Scott L Friedman

Summary

Affiliation: Mount Sinai School of Medicine
Country: USA

Publications

  1. ncbi request reprint Synergistic induction of apoptosis by acyclic retinoid and interferon-beta in human hepatocellular carcinoma cells
    Akihiro Obora
    First Department of Internal Medicine and Department of Pathobiochemistry, Gifu University School of Medicine, Japan
    Hepatology 36:1115-24. 2002
  2. pmc Hepatic stellate cells: protean, multifunctional, and enigmatic cells of the liver
    Scott L Friedman
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York 10029 6574, USA
    Physiol Rev 88:125-72. 2008
  3. pmc Tumor suppressor activity of KLF6 mediated by downregulation of the PTTG1 oncogene
    Ursula 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
  4. pmc Downregulation of KLF6 is an early event in hepatocarcinogenesis, and stimulates proliferation while reducing differentiation
    Sigal 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
  5. pmc Functional role of the KLF6 tumour suppressor gene in gastric cancer
    Jaya Sangodkar
    Department of Medicine, Mount Sinai School of Medicine, New York, NY, United States
    Eur J Cancer 45:666-76. 2009
  6. pmc Enhanced hepatocarcinogenesis in mouse models and human hepatocellular carcinoma by coordinate KLF6 depletion and increased messenger RNA splicing
    Diana Vetter
    Department of Medicine Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029 6574, USA
    Hepatology 56:1361-70. 2012
  7. pmc Wnt-pathway activation in two molecular classes of hepatocellular carcinoma and experimental modulation by sorafenib
    Anja Lachenmayer
    Mount Sinai Liver Cancer Program, Mount Sinai School of Medicine, New York, NY 10029, USA
    Clin Cancer Res 18:4997-5007. 2012
  8. pmc Ras pathway activation in hepatocellular carcinoma and anti-tumoral effect of combined sorafenib and rapamycin in vivo
    Pippa 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
  9. pmc Ras promotes growth by alternative splicing-mediated inactivation of the KLF6 tumor suppressor in hepatocellular carcinoma
    Steven Yea
    Division of Liver Diseases and Department of Medicine, Mount Sinai School of Medicine, New York, New York, USA
    Gastroenterology 134:1521-31. 2008
  10. ncbi request reprint Targeted inhibition of the KLF6 splice variant, KLF6 SV1, suppresses prostate cancer cell growth and spread
    Goutham Narla
    Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
    Cancer Res 65:5761-8. 2005

Detail Information

Publications111 found, 100 shown here

  1. ncbi request reprint Synergistic induction of apoptosis by acyclic retinoid and interferon-beta in human hepatocellular carcinoma cells
    Akihiro Obora
    First Department of Internal Medicine and Department of Pathobiochemistry, Gifu University School of Medicine, Japan
    Hepatology 36:1115-24. 2002
    ..In conclusion, these results provide a rationale for combined biochemoprevention of HCC using acyclic retinoid and IFN-beta...
  2. pmc Hepatic stellate cells: protean, multifunctional, and enigmatic cells of the liver
    Scott 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...
  3. pmc Tumor suppressor activity of KLF6 mediated by downregulation of the PTTG1 oncogene
    Ursula 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...
  4. pmc Downregulation of KLF6 is an early event in hepatocarcinogenesis, and stimulates proliferation while reducing differentiation
    Sigal 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...
  5. pmc Functional role of the KLF6 tumour suppressor gene in gastric cancer
    Jaya Sangodkar
    Department of Medicine, Mount Sinai School of Medicine, New York, NY, United States
    Eur J Cancer 45:666-76. 2009
    ....
  6. pmc Enhanced hepatocarcinogenesis in mouse models and human hepatocellular carcinoma by coordinate KLF6 depletion and increased messenger RNA splicing
    Diana Vetter
    Department of Medicine Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029 6574, USA
    Hepatology 56:1361-70. 2012
    ..Moreover, SV1 binds directly to KLF6 and accelerates its degradation. These findings represent a novel mechanism underlying the antagonism of tumor suppressor gene function by a splice variant of the same gene...
