G J Gores

Summary

Affiliation: Mayo Clinic
Country: USA

Publications

  1. ncbi Selectively targeting Mcl-1 for the treatment of acute myelogenous leukemia and solid tumors
    Gregory J Gores
    Division of Gastroenterology and Hepatology, Department of Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA
    Genes Dev 26:305-11. 2012
  2. ncbi Bax inhibition protects against free fatty acid-induced lysosomal permeabilization
    Ariel E Feldstein
    Department of Pediatric Gastroenterology and Cell Biology, Cleveland, USA
    Am J Physiol Gastrointest Liver Physiol 290:G1339-46. 2006
  3. ncbi Treatment endpoints for advanced cholangiocarcinoma
    Gregory J Gores
    Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Nat Clin Pract Gastroenterol Hepatol 1:4-5. 2004
  4. ncbi Induction of the mitochondrial permeability transition as a mechanism of liver injury during cholestasis: a potential role for mitochondrial proteases
    G J Gores
    Mayo Medical School, Clinic, and Foundation, 200 First Street SW, Rochester, MN 55905, USA
    Biochim Biophys Acta 1366:167-75. 1998
  5. ncbi Early detection and treatment of cholangiocarcinoma
    G J Gores
    Mayo Clinic, Foundation, and Medical School, Rochester, MN 55905, USA
    Liver Transpl 6:S30-4. 2000
  6. ncbi Mechanisms of lysophosphatidylcholine-induced hepatocyte lipoapoptosis
    Keisuke Kakisaka
    Division of Gastroenterology and Hepatology, College of Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA
    Am J Physiol Gastrointest Liver Physiol 302:G77-84. 2012
  7. ncbi Bile acids activate EGF receptor via a TGF-alpha-dependent mechanism in human cholangiocyte cell lines
    Nathan W Werneburg
    Mayo Medical School, Clinic, and Foundation, 200 First Street SW, Rochester, MN 55905, USA
    Am J Physiol Gastrointest Liver Physiol 285:G31-6. 2003
  8. ncbi Cholangiocarcinoma: current concepts and insights
    Gregory J Gores
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, MN 55905, USA
    Hepatology 37:961-9. 2003
  9. ncbi Cathepsin B inactivation attenuates hepatic injury and fibrosis during cholestasis
    Ali Canbay
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota 55905, USA
    J Clin Invest 112:152-9. 2003
  10. ncbi Cholangiocarcinoma: is transplantation an option? For whom?
    Gregory J Gores
    Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA
    J Hepatol 47:455-9. 2007

Research Grants

  1. MECHANISMS OF LIVER CELL INJURY
    Gregory J Gores; Fiscal Year: 2010
  2. Organelle Dysfunction and Apoptosis in Liver Epithelia
    Gregory Gores; Fiscal Year: 2009
  3. Mechanisms of Carcinogenesis in Biliary Epithelia
    Gregory J Gores; Fiscal Year: 2010
  4. Organelle Dysfunction and Apoptosis in Liver Epithelia
    Gregory J Gores; Fiscal Year: 2010
  5. Mechanisms of Carcinogenesis in Biliary Epithelia
    Gregory Gores; Fiscal Year: 2007
  6. Organelle Dysfunction and Apoptosis in Liver Epithelia
    Gregory Gores; Fiscal Year: 2007
  7. Mechanisms of Carcinogenesis in Biliary Epithelia
    Gregory Gores; Fiscal Year: 2005
  8. MECHANISMS OF LIVER CELL INJURY
    Gregory Gores; Fiscal Year: 2007
  9. MECHANISMS OF LIVER CELL INJURY
    Gregory J Gores; Fiscal Year: 2010

