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244 results on '"Costinean, Stefan"'

1. Author Correction: Astroblastomas exhibit radial glia stem cell lineages and differential expression of imprinted and X-inactivation escape genes

Author

Lehman, Norman L., Spassky, Nathalie, Sak, Müge, Webb, Amy, Zumbar, Cory T., Usubalieva, Aisulu, Alkhateeb, Khaled J., McElroy, Joseph P., Maclean, Kirsteen H., Fadda, Paolo, Liu, Tom, Gangalapudi, Vineela, Carver, Jamie, Abdullaev, Zied, Timmers, Cynthia, Parker, John R., Pierson, Christopher R., Mobley, Bret C., Gokden, Murat, Hattab, Eyas M., Parrett, Timothy, Cooke, Ralph X., Lehman, Trang D., Costinean, Stefan, Parwani, Anil, Williams, Brian J., Jensen, Randy L., Aldape, Kenneth, and Mistry, Akshitkumar M.

Published
2023
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2. Astroblastomas exhibit radial glia stem cell lineages and differential expression of imprinted and X-inactivation escape genes

Author

Lehman, Norman L., Spassky, Nathalie, Sak, Müge, Webb, Amy, Zumbar, Cory T., Usubalieva, Aisulu, Alkhateeb, Khaled J., McElroy, Joseph P., Maclean, Kirsteen H., Fadda, Paolo, Liu, Tom, Gangalapudi, Vineela, Carver, Jamie, Abdullaev, Zied, Timmers, Cynthia, Parker, John R., Pierson, Christopher R., Mobley, Bret C., Gokden, Murat, Hattab, Eyas M., Parrett, Timothy, Cooke, Ralph X., Lehman, Trang D., Costinean, Stefan, Parwani, Anil, Williams, Brian J., Jensen, Randy L., Aldape, Kenneth, and Mistry, Akshitkumar M.

Published
2022
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3. Disruption of miR-29 Leads to Aberrant Differentiation of Smooth Muscle Cells Selectively Associated with Distal Lung Vasculature.

Author

Cushing, Leah, Costinean, Stefan, Xu, Wei, Jiang, Zhihua, Madden, Lindsey, Kuang, Pingping, Huang, Jingshu, Weisman, Alexandra, Hata, Akiko, Croce, Carlo M, and Lü, Jining

Subjects
Muscle, Smooth, Vascular, Lung, Pulmonary Artery, Animals, Humans, Mice, Hypertension, Pulmonary, SKP Cullin F-Box Protein Ligases, Muscle Proteins, MicroRNAs, Cell Differentiation, Cell Proliferation, Gene Expression Regulation, Developmental, Kruppel-Like Transcription Factors, Muscle, Smooth, Vascular, Hypertension, Pulmonary, Gene Expression Regulation, Developmental, Developmental Biology, Genetics
Abstract

Differentiation of lung vascular smooth muscle cells (vSMCs) is tightly regulated during development or in response to challenges in a vessel specific manner. Aberrant vSMCs specifically associated with distal pulmonary arteries have been implicated in the pathogenesis of respiratory diseases, such as pulmonary arterial hypertension (PAH), a progressive and fatal disease, with no effective treatment. Therefore, it is highly relevant to understand the underlying mechanisms of lung vSMC differentiation. miRNAs are known to play critical roles in vSMC maturation and function of systemic vessels; however, little is known regarding the role of miRNAs in lung vSMCs. Here, we report that miR-29 family members are the most abundant miRNAs in adult mouse lungs. Moreover, high levels of miR-29 expression are selectively associated with vSMCs of distal vessels in both mouse and human lungs. Furthermore, we have shown that disruption of miR-29 in vivo leads to immature/synthetic vSMC phenotype specifically associated with distal lung vasculature, at least partially due to the derepression of KLF4, components of the PDGF pathway and ECM-related genes associated with synthetic phenotype. Moreover, we found that expression of FBXO32 in vSMCs is significantly upregulated in the distal vasculature of miR-29 null lungs. This indicates a potential important role of miR-29 in smooth muscle cell function by regulating FBXO32 and SMC protein degradation. These results are strongly supported by findings of a cell autonomous role of endogenous miR-29 in promoting SMC differentiation in vitro. Together, our findings suggested a vessel specific role of miR-29 in vSMC differentiation and function by targeting several key negative regulators.