  7. pmc Wnt-pathway activation in two molecular classes of hepatocellular carcinoma and experimental modulation by sorafenib
    Anja Lachenmayer
    Mount Sinai Liver Cancer Program, Mount Sinai School of Medicine, New York, NY 10029, USA
    Clin Cancer Res 18:4997-5007. 2012
    ..We aimed to characterize Wnt-pathway aberrations in HCC patients, and to investigate sorafenib as a potential Wnt modulator in experimental models of liver cancer...
  8. pmc Ras pathway activation in hepatocellular carcinoma and anti-tumoral effect of combined sorafenib and rapamycin in vivo
    Pippa 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...
  9. pmc Ras promotes growth by alternative splicing-mediated inactivation of the KLF6 tumor suppressor in hepatocellular carcinoma
    Steven 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...
  10. ncbi request reprint Targeted inhibition of the KLF6 splice variant, KLF6 SV1, suppresses prostate cancer cell growth and spread
    Goutham 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...
  11. pmc KLF6-SV1 overexpression accelerates human and mouse prostate cancer progression and metastasis
    Goutham 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...
  12. ncbi request reprint Functional inactivation of the KLF6 tumor suppressor gene by loss of heterozygosity and increased alternative splicing in glioblastoma
    Olga 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
    ....
  13. pmc Combination therapy for hepatocellular carcinoma: additive preclinical efficacy of the HDAC inhibitor panobinostat with sorafenib
    Anja Lachenmayer
    Mount Sinai Liver Cancer Program, Division of Liver Diseases, Department of Medicine, Tisch Cancer Institute, New York, NY 10029, USA
    J Hepatol 56:1343-50. 2012
    ..We analyzed the expression of 11 HDACs in human HCCs and assessed the efficacy of the pan-HDAC inhibitor panobinostat alone and in combination with sorafenib in preclinical models of liver cancer...
  14. pmc A novel murine model to deplete hepatic stellate cells uncovers their role in amplifying liver damage in mice
    Juan E Puche
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
    Hepatology 57:339-50. 2013
    ..Hepatic expression of interleukin-10 and interferon-gamma was increased after HSC depletion. No toxicity of GCV in either WT or Tg mice accounted for the differences in injury...
  15. pmc Dendritic cell regulation of carbon tetrachloride-induced murine liver fibrosis regression
    Jingjing Jiao
    Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, NY, USA
    Hepatology 55:244-55. 2012
    ..In contrast, transfer of DCs from MMP-9-deficient mice failed to improve fibrosis regression...
  16. ncbi request reprint KLF6 allelic loss is associated with tumor recurrence and markedly decreased survival in head and neck squamous cell carcinoma
    Miriam 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...
  17. pmc MicroRNA-based classification of hepatocellular carcinoma and oncogenic role of miR-517a
    Sara Toffanin
    Mount Sinai Liver Cancer Program, Division of Liver Diseases, Department of Medicine, Tisch Cancer Institute, New York, New York, USA
    Gastroenterology 140:1618-28.e16. 2011
    ..MicroRNAs (miRNAs) are involved in HCC pathogenesis, and their expression profiles have been used to classify cancers. We analyzed miRNA expression in human HCC samples to identify molecular subclasses and oncogenic miRNAs...
  18. pmc A DDX5 S480A polymorphism is associated with increased transcription of fibrogenic genes in hepatic stellate cells
    Jinsheng 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...
  19. ncbi request reprint A molecular signature to discriminate dysplastic nodules from early hepatocellular carcinoma in HCV cirrhosis
    Josep 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)...
  20. pmc Pivotal role of mTOR signaling in hepatocellular carcinoma
    Augusto 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...
  21. pmc A polymorphism that delays fibrosis in hepatitis C promotes alternative splicing of AZIN1, reducing fibrogenesis
    Andrew J Paris
    Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
    Hepatology 54:2198-207. 2011
    ..Conclusion: An SNP variant in the AZIN1 gene leads to enhanced generation of a novel alternative splice form that modifies the fibrogenic potential of HSCs...
