gms | German Medical Science

MAINZ//2011: 56. GMDS-Jahrestagung und 6. DGEpi-Jahrestagung

Deutsche Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie e. V.
Deutsche Gesellschaft für Epidemiologie e. V.

26. - 29.09.2011 in Mainz

Article

Send article

Second neoplasms and ovarian cancer

Meeting Abstract

Search Medline for

  • Manuela Marron - Institute of Medical Biostatistics, Epidemiology and Informatics (IMBEI), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany
  • Maria Blettner - Institute of Medical Biostatistics, Epidemiology and Informatics (IMBEI), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany
  • Hajo Zeeb - Bremen Institute for Prevention Research and Social Medicine (BIPS), Bremen, Germany
  • Ghislaine Scélo - International Agency for Research on Cancer (IARC), Lyon, France
  • Kari Hemminki - Division of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany
  • Jorgen H. Olsen - Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark
  • Eero Pukkala - Finnish Cancer Registry, Institute for Statistical and Epidemiology Cancer Research, Helsinki, Finland
  • Elisabete Weiderpass - The Cancer Registry of Norway, Oslo, and Department of Community Medicine, Tromso, Norway
  • Elizabeth Tracey - New South Wales Cancer Registry, Eveleigh, New South Wales, Australia
  • David H. Brewster - Scottish Cancer Registry, Information Services Division, NHS National Services Scotland, Edinburgh, United Kingdom
  • Sharon Tamaro - British Columbia Cancer Registry, Vancouver, British Columbia, Canada
  • Vera Pompe-Kirn - Cancer Registry of Slovenia, Institute of Oncology, Ljubljana, Slovenia
  • Erich V. Kliewer - Epidemiology and Cancer Registry, Cancer Care Manitoba, Winnipeg, Canada
  • Kee-Seng Chia - Center for Molecular Epidemiology, and Singapore Cancer Registry, Singapore
  • Jon M. Tonita - Saskatchewan Cancer Agency, Regina, Saskatchewan, Canada et. al.
  • Carmen Martos - Cancer Registry of Zaragoza, Aragon Health Science Institute, Zaragoza, Spain
  • Jon G Jonasson - Icelandic Cancer Registry, Icelandic Cancer Society, and Faculty of Medicine, University of Iceland, Reykjavik, Iceland
  • Hiroko Ohgaki - International Agency for Research on Cancer (IARC), Lyon, France
  • Paul Brennan - International Agency for Research on Cancer (IARC), Lyon, France
  • Paolo Boffetta - Icelandic Cancer Registry, Icelandic Cancer Society, and Faculty of Medicine, University of Iceland, Reykjavik, Iceland
  • The Tisch Cancer Institute, Mount Sinai School of Medicine, New York, USA

Mainz//2011. 56. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds), 6. Jahrestagung der Deutschen Gesellschaft für Epidemiologie (DGEpi). Mainz, 26.-29.09.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. Doc11gmds314

doi: 10.3205/11gmds314, urn:nbn:de:0183-11gmds3145

Published: September 20, 2011

© 2011 Marron et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

Text

Recent studies have suggested that different histological types of ovarian cancer develop via different pathways. Large epidemiological studies of first and second malignant neoplasms associated with ovarian cancer can quantify such risk and may provide etiologic clues in understanding these complex pathways.

We analyzed ovarian cancer data from 13 different cancer registries in Europe, Australia, Canada and Singapore from 1943-2000. Cumulative risks were calculated using a competing risk model, and standardized incidence ratios (SIR) for 34 cancers were estimated based on the observed numbers of second malignancies and the expected numbers obtained from population-specific incidence rates.

We observed 5,052 second malignant neoplasms in 107,038 ovarian cancer patients and 5,804 second ovarian cancers in 3,722,434 patients with cancer of other sites. Within 20 years from diagnosis of ovarian cancer, the cumulative risk of second malignant neoplasms was 4.8% (95% CI 4.6%-5.0%) before 1980 and 7.1% (6.1-8.0) after 1980. After sex cord-stromal, mucinous or endometrioid tumors of the ovary, the cumulative risk of second malignant neoplasms was higher [12.7% (11.2-14.3), 10.0% (9.0-11.0), 9.3% (7.9-10.7), respectively] than after germ-cell tumors, serous tumors or adenocarcinoma NOS [6.2% (3.7-8.7), 5.9% (5.5-6.3), 5.1% (4.9-5.4), respectively] within 20 years from diagnosis at age 45+. We observed increased SIRs for cancer of stomach [SIR=1.5 (95%CI 1.1-2.0)], small intestine [3.2(1.3-6.5)], colon [1.5(1.2-1.8)], rectum [1.9(1.4-2.4)], soft tissue sarcoma [3.2(1.5-5.8)], non-melanoma of skin [1.4(1.0-1.7)], breast [1.3(1.2-1.5)], other female genital organ [2.2(1.3-3.5)], bladder [2.3(1.7-3.1)], kidney [1.8(1.3-2.6)], myeloid leukemia [3.5(2.2-5.4)] and other leukemia [6.4(3.7-10.2)] after serous tumors of the ovary. There were increased SIRs for colon [2.2(1.7-2.7)], rectum [1.9(1.3-2.6)], lung [2.1(1.6-2.7)] and bladder cancer [1.8(1.0-2.8)] after mucinous tumors. After endometrioid tumors, we observed an excess risk for cancer of colon [2.1(1.5-2.9)], bone [12.1(1.5-43.6)], soft tissue sarcoma [5.2(1.1-15.3)], corpus uteri [3.3(2.2-4.7)] and kidney [2.3(1.1-4.4)]. There was an association with cancer of soft tissue sarcoma [3.2(1.0-7.4)], bladder [2.2(1.2-3.4)], kidney [2.1(1.2-3.3)], thyroid gland [3.1(1.5-5.6)] and myeloid leukemia [4.2(1.5-9.1)] after sex cord-stromal tumors. SIRs of second ovarian cancer were increased after stomach, small intestine, colon, gallbladder, pancreas, peritoneum, non-melanoma skin and breast cancer.

Women who survive ovarian cancer are at long-term risk of developing a second malignant neoplasm. The associations between specific types of ovarian cancer and other cancers may be attributed to late effects of radio- and chemotherapy, as well as to common genetic and environmental risk factors and pathways.