Research Topics
Genomes and Genes | SCOTT LAURENCE FRIEDMANSummaryAffiliation: Mount Sinai School of Medicine Country: USA Publications
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Publications
Transcriptional regulation of stellate cell activationScott L Friedman
Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
J Gastroenterol Hepatol 21:S79-83. 2006....
Mechanisms of hepatic fibrogenesisScott L Friedman
Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York 10029 6574, USA
Gastroenterology 134:1655-69. 2008..Clinical and translational implications of these advances have become clear, and have begun to impact significantly on the management and outlook of patients with chronic liver disease...
Therapy for fibrotic diseases: nearing the starting lineScott L Friedman
Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
Sci Transl Med 5:167sr1. 2013..Together, these advances herald an era of sustained focus on translating the biology of fibrosis into meaningful improvements in quality and length of life in patients with chronic fibrosing diseases...- Hepatocyte growth factor enhances alternative splicing of the Kruppel-like factor 6 (KLF6) tumor suppressor to promote growth through SRSF1Ursula Muñoz
Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
Mol Cancer Res 10:1216-27. 2012..Enhanced cell replication through increased KLF6 alternative splicing is a novel growth-promoting pathway of HGF that could contribute to the molecule's mitogenic activity in physiologic liver growth and hepatocellular carcinoma... - Impaired dermal wound healing in discoidin domain receptor 2-deficient mice associated with defective extracellular matrix remodelingElvira Olaso
Department of Cell Biology and Histology, University of the Basque Country School of Medicine, Leioa, Spain
Fibrogenesis Tissue Repair 4:5. 2011..abstract:.. - Characterization of the human Activin-A receptor type II-like kinase 1 (ACVRL1) promoter and its regulation by Sp1Eva M Garrido-Martin
Centro de Investigaciones Biologicas, Consejo Superior de Investigaciones Cientificas and Centro de Investigación Biomédica en Red de Enfermedades Raras, Ramiro de Maeztu 9, 28040 Madrid, Spain
BMC Mol Biol 11:51. 2010..Here, we have studied the different origins of ACVRL1 transcription, we have analyzed in silico its 5'-proximal promoter sequence and we have characterized the role of Sp1 in the transcriptional regulation of ACVRL1... - Cannabinoids provoke alcoholic steatosis through a conspiracy of neighborsScott L Friedman
Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
Cell Metab 7:187-8. 2008.... - Reversibility of hepatic fibrosis and cirrhosis--is it all hype?Scott L Friedman
Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029 6574, USA
Nat Clin Pract Gastroenterol Hepatol 4:236-7. 2007 - Hepatic fibrosis 2006: report of the Third AASLD Single Topic ConferenceScott L Friedman
Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
Hepatology 45:242-9. 2007.... - Mac the knife? Macrophages- the double-edged sword of hepatic fibrosisScott L Friedman
Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York 10029, USA
J Clin Invest 115:29-32. 2005..These findings underscore the potential importance of hepatic macrophages in regulating both stellate cell biology and ECM degradation during regression of hepatic fibrosis... - Reversal of hepatic fibrosis -- fact or fantasy?Scott L Friedman
Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
Hepatology 43:S82-8. 2006..These advances are sure to be captured in the next 25 years by Hepatology , and to profoundly impact the prognosis of patients with chronic liver disease... - Mechanisms of disease: Mechanisms of hepatic fibrosis and therapeutic implicationsScott L Friedman
Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
Nat Clin Pract Gastroenterol Hepatol 1:98-105. 2004..We are on the cusp of a new era in which antifibrotic therapies could become important in treating chronic fibrosing liver disease... - Hepatic fibrosis -- overviewScott L Friedman
Division of Liver Diseases, Box 1123, Mount Sinai School of Medicine, 1425 Madison Avenue, Room 11 70C, New York, NY 10029 6574, United States
Toxicology 254:120-9. 2008.... - Genomics and proteomics in liver fibrosis and cirrhosisRebekka A Hannivoort