  22. pmc Gene-expression signature of vascular invasion in hepatocellular carcinoma
    Beatriz Minguez
    Mount Sinai Liver Cancer Program, Division of Liver Diseases, Department of Medicine, Surgical Oncology, Department of Surgery, Department of Pathology, Department of Preventive Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
    J Hepatol 55:1325-31. 2011
    ..While macroscopic vascular invasion can be detected by radiological techniques, pre-operative detection of microscopic vascular invasion, which complicates 30-40% of patients with early tumors, remains elusive...
  23. ncbi request reprint Regulation of Kruppel-like factor 6 tumor suppressor activity by acetylation
    Dan 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...
  24. pmc Loss of matrix metalloproteinase-2 amplifies murine toxin-induced liver fibrosis by upregulating collagen I expression
    BRIAN D RADBILL
    Division of Nephrology, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
    Dig Dis Sci 56:406-16. 2011
    ..We therefore examined the impact of MMP-2 deficiency on liver fibrosis development during chronic CCl(4) liver injury and explored the effect of MMP-2 deficiency and overexpression on collagen I expression...
  25. pmc Antifibrotic activity of sorafenib in experimental hepatic fibrosis: refinement of inhibitory targets, dosing, and window of efficacy in vivo
    Feng Hong
    Division of Liver Diseases, Mount Sinai School of Medicine, Box 1123, 1425 Madison Ave, Room 1170C, New York, NY 10029, USA
    Dig Dis Sci 58:257-64. 2013
    ..Sorafenib, which is approved for treatment of HCC, has also shown promising antifibrotic activity, and therefore refinement of its dosing requirements and window of efficacy are important goals prior to antifibrotic clinical trials...
  26. pmc Glucokinase links Krüppel-like factor 6 to the regulation of hepatic insulin sensitivity in nonalcoholic fatty liver disease
    Lars P Bechmann
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY, USA
    Hepatology 55:1083-93. 2012
    ..Conclusion: KLF6 regulation of GCK contributes to the development of hepatic insulin resistance. The KLF6-IVS1-27A polymorphism, which generates more KLF6-SV1, combats this, lowering hepatic insulin resistance and blood glucose...
  27. pmc Kupffer cell activation by ambient air particulate matter exposure may exacerbate non-alcoholic fatty liver disease
    Hui 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...
  28. ncbi request reprint Roles of KLF6 and KLF6-SV1 in ovarian cancer progression and intraperitoneal dissemination
    Analisa 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)...
  29. pmc Klf6/copeb is required for hepatic outgrowth in zebrafish and for hepatocyte specification in mouse ES cells
    Xiao 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...
  30. pmc Carcinogen-induced hepatic tumors in KLF6+/- mice recapitulate aggressive human hepatocellular carcinoma associated with p53 pathway deregulation
    Mirko Tarocchi
    Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029 6574, USA
    Hepatology 54:522-31. 2011
    ..Whereas KLF6 overexpression in HCC cell lines and primary hepatocytes led to reduced MDM2 levels and increased p53 protein and transcriptional activity, reduction in KLF6 by small interfering RNA led to increased MDM2 and reduced p53...
  31. pmc Post-transcriptional activation of PPAR alpha by KLF6 in hepatic steatosis
    Lars P Bechmann
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY, United States Department of Gastroenterology and Hepatology, University Hospital Essen, Essen, Germany
    J Hepatol 58:1000-6. 2013
    ..We report here that Krüppel-like factor 6 (KLF6), a ubiquitous transcription factor that promotes adipocyte differentiation, also provokes the metabolic abnormalities of NAFLD by post-transcriptionally activating PPARα-signaling...
  32. pmc Autophagy releases lipid that promotes fibrogenesis by activated hepatic stellate cells in mice and in human tissues
    Virginia Hernandez-Gea
    Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029 6574, USA
    Gastroenterology 142:938-46. 2012
    ..We investigated whether autophagy also promotes loss of lipids in hepatic stellate cells to provide energy for their activation and extended these findings to other fibrogenic cells...