Published
2015

5. Supplementary Methods, Table 1, Figures 1-8 from RETRACTED: Loss of Metallothionein Predisposes Mice to Diethylnitrosamine-Induced Hepatocarcinogenesis by Activating NF-κB Target Genes

Author

Majumder, Sarmila, primary, Roy, Satavisha, primary, Kaffenberger, Thomas, primary, Wang, Bo, primary, Costinean, Stefan, primary, Frankel, Wendy, primary, Bratasz, Anna, primary, Kuppusamy, Periannan, primary, Hai, Tsonwin, primary, Ghoshal, Kalpana, primary, and Jacob, Samson T., primary

Published
2023
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6. Src homology 2 domain–containing inositol-5-phosphatase and CCAAT enhancer-binding protein β are targeted by miR-155 in B cells of Eμ-MiR-155 transgenic mice

Author

Costinean, Stefan, Sandhu, Sukhinder K, Pedersen, Irene M, Tili, Esmerina, Trotta, Rossana, Perrotti, Danilo, Ciarlariello, David, Neviani, Paolo, Harb, Jason, Kauffman, Lauren Rachel, Shidham, Aaditya, and Croce, Carlo Maria

Subjects
Hematology, Genetics, Biotechnology, Childhood Leukemia, Pediatric Cancer, Cancer, Rare Diseases, Pediatric, Lymphoma, Aetiology, 2.1 Biological and endogenous factors, Animals, CCAAT-Enhancer-Binding Protein-beta, Cell Transformation, Neoplastic, Down-Regulation, Gene Expression Regulation, Leukemic, Inositol Polyphosphate 5-Phosphatases, Interleukin-6, Lymphoma, B-Cell, Mice, Mice, Transgenic, MicroRNAs, Phosphoric Monoester Hydrolases, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Precursor Cells, B-Lymphoid, Signal Transduction, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Paediatrics and Reproductive Medicine, Immunology
Abstract

We showed that Emicro-MiR-155 transgenic mice develop acute lymphoblastic leukemia/high-grade lymphoma. Most of these leukemias start at approximately 9 months irrespective of the mouse strain. They are preceded by a polyclonal pre-B-cell proliferation, have variable clinical presentation, are transplantable, and develop oligo/monoclonal expansion. In this study, we show that in these transgenic mice the B-cell precursors have the highest MiR-155 transgene expression and are at the origin of the leukemias. We determine that Src homology 2 domain-containing inositol-5-phosphatase (SHIP) and CCAAT enhancer-binding protein beta (C/EBPbeta), 2 important regulators of the interleukin-6 signaling pathway, are direct targets of MiR-155 and become gradually more down-regulated in the leukemic than in the preleukemic mice. We hypothesize that miR-155, by down-modulating Ship and C/EBPbeta, initiates a chain of events that leads to the accumulation of large pre-B cells and acute lymphoblastic leukemia/high-grade lymphoma.

Published
2009

7. Src homology 2 domain-containing inositol-5-phosphatase and CCAAT enhancer-binding protein beta are targeted by miR-155 in B cells of Emicro-MiR-155 transgenic mice.

Author

Costinean, Stefan, Sandhu, Sukhinder K, Pedersen, Irene M, Tili, Esmerina, Trotta, Rossana, Perrotti, Danilo, Ciarlariello, David, Neviani, Paolo, Harb, Jason, Kauffman, Lauren Rachel, Shidham, Aaditya, and Croce, Carlo Maria

Subjects
Animals, Mice, Transgenic, Mice, Lymphoma, B-Cell, Cell Transformation, Neoplastic, Phosphoric Monoester Hydrolases, CCAAT-Enhancer-Binding Protein-beta, MicroRNAs, Interleukin-6, Signal Transduction, Down-Regulation, Gene Expression Regulation, Leukemic, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Precursor Cells, B-Lymphoid, Inositol Polyphosphate 5-Phosphatases, Transgenic, Lymphoma, B-Cell, Cell Transformation, Neoplastic, Gene Expression Regulation, Leukemic, Precursor Cells, B-Lymphoid, Immunology, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Paediatrics and Reproductive Medicine
Abstract