Detail Information

Publications124 found, 100 shown here

  1. ncbi Selectively targeting Mcl-1 for the treatment of acute myelogenous leukemia and solid tumors
    Gregory J Gores
    Division of Gastroenterology and Hepatology, Department of Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA
    Genes Dev 26:305-11. 2012
    ..120-125) demonstrates that Mcl-1 is essential for development and survival of acute myelogenous leukemia cells. These results provide new impetus for the generation of selective Mcl-1 inhibitors...
  2. ncbi Bax inhibition protects against free fatty acid-induced lysosomal permeabilization
    Ariel E Feldstein
    Department of Pediatric Gastroenterology and Cell Biology, Cleveland, USA
    Am J Physiol Gastrointest Liver Physiol 290:G1339-46. 2006
    ..Finally, paradigms that inhibit lysosomal permeabilization also reduced apoptosis. In conclusion, these data strongly support a regulatory role for Bax in FFA-mediated lysosomal permeabilization and subsequent cell death...
  3. ncbi Treatment endpoints for advanced cholangiocarcinoma
    Gregory J Gores
    Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Nat Clin Pract Gastroenterol Hepatol 1:4-5. 2004
  4. ncbi Induction of the mitochondrial permeability transition as a mechanism of liver injury during cholestasis: a potential role for mitochondrial proteases
    G J Gores
    Mayo Medical School, Clinic, and Foundation, 200 First Street SW, Rochester, MN 55905, USA
    Biochim Biophys Acta 1366:167-75. 1998
    ..In an experimental model of cholestasis, mitochondrial calpain-like protease activity increases 1.6-fold. We propose for the first time that activation of mitochondrial proteases may initiate the MPT and cell necrosis during cholestasis...
  5. ncbi Early detection and treatment of cholangiocarcinoma
    G J Gores
    Mayo Clinic, Foundation, and Medical School, Rochester, MN 55905, USA
    Liver Transpl 6:S30-4. 2000
    ..Outcomes are optimized by using preoperative radiation and chemotherapy and ensuring the absence of metastases by an exploratory laparotomy...
  6. ncbi Mechanisms of lysophosphatidylcholine-induced hepatocyte lipoapoptosis
    Keisuke Kakisaka
    Division of Gastroenterology and Hepatology, College of Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA
    Am J Physiol Gastrointest Liver Physiol 302:G77-84. 2012
    ..We concluded that LPC-induced lipoapoptosis is dependent on mechanisms largely indistinguishable from PA. These data suggest that FFA-mediated cytotoxicity is indirect via the generation of the toxic metabolite, LPC...
  7. ncbi Bile acids activate EGF receptor via a TGF-alpha-dependent mechanism in human cholangiocyte cell lines
    Nathan W Werneburg
    Mayo Medical School, Clinic, and Foundation, 200 First Street SW, Rochester, MN 55905, USA
    Am J Physiol Gastrointest Liver Physiol 285:G31-6. 2003
    ..In conclusion, bile acids activate EGFR via a TGF-alpha-dependent mechanism, and this EGFR activation promotes cellular growth...
  8. ncbi Cholangiocarcinoma: current concepts and insights
    Gregory J Gores
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, MN 55905, USA
    Hepatology 37:961-9. 2003
  9. ncbi Cathepsin B inactivation attenuates hepatic injury and fibrosis during cholestasis
    Ali Canbay
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota 55905, USA
    J Clin Invest 112:152-9. 2003
    ..These findings support a prominent role for the lysosomal pathway of apoptosis in tissue injury and link apoptosis to inflammation and fibrogenesis. Ctsb inhibition may be therapeutic in liver diseases...
  10. ncbi Cholangiocarcinoma: is transplantation an option? For whom?
    Gregory J Gores
    Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA
    J Hepatol 47:455-9. 2007
  11. ncbi The bile acid glycochenodeoxycholate induces trail-receptor 2/DR5 expression and apoptosis
    H Higuchi
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota 55905, USA
    J Biol Chem 276:38610-8. 2001
    ..Induction of TRAIL-R2/DR5 expression and apoptosis by bile acids provides new insights into the mechanisms of hepatocyte apoptosis and the regulation of TRAIL-R2/DR5 expression...
  12. ncbi NF-kappaB is activated in cholestasis and functions to reduce liver injury
    H Miyoshi
    Division of Gastroenterology and Hepatology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
    Am J Pathol 158:967-75. 2001