Department of Medicine Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
Fibrogenesis Tissue Repair 5:1. 2012..Thus, great opportunities and challenges lie ahead in the field of genomics and proteomics, which, if successful, could transform the diagnosis and treatment of chronic fibrosing liver diseases... - Toll-like receptor 4 signaling in liver injury and hepatic fibrogenesisJinsheng Guo
Division of Liver Diseases, Mount Sinai Hospital, Mount Sinai School of Medicine, New York, NY, USA
Fibrogenesis Tissue Repair 3:21. 2010..Further clarification of the function and endogenous ligands of TLR4 signaling in HSCs and other liver cells could uncover novel mechanisms of fibrogenesis and facilitate the development of therapeutic strategies... - Liver fibrosis -- from bench to bedsideScott L Friedman
Division of Liver Diseases, PO Box 1123, Mount Sinai School of Medicine, 1425 Madison Ave Room 1170F, New York, NY 10029, USA
J Hepatol 38:S38-53. 2003 - Evolving challenges in hepatic fibrosisScott L Friedman
Mount Sinai School of Medicine, Division of Liver Diseases, New York, NY 10029, USA
Nat Rev Gastroenterol Hepatol 7:425-36. 2010..As a result, focus is shifting towards overcoming key translational challenges in order to accelerate the development of new therapies for patients with chronic liver disease... - Tumor suppressor activity of KLF6 mediated by downregulation of the PTTG1 oncogeneUrsula E Lee
Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
FEBS Lett 584:1006-10. 2010..Whereas KLF6 downregulation by siRNA increased HepG2 proliferation, siRNA to PTTG1 was anti-proliferative. PTTG1 downregulation represents a novel tumor suppressor pathway of KLF6... - KLF6-SV1 overexpression accelerates human and mouse prostate cancer progression and metastasisGoutham Narla
Department of Genetics and Genomic Sciences, Mount Sinai School of Medicine, New York, New York 10029, USA
J Clin Invest 118:2711-21. 2008..Together, these findings demonstrate that KLF6-SV1 expression levels in PCa tumors at the time of diagnosis can predict the metastatic behavior of the tumor; thus, KLF-SV1 may represent a novel therapeutic target... - KLF6 degradation after apoptotic DNA damageMichaela S Banck
Department of Medicine, Division of Hematology Oncology, P O Box 1079, Mount Sinai School of Medicine, One Gustave Levy Place, Room 24 42A, New York, NY 10029, USA
FEBS Lett 580:6981-6. 2006..KLF6 was unchanged by apoptosis via the extrinsic/death-receptor pathway. Deregulation of KLF6 stability may alter its tumor suppressor function and/or the response of tumors to chemotherapeutics... - A molecular signature to discriminate dysplastic nodules from early hepatocellular carcinoma in HCV cirrhosisJosep M Llovet
Mount Sinai Liver Cancer Program, Department of Medicine, Mount Sinai School of Medicine, New York 10029, USA
Gastroenterology 131:1758-67. 2006..Small liver nodules approximately 2 cm are difficult to characterize by radiologic or pathologic examination. Our aim was to identify a molecular signature to diagnose early hepatocellular carcinoma (HCC)... - Scott L. Friedman, 59th President, AASLDMeena B Bansal
Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
Hepatology 48:1357-8. 2008 - Adenosine A(2A) receptors play a role in the pathogenesis of hepatic cirrhosisEdwin S L Chan
Division of Clinical Pharmacology, Department of Medicine, New York University School of Medicine, New York, NY 10016, USA
Br J Pharmacol 148:1144-55. 2006..6. These results demonstrate that hepatic adenosine A(2A) receptors play an active role in the pathogenesis of hepatic fibrosis, and suggest a novel therapeutic target in the treatment and prevention of hepatic cirrhosis... - Ras promotes growth by alternative splicing-mediated inactivation of the KLF6 tumor suppressor in hepatocellular carcinomaSteven Yea
Division of Liver Diseases and Department of Medicine, Mount Sinai School of Medicine, New York, New York, USA
Gastroenterology 134:1521-31. 2008..The molecular basis for stimulation of KLF6 splicing is unknown... - Hepatic stellate cells: protean, multifunctional, and enigmatic cells of the liverScott L Friedman
Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York 10029 6574, USA
