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  • Clinicopathologic Analysis With Immunohistochemistry for DNA Mismatch Repair Protein Expression in Synchronous Primary Endometrial and Ovarian Cancers

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Uterine Cancer
Clinicopathologic Analysis With Immunohistochemistry for DNA Mismatch Repair Protein Expression in Synchronous Primary Endometrial and Ovarian Cancers
  1. Yusuke Kobayashi, MD, PhD,
  2. Kanako Nakamura, MD,
  3. Hiroyuki Nomura, MD, PhD,
  4. Kouji Banno, MD, PhD,
  5. Haruko Irie, MD,
  6. Masataka Adachi, MD,
  7. Miho Iida, MD,
  8. Kiyoko Umene, MD,
  9. Yuya Nogami, MD,
  10. Kenta Masuda, MD,
  11. Iori Kisu, MD, PhD,
  12. Arisa Ueki, MD, PhD,
  13. Wataru Yamagami, MD, PhD,
  14. Fumio Kataoka, MD, PhD,
  15. Akira Hirasawa, MD, PhD,
  16. Eiichiro Tominaga, MD, PhD,
  17. Nobuyuki Susumu, MD, PhD and
  18. Daisuke Aoki, MD, PhD
  1. Department of Obstetrics and Gynecology, School of Medicine, Keio University, Tokyo, Japan.
  1. Address correspondence and reprint requests to Kouji Banno, MD, PhD, Department of Obstetrics and Gynecology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160–8582, Japan. E-mail: kbanno@z7.keio.jp.

Abstract

Objective Synchronous primary endometrial and ovarian cancers have been an important topic in clinical medicine because it is sometimes difficult to distinguish whether there are 2 primary tumors or a single primary tumor and an associated metastasis. In addition, although these tumors are recommended for either immunohistochemistry for DNA mismatch repair (MMR) proteins or a microsatellite instability test in the Bethesda guidelines as Lynch syndrome–associated cancers, few studies have completed these analyses. In this study, we characterized the clinicopathologic features and the expression pattern of MMR proteins in synchronous primary endometrial and ovarian cancers.

Methods Clinicopathologic features and the expression pattern of MMR proteins (MLH1, MSH2, and MSH6) were characterized and analyzed in 32 synchronous primary endometrial and ovarian cancers.

Results Most synchronous cancers are endometrioid type (endometrioid/endometrioid) (n = 24, 75%), grade 1 (n = 19, 59.4%), and diagnosed as stage I (n = 15, 46.9%) in both endometrium and ovary. It is worth mentioning that 75% of the patients (n = 24) had endometriosis, which was more common (n = 21, 87.5%) in endometrioid/endometrioid cancers, whereas only 3 cases (37.5%) were of different histology (P = 0.018). Loss of expression of at least 1 MMR protein was observed in 17 (53.1%) of the endometrial tumors and in 10 (31.3%) of ovarian tumors. Only 4 cases (12.5%) that had specific MMR protein loss showed the same type of loss for both endometrial and ovarian tumors, in which 3 of the cases were losses in MLH1. One case showed concordant MSH6 protein loss, although the cases did not meet the Amsterdam criteria II.

Conclusions These results suggest that most synchronous primary endometrial ovarian cancers are not hereditary cancers caused by germ line mutations but rather sporadic cancers.

  • Synchronous primary endometrial and ovarian cancers
  • DNA mismatch repair proteins
  • Lynch syndrome
  • Bethesda guideline

https://doi.org/10.1097/IGC.0000000000000377

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    Footnotes

    • The authors declare no conflicts of interest.

    • Supplemental digital content is available for this article. Direct URL citation appears in the printed text and is provided in the HTML and PDF versions of this article on the journal’s Web site (www.ijgc.net).