We showed that Emicro-MiR-155 transgenic mice develop acute lymphoblastic leukemia/high-grade lymphoma. Most of these leukemias start at approximately 9 months irrespective of the mouse strain. They are preceded by a polyclonal pre-B-cell proliferation, have variable clinical presentation, are transplantable, and develop oligo/monoclonal expansion. In this study, we show that in these transgenic mice the B-cell precursors have the highest MiR-155 transgene expression and are at the origin of the leukemias. We determine that Src homology 2 domain-containing inositol-5-phosphatase (SHIP) and CCAAT enhancer-binding protein beta (C/EBPbeta), 2 important regulators of the interleukin-6 signaling pathway, are direct targets of MiR-155 and become gradually more down-regulated in the leukemic than in the preleukemic mice. We hypothesize that miR-155, by down-modulating Ship and C/EBPbeta, initiates a chain of events that leads to the accumulation of large pre-B cells and acute lymphoblastic leukemia/high-grade lymphoma.

Published
2009

11. Supplementary Methods, Table 1, Figures 1-8 from Loss of Metallothionein Predisposes Mice to Diethylnitrosamine-Induced Hepatocarcinogenesis by Activating NF-κB Target Genes

Author

Majumder, Sarmila, primary, Roy, Satavisha, primary, Kaffenberger, Thomas, primary, Wang, Bo, primary, Costinean, Stefan, primary, Frankel, Wendy, primary, Bratasz, Anna, primary, Kuppusamy, Periannan, primary, Hai, Tsonwin, primary, Ghoshal, Kalpana, primary, and Jacob, Samson T., primary

Published
2023
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12. miR-15b/16-2 deletion promotes B-cell malignancies

Author

Lovat, Francesca, Fassan, Matteo, Gasparini, Pierluigi, Rizzotto, Lara, Cascione, Luciano, Pizzi, Marco, Vicentini, Caterina, Balatti, Veronica, Palmieri, Dario, Costinean, Stefan, and Croce, Carlo M.

Published
2015

15. MicroRNA-29b mediates altered innate immune development in acute leukemia

Author

Mundy-Bosse, Bethany L., Scoville, Steven D., Chen, Li, McConnell, Kathleen, Mao, Hsiaoyin C., Ahmed, Elshafa H., Zorko, Nicholas, Harvey, Sophia, Cole, Jordan, Zhang, Xiaoli, Costinean, Stefan, Croce, Carlo M., Larkin, Karilyn, Byrd, John C., Vasu, Sumithira, Blum, William, Yu, Jianhua, Freud, Aharon G., and Caligiuri, Michael A.

Subjects
Influence, Care and treatment, Analysis, Complications and side effects, Research, Health aspects, Killer cells -- Analysis -- Research, MicroRNA -- Analysis -- Research -- Influence, Cell differentiation -- Analysis, Leukemia -- Research -- Care and treatment -- Complications and side effects, Stem cell transplantation -- Analysis -- Research -- Health aspects, Stem cells -- Transplantation
Abstract

Introduction Acute myeloid leukemia (AML) is one of the most common types of leukemia diagnosed in adults. While many advancements have been made in the understanding of the genetic components [...], Natural killer (NK) cells can have potent antileukemic activity following haplo-mismatched, T cell-depleted stem cell transplantations for the treatment of acute myeloid leukemia (AML), but they are not successful in eradicating de novo AML. Here, we have used a mouse model of de novo AML to elucidate the mechanisms by which AML evades NK cell surveillance. NK cells in leukemic mice displayed a marked reduction in the cytolytic granules perforin and granzyme B. Further, as AML progressed, we noted the selective loss of an immature subset of NK cells in leukemic mice and in AML patients. This absence was not due to elimination by cell death or selective reduction in proliferation, but rather to the result of a block in NK cell differentiation. Indeed, NK cells from leukemic mice and humans with AML showed lower levels of TBET and EOMES, transcription factors that are critical for terminal NK cell differentiation. Further, the microRNA miR-29b, a regulator of T-bet and EOMES, was elevated in leukemic NK cells. Finally, deletion of miR-29b in NK cells reversed the depletion of this NK cell subset in leukemic mice. These results indicate that leukemic evasion of NK cell surveillance occurs through miR-mediated dysregulation of lymphocyte development, representing an additional mechanism of immune escape in cancer.

