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Your search keyword '"Leppa, Sirpa"' showing total 4 results
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4 results on '"Leppa, Sirpa"'

1. Enteropathy-associated T cell lymphoma subtypes are characterized by loss of function of SETD2

Author

Moffitt, Andrea B, Ondrejka, Sarah L, McKinney, Matthew, Rempel, Rachel E, Goodlad, John R, Teh, Chun Huat, Leppa, Sirpa, Mannisto, Susanna, Kovanen, Panu E, Tse, Eric, Au-Yeung, Rex KH, Kwong, Yok-Lam, Srivastava, Gopesh, Iqbal, Javeed, Yu, Jiayu, Naresh, Kikkeri, Villa, Diego, Gascoyne, Randy D, Said, Jonathan, Czader, Magdalena B, Chadburn, Amy, Richards, Kristy L, Rajagopalan, Deepthi, Davis, Nicholas S, Smith, Eileen C, Palus, Brooke C, Tzeng, Tiffany J, Healy, Jane A, Lugar, Patricia L, Datta, Jyotishka, Love, Cassandra, Levy, Shawn, Dunson, David B, Zhuang, Yuan, Hsi, Eric D, and Dave, Sandeep S

Subjects
Genetics, Cancer, Hematology, Lymphoma, Rare Diseases, Clinical Research, Biotechnology, Digestive Diseases, 2.1 Biological and endogenous factors, Aetiology, Animals, DNA Copy Number Variations, Enteropathy-Associated T-Cell Lymphoma, Female, Gene Expression Profiling, Gene Silencing, Histone-Lysine N-Methyltransferase, Humans, Male, Mice, Knockout, Middle Aged, Mutation, Sequence Analysis, DNA, T-Lymphocytes, Medical and Health Sciences, Immunology
Abstract

Enteropathy-associated T cell lymphoma (EATL) is a lethal, and the most common, neoplastic complication of celiac disease. Here, we defined the genetic landscape of EATL through whole-exome sequencing of 69 EATL tumors. SETD2 was the most frequently silenced gene in EATL (32% of cases). The JAK-STAT pathway was the most frequently mutated pathway, with frequent mutations in STAT5B as well as JAK1, JAK3, STAT3, and SOCS1 We also identified mutations in KRAS, TP53, and TERT Type I EATL and type II EATL (monomorphic epitheliotropic intestinal T cell lymphoma) had highly overlapping genetic alterations indicating shared mechanisms underlying their pathogenesis. We modeled the effects of SETD2 loss in vivo by developing a T cell-specific knockout mouse. These mice manifested an expansion of γδ T cells, indicating novel roles for SETD2 in T cell development and lymphomagenesis. Our data render the most comprehensive genetic portrait yet of this uncommon but lethal disease and may inform future classification schemes.

Published
2017

2. Translational suppression of syndecan-1 expression in Ha-ras transformed mouse mammary epithelial cells

Author

Markku Jalkanen, Leppa Sirpa Marianne, N E Hynes, and Jarkko Kirjavainen

Subjects
Syndecans, animal structures, Cell, Fluorescent Antibody Technique, Cell Line, Malignant transformation, Syndecan 1, Mice, Mammary Glands, Animal, Gene expression, medicine, Animals, Point Mutation, Molecular Biology, Membrane Glycoproteins, biology, Epithelial Cells, Cell Biology, Transfection, Molecular biology, Epithelium, carbohydrates (lipids), Cell Transformation, Neoplastic, Genes, ras, Phenotype, medicine.anatomical_structure, Proteoglycan, Cell culture, Protein Biosynthesis, embryonic structures, biology.protein, Proteoglycans, Syndecan-1, Research Article
Abstract

A cell surface proteoglycan, syndecan-1, has been shown to participate in the maintenance of the epithelial cell morphology. A point mutated activated c-Ha-ras gene under the control of the glucocorticoid inducible MMTV-LTR promoter was transfected into the mouse mammary epithelial cell line, NOG-8. The NOG-8 ras cells were used to study changes in syndecan-1 expression during epithelial transformation. NOG-8 ras cells, when induced to express Ha-ras, transformed and formed foci in monolayer cultures and colonies in suspension cultures. Expression of syndecan-1 at the cell surface was markedly reduced in cells showing the transformed phenotype. The accumulation of newly synthesized core protein of syndecan-1 was suppressed in these cells, whereas mRNA levels remained unchanged. This novel finding indicates that syndecan-1 expression is translationally suppressed in the Ha-ras-transformed epithelial cells. Hence, syndecan-1 loss during epithelial transformation could take place without altering syndecan gene transcription and, on the other hand, could be one of the critical events involved in malignant transformation.

Published
1993
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3. Syndecan expression regulates cell morphology and growth of mouse mammary epithelial tumor cells

Author

Markku Mali, Markku Jalkanen, Leppa Sirpa Marianne, and Heini M. Miettinen

Subjects
medicine.medical_specialty, animal structures, Syndecans, Cell division, Cell, Gene Expression, Biology, Cell morphology, Transfection, Dexamethasone, Epithelium, Syndecan 1, Mice, Internal medicine, medicine, Tumor Cells, Cultured, Animals, Testosterone, RNA, Messenger, Cloning, Molecular, Multidisciplinary, Membrane Glycoproteins, Cell growth, Mammary Neoplasms, Experimental, Blotting, Northern, Phenotype, Cell biology, carbohydrates (lipids), Actin Cytoskeleton, medicine.anatomical_structure, Endocrinology, embryonic structures, Proteoglycans, Cell Division, Research Article
Abstract

S115 mouse mammary epithelial cells lose their epithelial morphology and become tumorigenic when exposed to steroids. We have recently reported that testosterone exposure results in the suppression of syndecan expression, suggesting that this cell surface proteoglycan may influence S115 cell phenotype. We now report that a similar suppression and morphological response of S115 cells can be achieved by glucocorticoid exposure. We introduced into S115 cells an exogenous gene construct containing the full-length human syndecan cDNA under the control of a glucocorticoid-inducible retroviral promoter, in order to study the effect of syndecan expression on S115 cell behavior. Glucocorticoid-induced re-expression of syndecan in S115 cells restored an epithelial phenotype, while control transfectants and parental S115 cells exhibited an altered, nonepithelial phenotype. Moreover, the S115 cells expressing exogenous syndecan revealed a reduced ability to form colonies in soft agar. Therefore, the maintenance of epithelial morphology and normal growth of S115 cells are dependent on syndecan expression.

Published
1992

4. Syndecan, a regulator of cell behaviour, is lost in malignant transformation

Author

Markku Jalkanen, Jarkko Kirjavainen, Leppa Sirpa Marianne, Pirjo Inki, and Klaus Elenius

Subjects
Cell Transformation, Neoplastic, Membrane Glycoproteins, Syndecans, Gene Expression Regulation, Philosophy, Cell regulation, Animals, Cell behaviour, Proteoglycans, Anatomy, Biochemistry, Humanities, Extracellular Matrix
Abstract

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Published
1991

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