  33. pmc Anti-fibrotic activity and enhanced interleukin-6 production by hepatic stellate cells in response to imatinib mesylate
    Youngchul Kim
    Division of Liver Diseases, Department of Medicine, The Mount Sinai School of Medicine, New York, NY 10029 6574, USA
    Liver Int 32:1008-17. 2012
    ..The hepatic stellate cell (HSC) is a key target of anti-fibrotic therapies. Imatinib mesylate is a small molecule receptor tyrosine kinase inhibitor indicated for treatment of chronic myelogenous leukaemia and GI stromal tumours...
  34. pmc Experimental models of hepatocellular carcinoma
    Philippa 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...
  35. ncbi request reprint Krüppel-like factor-6 promotes preadipocyte differentiation through histone deacetylase 3-dependent repression of DLK1
    Dan 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
    ....
  36. ncbi request reprint Genomics and signaling pathways in hepatocellular carcinoma
    Augusto 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...
  37. ncbi request reprint A germline DNA polymorphism enhances alternative splicing of the KLF6 tumor suppressor gene and is associated with increased prostate cancer risk
    Goutham Narla
    Department of Medicine, Mount Sinai School of Medicine, New York, New York, USA
    Cancer Res 65:1213-22. 2005
    ....
  38. pmc Role of the microenvironment in the pathogenesis and treatment of hepatocellular carcinoma
    Virginia Hernandez-Gea
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York HCC Translational Research Laboratory, Barcelona Clinic Liver Cancer Group, Institut d Investigacions Biomediques August Pi i Sunyer, Liver Unit, Hospital Clinic, University of Barcelona, Catalonia, Spain
    Gastroenterology 144:512-27. 2013
    ..Increasing our understanding of how stromal components interact with cancer cells and the signaling pathways involved could help identify new therapeutic and chemopreventive targets...
  39. pmc Prognostic gene expression signature for patients with hepatitis C-related early-stage cirrhosis
    Yujin Hoshida
    Mount Sinai Liver Cancer Program, Tisch Cancer Institute, Division of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York Electronic address
    Gastroenterology 144:1024-30. 2013
    ..We investigated whether a liver-derived 186-gene signature previously associated with outcomes of patients with HCC is prognostic for patients with newly diagnosed cirrhosis but without HCC...
  40. pmc Reduced hepatic stellate cell expression of Kruppel-like factor 6 tumor suppressor isoforms amplifies fibrosis during acute and chronic rodent liver injury
    Zahra Ghiassi-Nejad
    Department of Gastroenterology and Hepatology, Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
    Hepatology 57:786-96. 2013
    ..Stellate cells overexpressing either KLF6(WT) or KLF6(SV1) were more susceptible to apoptotic stress based on poly (ADP-ribose) polymerase (PARP) cleavage...
  41. doi request reprint Autophagy fuels tissue fibrogenesis
    Virginia Hernandez-Gea
    Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, NY, USA
    Autophagy 8:849-50. 2012
    ..Our results provide a novel framework for understanding pathways underlying fibrogenic cell responses to tissue injury...
  42. ncbi request reprint KLF6 degradation after apoptotic DNA damage
    Michaela 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...
  43. ncbi request reprint Enhanced oral tolerance in transgenic mice with hepatocyte secretion of IL-10
    Rifaat 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...
  44. pmc 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...
  45. pmc Interleukin-6 protects hepatocytes from CCl4-mediated necrosis and apoptosis in mice by reducing MMP-2 expression
    Meena 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...
  46. ncbi request reprint Sex steroids have differential effects on growth and gene expression in primary human prostatic epithelial cell cultures derived from the peripheral versus transition zones
    Alexander 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...
  47. pmc Adenosine A(2A) receptors play a role in the pathogenesis of hepatic cirrhosis
    Edwin 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...
  48. doi request reprint Cannabinoids provoke alcoholic steatosis through a conspiracy of neighbors
    Scott L Friedman
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
    Cell Metab 7:187-8. 2008
    ....
  49. ncbi request reprint Frequent inactivation of the tumor suppressor Kruppel-like factor 6 (KLF6) in hepatocellular carcinoma
    Sigal 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...
  50. pmc Developmental regulation of yolk sac hematopoiesis by Kruppel-like factor 6
    Nobuyuki 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...
