We previously proposed a dualistic model for ovarian serous carcinogenesis. One pathway involves the stepwise development of invasive micropapillary serous carcinoma (MPSC) from serous borderline tumor (atypical proliferative serous tumor) to noninvasive and then invasive MPSC. The carcinomas that develop in this fashion are characterized by low-grade nuclei and frequent K-ras mutations. They generally pursue an indolent course. In the other pathway conventional serous carcinoma (CSC) develops from the ovarian surface epithelium without what appears to be intermediate stages. These tumors display high-grade nuclei, wild-type K-ras, and are very aggressive. Some of these CSCs display micropapillary architecture and simulate invasive MPSCs. This raises the possibility that these CSCs develop from an invasive MPSC. To address this question we reviewed 31 moderately and poorly differentiated CSCs and identified 7 with morphological features of invasive MPSC. These seven tumors exhibited micropapillary architecture in at least 25% of the tumor but contained high-grade nuclei. The 31 tumors were assessed for K-ras mutations using digital polymerase chain reaction-based analysis. Despite their micropapillary architecture, all 7 CSCs with micropapillary features contained wild-type K-ras as did the other 24 pure CSCs. The results indicate that CSCs with micropapillary features are not derived from invasive MPSCs. The molecular findings also support the view that ovarian serous carcinomas should be graded as low- and high-grade tumors.

BACKGROUND.Patients with head and neck squamous cell carcinoma (HNSCC) often present with metastatic disease. The diagnosis of metastatic lesions usually is determined by fine-needle aspiration. Human papillomavirus (HPV) is now being considered as a causative agent in a subset of HNSCC. The objectives of this study were, first; to search for the presence of HPV DNA by in situ hybridization (ISH) in metastatic lesions from HNSCC using alcohol-fixed, archival, cytopathologic material; second, to characterize the cytologic features of HPV-positive metastatic lesions of HNSCC; and, third, to determine whether there is a correlation between the presence of HPV DNA and the origin of metastatic lesions. METHODS.The authors performed chromogenic ISH analysis for HPV DNA on fine-needle aspiration materials from metastatic lesions from 26 patients with HNSCC. Along with the ISH analysis, a detailed cytologic review was performed, and cytopathologic features were recorded. The HPV DNA status in metastatic lesion was correlated with cytopathologic features and primary tumor location. RESULTS.The integration of HPV DNA was visualized microscopically on tumor cell nuclei in 15% of aspirates. The anatomic locations of the study samples were as follows: 16 lymph node aspirates (11 cervical lymph nodes and 5 lymph nodes at other sites other), 5 tracheostomy sites, and 5 miscellaneous sites located on the head and neck area. Cytologic review revealed 13 keratinized and 13 nonkeratinized metastatic tumors. HPV DNA was detected in four metastatic sites (three lymph nodes and one tracheostomy site). All HPV DNA-positive tumors were of the nonkeratinizing type (P Ͻ 0.05; Fisher exact test). The origins of HPV-positive tumors included two laryngeal sites, one nasopharyngeal site, and one oral cavity site. CONCLUSIONS.The current findings showed that archival cytology slides can be used for HPV DNA detection with ISH. The results also showed that HPV DNAcontaining HNSCC has distinctively nonkeratinizing cytologic features. The authors concluded that HPV DNA not only is involved in the initiation of tumoral processes but also plays an important role in the development of metastatic disease.

Introduction:Differentiation between pancreatic ductal adenocarcinoma (PDAC) from benign mimickers is a well-known problem in cytological materials. Recent studies incorporated biological markers into this question and some studies showed that expression of S100P, IMP3, and maspin as well as nonexpression of von Hippel-Lindau gene product (pVHL) were significantly correlated with PDAC. In this study, we aimed to investigate diagnostic value of maspin, IMP3, S100P, and pVHL immunostaining in fine needle aspiration biopsies (FNABs) of pancreatic lesions.Materials and Method:In all, 33 cases of FNAB cell blocks of PDAC and 34 cases of surgical non-neoplastic pancreas specimens which were retrieved from the archives slides from 2007 to 2011 were included in this study. All the cases were stained with maspin, IMP3, S100P, and pVHL. Expression patterns of markers were scored and compared with benign mimickers. Test performance of each antibody and possible antibody combinations were also evaluated.Results:The study was composed of 33 PDAC and 34 control cases (8 chronic pancreatitis, 3 mucinous cystic neoplasm, and 23 nontumoral pancreatic tissue of PDAC). Diagnostic sensitivity for malignancy in S100P, IMP3, and maspin was 84.8%, 81.8%, and 87.5%, respectively. Specificity of these three markers was 100%. Sensitivity and specificity of pVHL for detecting nontumoral pancreatic tissue were 100% and 81.8%, respectively. When maspin, IMP3, and S100P expression were used together as triple test, sensitivity was 62.5% and specificity 100%. However, when any two of each three markers were evaluated (triple test/dual response), sensitivity reached 93.8% and specificity 100%.Conclusion:We observed that dual response in triple test (positive staining with two of these three markers) of maspin, IMP3, and S100P immunocytochemistry is very sensitive and specific in differential diagnosis of PDA and non-neoplastic pancreatic lesions. pVHL may have an additional role, when triple assessment is not satisfactory.

Multinodular hydropic leiomyoma (MHL) of the uterus is one of the rarest variants of uterine leiomyomas and can create some diagnostic problems. Only five cases have been reported previously. We describe an MHL with perinodular hydropic degeneration in a 48-year-old woman. Gross examination revealed a large and predominantly intramural, edematous multinodular uterine tumor and extrauterine, small grape-like nodules overlying the lateral surface of the uterine serosa. Histologically, the tumor was composed of extra-intrauterine benign, small smooth muscle nodules with perinodular hydropic degeneration, prominent intramural dissecting growth pattern, and satellite nodules closely resembling vascular invasion. Immunohistochemically, these cells stained for desmin, smooth muscle actin and vimentin. The patient had no evidence of disease for 18 months after hysterectomy. Multinodular hydropic leiomyoma is a clinically benign tumor and should not be confused with intravenous leiomyomatosis and some other unusual leiomyoma variants.