Published
2016
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16. Retraction Notice to: miR-221&222 Regulate TRAIL Resistance and Enhance Tumorigenicity through PTEN and TIMP3 Downregulation

Author

Garofalo, Michela, primary, Di Leva, Gianpiero, additional, Romano, Giulia, additional, Nuovo, Gerard, additional, Suh, Sung-Suk, additional, Ngankeu, Apollinaire, additional, Taccioli, Cristian, additional, Pichiorri, Flavia, additional, Alder, Hansjuerg, additional, Secchiero, Paola, additional, Gasparini, Pierluigi, additional, Gonelli, Arianna, additional, Costinean, Stefan, additional, Acunzo, Mario, additional, Condorelli, Gerolama, additional, and Croce, Carlo Maria, additional

Published
2022
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21. Regulation of acute graft-versus-host disease by microRNA-155

Author

Ranganathan, Parvathi, Heaphy, Catherine E.A., Costinean, Stefan, Stauffer, Nicole, Na, Caroline, Hamadani, Mehdi, Santhanam, Ramasamy, Mao, Charlene, Taylor, Patricia A., Sandhu, Sukhinder, He, Gang, Shana'ah, Arwa, Nuovo, Gerard J., Lagana, Alessandro, Cascione, Luciano, Obad, Susanna, Broom, Oliver, Kauppinen, Sakari, Byrd, John C., Caligiuri, Michael, Perrotti, Danilo, Hadley, Gregg A., Marcucci, Guido, Devine, Steven M., Blazar, Bruce R., Croce, Carlo M., and Garzon, Ramiro

Published
2012
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26. Modulation of mismatch repair and genomic stability by miR-155

Author

Valeri, Nicola, Gasparini, Pierluigi, Fabbri, Muller, Braconi, Chiara, Veronese, Angelo, Lovat, Francesca, Adair, Brett, Vannini, Ivan, Fanini, Francesca, Bottoni, Arianna, Costinean, Stefan, Sandhu, Sukhinder K., Nuovo, Gerard J, Alder, Hansjuerg, Gafa, Roberta, Calore, Federica, Ferracin, Manuela, Lanza, Giovanni, Volinia, Stefano, Negrini, Massimo, McIlhatton, Michael A., Amadori, Dino, Fishel, Richard, and Croce, Carlo M.

Published
2010

30. Pluripotent Stem Cell miRNAs and Metastasis in Invasive Breast Cancer

Author

Volinia, Stefano, Nuovo, Gerard, Drusco, Alessandra, Costinean, Stefan, Abujarour, Ramzey, Desponts, Caroline, Garofalo, Michela, Baffa, Raffaele, Aeqilan, Rami, Maharry, Kati, Garzon, Maria Elena Sana Ramiro, Di Leva, Gianpiero, Gasparini, Pierluigi, Dama, Paola, Marchesini, Jlenia, Galasso, Marco, Manfrini, Marco, Zerbinati, Carlotta, Corrà, Fabio, Wise, Timothy, Wojcik, Sylwia E., Previati, Maurizio, Pichiorri, Flavia, Zanesi, Nicola, Alder, Hansjuerg, Palatini, Jeff, Huebner, Kay F., Shapiro, Charles L., Negrini, Massimo, Vecchione, Andrea, Rosenberg, Anne L., and Croce, Carlo M.

