Intraoperative Lymph Node Assessment (Touch Preparation Only) for Metastatic Breast Carcinoma in Neoadjuvant and Non-neoadjuvant Settings.

CONTEXT.­: Touch preparation (TP) alone is discouraged for intraoperative lymph node (LN) assessment in the neoadjuvant setting (NAS) owing to overall low sensitivity in detecting metastatic breast cancer. OBJECTIVE.­: To compare the sensitivity, specificity, and negative predictive value of intraoperative LN assessment via TP and examine potential causes of discrepancies along with the clinical, radiologic, and pathologic parameters in the NAS and non-neoadjuvant setting (NNAS). DESIGN.­: A total of 99 LNs from 47 neoadjuvant patients and 108 LNs from 56 non-neoadjuvant patients were identified. Discordant cases were reviewed retrospectively to reveal the discrepancy reasons. Clinical, radiologic, and pathologic data were obtained from chart review and the pathology CoPath database. RESULTS.­: The sensitivity, specificity, and negative predictive value of TP in NAS and NNAS were 34.2% versus 37.5%, 100% versus 100%, and 70.9% versus 90.2%, respectively. In NAS, discrepancy reasons were interpretation challenge due to lobular histotype, poor TP quality secondary to therapy-induced histomorphologic changes, and undersampling due to small tumor deposits (≤2 mm); the latter was the major reason in NNAS. More cases with macrometastasis were missed in NAS compared to NNAS (14 of 25 versus 1 of 10). The parameters associated with discrepancy were lobular histotype, histologic grade 2, estrogen receptor positivity, HER2 human epidermal growth factor receptor 2 negativity, multifocality, and pathologic tumor size greater than 10 mm in NAS; and lymphovascular space involvement and pathologic tumor size greater than 20 mm in NNAS. CONCLUSIONS.­: In NAS, intraoperative TP alone should be used very cautiously owing to a high false-negative rate of macrometastasis, especially for patients with invasive lobular carcinoma and known axillary LN metastasis before neoadjuvant therapy.

Vaginal myofibroblastoma with prostatic glands: is there an association with tamoxifen use? A case report.

BACKGROUND: Both ectopic prostate tissue in the female genital tract and vaginal myofibroblastoma have rarely been reported in the literature. Tamoxifen use has been associated with the development of vaginal myofibroblastoma. CASE: A 76-year-old, multiparous woman who had taken tamoxifen for breast cancer presented with postmenopausal bleeding and a vaginal mass. Endometrial work-up revealed a benign polyp, and the polypoid tumor in the vagina was found to be a myofibroblastoma harboring ectopic prostatic glands. CONCLUSION: To our knowledge this is the first case of these two rare pathologic entities occurring together. Of note, this patient also had a history of tamoxifen therapy, like some of the previous patients with vaginal myofibroblastoma.

Diagnostic utility of p16 immunocytochemistry for Trichomonas in urine cytology.

We present a case in which p16 immunocytochemistry helped establish the diagnosis of Trichomonas in urine from a male patient. Based on this finding, we recommend p16 immunocytochemistry as a diagnostic tool for unexpected patients or specimen types in which potential trichomonads are identified following routine cytologic evaluation.

Distinctive gene expression profiles by cDNA microarrays in endometrioid and serous carcinomas of the endometrium.

