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Fulltext Identification of 12 new susceptibility loci for different histotypes of epithelial ovarian cancer

Phelan CM, Kuchenbaecker KB, Tyrer JP, Kar SP, Lawrenson K, Winham SJ, et al.

Nat Genet, 2017 May;49(5):680-691.
PMID: 28346442 DOI: 10.1038/ng.3826

To identify common alleles associated with different histotypes of epithelial ovarian cancer (EOC), we pooled data from multiple genome-wide genotyping projects totaling 25,509 EOC cases and 40,941 controls. We identified nine new susceptibility loci for different EOC histotypes: six for serous EOC histotypes (3q28, 4q32.3, 8q21.11, 10q24.33, 18q11.2 and 22q12.1), two for mucinous EOC (3q22.3 and 9q31.1) and one for endometrioid EOC (5q12.3). We then performed meta-analysis on the results for high-grade serous ovarian cancer with the results from analysis of 31,448 BRCA1 and BRCA2 mutation carriers, including 3,887 mutation carriers with EOC. This identified three additional susceptibility loci at 2q13, 8q24.1 and 12q24.31. Integrated analyses of genes and regulatory biofeatures at each locus predicted candidate susceptibility genes, including OBFC1, a new candidate susceptibility gene for low-grade and borderline serous EOC.

Matched MeSH terms: Neoplasms, Glandular and Epithelial/genetics*; Neoplasms, Glandular and Epithelial/pathology
Fulltext Clinical behaviour, pathological findings, survival and prognostic factors in young woman in comparison to menopausal women with Epithelial ovarian malignancy

Rusinahayati, M., Sivanesaratnam, V., Jayalashmi, Noraihan, M. N.

Malaysian Journal of Medicine and Health Sciences, 2010;6(1):19-32.
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Objective: The purpose of this study was to evaluate the clinical behaviour, pathological findings, survival and prognostic factors in young women in comparison to menopausal women with epithelial ovarian malignancy. Methods: A retrospective analysis of 141 patients (67 for age below 40 years and 74 menopausal) treated between 1980 and 2000 was conducted. Results: Irrespective of the stage, the most common clinical presentation was abdominal distension in both young (78%) and menopausal women (66%). In young women, 52% presented at an early stage of the disease and in menopausal women this was seen in 22% (p-value

Matched MeSH terms: Neoplasms, Glandular and Epithelial
Invadopodia proteins, cortactin, N-WASP and WIP differentially promote local invasiveness in ameloblastoma

Siar CH, Rahman ZA, Tsujigiwa H, Mohamed Om Alblazi K, Nagatsuka H, Ng KH

J Oral Pathol Med, 2016 Sep;45(8):591-8.
PMID: 26752341 DOI: 10.1111/jop.12417

BACKGROUND: Cell migration and invasion through interstitial tissues are dependent upon several specialized characteristics of the migratory cell notably generation of proteolytic membranous protrusions or invadopodia. Ameloblastoma is a benign odontogenic epithelial neoplasm with a locally infiltrative behaviour. Cortactin and MMT1-MMP are two invadopodia proteins implicated in its local invasiveness. Other invadopodia regulators, namely N-WASP, WIP and Src kinase remain unclarified. This study addresses their roles in ameloblastoma.
MATERIALS AND METHOD: Eighty-seven paraffin-embedded ameloblastoma cases (20 unicystic, 47 solid/multicystic, 3 desmoplastic and 17 recurrent) were subjected to immunohistochemistry for expression of cortactin, N-WASP, WIP, Src kinase and F-actin, and findings correlated with clinicopathological parameters.
RESULTS: Invadopodia proteins (except Src kinase) and F-actin were widely detected in ameloblastoma (cortactin: n = 73/87, 83.9%; N-WASP: n = 59/87; 67.8%; WIP: n = 77/87; 88.5%; and F-actin: n = 87/87, 100%). Protein localization was mainly cytoplasmic and/or membranous, and occasionally nuclear for F-actin. Cortactin, which functions as an actin-scaffolding protein, demonstrated significantly higher expression levels within ameloblastoma tumoral epithelium than in stroma (P < 0.05). N-WASP, which coordinates actin polymerization and invadopodia-mediated extracellular matrix degradation, was overexpressed in the solid/multicystic subtype (P < 0.05). WIP, an upstream regulator of N-WASP, and F-actin were significantly upregulated along the tumour invasive front compared to tumour centres (P < 0.05). Except for males with cortactin overexpression, other clinical parameters (age, ethnicity and anatomical site) showed no significant correlations.
CONCLUSIONS: Present results suggest that local invasiveness of ameloblastoma is dependent upon the migratory potential of its tumour cells as defined by their distribution of cortactin, N-WASP and WIP in correlation with F-actin cytoskeletal dynamics.