  51. ncbi request reprint Transcriptional regulation of stellate cell activation
    Scott L Friedman
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
    J Gastroenterol Hepatol 21:S79-83. 2006
    ....
  52. ncbi request reprint Cellular basis of hepatic fibrosis and its role in inflammation and cancer
    Peri Kocabayoglu
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
    Front Biosci (Schol Ed) 5:217-30. 2013
    ....
  53. pmc Endoplasmic reticulum stress induces fibrogenic activity in hepatic stellate cells through autophagy
    Virginia Hernandez-Gea
    Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
    J Hepatol 59:98-104. 2013
    ..The aim of our study was to determine the impact of oxidant and ER stress on stellate cell activation...
  54. ncbi request reprint 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...
  55. doi request reprint Scott L. Friedman, 59th President, AASLD
    Meena B Bansal
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
    Hepatology 48:1357-8. 2008
  56. doi request reprint Fibrosis in the liver: acute protection and chronic disease
    Youngmin Lee
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York, USA
    Prog Mol Biol Transl Sci 97:151-200. 2010
    ..Hepatic fibrosis and cirrhosis have emerged as treatable and potentially reversible consequence of chronic liver disease...
  57. ncbi request reprint Molecular diagnosis of chronic liver disease and hepatocellular carcinoma: the potential of gene expression profiling
    Eric 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...
  58. ncbi request reprint Mechanisms of disease: Mechanisms of hepatic fibrosis and therapeutic implications
    Scott 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...
  59. pmc Mechanisms of hepatic fibrogenesis
    Scott 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...
  60. ncbi request reprint Prostaglandin E2 inhibits transforming growth factor beta 1-mediated induction of collagen alpha 1(I) in hepatic stellate cells
    Alex Y Hui
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
    J Hepatol 41:251-8. 2004
    ..We assessed the impact of COX-2 inhibition and PGE(2) on the regulation of TGF-beta 1-stimulated matrix synthesis in an immortalized human HSC line, LX-1 and corroborated these findings in primary stellate cells...
  61. ncbi request reprint Hepatic fibrogenesis
    Jinsheng 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
    ....
  62. pmc Mac the knife? Macrophages- the double-edged sword of hepatic fibrosis
    Scott 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...
  63. doi request reprint Hepatic fibrosis -- overview
    Scott 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
    ....
  64. ncbi request reprint Diagnosis of hepatic fibrosis in patients with chronic hepatitis C
    Efsevia 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...
  65. ncbi request reprint 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
  66. ncbi request reprint Cytochrome P450 2E1-derived reactive oxygen species mediate paracrine stimulation of collagen I protein synthesis by hepatic stellate cells
    Natalia 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...
  67. pmc Krüppel cripples prostate cancer: KLF6 progress and prospects
    Goutham Narla
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, New York, USA
    Am J Pathol 162:1047-52. 2003
  68. ncbi request reprint Hepatocyte growth factor enhances alternative splicing of the Kruppel-like factor 6 (KLF6) tumor suppressor to promote growth through SRSF1
    Ursula 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...
  69. doi request reprint Fibrosis-dependent mechanisms of hepatocarcinogenesis
    David Y Zhang
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
    Hepatology 56:769-75. 2012
    ..Clarifying fibrosis-dependent tumorigenic mechanisms will help rationalize antifibrotic therapies as a strategy to prevent and treat HCC...
  70. ncbi request reprint 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
  71. ncbi request reprint Immune stimulation of hepatic fibrogenesis by CD8 cells and attenuation by transgenic interleukin-10 from hepatocytes
    Rifaat Safadi
    Division of Liver Diseases, The Mount Sinai School of Medicine, New York, New York, USA
    Gastroenterology 127:870-82. 2004
    ..Immunomodulatory cytokines, including interleukin-10 (IL-10), may mediate hepatic fibrosis...
  72. doi request reprint Pathogenesis of liver fibrosis
    Virginia 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...