    ..Liver histology also demonstrated increased liver injury in the BDL mice treated with the Ad5IkappaBsr. In conclusion, NF-kappaB is activated in hepatocytes during obstructive cholestasis and functions to reduce liver injury...
  13. ncbi The bile acid-activated phosphatidylinositol 3-kinase pathway inhibits Fas apoptosis upstream of bid in rodent hepatocytes
    Y Takikawa
    Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota 55905, USA
    Gastroenterology 120:1810-7. 2001
    ..Potentiation of this survival pathway in cholestasis has the potential to attenuate liver injury...
  14. ncbi Cathepsin B knockout mice are resistant to tumor necrosis factor-alpha-mediated hepatocyte apoptosis and liver injury: implications for therapeutic applications
    M E Guicciardi
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota 55905, USA
    Am J Pathol 159:2045-54. 2001
    ..The present data demonstrate that a cat B-mitochondrial apoptotic pathway plays a pivotal role in TNF-alpha-induced hepatocyte apoptosis and liver injury...
  15. ncbi Cholangiocarcinomas express Fas ligand and disable the Fas receptor
    F G Que
    Division of Gastroenterologic and General Surgery, Mayo Medical School, Clinic, and Foundation, Rochester, MN 55905, USA
    Hepatology 30:1398-404. 1999
    ..Reduction of I-FLICE expression in cholangiocarcinoma cells restored Fas-mediated apoptosis. Therapeutic maneuvers to inhibit expression of I-FLICE may aid in the treatment of cholangiocarcinoma...
  16. ncbi Cathepsin B contributes to TNF-alpha-mediated hepatocyte apoptosis by promoting mitochondrial release of cytochrome c
    M E Guicciardi
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota 55905, USA
    J Clin Invest 106:1127-37. 2000
    ..Collectively, these observations suggest that caspase-mediated release of cat B from lysosomes enhances mitochondrial release of cytochrome c and subsequent caspase activation in TNF-alpha-treated hepatocytes...
  17. ncbi Nitric oxide-mediated inhibition of DNA repair potentiates oxidative DNA damage in cholangiocytes
    M Jaiswal
    Center for Basic Research in Digestive Diseases, Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota, USA
    Gastroenterology 120:190-9. 2001
    ..CONCLUSIONS: Collectively, these data implicate NO-mediated inhibition of 8-oxodG base excision DNA repair processes as a mechanism potentiating DNA damage in human inflammatory diseases involving the biliary tract...
  18. ncbi Free fatty acids induce JNK-dependent hepatocyte lipoapoptosis
    Harmeet Malhi
    Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
    J Biol Chem 281:12093-101. 2006
    ..Collectively the data indicate that saturated FFAs induce JNK-dependent hepatocyte lipoapoptosis by activating the proapoptotic Bcl-2 proteins Bim and Bax, which trigger the mitochondrial apoptotic pathway...
  19. ncbi GUDC inhibits cytochrome c release from human cholangiocyte mitochondria
    F G Que
    Division of Gastroenterologic and General Surgery, Mayo Medical School, Rochester, Minnesota 55905, USA
    J Surg Res 83:100-5. 1999
    ..These preliminary results are consistent with our hypothesis that the beneficial effect of UDC on PBC may involve decreased apoptosis after GUDC uptake by cholangiocytes...
  20. ncbi Apoptosis in cancer: cause and cure
    S H Kaufmann
    Division of Oncology Research and Department of Molecular Pharmacology, Mayo Graduate School, Rochester, Minnesota, USA
    Bioessays 22:1007-17. 2000
    ..In this essay, we review recent developments in the fields of carcinogenesis and molecular therapeutics in light of new understanding of apoptotic pathways...
  21. ncbi Cathepsin B inactivation attenuates hepatocyte apoptosis and liver damage in steatotic livers after cold ischemia-warm reperfusion injury
    E S Baskin-Bey
    Mayo Clinic College of Medicine, 200 First St SW, Rochester, Minnesota 55905, USA
    Am J Physiol Gastrointest Liver Physiol 288:G396-402. 2005
    ..In conclusion, these findings support a prominent role for the lysosomal pathway of apoptosis in steatotic livers following CI/WR injury...
  22. ncbi GLI3-dependent repression of DR4 mediates hedgehog antagonism of TRAIL-induced apoptosis
    S Kurita
    Division of Gastroenterology and Hepatology, Mayo Clinic, College of Medicine, Rochester, MN, USA
    Oncogene 29:4848-58. 2010
    ..In conclusion, these data provide evidence of a regulatory mechanism, which modulates TRAIL signaling in cancer cells and suggest new therapeutic approaches for TRAIL-resistant neoplasms...
