Family history of cancer, Ashkenazi Jewish ancestry, and pancreatic cancer risk

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Abstract

Background

Individuals with a family history of cancer may be at increased risk of pancreatic cancer. Ashkenazi Jewish (AJ) individuals carry increased risk for pancreatic cancer and other cancer types.

Methods

We examined the association between family history of cancer, AJ heritage, and incident pancreatic cancer in 49 410 male participants of the prospective Health Professionals Follow-up Study. Hazard ratios (HRs) were estimated using multivariable-adjusted Cox proportional hazards models.

Results

During 1.1 million person-years (1986–2016), 452 participants developed pancreatic cancer. Increased risk of pancreatic cancer was observed in individuals with a family history of pancreatic (HR, 2.79; 95% confidence interval [CI], 1.28–6.07) or breast cancer (HR, 1.40; 95% CI, 1.01–1.94). There was a trend towards higher risk of pancreatic cancer in relation to a family history of colorectal cancer (HR, 1.21; 95% CI, 0.95–1.55) or AJ heritage (HR, 1.29; 95% CI, 0.94–1.77). The risk was highly elevated among AJ men with a family history of breast or colorectal cancer (HR, 2.61 [95% CI, 1.41–4.82] and 1.92 [95% CI, 1.05–3.49], respectively).

Conclusion

Family history of pancreatic cancer was associated with increased risk of this malignancy. Family history of breast or colorectal cancer was associated with the increased risk among AJ men.

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Most cited references 36

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Exomic sequencing identifies PALB2 as a pancreatic cancer susceptibility gene.

Siân Jones, Ralph H. Hruban, Mihoko Kamiyama … (2009)

Through complete sequencing of the protein-coding genes in a patient with familial pancreatic cancer, we identified a germline, truncating mutation in PALB2 that appeared responsible for this patient's predisposition to the disease. Analysis of 96 additional patients with familial pancreatic cancer revealed three distinct protein-truncating mutations, thereby validating the role of PALB2 as a susceptibility gene for pancreatic cancer. PALB2 mutations have been previously reported in patients with familial breast cancer, and the PALB2 protein is a binding partner for BRCA2. These results illustrate that complete, unbiased sequencing of protein-coding genes can lead to the identification of a gene responsible for a hereditary disease.

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Test of the National Death Index and Equifax Nationwide Death Search.

Janet W. Rich-Edwards, M Stampfer, K Corsano (1994)

The authors compared the ability of the National Death Index and the Equifax Nationwide Death Search to ascertain deaths of participants in the Nurses' Health Study. Each service was sent information on 197 participants aged 60-68 years in 1989 whose deaths were reported by kin or postal authorities and 1,997 participants of the same age who were known to be alive. Neither service was aware of the authors' information regarding participants' vital status. The sensitivity of the National Death Index was 98 percent and that of Equifax was 79 percent. Sensitivity was similar for women aged 65-68 years; however, for women aged 61-64 years, the sensitivity of the National Death Index was 97.7 percent compared with 60.2 percent for Equifax. The specificity of both services was approximately 100 percent. The contrast between the sources of these databases and the matching algorithms they employ has implications for researchers and for those planning health data systems.

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Periodontal disease, tooth loss, and cancer risk in male health professionals: a prospective cohort study.

Dominique S Michaud, Yan Liu, Mara Meyer … (2008)

