Distinction of primary ovarian epithelial tumors from metastatic adenocarcinomas is challenging for tumors exhibiting mucinous, endometrioid, or mixed endometrioid/mucinous differentiation. Metastatic carcinomas with these types of differentiation can be derived from several sites, including the gastrointestinal tract and the uterus. Most endocervical adenocarcinomas exhibit mucinous and/or endometrioid differentiation; they infrequently metastasize to the ovaries but may simulate primary ovarian tumors [both atypical proliferative (borderline) and carcinoma]. Most are high-risk human papillomavirus (HPV)-related and demonstrate diffuse p16 over-expression due to complex molecular mechanisms by which high-risk HPV transforming proteins interact with cell cycle regulatory proteins. The performance of this expression pattern for identifying metastatic endocervical adenocarcinomas in the ovaries among primary ovarian tumors and other metastatic adenocarcinomas having mucinous and/or endometrioid/endometrioidlike differentiation has not been evaluated. Immunohistochemical expression of p16 was assessed in 195 tumors, including 98 primary ovarian tumors (51 mucinous, 47 endometrioid, and 4 mixed mucinous-endometrioid tumors), 93 metastatic adenocarcinomas of known primary sites (colorectum: 34, endocervix: 19, pancreaticobiliary tract: 17, appendix: 7, stomach: 5), 11 metastatic adenocarcinomas of unknown origin (7 established as noncervical), and 4 adenocarcinomas of uncertain (primary ovarian vs. metastatic) origin. The HPV status of the endocervical adenocarcinomas was determined by in situ hybridization and polymerase chain reaction (when in situ hybridization was negative). Expression was assessed based on the percentage of moderately to strongly positive cells, estimated to the nearest 10%. Mean and median expression values for HPV-positive endocervical adenocarcinomas (99%, 100%; range 90% to 100%) were substantially higher than those for primary ovarian mucinous (5%, 0%; range 0% to 70%) and endometrioid (20%, 10%; range 0% to 100%) tumors, HPV-unrelated endocervical adenocarcinomas (0%, 0%; range 0% to 60%), metastatic adenocarcinomas of unknown origin (11%, 0%; range 0% to 30%), and adenocarcinomas of uncertain (primary ovarian vs. metastatic) origin (40%, 35%; range 0% to 90%); only the 15 HPV-positive endocervical adenocarcinomas and 6 other tumors had values of 80% or greater. Diffuse (>75% positive tumor cells) moderate to strong p16 expression is a sensitive (100%) and specific (97%) marker for identifying HPV-related endocervical adenocarcinomas metastatic to the ovary among the primary ovarian tumors and metastatic adenocarcinomas from other sites that are in the differential diagnosis of ovarian tumors having mucinous and/or endometrioid/endometrioidlike differentiation. p16 is useful as part of a panel of immunohistochemical markers for distinguishing primary ovarian tumors from metastases and, when diffusely positive, can suggest the cervix as a potential primary site for metastatic adenocarcinomas...
CT-guided FNAB of PPS tumors is helpful to predict the nature of the PPS tumors (especially benign), which allows the surgeon and patient to plan for treatment, accordingly.
BACKGROUND CD56 antigen or NCAM (neural cell adhesion molecule) has an established role in the diagnosis of non‐Hodgkin lymphoma (NHL)‐natural killer cell type and other hematologic malignancies. Therefore, it is included routinely in the panel of antibodies for flow cytometric (FC) analysis of suspected lymphomatous tissue specimens obtained from fine‐needle aspiration biopsy (FNAB). The authors evaluated the role of CD56 expression on FC of neuroendocrine (NE) tumors. An initial diagnosis of NHL was suspected based on an on‐site FNAB evaluation. METHODS Ten FNABs were identified from the cytopathology files at The Johns Hopkins Hospital, Baltimore, MD (2000–2001). Flow cytometric analysis was negative for NHL but revealed a CD56‐positive nonlymphoid cell population. An FNAB evaluation was performed on air‐dried Diff‐Quik–stained smears and FC analysis used a fixed panel of 12 antibodies (B‐cell markers, T‐cell markers, CD33, CD56, and CD71). Immunoperoxidase staining (IPOX) was performed on the cell block sections from four of the tissue specimens using epithelial and NE markers, CD56, desmin, and O13 antibodies. Sites of FNAB included the lung (five cases), liver (one case), lymph node (three cases), and peritoneum (one case). Only one patient had a history of cancer at the time of FNAB. RESULTS All cytologic diagnoses were confirmed by histopathologic follow‐up on resection or biopsy or both. Diagnoses included small cell carcinoma (eight cases), Merkel cell carcinoma (one case), and primitive neuroectodermal tumor/Ewing sarcoma (one case). All tissue specimens that underwent IPOX stained strongly with NE markers, with one tissue section staining only with O13. CONCLUSIONS CD56 expression by FC in the presence of negative immunostaining with lymphoid markers represented a unique yet highly specific method for the diagnosis of NE tumors by FNAB. This procedure eliminated the need for further IPOX studies on the already limited cytologic sample and provided a timely and accurate diagnosis. Cancer (Cancer Cytopathol) 2003;99:240–6. © 2003 American Cancer Society.