  23. ncbi Bid antisense attenuates bile acid-induced apoptosis and cholestatic liver injury
    H Higuchi
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota 55905, USA
    J Pharmacol Exp Ther 299:866-73. 2001
    ..These results suggest that bile acid cytotoxicity is Bid-dependent despite the absence of Fas. Bid antisense therapy is a promising approach for the treatment of cholestatic liver injury...
  24. ncbi Viral fusogenic membrane glycoprotein expression causes syncytia formation with bioenergetic cell death: implications for gene therapy
    H Higuchi
    Center for Basic Research in Digestive Diseases, Mayo Clinic, Rochester Minnesota 55905, USA
    Cancer Res 60:6396-402. 2000
    ..This form of cell death should be effective in vivo and enhance the bystander effect, suggesting that FMG-based gene therapy deserves further study for the treatment of hepatocellular and other cancers...
  25. ncbi Hepatocyte apoptosis is a pathologic feature of human alcoholic hepatitis
    S Natori
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic and Foundation, Rochester, MN 55905, USA
    J Hepatol 34:248-53. 2001
    ..CONCLUSIONS: The present results demonstrate that hepatocyte apoptosis is significantly increased in human AH and justify therapeutic strategies aimed at inhibiting apoptosis in this disease...
  26. ncbi Liver transplantation with neoadjuvant chemoradiation is more effective than resection for hilar cholangiocarcinoma
    David J Rea
    Division of Gstroenterologic and General Surgery, Mayo Clinic College of Medicine, Rochester, MN, USA
    Ann Surg 242:451-8; discussion 458-61. 2005
    ....
  27. ncbi Bid is upstream of lysosome-mediated caspase 2 activation in tumor necrosis factor alpha-induced hepatocyte apoptosis
    M Eugenia Guicciardi
    Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
    Gastroenterology 129:269-84. 2005
    ....
  28. ncbi Kupffer cell-derived cyclooxygenase-2 regulates hepatocyte Bcl-2 expression in choledocho-venous fistula rats
    E O Souto
    Division of Gastroenterology and Hepatology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
    Am J Physiol Gastrointest Liver Physiol 280:G805-11. 2001
    ..These data suggest Kupffer cell-derived prostanoids may regulate Bcl-2 expression in the hepatocyte...
  29. ncbi Nuclear serine protease activity contributes to bile acid-induced apoptosis in hepatocytes
    P Kwo
    Center for Basic Research in Digestive Diseases, Mayo Clinic, Rochester, Minnesota 55905, USA
    Am J Physiol 268:G613-21. 1995
    ..These data may be important in understanding apoptosis in other cell types and in providing insight into the mechanisms of liver injury during cholestasis...
  30. ncbi Increases of intracellular magnesium promote glycodeoxycholate-induced apoptosis in rat hepatocytes
    T Patel
    Center for Basic Research in Digestive Diseases, Mayo Clinic, Rochester, Minnesota 55905
    J Clin Invest 94:2183-92. 1994
    ..These data suggest for the first time that changes of Mgi2+ may participate in the program of cellular events culminating in apoptosis...
  31. ncbi Imatinib mesylate induces apoptosis in human cholangiocarcinoma cells
    Mihnea V Chiorean
    Division of Gastroenterology and Hepatology, and Division of Oncology Research, Mayo Clinic College of Medicine, Rochester, MN, USA
    Liver Int 24:687-95. 2004
    ....
  32. ncbi Tumor necrosis factor-alpha-associated lysosomal permeabilization is cathepsin B dependent
    Nathan W Werneburg
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota 55905, USA
    Am J Physiol Gastrointest Liver Physiol 283:G947-56. 2002
    ..C(6) ceramide did not permeabilize lysosomes. In conclusion, these data implicate a sphingosine-Cat B interaction inducing lysosomal destabilization during TNF-alpha cytotoxic signaling...
  33. ncbi Cholestasis increases tumor necrosis factor-related apoptotis-inducing ligand (TRAIL)-R2/DR5 expression and sensitizes the liver to TRAIL-mediated cytotoxicity
    Hajime Higuchi
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, 200 First Street SW, Rochester, MN 55905, USA
    J Pharmacol Exp Ther 303:461-7. 2002
    ..In conclusion, these data define conditions under which TRAIL is hepatotoxic...
  34. ncbi Endoscopic application of photodynamic therapy for cholangiocarcinoma
    A Rumalla
    Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA
