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Granulosa cell tumor (GCT) with synchronous mature teratoma is extremely rare and only eight cases are documented in the literature. GCT is low-grade malignancy and need a close follow up for recurrences which may be late. We report a case of GCT and mature teratoma occurring synchronously in the same ovary in a perimenopausal woman.

Background: Metastasis to the breast of an extra-mammary origin is very rare. FNAC plays an important role in differentiating non-mammary breast metastasis from primary malignancy. This study aimed to analyze the cytomorphological criteria and its pitfalls in differentiating metastatic lesion of the breast from primary malignancy. Methodology: Retrospective analysis of 891 FNACs of the breast was performed for a time span of 3 years. A total of 12 cases were diagnosed on FNAC as secondary neoplasms to the breast. Clinical and radiological data, along with Pap and MGG stained smears of each case were examined and correlated with the histopathology of the primary tumor. Statistical analysis was carried out. All cases of primary breast malignancies were excluded from our study. Results: In 10 out of 12 cases, primary malignancies were identified as Plasma cell myeloma (one case), B-acute lymphoblastic leukemia (two cases), acute myeloid leukemia (one case); chronic myeloid leukemia (one case), Burkitt's lymphoma of the ovary (one case), Diffuse large B-cell lymphoma (one case), esophageal squamous cell carcinoma (one case), spindle cell sarcoma (one case) and squamous cell carcinoma of the cervix (one case). The remaining two cases in our study were misdiagnosed on cytology as metastasis and turned out to be breast primaries on histopathology. Conclusion: Our case series highlights the importance of FNAC to differentiate secondary lesions from primary breast malignancy and thus helps to avoid unnecessary surgery to the patient. It emphasizes on the need to keep in mind the possibility of metastatic breast neoplasms in the presence of unusual cytological features on FNAC. [ABSTRACT FROM AUTHOR]

Background: The incidence of gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) is on the rise. Although the clinicopathologic characteristics of NENs have been previously reviewed in the literature, the data published in the Indian literature so far are sparse. This study aims to review the clinicopathological features of GEP-NENs, diagnosed at our institution, and that were classified and graded according to the World Health Organization 2010 classification system. Materials and Methods: One hundred patients with GEP-NENs presenting to our institute from August 2012 to May 2016 were analyzed retrospectively. Demographic data and tumor characteristics were expressed as number, percentage, and mean value. Tumor grade was correlated to metastasis through the Chi-square test. P < 0.05 was considered statistically significant. Results: Of the 100 cases studied, 58 were male and 42 were female. The most common primary site was the pancreas (n = 36), followed by the small intestine (n = 19), esophagus (n = 17), stomach (n = 15), colon (n = 6), rectum (n = 4), and appendix (n = 3). The incidence of neuroendocrine tumor (NET) Grade 1 (NET G1) was higher (n = 40) compared to NET Grade 2 (NET G2) (n = 25) and neuroendocrine carcinoma Grade 3 (NEC G3) (n = 35). Overall in these 100 cases, NET G1 tumors and NET G2 tumors were most common in the pancreas (n = 18/36) and (n = 13/36), respectively. NEC G3 tumors were most common in the esophagus (n = 16/17). The most common site of distant metastasis was the liver (n = 23/26). Conclusion: We elucidated the epidemiological and clinicopathological features of patients presenting to our institute with GEP-NENs. [ABSTRACT FROM AUTHOR]

Byline: Melissa L. Gruys, Susan M. Stewart, Trupti Patel The current paper provides a summary and highlights issues that are specific to female expatriates completing assignments in 12 different countries from four regions around the world. The regions and countries reviewed include North America (USA, Mexico, Canada), Europe (Spain, France, Italy), Middle East (Saudi Arabia, Israel, Afghanistan) and Asia (Korea, China, Japan). The information provided will be of assistance to female expatriates who are making preparations to travel to any of the countries reviewed and might also help decision-makers focus on how women can be effectively utilised in global business assignments and transactions.

Objective:The objective of our review is to highlight the significance of microsatellite hypervariation in diagnostics of hematologic malignancies. Methods:For the past few decades, extensive experiments in cancer research have explored all the possible pathways and a number of deleterious mutations that either make the tumor suppressor genes (TSGs) dysfunctional or cause the proto-oncogenes to behave abnormally by changing the cellular phenotype hence rendering disease. To prevent the deleterious effects of mutations and to protect the genomic integrity, our system possesses multiple repair mechanisms. DNA Mismatch Repair (MMR) and Direct Reversal of Damage (DRD) are two repair mechanisms which help in removal of faulty base pairs and alkyl adduct formation respectively to avoid long term effects of toxicity, tumorigenesis and mutagenesis. There are nine major MMR genes – MutS homolog (MSH2, MSH3, MSH4, MSH5, MSH6), MutL homolog (MLH1, MLH3), human post-meiotic segregation genes (PMS1, PMS2), and three major damage reversal genes – O6-methylguanine-DNA-methyltransferase (MGMT), ABH2 and DEPC1. Results:Any malfunction in DNA repair machinery can cause microsatellite instability (MSI), a form of genomic abnormality with hyper mutable repeats that is directly associated with cancer. Microsatellites are short, repetitive sequences, non-randomly distributed and localized in 3'-UTR (Untranslated Region), introns, coding regions and promoters. Besides MSI, evidence on promoter hypermethylation of selected repair genes also points toward a prominent reason for cancer initiation and progression. Conclusion:The presence of specific microsatellite marker hyper-mutability and consistent promoter hypermethylation in leukemia or lymphoma can be considered as a part of routine diagnostic test in clinical laboratories. [ABSTRACT FROM AUTHOR]

Background: Enhancer of zeste homolog 2 (EZH2) is a catalytic subunit of Polycomb Repressor Complex 2. PRC2 catalyzes methylation of H3K27me and it silences specific gene transcriptions. EZH2 is known to play a vital role in cancer initiation, development, progression, metastasis, and drug resistance. The expression of EZH2 is regulated by a variety of oncogenic transcription factors, tumor suppressor micro-RNAs, and cancer-associated non-coding RNAs. Post-translational modifications also control EZH2 activity. The altered expression of EZH2 has major implication in altering cellular plasticity and, hence, understanding various deleterious mutations can help comprehend its role in cancer metastasis. Objectives: The aim of this study is to summarize the data from COSMIC into useful information from the perspective of severity of the mutations in EZH2 and their contributory role as a potential biomarker in diagnosis and therapeutics associated cancers. Methods: Data mining was carried out for various SNPs in EZH2 SET domain from COSMIC, and the severity of each mutation on the functionality of the enzyme was analyzed, using multiple online in-silico tools. The frequently deleterious SNPs were further subjected to advanced tools to understand the changes which render the enzyme functionally erratic during cancer. Results: The results obtained enhanced the understanding of EZH2 mutation and predicted the plausible biomarkers that could be targeted for the purpose of diagnosis and therapeutics. About 14 prospective biomarkers for various cancers were identified and, further, their role in altering the EZH2 function was discussed. Conclusions: The various predictive and prognostic impacts of these SNPs in the selected residues are discussed which can be efficiently targeted for an improved cancer diagnosis and designing appropriate treatment strategies. [ABSTRACT FROM AUTHOR]