The biologic role that estrogen receptor (ER) and progesterone receptor (PR) play in ovarian sex cord-stromal tumors is poorly understood. Furthermore, immunohistochemical data on these hormone receptors in this group of neoplasms are limited and conflicting, with many reports suggesting that expression of ERalpha and/or PR is either infrequent or present at low levels in granulosa and Sertoli cell tumors. Immunohistochemical staining for ERalpha and PR was performed in 69 ovarian sex cord-stromal tumors: 41 adult granulosa cell tumors and 28 Sertoli-Leydig cell tumors. Extent of expression was scored based on the percentage of positive cells: 0, 5% or less; 1+, 6% to 25%; 2+, 26% to 50%; 3+, 51% to 75%; and 4+, 76% to 100%. Estrogen receptor alpha and PR were frequently expressed in adult granulosa cell tumors (66% and 98%, respectively) and Sertoli-Leydig cell tumors (79% and 86%, respectively). Diffuse (3+ or 4+) expression of PR was more common in adult granulosa cell tumors (68% vs. 36%; P = 0.013), whereas diffuse (3+ or 4+) expression of ERalpha was more frequent in Sertoli-Leydig cell tumors (50% vs. 20%; P = 0.010). In cases positive for both markers, adult granulosa cell tumors exhibited a focal (1+ or 2+) ERalpha/diffuse (3+ or 4+) PR coordinate profile more commonly than Sertoli-Leydig cell tumors (52% vs. 18%; P = 0.02), whereas Sertoli-Leydig cell tumors displayed a diffuse (3+ or 4+) ERalpha/focal (1+ or 2+) PR profile more frequently than adult granulosa cell tumors (36% vs. 0%; P = 0.0007). We conclude that expression of hormone receptors (based only on frequency of immunostaining) does not allow for distinction from other tumors in the differential diagnosis that are known to be frequently positive for ERalpha and PR such as endometrioid neoplasms. Most adult granulosa cell tumors and Sertoli-Leydig cell tumors share overlapping patterns of expression of ERalpha and PR with each other, but a subset of cases in each tumor category exhibits unique ERalpha/PR immunoprofiles (eg, focal ERalpha/diffuse PR in adult granulosa cell tumors and diffuse ERalpha/focal PR in Sertoli-Leydig cell tumors). These patterns of expression of ERalpha and PR may aid our understanding of the biologic differences between granulosa and Sertoli cell tumors.
Background Patients with human epidermal growth factor receptor 2 (HER2)‐positive breast cancer are treated with trastuzumab‐based neoadjuvant therapy (NAT); some patients with residual disease post‐NAT show loss of HER2 amplification and has been inconsistently associated with oncologic outcomes. Methods We queried our multi‐institutional cancer registry for women with HER2‐positive breast cancer undergoing NAT from 2011 to 2018. Clinicopathologic, treatment‐related, and outcomes data were collected. Kaplan–Meier and Cox proportional hazards analysis were used to evaluate oncologic outcomes. Results A total of 348 patients were identified; 166 (48%) had a pathologic complete response. Of the 182 patients with residual disease, 87 (48%) were HER2‐positive, 34 (19%) were HER2‐negative, and 61 (33%) were HER2‐unknown, with a median follow‐up of 44 months. There were no factors associated with HER2 loss apart from age. On Kaplan–Meier analysis, estimated 5‐year recurrence‐free survival (RFS) and overall survival (OS) for patients with HER2‐positive residual disease was 81% and 92%, respectively, and 74% (log rank p = 0.75) and 81% (p = 0.35) in patients with HER2‐negative residual disease. Conclusion The loss of HER2‐positivity following NAT is not associated with worse 5‐year RFS or OS. We do not recommend retesting HER2 status following NAT for the purpose of clinical management; these patients should complete targeted adjuvant therapy.
This study identifies a set of genes associated with the progression of IPMN to malignancy. These genes are potential markers that could be used to identify IPMN requiring surgical resection.
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