  73. pmc Mechanisms of hepatic fibrogenesis
    Ursula E Lee
    Division of Liver Diseases, Mount Sinai School of Medicine, 1425 Madison Ave, Room 11 76, New York, NY 10029, USA
    Best Pract Res Clin Gastroenterol 25:195-206. 2011
    ..Uncovering the intricate mechanisms that underlie liver fibrogenesis forms the basis for efforts to develop targeted therapies to reverse the fibrotic response and improve the outcomes of patients with chronic liver disease...
  74. doi request reprint Evolving challenges in hepatic fibrosis
    Scott 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...
  75. ncbi request reprint Liver fibrosis -- from bench to bedside
    Scott 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
  76. ncbi request reprint Treatment of hepatic fibrosis: almost there
    Efsevia 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...
  77. pmc Hepatic fibrosis
    Jingjing 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...
  78. ncbi request reprint Molecular basis of hepatic fibrosis
    Alex 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
    ....
  79. ncbi request reprint Suppression of glioblastoma tumorigenicity by the Kruppel-like transcription factor KLF6
    Alec 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...
  80. ncbi request reprint Kruppel-like factor 6 (KLF6) is a tumor-suppressor gene frequently inactivated in colorectal cancer
    Helen L Reeves
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
    Gastroenterology 126:1090-103. 2004
    ....
  81. ncbi request reprint Activation of hepatic stellate cells--a key issue in liver fibrosis
    Helen L Reeves
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029 6574, USA
    Front Biosci 7:d808-26. 2002
    ....
  82. pmc Toll-like receptor 4 signaling in liver injury and hepatic fibrogenesis
    Jinsheng 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...
  83. pmc Advances in antifibrotic therapy
    Zahra 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...
  84. ncbi request reprint Hepatic fibrosis 2006: report of the Third AASLD Single Topic Conference
    Scott L Friedman
    Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY 10029, USA
    Hepatology 45:242-9. 2007
    ....
  85. doi request reprint Dendritic cells in alcoholic liver injury and fibrosis
    Costica Aloman
    Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
    Alcohol Clin Exp Res 35:776-81. 2011
    ..Understanding the mechanism by which DC modulate liver function after alcohol consumption may help uncover novel therapeutic strategies for the treatment of these conditions...
  86. ncbi request reprint Cyclin-dependent kinase inhibition by the KLF6 tumor suppressor protein through interaction with cyclin D1
    Sharon 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...
  87. ncbi request reprint Discoidin domain receptor 2 regulates fibroblast proliferation and migration through the extracellular matrix in association with transcriptional activation of matrix metalloproteinase-2
    Elvira 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...
  88. ncbi request reprint Stimulation and proliferation of primary rat hepatic stellate cells by cytochrome P450 2E1-derived reactive oxygen species
    Natalia 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...
  89. ncbi request reprint Discoidin domain receptor 2 interacts with Src and Shc following its activation by type I collagen
    Kazuo 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...
  90. ncbi request reprint Molecular mechanism for growth suppression of human hepatocellular carcinoma cells by acyclic retinoid
    Rie Matsushima-Nishiwaki
    First Department of Internal Medicine, Gifu University School of Medicine, Gifu, Japan
    Carcinogenesis 24:1353-9. 2003
    ..These events provide a novel molecular basis for the antitumor activity of acyclic retinoid against HCC...
  91. ncbi request reprint Phosphorylation of retinoid X receptor suppresses its ubiquitination in human hepatocellular carcinoma
    Seiji Adachi
    Department of Molecular Pathobiochemistry, Gifu University School of Medicine, Gifu, Japan
    Hepatology 35:332-40. 2002
    ..In conclusion, switching of the ubiquitin/proteasome-dependent degradation of RXRalpha by phosphorylation at serine 260 may be responsible for the aberrant growth of HCC and its suppression by retinoids...
  92. pmc Leptin in hepatic fibrosis: evidence for increased collagen production in stellate cells and lean littermates of ob/ob mice
    Neeraj K Saxena
    Hepatology Section, University of Maryland School of Medicine, Baltimore, MD 21201 1595, USA
    Hepatology 35:762-71. 2002
    ..Up-regulation of leptin signaling in liver injury could contribute to enhanced fibrogenesis, particularly in states in which leptin levels are high...