Physiol Rev 88:125-72. 2008..As interest in this cell type intensifies, more surprises and mysteries are sure to unfold that will ultimately benefit our understanding of liver physiology and the diagnosis and treatment of liver disease... - Regulation of hepatic stellate cell activation and growth by transcription factor myocyte enhancer factor 2Xuemin Wang
Liver Research Center, Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence 02903, USA
Gastroenterology 127:1174-88. 2004..Transcriptional regulation plays a key role in this process. We studied the role of transcription factor myocyte enhancer factor 2 (MEF2) during HSC activation... - Interleukin-6 protects hepatocytes from CCl4-mediated necrosis and apoptosis in mice by reducing MMP-2 expressionMeena B Bansal
Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY, USA
J Hepatol 42:548-56. 2005..Because studies suggest matrix metalloproteinase-2 (MMP-2) may promote liver injury, we examined whether IL-6 exerted its protective effects via regulation of MMP-2... - Advances in antifibrotic therapyZahra Ghiassi-Nejad
Division of Liver Diseases, Box 1123, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, NY 10029, USA
Expert Rev Gastroenterol Hepatol 2:803-16. 2008..Thus, features of injury and stellate cell activation provide a useful template for classifying these emerging agents and point to a new class of therapies for patients with fibrosing liver disease... - Downregulation of KLF6 is an early event in hepatocarcinogenesis, and stimulates proliferation while reducing differentiationSigal Kremer Tal
Division of Liver Diseases and Department of Medicine, Mount Sinai School of Medicine, New York, NY, USA
J Hepatol 46:645-54. 2007..Hepatocellular carcinoma (HCC) has the most rapidly rising cancer incidence in the US and Europe. The KLF6 tumor suppressor is frequently inactivated in HCC by loss-of-heterozygosity (LOH) and/or mutation... - Krüppel cripples prostate cancer: KLF6 progress and prospectsGoutham Narla
Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York, USA
Am J Pathol 162:1047-52. 2003 - Molecular diagnosis of chronic liver disease and hepatocellular carcinoma: the potential of gene expression profilingEric R Lemmer
Mount Sinai Liver Cancer Program, Division of Liver Disease, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
Semin Liver Dis 26:373-84. 2006..Continued progress is anticipated in the practical application of gene array methods to refine diagnosis and therapy of HCC... - Roles of KLF6 and KLF6-SV1 in ovarian cancer progression and intraperitoneal disseminationAnalisa Difeo
Department of Human Genetics, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, New York 10029, USA
Clin Cancer Res 12:3730-9. 2006..We investigated the role of the KLF6 tumor suppressor gene and its alternatively spliced isoform KLF6-SV1 in epithelial ovarian cancer (EOC)... - Activation of hepatic stellate cells--a key issue in liver fibrosisHelen L Reeves
Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029 6574, USA
Front Biosci 7:d808-26. 2002.... - Cytochrome P450 2E1-derived reactive oxygen species mediate paracrine stimulation of collagen I protein synthesis by hepatic stellate cellsNatalia Nieto
Department of Pharmacology and Biological Chemistry, Mount Sinai School of Medicine, New York, New York 10029, USA
J Biol Chem 277:9853-64. 2002..These co-culture models may be useful for understanding the impact of CYP2E1-derived ROS on stellate cell function and activation... - Frequent inactivation of the tumor suppressor Kruppel-like factor 6 (KLF6) in hepatocellular carcinomaSigal Kremer-Tal
Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
Hepatology 40:1047-52. 2004..In conclusion, we propose that KLF6 is deregulated by loss and/or mutation in HCC, and its inactivation may contribute to pathogenesis in a significant number of these tumors... - Hepatic fibrogenesisJinsheng Guo
Division of Liver Diseases, Mount Sinai Hospital, Mount Sinai School of Medicine, New York, New York 10029, USA
Semin Liver Dis 27:413-26. 2007.... - Suppression of glioblastoma tumorigenicity by the Kruppel-like transcription factor KLF6Alec C Kimmelman
The Derald H Ruttenberg Cancer Center, The Mount Sinai School of Medicine, New York, NY 10029, USA
