information from questionnaires is ongoing, along with biospecimen collection. To date, 13,147 patients have been screened for family history, of whom 476 (50% male) probands and 1,912 of their adult (99% unaffected) relatives have been enrolled. Of these, 379 kindreds meet criteria for FPC, having at least two first-degree relatives with pancreatic cancer. Cumulative incidence curves using available age of diagnosis (onset) among and affected relatives were compared with those for incident pancreatic cancer cases reported to 13 U.S. Surveillance Epidemiology and End Results (SEER) sites from 1973 to 2000 (N = 72,700). The mean age ± SD at diagnosis among 466 PACGENE probands and 670 affected relatives was 64.1 ± 11.8 and was 65.4 ± 11.6 for the subset of 369 FPC probands and 429 relatives. Both samples were significantly younger than the mean age at diagnosis in the SEER population (70.0 ± 12.1 years; differences in curves versus SEER, P <0.001). Age at diagnosis (excluding probands) in FPC kindreds does not decrease with increasing number of affected individuals. In our sample, younger age at diagnosis was observed whether we grouped probands by recruitment sites that predominantly recruited through high-risk referrals, or through screening all pancreatic cancer patients for family history. Linkage studies are ongoing. The PACGENE Consortium will be a valuable family-based resource that will greatly enhance genetic epidemiology research in pancreatic cancer.

Original languageEnglish
Pages (from-to)704-710
Number of pages7
JournalCancer Epidemiology Biomarkers and Prevention
Volume15
Issue number4
DOIs
StatePublished - Apr 2006

Fingerprint

Molecular Epidemiology
Pancreatic Neoplasms
Epidemiology
Referral and Consultation
Genetic Research
Age of Onset
Internet
Life Style
Adenocarcinoma
Demography
Databases
Pathology
Physicians

All Science Journal Classification (ASJC) codes

  • Epidemiology
  • Oncology

Cite this

Petersen, G. M., De Andrade, M., Goggins, M., Hruban, R. H., Bondy, M., Korczak, J. F., ... Klein, A. P. (2006). Pancreatic cancer genetic epidemiology consortium. Cancer Epidemiology Biomarkers and Prevention, 15(4), 704-710. https://doi.org/10.1158/1055-9965.EPI-05-0734

Pancreatic cancer genetic epidemiology consortium. / Petersen, Gloria M.; De Andrade, Mariza; Goggins, Michael; Hruban, Ralph H.; Bondy, Melissa; Korczak, Jeannette F.; Gallinger, Steven; Lynch, Henry T.; Syngal, Sapna; Rabe, Kari G.; Seminara, Daniela; Klein, Alison P.

In: Cancer Epidemiology Biomarkers and Prevention, Vol. 15, No. 4, 04.2006, p. 704-710.

Research output: Contribution to journalArticle

Petersen, GM, De Andrade, M, Goggins, M, Hruban, RH, Bondy, M, Korczak, JF, Gallinger, S, Lynch, HT, Syngal, S, Rabe, KG, Seminara, D & Klein, AP 2006, 'Pancreatic cancer genetic epidemiology consortium', Cancer Epidemiology Biomarkers and Prevention, vol. 15, no. 4, pp. 704-710. https://doi.org/10.1158/1055-9965.EPI-05-0734
Petersen GM, De Andrade M, Goggins M, Hruban RH, Bondy M, Korczak JF et al. Pancreatic cancer genetic epidemiology consortium. Cancer Epidemiology Biomarkers and Prevention. 2006 Apr;15(4):704-710. https://doi.org/10.1158/1055-9965.EPI-05-0734
Petersen, Gloria M. ; De Andrade, Mariza ; Goggins, Michael ; Hruban, Ralph H. ; Bondy, Melissa ; Korczak, Jeannette F. ; Gallinger, Steven ; Lynch, Henry T. ; Syngal, Sapna ; Rabe, Kari G. ; Seminara, Daniela ; Klein, Alison P. / Pancreatic cancer genetic epidemiology consortium. In: Cancer Epidemiology Biomarkers and Prevention. 2006 ; Vol. 15, No. 4. pp. 704-710.
@article{011b62f9ab95446db0ed035627b33849,
title = "Pancreatic cancer genetic epidemiology consortium",
abstract = "We have organized the Pancreatic Cancer Genetic Epidemiology (PACGENE) Consortium to identify susceptibility genes in familial pancreatic cancer (FPC). The Consortium comprises seven data collection centers, a statistical genetics core, and a pathology/archival genotyping core. We recruit kindreds containing two or more affected blood relatives ascertained through incident pancreatic adenocarcinoma cases, physician referrals, and/or through Internet recruitment. Accrual to a database containing core clinical, demographic, lifestyle, and family history information from questionnaires is ongoing, along with biospecimen collection. To date, 13,147 patients have been screened for family history, of whom 476 (50{\%} male) probands and 1,912 of their adult (99{\%} unaffected) relatives have been enrolled. Of these, 379 kindreds meet criteria for FPC, having at least two first-degree relatives with pancreatic cancer. Cumulative incidence curves using available age of diagnosis (onset) among and affected relatives were compared with those for incident pancreatic cancer cases reported to 13 U.S. Surveillance Epidemiology and End Results (SEER) sites from 1973 to 2000 (N = 72,700). The mean age ± SD at diagnosis among 466 PACGENE probands and 670 affected relatives was 64.1 ± 11.8 and was 65.4 ± 11.6 for the subset of 369 FPC probands and 429 relatives. Both samples were significantly younger than the mean age at diagnosis in the SEER population (70.0 ± 12.1 years; differences in curves versus SEER, P <0.001). Age at diagnosis (excluding probands) in FPC kindreds does not decrease with increasing number of affected individuals. In our sample, younger age at diagnosis was observed whether we grouped probands by recruitment sites that predominantly recruited through high-risk referrals, or through screening all pancreatic cancer patients for family history. Linkage studies are ongoing. The PACGENE Consortium will be a valuable family-based resource that will greatly enhance genetic epidemiology research in pancreatic cancer.",
author = "Petersen, {Gloria M.} and {De Andrade}, Mariza and Michael Goggins and Hruban, {Ralph H.} and Melissa Bondy and Korczak, {Jeannette F.} and Steven Gallinger and Lynch, {Henry T.} and Sapna Syngal and Rabe, {Kari G.} and Daniela Seminara and Klein, {Alison P.}",
year = "2006",
month = "4",
doi = "10.1158/1055-9965.EPI-05-0734",
language = "English",
volume = "15",
pages = "704--710",
journal = "Cancer Epidemiology Biomarkers and Prevention",
issn = "1055-9965",
publisher = "American Association for Cancer Research Inc.",
number = "4",