  93. pmc The Kruppel-like factor 6 genotype is associated with fibrosis in nonalcoholic fatty liver disease
    Luca Miele
    Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, United Kingdom
    Gastroenterology 135:282-291.e1. 2008
    ..Based on its role in liver growth and repair, we explored whether Kruppel-like factor 6 (KLF6) plays a role in NAFLD progression...
  94. ncbi request reprint Proangiogenic role of tumor-activated hepatic stellate cells in experimental melanoma metastasis
    Elvira Olaso
    University of the Basque Country, School of Medicine and Dentistry, Bizkaia, Spain
    Hepatology 37:674-85. 2003
    ....
  95. doi request reprint Insulin-like growth factor-i regulates Kruppel-like factor-6 gene expression in a p53-dependent manner
    Itay Bentov
    Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel
    Endocrinology 149:1890-7. 2008
    ..Stimulation of KLF6 expression by IGF-I in a p53-dependent manner may constitute a novel mechanism of action of IGF-I, with implications in normal cell cycle progression and cancer biology...
  96. pmc Focal gains of VEGFA and molecular classification of hepatocellular carcinoma
    Derek Y Chiang
    Department of Medical Oncology and Center for Cancer Genome Discovery, Dana Farber Cancer Institute, Boston, MA 02115, USA
    Cancer Res 68:6779-88. 2008
    ..Furthermore, the prevalence of VEGFA high-level gains in multiple tumor types suggests indications for clinical trials of antiangiogenic therapies...
  97. pmc Activation of hepatic stellate cells after phagocytosis of lymphocytes: A novel pathway of fibrogenesis
    Nidal Muhanna
    Liver and Gastroenterology Units Division of Medicine, Hadassah Hospital, Jerusalem, Israel
    Hepatology 48:963-77. 2008
    ..LX2 knockdown of either Cdc42 or Rac1 [members of the Rho-guanosine triphosphatase (GTPase) family] prevented both phagocytosis and the activation of HSC by HCV-derived lymphocytes...
  98. ncbi request reprint Beneficial effect of glatiramer acetate (Copaxone) on immune modulation of experimental hepatic fibrosis
    Amjad Horani
    Liver and Gastroenterology Units, Div of Medicine, Hadassah University Hospital, 91120 Jerusalem, Israel
    Am J Physiol Gastrointest Liver Physiol 292:G628-38. 2007
    ..In an animal model of hepatic fibrosis, GA has an antifibrotic effect associated with decreased CD8 cells and reduced serum IL-4 levels and increased NK cells, CD4(+)CD25(+)FoxP3(+) cells, TRAIL, and elevated serum IL-10 levels...
  99. pmc Targeted and regulable expression of transgenes in hepatic stellate cells and myofibroblasts in culture and in vivo using an adenoviral Cre/loxP system to antagonise hepatic fibrosis
    Kohji Kinoshita
    First Department of Surgery, Hyogo College of Medicine, Nishinomiya, Japan
    Gut 56:396-404. 2007
    ..Activated hepatic stellate cells (HSCs) are an attractive target for antifibrotic therapy based on their key role in extracellular matrix accumulation during liver injury...
  100. ncbi request reprint Stellate cell apoptosis by a soluble mediator from immortalized human hepatocytes
    Arnab Basu
    Department of Internal Medicine, Saint Louis University, St Louis, MO 63110, USA
    Apoptosis 11:1391-400. 2006
    ..Taken together, our results suggested that a soluble mediator secreted from immortalized human hepatocytes plays an important role in hepatic stellate cell growth regulation...
  101. ncbi request reprint Anti-fibrotic activity of NK cells in experimental liver injury through killing of activated HSC
    Alaa Melhem
    Division of Medicine, Liver and Gastroenterology Units, Hadassah University Hospital, POB 12000, 91120 Jerusalem, Israel
    J Hepatol 45:60-71. 2006
    ..We have investigated the role of natural killer (NK) cells in hepatic fibrogenesis. Mouse NK cells express both inhibitory/activating-killing-immunoglobulin-related-receptors (iKIR/aKIR) specific for Class-I-molecules...