Most endocervical adenocarcinomas are associated with human papillomavirus (HPV) infection. Studies suggest that synchronous endocervical and ovarian tumors can contain identical HPV subtypes and that, in this setting, the ovarian tumors likely represent metastases from the endocervical adenocarcinoma rather than 2 independent primaries. However, there are still relatively few reports in the literature.
We describe 2 patients with HPV-related endocervical adenocarcinoma or adenocarcinoma in situ who had metastatic ovarian tumors that simulated primary ovarian neoplasms. After total hysterectomy and bilateral salpingo-oophorectomy, patient 1, in her mid-40s, was diagnosed with endocervical adenocarcinoma in situ and patient 2, in her early 50s, was diagnosed with endocervical adenocarcinoma showing early focal stromal invasion. The ovarian tumors in both cases simulated independent borderline mucinous tumors without evidence of surface involvement or spread beyond the ovary. However, in both cases, the cervical and ovarian tumors showed diffuse, strong P16 staining and contained identical high-risk HPV subtypes (subtypes 16 and 18 in patient 1 and subtype 16 in patient 2). Patient 1 was treated with radiation therapy and remains recurrence free 5 years after diagnosis, and patient 2 has recently completed combined modality treatment with radiation therapy and cisplatin chemotherapy and remains recurrence free 10 months after diagnosis.
A high index of suspicion and ancillary testing, including P16 immunostaining and molecular genetic testing for HPV, is required to properly diagnose and subclassify HPV-related endocervical adenocarcinoma metastatic to the ovary.
Ancillary testing for P16 and HPV is required to diagnose early invasive or noninvasive HPV-related endocervical adenocarcinoma with ovarian metastasis.
1Department of Pathology and Molecular Medicine, Queen's University, Kingston General Hospital, Kingston; and 2Department of Laboratory Medicine and Pathology, Mount Sinai Hospital, Toronto, Ontario, Canada.
Reprint requests to: Timothy Childs, MD, PhD, Department of Pathology and Molecular Medicine, Queen's University and Kingston General Hospital, 76 Stuart St, Kingston, Ontario, K7L 2V7, Canada. E-mail: firstname.lastname@example.org
The authors have declared they have no conflict of interest