Matched MeSH terms: Neoplasms, Glandular and Epithelial/metabolism
Collision tumor of the ovary: Fibroma and mature cystic teratoma

Tan GC, Chandramaya SF, Noordin A, S Tay PY

Indian J Pathol Microbiol, 2021 1 13;64(1):171-173.
PMID: 33433434 DOI: 10.4103/IJPM.IJPM_670_19

Collision tumor consists of two tumors occurring in the same organ without intermixture of the two cell types. The most common type of collision tumor in ovary is between teratoma and surface epithelial tumor. A 38-year-old woman presented with complained of lower abdominal pain and tightness, and a solid partially cystic left ovarian mass with minimal ascites was detected. Left salpingo-oophorectomy was performed. The ovarian mass measured 15 × 12 × 7 cm with a pedunculated mass on its surface which measured 6 × 2.5 × 2.5 cm. Histologically, it was a collision tumor of fibroma and mature cystic teratoma. Fibroma becomes more edematous as their size increases, which is frequently accompanied by the escape of increasing quantities of fluid from the tumor surfaces. Ascites is often detected when the fibroma is more than a diameter of 10 cm. It is important to identify the different components of a collision tumor for proper management.

Matched MeSH terms: Neoplasms, Glandular and Epithelial
Epstein-Barr virus-encoded latent membrane protein-1 upregulates 14-3-3σ and Reprimo to confer G(2)/M phase cell cycle arrest

Yeo KS, Mohidin TB, Ng CC

C. R. Biol., 2012 Dec;335(12):713-21.
PMID: 23312294 DOI: 10.1016/j.crvi.2012.11.002

Epstein-Barr virus (EBV) is a ubiquitous tumor-causing virus which infects more than 90% of the world population asymptomatically. Recent studies suggest that LMP-1, -2A and -2B cooperate in the tumorigenesis of EBV-associated epithelial cancers such as nasopharygeal carcinoma, oral and gastric cancer. In this study, LMPs were expressed in the HEK293T cell line to reveal their oncogenic mechanism via investigation on their involvement in the regulation of the cell cycle and genes that are involved. LMPs were expressed in HEK293T in single and co-expression manner. The transcription of cell cycle arrest genes were examined via real-time PCR. Cell cycle progression was examined via flow cytometry. 14-3-3σ and Reprimo were upregulated in all LMP-1 expressing cells. Moreover, cell cycle arrest at G(2)/M progression was detected in all LMP-1 expressing cells. Therefore, we conclude that LMP-1 may induce cell cycle arrest at G(2)/M progression via upregulation of 14-3-3σ and Reprimo.

Matched MeSH terms: Neoplasms, Glandular and Epithelial/virology
Epstein-Barr virus: more than 50 years old and still providing surprises

Young LS, Yap LF, Murray PG

Nat Rev Cancer, 2016 12;16(12):789-802.
PMID: 27687982 DOI: 10.1038/nrc.2016.92

It is more than 50 years since the Epstein-Barr virus (EBV), the first human tumour virus, was discovered. EBV has subsequently been found to be associated with a diverse range of tumours of both lymphoid and epithelial origin. Progress in the molecular analysis of EBV has revealed fundamental mechanisms of more general relevance to the oncogenic process. This Timeline article highlights key milestones in the 50-year history of EBV and discusses how this virus provides a paradigm for exploiting insights at the molecular level in the diagnosis, treatment and prevention of cancer.

Matched MeSH terms: Neoplasms, Glandular and Epithelial/virology