Oncogene 23:5077-83. 2004..Our results provide the first evidence of functional tumor suppression by KFL6, and its loss may contribute to glial tumor progression... - Pivotal role of mTOR signaling in hepatocellular carcinomaAugusto Villanueva
Mount Sinai Liver Cancer Program, Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
Gastroenterology 135:1972-83, 1983.e1-11. 2008..We evaluated mTOR signaling in human HCC, as well as the antitumoral effect of a dual-level blockade of the mTOR pathway... - Kruppel-like factor 6 (KLF6) is a tumor-suppressor gene frequently inactivated in colorectal cancerHelen L Reeves
Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
Gastroenterology 126:1090-103. 2004.... - Kupffer cell activation by ambient air particulate matter exposure may exacerbate non-alcoholic fatty liver diseaseHui Hui Tan
Department of Medicine, The Mount Sinai School of Medicine, New York, NY, USA
J Immunotoxicol 6:266-75. 2009..050). In conclusion, ambient PM(2.5) exposure may be a significant risk factor for NAFLD progression... - A DDX5 S480A polymorphism is associated with increased transcription of fibrogenic genes in hepatic stellate cellsJinsheng Guo
Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York 10029, USA
J Biol Chem 285:5428-37. 2010..The enhanced fibrogenic activity of the DDX5 risk variant is linked to a reduced repressive function toward these target genes... - Downregulation of hepatic stellate cell activation by retinol and palmitate mediated by adipose differentiation-related protein (ADRP)Ting Fang Lee
Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York 10029, USA
J Cell Physiol 223:648-57. 2010..Tissue inhibitor of metalloproteinase-1 was not affected. Thus, ADRP upregulation mediated by retinol and palmitate promotes downregulation of HSC activation and is functionally linked to the expression of fibrogenic genes... - Molecular basis of hepatic fibrosisAlex Y Hui
Division of Liver Diseases, Mount Sinai School of Medicine, 1425 Madison Avenue, Room 11 76, New York, NY 10029 6574, USA
Expert Rev Mol Med 5:1-23. 2003.... - Immune stimulation of hepatic fibrogenesis by CD8 cells and attenuation by transgenic interleukin-10 from hepatocytesRifaat Safadi
Division of Liver Diseases, The Mount Sinai School of Medicine, New York, New York, USA
Gastroenterology 127:870-82. 2004..In this model, fibrosis may be a CD8+ T-cell-mediated disease that is attenuated by rIL-10... - Klf6/copeb is required for hepatic outgrowth in zebrafish and for hepatocyte specification in mouse ES cellsXiao Zhao
Division of Liver Diseases Department of Medicine, Black Family Stem Cell Institute, Mount Sinai School of Medicine, New York, NY 10029, USA
Dev Biol 344:79-93. 2010..Collectively, these findings indicate that copeb/Klf6 is essential for the development of endoderm-derived organs... - Developmental regulation of yolk sac hematopoiesis by Kruppel-like factor 6Nobuyuki Matsumoto
Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, 1425 Madison Ave, Rm 1170F, New York, NY 10029, USA
Blood 107:1357-65. 2006..Forced expression of KLF6 using a tet-inducible system enhanced the hematopoietic potential of wild-type EBs. Collectively, these findings implicate Klf6 in ES-cell differentiation and hematopoiesis... - KLF6 allelic loss is associated with tumor recurrence and markedly decreased survival in head and neck squamous cell carcinomaMiriam S Teixeira
Department of Genetics and Genomic Sciences, Mount Sinai School of Medicine, New York, NY 10029, USA
Int J Cancer 121:1976-83. 2007..Taken together, these findings suggest that KLF6 LOH represents a clinically-relevant biomarker predicting patient survival and tumor recurrence and that dysregulation of KLF6 function plays an important role in HNSCC progression... - Genomics and signaling pathways in hepatocellular carcinomaAugusto Villanueva
Mount Sinai Liver Cancer Program, Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York 10029, USA
Semin Liver Dis 27:55-76. 2007..This review summarizes the most relevant information regarding structural and functional alterations in HCC and describes some of the key signaling pathways implicated in hepatocarcinogenesis... - Regulation of Kruppel-like factor 6 tumor suppressor activity by acetylationDan Li
