Border: pushing/infiltrative. Lymphocytic reaction: prominent/sparse.
Capsule/serosa/paratubal connective tissue/contiguous fallopian tube/ uterus. Involvement of fallopian tube is usually secondary to primary ovarian disease wherein the bulk of tumour will usually reside. Note that extension of tumour along the tubal mucosa can sometimes mimic carcinoma in situ and a tubal origin. Spread to uterus is usually as a serosal plaque of friable tumour with invasion of outer myometrium and/or its underlying vessels.
Extensive sampling of ovarian epithelial cystic lesions is necessary (1 block/cm diameter) as there can be marked heterogeneity and coexistence of benign, borderline and malignant features, e.g. mucinous lesions. In this respect more blocks are required than in an obviously malignant homogeneous tumour and nodular/solid areas should be preferentially sampled in an otherwise cystic lesion. Microinvasion <10mm2 (or approximately 3 mm diameter) can be difficult to distinguish from crypt epithelial complexity and invagination into stroma (desmoplasia is a useful feature in carcinoma). It is occasionally seen in otherwise borderline serous tumours but does not alter the prognosis. Invasion >5mm may help to discriminate between mucinous and endometrioid borderline and carcinoma lesions with a worse clinical outcome.
Invasion of stroma and/or capsule remains the hallmark of carcinoma but not infrequently its presence is difficult to assess or it is not evident. This is particularly problematic in mucinous lesions, where a designation of non-invasive carcinoma or intraepithelial carcinoma may be made on the basis of epithelial complexity with a confluent glandular pattern and cellular atypia alone, e.g. nuclear stratification >4 deep, cribriform epithelial pattern or stroma-free papillae of epithelial cells. Further sampling is necessary to exclude frankly invasive areas warranting the more usual designation of adenocarcinoma.
Minimal staging requires removal of the ovarian primary lesion, biopsy of the contralateral ovary, biopsy of omentum and peritoneal surfaces, and peritoneal washings for cytology if ascitic fluid is not present.
The TNM classification applies to malignant surface epithelial-stromal tumours, including those of borderline malignancy. Non-epithelial ovarian cancers may also be classified using this scheme. FIGO is based on surgical staging, TNM on clinical and/or pathological classification.
pT1 growth limited to the ovaries a. one ovary, capsule intact, no serosal disease or malignant cells in ascites or peritoneal washings b. two ovaries, capsule intact, no serosal disease or malignant cells in ascites or peritoneal washings c. one or both ovaries with any of: capsule rupture*, serosal disease or malignant cells in ascites or peritoneal washings.
pT2 growth involving one or both ovaries with pelvic tumour extension and/or implants a. uterus, and/or tube(s)
b. other pelvic tissues c. 2a or 2b plus malignant cells in ascites or peritoneal washings pT3 growth involving one or both ovaries with metastases to abdominal peritoneum^ and/or regional nodes a. microscopic peritoneal metastasis beyond pelvis b. macroscopic peritoneal metastasis <2 cm in greatest dimension beyond pelvis c. peritoneal metastasis >2 cm in greatest dimension and/or regional lymph node metastasis (N1)
pT4/M1 growth involving one or both ovaries with distant metastases, e.g. liver parenchyma or positive pleural fluid cytology.
The commonest pattern of spread is the contralateral ovary, peritoneum, para-aortic and pelvic lymph nodes and liver. Lung is the preferred extra-abdominal site and occasionally unusual sites, e.g. breast.
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