Studies suggest that tooth loss and periodontal disease might increase the risk of developing various cancers; however, smoking might have confounded the reported associations. We aimed to assess whether periodontal disease or tooth loss is associated with cancer risk. The analysis was done in a prospective study (the Health Professionals Follow-Up Study [HPFS]), which was initiated in 1986 when US male health professionals aged 40-75 years responded to questionnaires posted by the Department of Nutrition, Harvard University School of Public Health, Boston, MA, USA. In addition to the baseline questionnaires, follow-up questionnaires were posted to all living participants every 2 years and dietary questionnaires every 4 years. At baseline, participants were asked whether they had a history of periodontal disease with bone loss. Participants also reported number of natural teeth at baseline and any tooth loss during the previous 2 years was reported on the follow-up questionnaires. Smoking status and history of smoking were obtained at baseline and in all subsequent questionnaires. Additionally at baseline, participants reported their mean frequency of food intake over the previous year on a 131-item semiquantitative food-frequency questionnaire. Participants reported any new cancer diagnosis on the follow-up questionnaires. Endpoints for this study were risk of total cancer and individual cancers with more than 100 cases. Multivariate hazard ratios (HRs) and 95% CIs were calculated by use of Cox proportional hazard models according to periodontal disease status and number of teeth at baseline. In the main analyses, 48 375 men with median follow-up of 17.7 years (1986 to Jan 31, 2004) were eligible after excluding participants diagnosed with cancer before 1986 (other than non-melanoma skin cancer, n=2076) and those with missing data on periodontal disease (n=1078). 5720 incident cancer cases were documented (excluding non-melanoma skin cancer and non-aggressive prostate cancer). The five most common cancers were colorectal (n=1043), melanoma of the skin (n=698), lung (n=678), bladder (n=543), and advanced prostate (n=541). After adjusting for known risk factors, including detailed smoking history and dietary factors, participants with a history of periodontal disease had an increased risk of total cancer (HR 1.14 [95% CI 1.07-1.22]) compared with those with no history of periodontal disease. By cancer site, significant associations for those with a history of periodontal disease were noted for lung (1.36 [1.15-1.60]), kidney (1.49 [1.12-1.97]), pancreas (1.54 [1.16-2.04]; findings previously published), and haematological cancers (1.30 [1.11-1.53]). Fewer teeth at baseline (0-16) was associated with an increase in risk of lung cancer (1.70 [1.37-2.11]) for those with 0-16 teeth versus those with 25-32 teeth. In never-smokers, periodontal disease was associated with significant increases in total (1.21 [1.06-1.39]) and haematological cancers (1.35 [1.01-1.81]). By contrast, no association was noted for lung cancer (0.96 [0.46-1.98]). Periodontal disease was associated with a small, but significant, increase in overall cancer risk, which persisted in never-smokers. The associations recorded for lung cancer are probably because of residual confounding by smoking. The increased risks noted for haematological, kidney, and pancreatic cancers need confirmation, but suggest that periodontal disease might be a marker of a susceptible immune system or might directly affect cancer risk.

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Author and article information

Contributors

Brian M. Wolpin: +1-617-632-6942 , bwolpin@partners.org

Journal

Journal ID (nlm-ta): Br J Cancer

Journal ID (iso-abbrev): Br. J. Cancer

Title: British Journal of Cancer

Publisher: Nature Publishing Group UK (London )

ISSN (Print): 0007-0920

ISSN (Electronic): 1532-1827

Publication date (Electronic): 14 March 2019

Publication date (Print): 16 April 2019

Volume: 120

Issue: 8

Pages: 848-854

Affiliations

[1 ]ISNI 0000 0001 2106 9910, GRID grid.65499.37, Department of Oncologic Pathology, , Dana-Farber Cancer Institute and Harvard Medical School, ; 450 Brookline Avenue, Boston, MA 02215 USA

[2 ]ISNI 0000 0001 2106 9910, GRID grid.65499.37, Department of Medical Oncology, , Dana-Farber Cancer Institute and Harvard Medical School, ; 450 Brookline Avenue, Boston, MA 02215 USA

[3 ]ISNI 000000041936754X, GRID grid.38142.3c, Department of Epidemiology, , Harvard T.H. Chan School of Public Health, ; 677 Huntington Avenue, Boston, MA 02115 USA

[4 ]ISNI 0000 0004 0378 8294, GRID grid.62560.37, Division of Gastroenterology, Hepatology, and Endoscopy, , Brigham and Women’s Hospital and Harvard Medical School, ; 75 Francis Street, Boston, MA 02115 USA

