Familial risks of ovarian cancer by age at diagnosis, proband type and histology

PLoS One. 2018 Oct 3;13(10):e0205000. doi: 10.1371/journal.pone.0205000. eCollection 2018.

Abstract

Ovarian cancer is a heterogeneous disease. Data regarding familial risks for specific proband, age at diagnosis and histology are limited. Such data can assist genetic counseling and help elucidate etiologic differences among various histologic types of ovarian malignancies. By using the Swedish Family-Cancer Database, we calculated relative risks (RRs) for detailed family histories using a two-way comparison, which implied e.g. estimation of RRs for overall ovarian cancer when family history was histology-specific ovarian cancer, and conversely, RRs for histology-specific ovarian cancer when family history was overall ovarian cancer. In families of only mother, only sisters or both mother and sisters diagnosed with ovarian cancer, cancer risks for ovary were 2.40, 2.59 and 10.40, respectively; and were higher for cases diagnosed before the age of 50 years. All histological types showed a familial risk in two-way analyses, except mucinous and sex cord-stromal tumors. RRs for concordant histology were found for serous (2.47), endometrioid (3.59) and mucinous ovarian cancers (6.91). Concordant familial risks were highest for mucinous cancer; for others, some discordant associations, such as endometrioid-undifferentiated (9.27) and serous-undifferentiated (4.80), showed the highest RRs. Familial risks are high for early-onset patients and for those with multiple affected relatives. Sharing of different histological types of ovarian cancer is likely an indication of the complexity of the underlying mechanisms.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Child
  • Child, Preschool
  • Female
  • Humans
  • Infant
  • Infant, Newborn
  • Male
  • Middle Aged
  • Mothers
  • Ovarian Neoplasms / epidemiology*
  • Pedigree*
  • Risk
  • Siblings
  • Young Adult

Grants and funding

This work was supported by the German Cancer Aid; and the Swedish Research Council for Health, Working Life and Welfare (in Swedish: FORTE; Reg. no. 2013-1836), and FORTE (Reg. no. 2014-0804) and the Swedish Research Council (2012-2378 and 2014-10134); and ALF funding from Region Skåne. This research was also supported by the China Scholarship Council (201606100057 to GZ). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.