Endometrial carcinomas are classified by their morphology into two major subtypes. Endometrioid carcinomas (type I) are generally estrogen dependent, well-differentiated, superficially invasive, and have a good outcome. Serous carcinomas (type II) are hormone independent, frequently deeply invasive and widely metastatic, and have a poor prognosis. Microarray technology and analysis allows us to determine if the global gene expression profiles of these two subtypes correlate with their morphologic phenotype. Fresh tissue from 18 endometrial carcinomas was studied: 7 well-, 2 moderately, and one poorly differentiated endometrioid, 4 serous carcinomas, and 4 high-grade mixed endometrioid-serous carcinomas. Labeled cDNA probes were synthesized (Cy5 for tumor, Cy3 for reference) and applied to microarrays containing 18,098 cDNA clones or ESTs. A pool of equal amounts of total RNA from each tumor served as the reference RNA. By unsupervised cluster analysis, the endometrioid carcinomas clustered together and were separate from the serous carcinomas. The high-grade mixed carcinomas clustered with the serous carcinomas. Using a statistical algorithm based on gene expression pattern and conducting a supervised analysis of the two defined groups, we have identified 315 genes that statistically differentiate type I from type II endometrial carcinomas. In addition to corroborating the predicted overexpression of known markers (e.g., ras and catenin in endometrioid carcinomas), the cDNA microarray technique has revealed novel alterations in gene expression relevant to cell cycle, cell adhesion, signal transduction, apoptosis, and tumor progression not previously implicated in endometrial carcinomas. For serous carcinomas, these include aldolase, desmoplakin, integrin-linked kinase, PKC, and metallopeptidase. In conclusion, the gene expression profiles of type I and type II endometrial carcinomas are different. Refinement of these profiles will permit more accurate diagnostic tumor classification and the development of prognosis assays.

Vimentin and leukocyte common antigen-negative molding cells in pleural effusions of patients with small cell lung carcinoma.

OBJECTIVE: To determine whether the presence of vimentin and leukocyte common antigen (LCA)-negative molding cells (VLNMC) could help in identifying rare small cell lung carcinoma (SCLC) cells. STUDY DESIGN: Thirty-four cell blocks of pleural effusions (PEs) from 26 patients with confirmed SCLC were stained immunohistochemically with vimentin and LCA antibodies and compared with hematoxylin and eosin-stained preparations. RESULTS: VLNMC were present in 22/22 PEs originally diagnosed as positive or atypical/suspicious for SCLC. Focal vimentin staining was seen in SCLC in 10/22 cases, and 1 case showed many vimentin-positive SCLC cells. One of 11 PEs originally interpreted as negative showed rare groups of VLNMC. This was supported by a subsequent PE obviously positive for SCLC. CONCLUSION: Immunoperoxidase stains for vimentin and LCA highlight SCLC in PEs as VLNMC; however, morphologic criteria must prevail in making the final diagnosis.

Expression of COX-2, Ki-67, cyclin D1, and P21 in endometrial endometrioid carcinomas.

COX-2, the isoform of cyclooxygenase inducible by cytokines, mitogens, and growth factors, appears to play an important role in inflammation and carcinogenesis. In the colon, COX-2 overexpression results in cell cycle alterations, and NSAIDs have proven effective in cancer chemoprevention. HNPCC (hereditary nonpolyposis colon cancer) is a clinically defined cancer susceptibility syndrome in which women are also at significantly increased risk for the development of endometrial carcinoma. The purpose of this study was to evaluate expression of COX-2 in benign and malignant endometrium in the context of other cell cycle and proliferation markers, including Ki-67, cyclin D1, and the cyclin-dependent kinase inhibitor, p21. Immunostains with COX-2, Ki-67, cyclin D1, and p21 antibodies were performed on formalin-fixed and paraffin-embedded tissue sections from 40 cases: 10 benign (5 atrophic and 5 proliferative) endometria, 6 hyperplasias (complex without atypia), and 24 endometrioid carcinomas (9 well, 4 moderately, and 11 poorly differentiated). Ki-67 was positive in all proliferative and neoplastic endometria. Cyclin D1 and p21 were both overexpressed in endometrial hyperplasia and endometrioid carcinomas. COX-2 was negative in the nonneoplastic endometrium, stained minimally in the well-differentiated endometrioid carcinomas, and stained most strongly in the moderately and poorly differentiated endometrioid carcinomas. Because cyclin D1 may function as an oncogene, its effects may dominate the usual inhibitory effect of a rising p21. Alternatively, it has been shown that p21 can promote cell cycle function by stabilizing cell cycle complexes. The overexpression of COX-2 in poorly differentiated endometrioid carcinoma and lack of expression in hyperplasia and well-differentiated carcinoma suggests that in this form of cancer, COX-2 may play a role in tumor progression rather than tumor initiation.