[5 ]ISNI 0000 0004 0378 8294, GRID grid.62560.37, Program in MPE Molecular Pathological Epidemiology, Department of Pathology, , Brigham and Women’s Hospital and Harvard Medical School, ; 75 Francis Street, Boston, MA 02115 USA

[6 ]GRID grid.66859.34, Broad Institute of Massachusetts Institute of Technology and Harvard, ; 415 Main Street, Cambridge, MA 02142 USA

[7 ]ISNI 0000 0004 0378 8294, GRID grid.62560.37, Department of Medicine, , Brigham and Women’s Hospital and Harvard Medical School, ; 75 Francis Street, Boston, MA 02115 USA

[8 ]ISNI 000000041936754X, GRID grid.38142.3c, Department of Biostatistics, , Harvard T.H. Chan School of Public Health, ; 677 Huntington Avenue, Boston, MA 02115 USA

[9 ]ISNI 0000 0004 0378 8294, GRID grid.62560.37, Channing Division of Network Medicine, Department of Medicine, , Brigham and Women’s Hospital and Harvard Medical School, ; 181 Longwood Avenue, Boston, MA 02115 USA

[10 ]ISNI 000000041936754X, GRID grid.38142.3c, Department of Nutrition, , Harvard T.H. Chan School of Public Health, ; 677 Huntington Avenue, Boston, MA 02115 USA

[11 ]GRID grid.433818.5, Yale Cancer Center, ; 333 Cedar Street, New Haven, CT 06510 USA

[12 ]ISNI 0000000419368710, GRID grid.47100.32, Department of Medicine, , Yale School of Medicine, ; 333 Cedar Street, New Haven, CT 06510 USA

[13 ]GRID grid.490524.e, Smilow Cancer Hospital, ; 20 York Street, New Haven, CT 06519 USA

Article

Publisher ID: 426

DOI: 10.1038/s41416-019-0426-5

PMC ID: 6474278

PubMed ID: 30867564

SO-VID: af8edf44-6bfc-4053-8696-518d9a6c30ed

License:

This work is published under the standard license to publish agreement. After 12 months the work will become freely available and the license terms will switch to a Creative Commons Attribution 4.0 International (CC BY 4.0).

History

Date received : 13 November 2018

Date revision received : 25 February 2019

Date accepted : 27 February 2019

Funding

Funded by: U.S. National Institutes of Health (R01 CA205406) and the Broman Fund for Pancreatic Cancer Research

Funded by: U.S. National Institutes of Health (R01 CA124908 and P50 CA127003), the Robert T. and Judith B. Hale Fund for Pancreatic Cancer, Perry S. Levy Fund for Gastrointestinal Cancer Research, and Pappas Family Research Fund for Pancreatic Cancer

Funded by: U.S. National Institutes of Health (R35 CA197735)

Funded by: Hale Center for Pancreatic Cancer Research, NIH/National Cancer Institute (NCI) U01 CA210171, Department of Defense CA130288, Lustgarten Foundation, Stand Up to Cancer, Pancreatic Cancer Action Network, Noble Effort Fund, Wexler Family Fund, and Promises for Purple.

Custom metadata

ScienceOpen disciplines: Oncology & Radiotherapy

Keywords: risk factors,cancer epidemiology,pancreatic cancer

Data availability:

ScienceOpen disciplines: Oncology & Radiotherapy

Keywords: risk factors, cancer epidemiology, pancreatic cancer

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Family history of cancer, Ashkenazi Jewish ancestry, and pancreatic cancer risk

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Abstract

Background

Methods

Results

Conclusion

Related collections

Karger: Oncology

Most cited references 36

Exomic sequencing identifies PALB2 as a pancreatic cancer susceptibility gene.

Test of the National Death Index and Equifax Nationwide Death Search.

Periodontal disease, tooth loss, and cancer risk in male health professionals: a prospective cohort study.

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Cited by 3

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