Published
2014
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32. Essential metabolic, anti-inflammatory, and anti-tumorigenic functions of miR-122 in liver

Author

Hsu, Shu-hao, Wang, Bo, Kota, Janaiah, Yu, Jianhua, Costinean, Stefan, Kutay, Huban, Yu, Lianbo, Bai, Shoumei, La Perle, Krista, Chivukula, Raghu R., Mao, Hsiaoyin, Wei, Min, Clark, K. Reed, Mendell, Jerry R., Caligiuri, Michael A., Jacob, Samson T., Mendell, Joshua T., and Ghoshal, Kalpana

Subjects
Physiological aspects, Tumor necrosis factor -- Physiological aspects, Anti-inflammatory agents -- Physiological aspects, MicroRNA -- Physiological aspects, Liver diseases -- Physiological aspects, Tumors -- Physiological aspects, Hepatitis C virus -- Physiological aspects, Cholesterol -- Physiological aspects, Anti-inflammatory drugs -- Physiological aspects
Abstract

miR-122, an abundant liver-specific microRNA (miRNA), regulates cholesterol metabolism and promotes hepatitis C virus (HCV) replication. Reduced miR-122 expression in hepatocellular carcinoma (HCC) correlates with metastasis and poor prognosis. Nevertheless, [...]

Published
2012
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39. Common fragile site tumor suppressor genes and corresponding mouse models of cancer

Author

Drusco, Alessandra, Pekarsky, Yuri, Costinean, Stefan, Antenucci, Anna, Conti, Laura, Volinia, Stefano, Aqeilan, Rami I., Huebner, Kay, and Zanesi, Nicola

Subjects
Physiological aspects, Complications and side effects, Genetic aspects, Research, Chromosome abnormalities -- Complications and side effects -- Research, Cancer -- Genetic aspects -- Research, Tumor suppressor genes -- Physiological aspects -- Research
Abstract

1. Introduction Fragile sites can be defined as heritable-specific loci on human chromosomes that exhibit nonrandom gaps or breaks when chromosomes are exposed to specific cell culture conditions [1]. Classification [...], Chromosomal common fragile sites (CFSs) are specific mammalian genomic regions that show an increased frequency of gaps and breaks when cells are exposed to replication stress in vitro. CFSs are also consistently involved in chromosomal abnormalities in vivo related to cancer. Interestingly, several CFSs contain one or more tumor suppressor genes whose structure and function are often affected by chromosomal fragility. The two most active fragile sites in the human genome are FRA3B and FRA16D where the tumor suppressor genes FHIT and WWOX are located, respectively. The best approach to study tumorigenic effects of altered tumor suppressors located at CFSs in vivo is to generate mouse models in which these genes are inactivated. This paper summarizes our present knowledge on mouse models of cancer generated by knocking out tumor suppressors of CFS.

Published
2011
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40. Reprogramming of miRNA networks in cancer and leukemia

Author

Volinia, Stefano, Galasso, Marco, Costinean, Stefan, Tagliavini, Luca, Gamberoni, Giacomo, Drusco, Alessandra, Marchesini, Jlenia, Mascellani, Nicoletta, Sana, Maria Elena, Jarour, Ramzey Abu, Desponts, Caroline, Teitell,Michael, Baffa, Raffaele, Aqeilan, Rami, Iorio, Marilena V., Taccioli, Cristian, Garzon, Ramiro, Di Leva, Gianpiero, Fabbri, Muller, Catozzi, Marco, Previati, Maurizio, Ambs, Stefan, Palumbo, Tiziana, Garofalo, Michela, Veronese, Angelo, Bottoni, Arianna, Gasparini, Pierluigi, Harris, Curtis C., Visone, Rosa, Pekarsky, Yuri, Chapelle, Albert de la, Bloomston, Mark, Dillhoff, Mary, Rassenti, Laura Z., Kipps, Thomas J., Huebner, Kay, Pichiorri, Flavia, Lenze, Dido, Cairo, Stefano, Buendia, Marie-Annick, Pineau, Pascal, Dejean, Anne, Zanesi, Nicola, Rossi, Simona, Calin, George A., Chang-Gong Liu, Palatini, Jeff, Negrini, Massimo, Vecchione, Andrea, Rosenberg, Anne, and Croce, Carlo M.

Subjects
MicroRNA -- Research, Cancer -- Genetic aspects, Gene expression -- Analysis, Cancer -- Research, Health
Published
2010

42. miR-29ab1-deficiency Identifies a Negative Feedback Loop Controlling Th1 Bias that is Dysregulated in Multiple Sclerosis1

Author

Smith, Kristen M., Guerau-de-Arellano, Mireia, Costinean, Stefan, Williams, Jessica L., Bottoni, Arianna, Cox, Gina Mavrikis, Satoskar, Abhay R., Croce, Carlo M., Racke, Michael K., Lovett-Racke, Amy E., and Whitacre, Caroline C.

