Metastatic tumors to the ovary account for approximately 10 – 15% of ovarian malignancies  with the majority of the metastatic tumors arising from the genital tract. Cervical cancer is a very rare cause of ovarian metastasis  and the risk is more likely in advanced disease vis-à-vis early stage cervical cancer . Most of the advanced cases described have bulky exophytic growths with extensive corpus uteri involvement. Metastases to ovaries occur in 0.5% of cases of SCC and 1.7% of cases of adenocarcinoma, so ovarian preservation at the time of surgery may incur a small risk of occult disease .
In a large autopsy series by Tabata et al  ovarian metastases were found in 104 out of 597 (17.4%) cases of SCC as opposed to 28.6% cases of adenocarcinoma while Toki et al  reported ovarian metastasis in only one case of 524 SCCs. Most of the ovarian metastases reported are microscopic, unilateral, confined to ovarian parenchyma and detected postoperatively [1, 8–11]. Independent risk factors for ovarian metastasis include age, stage, non squamous histology, unaffected peripheral stromal thickness  and uterine corpus involvement .
Possible routes of spread to the ovary from cervical cancer include hematologic metastasis , or lymphatic drainage and transtubal drainage  and involvement of the corpus may potentiate these mechanisms. Reverse transcriptase in situ polymerase chain reaction for human papillomavirus ribonucleic acid is a reliable method to differentiate metastatic cervical carcinoma from either a new primary tumor or a metastasis from another cancer . In the female genital tract, p63 is expressed in the basal and parabasal layers of mature cervical, vaginal, and vulval squamous epithelium, and is useful to establish the diagnosis of cervical squamous cell carcinoma .
Endophytic cervical squamous cell carcinoma with normal endocervical, endometrial and fallopian tube epithelia, extensive lymphovascular invasion of the entire genital tract and bilateral parenchymal involvement of the ovaries is an extremely rare presentation. Endophytic tumors may appear normal speculoscopically and colposcopically. The growth occurs in the cervical canal with direct infiltration into the wall causing diffuse enlargement and hardening of the cervix. The mucosal surface may be covered by normal epithelium, and the underlying malignant cells may escape detection by cytologic smear. These endophytic tumors may produce a barrel-shaped cervix, which has a diameter greater than 4 cm. Rectal examination can be helpful in such cases to palpate the enlarged uterine cervix and the role of MRI is usually complementary. Actual pathophysiological mechanisms leading to abnormal bleeding in carcinoma cervix are poorly understood, but are probably due to the presence and dilatation of abnormal surface vessels on the lesion .
Since the ovaries in our case demonstrated solid tumor bilaterally, primary solid ovarian neoplasms such as Brenner tumor, non cystic ovarian teratoma, dysgerminoma, granulosa cell tumor and lymphoma were excluded with the help of IHC markers. Apart from these, ovarian endometrioid adenocarcinoma resembling sex cord stromal tumor which demonstrates CK7 and epithelial membrane antigen positivity  was differentiated by negativity in our case. Endometrioid adenocarcinoma with squamous differentiation may show keratin granulomas over the surface of the ovary and if viable tumor cells are observed in the granulomas, these lesions should be regarded as conventional metastatic foci . There were no keratin granulomas or peritoneal deposits in our case. Further the endophytic nature required differentiation from mesonephric adenocarcinoma with sarcomatous component . Absence of sarcomatous component in the cervical biopsy helped exclude this lesion. Non-involvement of endometrium with invasive squamous cell carcinoma, along with demonstration of secretory changes and concomitant exogenous hormone induced features warranted that a FIGO grade 1 endometrioid adenocarcinoma and/or intestinal-type metaplasia be ruled out . This was eliminated by CA 125, AB-PAS and CDX-2 IHC marker negativity within the endometrium while p63 and high molecular weight cytokeratin CK5/6 positivity in the cervix and metastatic ovarian deposits.
Differentiation between metastatic SCC from the cervix and primary SCC of the ovary usually has been aided by the knowledge of the presence of a cervical tumor. Before the diagnosis of a primary SCC of the ovary is made, the possibility of spread from a cervical tumor, even one that is occult should be considered unless overt features of primary neoplasia are immediately obvious. As most SCCs of the ovary arise in the background of a pre-existing neoplasm such as dermoid or endometriotic cyst, thorough sampling to identify such a component may be crucial in determining the primary nature of the neoplasm. Although the evidence strongly points to the ovarian tumor being metastatic when both organs have been involved by SCC, the rare association of SCC of the ovary with SCC in situ of the cervix leaves open the possibility of independent primary neoplasms in some cases .