Pleomorphic adenoma of the breast is a rare tumor, with fewer than 100 patients described in the English literature, mainly as case reports and small case series. Histologically, breast pleomorphic adenoma resembles its more common salivary gland counterpart; however, it can present diagnostic challenges, particularly on core needle biopsy and fine-needle aspiration. The differential diagnosis includes benign and malignant tumors, which carry major treatment implications, from the extent of surgical intervention to the potential use of chemotherapy. Herein we describe a tumor that was initially diagnosed as a triple-negative matrix-producing metaplastic carcinoma, but a secondary review led to the diagnosis of pleomorphic adenoma of the breast. Prior to the secondary review, the patient underwent an excisional biopsy, sentinel lymph node biopsy, and one round of chemotherapy. This report adds to the limited literature surrounding this entity and discusses the differential diagnosis along with histopathologic and immunohistochemical findings that aid in the diagnosis and reviews the radiologic findings observed throughout the patient's clinical course. This patient underscores the difficulty of diagnosis and highlights the need for multidisciplinary consideration and communication to avoid overtreatment.
Detailed Reanalysis of 500 Breast Cancers With Equivocal HER2 Immunohistochemistry and Borderline ERBB2 Fluorescence In Situ Hybridization Results
Abstract Objectives We investigated the impact of our laboratory’s reflex testing process for resolving ERBB2 (HER2) status on breast cancer samples that require additional workup after fluorescence in situ hybridization (FISH), per guideline recommendations published in 2018 by the American Society of Clinical Oncology (ASCO) and the College of American Pathologists (CAP). Methods In total, 500 breast cancer specimens with ERBB2 FISH results in groups 2 through 4 (all reported as immunohistochemistry [IHC] equivocal [2+] at external laboratories) were resubmitted for IHC testing in our laboratory. Per the ASCO/CAP guideline, FISH was rescored when internal IHC was also equivocal (2+), targeted to tumor areas demonstrating more intense IHC staining, if observed. Results Reflex IHC/FISH testing changed the final reported ERBB2 status in 185 of 500 (37.0%) samples. Result changes included discordant IHC (n = 4 score 0, n = 132 score 1+, and n = 16 score 3+) and discordant FISH (n = 33). Numerical differences in FISH scores were comparable for targeted vs nontargeted FISH rescoring (P = .086 for ERBB2 copy number; P = .49 for ERBB2 ratio). Two cases showed larger differences in FISH scores, suggesting heterogeneity. Conclusions Retesting of breast cancer samples with equivocal IHC frequently changes IHC results, but targeted reanalysis of borderline FISH results rarely identifies significant differences in ERBB2 copy number or ratio.
PLEKHA7, an Apical Adherens Junction Protein, Suppresses Inflammatory Breast Cancer in the Context of High E-Cadherin and p120-Catenin Expression
Inflammatory breast cancer is a highly aggressive form of breast cancer that forms clusters of tumor emboli in dermal lymphatics and readily metastasizes. These cancers express high levels of E-cadherin, the major mediator of adherens junctions, which enhances formation of tumor emboli. Previous studies suggest that E-cadherin promotes cancer when the balance between apical and basolateral cadherin complexes is disrupted. Here, we used immunohistochemistry of inflammatory breast cancer patient samples and analysis of cell lines to determine the expression of PLEKHA7, an apical adherens junction protein. We used viral transduction to re-express PLEKHA7 in inflammatory breast cancer cells and examined their aggressiveness in 2D and 3D cultures and in vivo. We determined that PLEKHA7 was deregulated in inflammatory breast cancer, demonstrating improper localization or lost expression in most patient samples and very low expression in cell lines. Re-expressing PLEKHA7 suppressed proliferation, anchorage independent growth, spheroid viability, and tumor growth in vivo. The data indicate that PLEKHA7 is frequently deregulated and acts to suppress inflammatory breast cancer. The data also promote the need for future inquiry into the imbalance between apical and basolateral cadherin complexes as driving forces in inflammatory breast cancer.
Association of Event-Free and Distant Recurrence–Free Survival With Individual-Level Pathologic Complete Response in Neoadjuvant Treatment of Stages 2 and 3 Breast Cancer
Abstract Objective Parenchymal breast cysts are considered to be rare in men and are sparsely described in the literature. The purpose of this study was to review our institution’s experience with male breast cysts in an effort to improve overall understanding and management of this rare entity. Methods An institutional review board–exempt retrospective study was performed. Radiology reports for males who underwent mammogram and/or breast ultrasound at any of our institution’s primary or satellite locations from January 1995 to January 2020 were screened to find males with breast cysts. If cysts were reported and images were available, case review was performed to confirm parenchymal breast cyst(s) and patient characteristics were collated. Results Of 5425 male cases presenting for breast imaging, 19 (0.4%) cases of male breast cysts were confirmed, with a mean patient age of 41.6 years (range: 2–81 years). The most common indication leading to cyst discovery was a palpable lump, corresponding to the site of the cyst in 5 (26.3%) patients and near the site where cyst(s) were ultimately discovered in 7 (36.8%) patients. There were 8 (42.1%) instances of cysts without concurrent gynecomastia. Three (15.8%) men underwent needle sampling. There were no cases of atypia or malignancy on needle biopsy or on subsequent clinical follow-up, with median clinical follow-up of 70.3 months (range: 3.3–259.4 months). Conclusion Male breast parenchymal cysts are rare, but their prevalence is likely underestimated. If detected incidentally or upon targeted evaluation, biopsy may be averted if classic benign cyst features are identified.
Genomic profiling proves metastasis of cutaneous melanoma to vitreal fluid
Cutaneous melanoma metastases can contribute to visual disturbances through a variety of factors, including metastasis to the vitreal fluid. The optimum management of metastatic cutaneous melanoma to the vitreal fluid is unknown, but can include radiation therapy or systemic therapy including immunotherapy. A high degree of suspicion is necessary to consider this complication while working with patients with cutaneous melanoma.
Breast MRI phenotype and background parenchymal enhancement may predict tumor response to neoadjuvant endocrine therapy