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EP409/#609  Defect of MIS in placental site trophoblastic tumors and epithelioid trophoblastic tumors
  1. Hyun Jin Choi1,
  2. Min Chul Choi2,
  3. Chi-Son Chang3 and
  4. Hyun Soo Kim4
  1. 1Chung-Ang University GwangMyeong Hospital, Obstetrics and Gynecology, Gwangmyeong-si, Korea, Republic of
  2. 2CHA Bundang Medical center, Obgy, Seongnam-si, Korea, Republic of
  3. 3Chung-Ang University GwangMyeong Hospital, Obgy, Gwangmyeong-si, Korea, Republic of
  4. 4Samsung Medical Center, Sungkyunkwan University School of Medicine, Pathology and Translational Genomics, Seoul, Korea, Republic of


Introduction This study aims to evaluate mismatch repair defect (MMRd) in placental trophoblastic tumors (PSTTs) and epithelial trophoblastic tumors (ETTs).

Methods This study was performed in three academic hospitals retrospectively. Serial histology sections from 15 patients diagnosed with a PSTT or ETT were immunohistochemically stained using the MLH1/MSH2/MSH6/PMS2 to test MMRd. MMRd was determined by one pathologist. Less than 10% of expression in IHC was considered as MMRd.

Results We obtained IHC stain of MLH1/MSH2/MSH6/PMS2 from 15 patients’ samples. There were nine PSTT and six ETT patients. Sample from PSTT patients showed one MLH1 defect and one PMS2 defect. Sample from ETT patients showed PMS2 defect in five out of six samples. One sample showed defects in MLH1, MSH6, and PMS6.

Conclusion/Implications Gestational trophoblastic tumors especially in ETT showed high MMRd. This study explains the high response rate in PSTT and ETT to immune checkpoint inhibitors. This type of tumor may be a good target of immune checkpoint inhibitors.

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