Subjects
Feedback, Physiological, Mice, Knockout, Chromatin Immunoprecipitation, Encephalomyelitis, Autoimmune, Experimental, Multiple Sclerosis, Cell Differentiation, Th1 Cells, Blotting, Northern, Flow Cytometry, Lymphocyte Activation, Article, Mice, Inbred C57BL, Mice, MicroRNAs, Animals, Humans
Abstract

Th cell programming and function is tightly regulated by complex biological networks to prevent excessive inflammatory responses and autoimmune disease. The importance of microRNAs (miRNAs) in this process is highlighted by the preferential Th1 polarization of Dicer-deficient T cells that lack miRNAs. Using genetic knockouts, we demonstrate that loss of endogenous miR-29, derived from the miR-29ab1 genomic cluster, results in unrestrained T-bet expression and IFN-γ production. miR-29b regulates T-bet and IFN-γ via a direct interaction with the 3' untranslated regions, and IFN-γ itself enhances miR-29b expression, establishing a novel regulatory feedback loop. miR-29b is increased in memory CD4(+) T cells from multiple sclerosis (MS) patients, which may reflect chronic Th1 inflammation. However, miR-29b levels decrease significantly upon T cell activation in MS patients, suggesting that this feedback loop is dysregulated in MS patients and may contribute to chronic inflammation. miR-29 thus serves as a novel regulator of Th1 differentiation, adding to the understanding of T cell-intrinsic regulatory mechanisms that maintain a balance between protective immunity and autoimmunity.

Published
2012

46. MicroRNA Profiles Discriminate among Colon Cancer Metastasis

Author

Drusco, Alessandra, primary, Nuovo, Gerard J., additional, Zanesi, Nicola, additional, Di Leva, Gianpiero, additional, Pichiorri, Flavia, additional, Volinia, Stefano, additional, Fernandez, Cecilia, additional, Antenucci, Anna, additional, Costinean, Stefan, additional, Bottoni, Arianna, additional, Rosito, Immacolata A., additional, Liu, Chang-Gong, additional, Burch, Aaron, additional, Acunzo, Mario, additional, Pekarsky, Yuri, additional, Alder, Hansjuerg, additional, Ciardi, Antonio, additional, and Croce, Carlo M., additional

Published
2014
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48. Abstract LB-241: Silencing of microRNA-31 prevents esophageal neoplasia in zinc deficient rats.

Author

Taccioli, Cristian, primary, Chen, Hongping, additional, Garofalo, Michela, additional, Jiang, Yubao, additional, Di Leva, Gianpiero, additional, Alder, Hansjuerg, additional, Middleton, Justin, additional, Smalley, Karl J., additional, Bottoni, Arianna, additional, Costinean, Stefan, additional, Farber, John L., additional, Croce, Carlo M., additional, and Fong, Louise Y Y, additional

Published
2013
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49. miR-29ab1 Deficiency Identifies a Negative Feedback Loop Controlling Th1 Bias That Is Dysregulated in Multiple Sclerosis

Author

Smith, Kristen M., primary, Guerau-de-Arellano, Mireia, additional, Costinean, Stefan, additional, Williams, Jessica L., additional, Bottoni, Arianna, additional, Mavrikis Cox, Gina, additional, Satoskar, Abhay R., additional, Croce, Carlo M., additional, Racke, Michael K., additional, Lovett-Racke, Amy E., additional, and Whitacre, Caroline C., additional

Published
2012
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50. Abstract 909: Activation of NF-κB and its downstream targets play a key role in the dramatic induction of hepatocarcinogenesis in metallothionein null mice

Author

Kaffenberger, Thomas, primary, Roy, Satavisha, additional, Wang, Bo, additional, Costinean, Stefan, additional, Frankel, Wendy, additional, Bratasz, Anna, additional, Kuppusamy, Periannan, additional, Hai, Tsonwin, additional, Ghoshal, Kalpana, additional, Jacob, Samson, additional, and Majumder, Sarmila, additional

Published
2011
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