Department of Human Genetics, Mount Sinai School of Medicine, New York, NY 10029-6574, USA
Cancer Res 65:9216-25. 2005..These data indicate that acetylation may regulate KLF6 function, and its loss in some tumor-derived mutants could contribute to its failure to suppress growth in prostate cancer... - Krüppel-like factor-6 promotes preadipocyte differentiation through histone deacetylase 3-dependent repression of DLK1Dan Li
Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
J Biol Chem 280:26941-52. 2005.... - A germline DNA polymorphism enhances alternative splicing of the KLF6 tumor suppressor gene and is associated with increased prostate cancer riskGoutham Narla
Department of Medicine, Mount Sinai School of Medicine, New York, New York, USA
Cancer Res 65:1213-22. 2005.... - Sex steroids have differential effects on growth and gene expression in primary human prostatic epithelial cell cultures derived from the peripheral versus transition zonesAlexander Kirschenbaum
Division of Endocrinology, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
Carcinogenesis 27:216-24. 2006..Finally, we demonstrate divergent responses to sex hormones in the two basal cell populations. The gene expression pattern in the PZ cells may partially explain the predominance of prostate cancer development in this region... - Treatment of hepatic fibrosis: almost thereEfsevia Albanis
Division of Liver Diseases, Mount Sinai School of Medicine, Box 1123, 1425 Madison Avenue, Room 1170F, New York, NY 10029-6574, USA
Curr Gastroenterol Rep 5:48-56. 2003..This review describes the ways in which insights into the cellular basis of hepatic fibrosis are leading to realistic strategies for antifibrotic treatment that may revolutionize the management of patients with chronic liver disease... - Ras pathway activation in hepatocellular carcinoma and anti-tumoral effect of combined sorafenib and rapamycin in vivoPippa Newell
Mount Sinai Liver Cancer Program, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, NY 10029, USA
J Hepatol 51:725-33. 2009..We investigated the molecular alterations of the Ras pathway in HCC and the antineoplastic effects of sorafenib in combination with rapamycin, an inhibitor of mTOR pathway, in experimental models... - Hepatic fibrosisJingjing Jiao
Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York 10029 6574, USA
Curr Opin Gastroenterol 25:223-9. 2009..This review will summarize the most significant work that contributed to the understanding of liver fibrosis progression and resolution, which in turn has yielded new areas of therapeutic targeting... - Functional role of the KLF6 tumour suppressor gene in gastric cancerJaya Sangodkar
Department of Medicine, Mount Sinai School of Medicine, New York, NY, United States
Eur J Cancer 45:666-76. 2009.... - Cyclin-dependent kinase inhibition by the KLF6 tumor suppressor protein through interaction with cyclin D1Sharon Benzeno
Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
Cancer Res 64:3885-91. 2004..Our data suggest that KLF6 converges with the Rb pathway to inhibit cyclin D1/cdk4 activity, resulting in growth suppression... - Functional inactivation of the KLF6 tumor suppressor gene by loss of heterozygosity and increased alternative splicing in glioblastomaOlga Camacho-Vanegas
Department of Genetics and Genomic Sciences, Mount Sinai School of Medicine, New York, NY 10029, USA
Int J Cancer 121:1390-5. 2007.... - Diagnosis of hepatic fibrosis in patients with chronic hepatitis CEfsevia Albanis
Division of Liver Diseases, Mount Sinai Medical Center, 1425 Madison Avenue, New York, NY 10029, USA
Clin Liver Dis 10:821-33. 2006..More accurate and noninvasive methods to diagnose and monitor fibrosis are needed, because these trials will require serial evaluations of liver fibrosis to assess a compound's antifibrotic effect... - Prostaglandin E2 inhibits transforming growth factor beta 1-mediated induction of collagen alpha 1(I) in hepatic stellate cellsAlex Y Hui
Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
