Fourteen steroid cell tumors (SCTs) of the ovary were studied by immunohistochemistry including inhibin, calretinin, CD99, Melan A, androgen receptor, and AE1/3. Twelve tumors were primary and 2 were recurrent. The primary tumors included 5 stromal luteomas (SL), 5 SCTs, not otherwise specified, and 2 Leydig cell tumors, 1 of the hilar type and 1 of the nonhilar type. All tumors were classified according to the predominant cell type. Six tumors were eosinophilic cell type, 3 clear-cell type, and 5 were mixed eosinophilic-clear-cell type. Inhibin, calretinin, and CD99 were positive in all 14 tumors. Twelve of 14 tumors (86%) were positive for Melan A and 9 of 14 (64%) for androgen receptor. AE 1/3 immunopositivity was found in 5 of 14 tumors (36%). Immunohistochemistry helps in the distinction between SCTs of the ovary and other primary or metastatic ovarian neoplasms with eosinophilic and clear-cell histology. In addition, immunohistochemistry can confirm the presence of recurrent SCT, if no sufficient clinical history is provided. As some SCTs can be positive for epithelial markers and histologically similar epithelial tumors can be positive for sex cord stromal markers, the use of multiple immunohistochemical stains is recommended.
Magee Equations™ are multivariable models that can estimate oncotype DX® Recurrence Score, and Magee Equation 3 has been shown to have chemopredictive value in the neoadjuvant setting as a standalone test. The current study tests the accuracy of Magee Decision Algorithm™ using a large in-house database. According to the algorithm, if all Magee Equation scores are <18, or 18-25 with a mitosis score of 1, then oncotype testing is not required as the actual oncotype recurrence score is expected to be ≤25 (labeled "do not send"). If all Magee Equation scores are 31 or higher, then also oncotype testing is not required as the actual score is expected to be >25 (also "do not send"). All other cases could be considered for testing (labeled "send"). Of the 2196 ER+, HER2-negative cases sent for oncotype testing, 1538 (70%) were classified as "do not send" and 658 (30%) as "send". The classification accuracy in the "do not send" group was 95.1%. Of the 75 (4.9%) discordant cases (expected score ≤25 by decision algorithm but the actual oncotype score >25), 26 received endocrine therapy alone. None of these 26 patients experienced distant recurrence (average follow-up of 73 months). The Magee Decision Algorithm accurately identifies cases that will not benefit from oncotype testing. Such cases constitute~70% of the routine clinical oncotype requests, an estimated saving of $300,000 per 100 test requests. The occasional discordant cases (expected ≤25, but actual oncotype score >25) appears to have an excellent outcome on endocrine therapy alone.
Pleomorphic lobular carcinoma of the breast is a high nuclear grade variant of lobular carcinoma. E-cadherin, a tumor-invasion suppressor gene, codes for a transmembrane protein that functions in intercellular adhesion. The E-cadherin protein internal domain binds with alpha, beta, gamma, and p120 catenins to anchor the E-cadherin complex to the actin cytoskeleton of the cell. The E-cadherin gene is routinely mutated in lobular neoplasia. This study examines the morphomolecular spectrum of the components of the E-cadherin-catenin complex in lobular neoplasia. Fifteen cases of pleomorphic lobular neoplasia, 8 cases of classic lobular neoplasia and 4 ductal carcinomas were studied. Normal breast epithelium and invasive ductal carcinomas all showed intense linear cell membrane immunostaining with antibodies to E-cadherin, alpha, beta, gamma, and P120 catenins. Membrane immunostaining of the catenin antibodies in lobular neoplasia was negative, except for rare cases that displayed beaded or dotlike patterns. Cytoplasmic immunostaining patterns for all lobular lesions included coarse paranuclear granules of beta catenin or diffuse intense cytoplasmic staining for P120 catenin. These immunostaining patterns demonstrate that catenins alpha, beta, gamma, and p120 are routinely dislocated from the cell membrane into the cytoplasm in lobular neoplasia and that the disrupted catenin patterns parallel absence of membrane E-cadherin in all cases. The diffuse cytoplasmic immunostaining of p120 in lobular neoplasia may be useful diagnostically as a positive marker for lobular neoplasia.
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