}

TY - JOUR

T1 - Pancreatic cancer genetic epidemiology consortium

AU - Petersen, Gloria M.

AU - De Andrade, Mariza

AU - Goggins, Michael

AU - Hruban, Ralph H.

AU - Bondy, Melissa

AU - Korczak, Jeannette F.

AU - Gallinger, Steven

AU - Lynch, Henry T.

AU - Syngal, Sapna

AU - Rabe, Kari G.

AU - Seminara, Daniela

AU - Klein, Alison P.

PY - 2006/4

Y1 - 2006/4

N2 - We have organized the Pancreatic Cancer Genetic Epidemiology (PACGENE) Consortium to identify susceptibility genes in familial pancreatic cancer (FPC). The Consortium comprises seven data collection centers, a statistical genetics core, and a pathology/archival genotyping core. We recruit kindreds containing two or more affected blood relatives ascertained through incident pancreatic adenocarcinoma cases, physician referrals, and/or through Internet recruitment. Accrual to a database containing core clinical, demographic, lifestyle, and family history information from questionnaires is ongoing, along with biospecimen collection. To date, 13,147 patients have been screened for family history, of whom 476 (50% male) probands and 1,912 of their adult (99% unaffected) relatives have been enrolled. Of these, 379 kindreds meet criteria for FPC, having at least two first-degree relatives with pancreatic cancer. Cumulative incidence curves using available age of diagnosis (onset) among and affected relatives were compared with those for incident pancreatic cancer cases reported to 13 U.S. Surveillance Epidemiology and End Results (SEER) sites from 1973 to 2000 (N = 72,700). The mean age ± SD at diagnosis among 466 PACGENE probands and 670 affected relatives was 64.1 ± 11.8 and was 65.4 ± 11.6 for the subset of 369 FPC probands and 429 relatives. Both samples were significantly younger than the mean age at diagnosis in the SEER population (70.0 ± 12.1 years; differences in curves versus SEER, P <0.001). Age at diagnosis (excluding probands) in FPC kindreds does not decrease with increasing number of affected individuals. In our sample, younger age at diagnosis was observed whether we grouped probands by recruitment sites that predominantly recruited through high-risk referrals, or through screening all pancreatic cancer patients for family history. Linkage studies are ongoing. The PACGENE Consortium will be a valuable family-based resource that will greatly enhance genetic epidemiology research in pancreatic cancer.

AB - We have organized the Pancreatic Cancer Genetic Epidemiology (PACGENE) Consortium to identify susceptibility genes in familial pancreatic cancer (FPC). The Consortium comprises seven data collection centers, a statistical genetics core, and a pathology/archival genotyping core. We recruit kindreds containing two or more affected blood relatives ascertained through incident pancreatic adenocarcinoma cases, physician referrals, and/or through Internet recruitment. Accrual to a database containing core clinical, demographic, lifestyle, and family history information from questionnaires is ongoing, along with biospecimen collection. To date, 13,147 patients have been screened for family history, of whom 476 (50% male) probands and 1,912 of their adult (99% unaffected) relatives have been enrolled. Of these, 379 kindreds meet criteria for FPC, having at least two first-degree relatives with pancreatic cancer. Cumulative incidence curves using available age of diagnosis (onset) among and affected relatives were compared with those for incident pancreatic cancer cases reported to 13 U.S. Surveillance Epidemiology and End Results (SEER) sites from 1973 to 2000 (N = 72,700). The mean age ± SD at diagnosis among 466 PACGENE probands and 670 affected relatives was 64.1 ± 11.8 and was 65.4 ± 11.6 for the subset of 369 FPC probands and 429 relatives. Both samples were significantly younger than the mean age at diagnosis in the SEER population (70.0 ± 12.1 years; differences in curves versus SEER, P <0.001). Age at diagnosis (excluding probands) in FPC kindreds does not decrease with increasing number of affected individuals. In our sample, younger age at diagnosis was observed whether we grouped probands by recruitment sites that predominantly recruited through high-risk referrals, or through screening all pancreatic cancer patients for family history. Linkage studies are ongoing. The PACGENE Consortium will be a valuable family-based resource that will greatly enhance genetic epidemiology research in pancreatic cancer.

UR - http://www.scopus.com/inward/record.url?scp=33646231772&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33646231772&partnerID=8YFLogxK

U2 - 10.1158/1055-9965.EPI-05-0734

DO - 10.1158/1055-9965.EPI-05-0734

M3 - Article

VL - 15

SP - 704

EP - 710

JO - Cancer Epidemiology Biomarkers and Prevention

JF - Cancer Epidemiology Biomarkers and Prevention

SN - 1055-9965

IS - 4

ER -