J Hepatol 41:251-8. 2004..Based on these findings, it will be important to determine whether inhibiting COX-derived PGE(2) synthesis alters the progression of liver fibrosis in vivo... - Targeted inhibition of the KLF6 splice variant, KLF6 SV1, suppresses prostate cancer cell growth and spreadGoutham Narla
Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
Cancer Res 65:5761-8. 2005..Together, these findings begin to highlight a dynamic and functional antagonism between wtKLF6 and its splice variant KLF6 SV1 in tumor growth and dissemination... - Pathogenesis of liver fibrosisVirginia Hernandez-Gea
Mount Sinai School of Medicine, New York, New York 10029, USA
Annu Rev Pathol 6:425-56. 2011..As pathways of fibrogenesis are increasingly clarified, the key challenge will be translating new advances into the development of antifibrotic therapies for patients with chronic liver disease... - Stimulation and proliferation of primary rat hepatic stellate cells by cytochrome P450 2E1-derived reactive oxygen speciesNatalia Nieto
Department of Biochemistry, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA
Hepatology 35:62-73. 2002..Thus, besides perturbing the homeostasis of hepatocytes, CYP2E1-derived diffusible oxidants may also interact with stellate cells and contribute to hepatic fibrosis... - Enhanced oral tolerance in transgenic mice with hepatocyte secretion of IL-10Rifaat Safadi
Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
J Immunol 175:3577-83. 2005..In contrast to hepatic TG expression of rIL-10, systemic administration of rIL-10 had only a modest effect on tolerance. IL-10, when transgenically expressed in the liver enhances mucosal tolerance to an oral Ag... - Discoidin domain receptor 2 interacts with Src and Shc following its activation by type I collagenKazuo Ikeda
Department of Medicine, Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York 10029, USA
J Biol Chem 277:19206-12. 2002..The data support a model in which Src and the DDR2 receptor cooperate in a regulated fashion to direct the phosphorylation of both the receptor and its targets... - Discoidin domain receptor 2 regulates fibroblast proliferation and migration through the extracellular matrix in association with transcriptional activation of matrix metalloproteinase-2Elvira Olaso
Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
J Biol Chem 277:3606-13. 2002..These data establish a role for DDR2 in critical events during wound repair... - The answer: angiotensin II. The question: what do inflammation, oxidant stress and fibrogenesis have in common?Scott L Friedman
Mount Sinai School of Medicine, Box 1123, 1425 Madison Ave, Room 11 70F, New York, NY 10029, USA
J Hepatol 40:1050-2. 2004 - Experimental models of hepatocellular carcinomaPhilippa Newell
Division of Liver Diseases, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, NY 10029, USA
J Hepatol 48:858-79. 2008..These models will be instrumental in the evaluation of compounds targeting specific molecular pathways in future preclinical studies...
Research Grants
- The Role of KLF6 in Hepatic FibrosisScott Friedman; Fiscal Year: 2009..These innovative studies could lead to new insights into stellate cell activation that may offer novel approaches to treating hepatic fibrosis, for which there are currently no effective therapies. ..
- The Role of KLF6 in Hepatic FibrosisScott Friedman; Fiscal Year: 2007..These innovative studies could lead to new insights into stellate cell activation that may offer novel approaches to treating hepatic fibrosis, for which there are currently no effective therapies. ..
- Role of KLF6 Tumor Suppressor in Hepatocellular CancerScott Friedman; Fiscal Year: 2007..abstract_text> ..
- TRAINING PROGRAM IN INVESTIGATIVE GASTROENTEROLOGYScott Friedman; Fiscal Year: 2007....
- The Role of KLF6 Tumor Suppressor in Hepatocellular CancerScott Friedman; Fiscal Year: 2009..abstract_text> ..
- THE ROLE OF STELLATE CELLS IN HEPATIC FIBROSISScott Friedman; Fiscal Year: 2003..The findings could lead to new treatments for this debilitating and incurable condition. ..
- DDR2 RECEPTOR TYROSINE KINASE IN HEPATIC FIBROSISScott Friedman; Fiscal Year: 2004..The findings could lead to new treatments for this debilitating and incurable condition. ..
- The Role of KLF6 Tumor Suppressor in Hepatocellular CancerSCOTT LAURENCE FRIEDMAN; Fiscal Year: 2010..abstract_text> ..