Gynecologic oncology reports · 2026
Characterizing therapeutic target antigen expression in anaplastic carcinoma of the ovary.
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Sullivan Mackenzie W, Chui M Herman, Kanbergs Alexa N, Green Hunter, Gill Kaitlyn, Selenica Pier, Jungbluth Achim A, Long Kara C, Sonoda Yukio, Mueller Jennifer J, Tarney Christopher, Grisham Rachel N, Makker Vicky, Abu-Rustum Nadeem R, Weigelt Britta, O'Cearbhaill Roisín E
Аннотация
OBJECTIVE: Novel treatment strategies are needed for patients with anaplastic carcinoma of the ovary given the high incidence of chemoresistance to conventional systemic therapies. Here we sought to evaluate HER2, FOLR1, TROP2, and mismatch repair protein expression as well as the tumor mutational burden of anaplastic carcinoma of the ovary.
METHODS: We retrospectively identified a total of 9 anaplastic ovarian carcinomas in institutional databases from 2013 to 2023, including one case from a collaborating institution. Cases with adequate tissue available underwent immunohistochemical analysis for HER2, FOLR1, TROP2, and mismatch repair proteins MLH1, MSH2, MSH6, and PMS2. Tumor mutational burden was obtained from tumor-normal panel sequencing.
RESULTS: Anaplastic carcinoma of the ovary demonstrated low or absent expression of FOLR1, HER2, and TROP2 protein. FOLR1 expression in the two cases was weak and below currently used clinical cutoffs for mirvetuximab soravtansine eligibility. HER2 expression was low in the two anaplastic carcinomas (1-2+). TROP2 expression was low in one case (H-score of 60) and negative in the other five. All cases were mismatch repair proficient by immunohistochemistry and had low tumor mutational burden (median, 3.3 mut/Mb; range, 0.8-6.9).
CONCLUSION: Only a subset of anaplastic carcinomas of the ovary express targetable tumor antigens at low levels, suggesting that these may have limited benefit from antibody-drug conjugates. Likewise, due to mismatch repair proficiency and low tumor mutational burden, immunotherapy is unlikely to be effective in this rare disease.
METHODS: We retrospectively identified a total of 9 anaplastic ovarian carcinomas in institutional databases from 2013 to 2023, including one case from a collaborating institution. Cases with adequate tissue available underwent immunohistochemical analysis for HER2, FOLR1, TROP2, and mismatch repair proteins MLH1, MSH2, MSH6, and PMS2. Tumor mutational burden was obtained from tumor-normal panel sequencing.
RESULTS: Anaplastic carcinoma of the ovary demonstrated low or absent expression of FOLR1, HER2, and TROP2 protein. FOLR1 expression in the two cases was weak and below currently used clinical cutoffs for mirvetuximab soravtansine eligibility. HER2 expression was low in the two anaplastic carcinomas (1-2+). TROP2 expression was low in one case (H-score of 60) and negative in the other five. All cases were mismatch repair proficient by immunohistochemistry and had low tumor mutational burden (median, 3.3 mut/Mb; range, 0.8-6.9).
CONCLUSION: Only a subset of anaplastic carcinomas of the ovary express targetable tumor antigens at low levels, suggesting that these may have limited benefit from antibody-drug conjugates. Likewise, due to mismatch repair proficiency and low tumor mutational burden, immunotherapy is unlikely to be effective in this rare disease.