    Gastrointest Endosc 53:500-4. 2001
    ..CONCLUSIONS: Photodynamic therapy for cholangiocarcinoma is safe and technically feasible with a preloaded biliary catheter and a monorail technique for catheter positioning...
  35. ncbi Inhibition of epidermal growth factor receptor kinase induces protease-dependent apoptosis in human colon cancer cells
    W E Karnes
    Division of Gastroenterology, Mayo Clinic, Rochester, Minnesota 55905, USA
    Gastroenterology 114:930-9. 1998
    ....
  36. ncbi Cholangiocarcinoma
    N Torok
    Division of Gastroenterology and Hepatobiology, Center for Basic Research in Digestive Diseases, Mayo Clinic/Foundation/Medical School, Rochester, MN 55905, USA
    Semin Gastrointest Dis 12:125-32. 2001
    ..Successful treatment outcome of these patients highlights the need for an early diagnosis of cholangiocarcinoma using the approaches described above...
  37. ncbi Caspase inhibition reduces apoptotic death of cryopreserved porcine hepatocytes
    T Yagi
    Division of Transplantation Surgery, Mayo Clinic, Rochester, MN 55905, USA
    Hepatology 33:1432-40. 2001
    ..These results demonstrate the following: 1) Caspase 3-like protease activation and apoptosis occurs in porcine hepatocytes during cryopreservation; and 2) mitochondrial injury in this process is reduced by caspase inhibition...
  38. ncbi Liver transplantation for gastroenteropancreatic neuroendocrine cancers: Defining selection criteria to improve survival
    Frederike G I van Vilsteren
    Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Liver Transpl 12:448-56. 2006
    ..In conclusion, liver transplantation for patients with hepatic metastases from GEP is a viable therapeutic option in highly selected patients...
  39. ncbi Sustained IL-6/STAT-3 signaling in cholangiocarcinoma cells due to SOCS-3 epigenetic silencing
    Hajime Isomoto
    Miles and Shirley Fiterman Center for Digestive Diseases, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA
    Gastroenterology 132:384-96. 2007
    ..Because suppressor of cytokine signaling 3 (SOCS) controls the IL-6/STAT-3 signaling pathway by a classic feedback loop, the aims of this study were to examine SOCS-3 regulation in human cholangiocarcinoma...
  40. ncbi JNK1-dependent PUMA expression contributes to hepatocyte lipoapoptosis
    Sophie C Cazanave
    Miles and Shirley Fitterman Center for Digestive Diseases, Division of Gastroenterology and Hepatology, College of Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA
    J Biol Chem 284:26591-602. 2009
    ..Collectively, the data implicate JNK1-dependent PUMA expression as a mechanism contributing to hepatocyte lipoapoptosis...
  41. ncbi Cholangiocarcinoma: modern advances in understanding a deadly old disease
    Harmeet Malhi
    Mayo Clinic College of Medicine, Rochester, MN, USA
    J Hepatol 45:856-67. 2006
    ..Future targeted therapies will depend on a better understanding of the cellular and molecular biology of cholangiocarcinomas...
  42. ncbi Treatment of cholangiocarcinoma complicating primary sclerosing cholangitis: the Mayo Clinic experience
    M Kaya
    Division of Gastroenterology and Hepatology, Mayo Clinic and General Foundation, Rochester, Minnesota 55905, USA
    Am J Gastroenterol 96:1164-9. 2001
    ..However, these therapies are rarely applied to these patients because of the advanced nature of the disease at the time of diagnosis. Efforts should be directed at earlier identification of potential surgical candidates...
  43. ncbi Mcl-1 mediates tumor necrosis factor-related apoptosis-inducing ligand resistance in human cholangiocarcinoma cells
    Makiko Taniai
    Mayo Clinic School of Medicine, Rochester, Minnesota 55905, USA
    Cancer Res 64:3517-24. 2004
    ..In conclusion, these studies not only demonstrate that Mcl-1 mediates TRAIL resistance in cholangiocarcinoma cells by blocking the mitochondrial pathway of cell death but also identify two strategies for circumventing this resistance...
  44. ncbi The utility of Lens culinaris agglutinin-reactive alpha-fetoprotein in the diagnosis of hepatocellular carcinoma: evaluation in a United States referral population
    Apinya Leerapun
    Miles and Shirley Fiterman Center for Digestive Diseases, Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
    Clin Gastroenterol Hepatol 5:394-402; quiz 267. 2007
    ..We evaluated the utility of AFP-L3% for diagnosis of HCC in a US referral population...
  45. ncbi Transcriptional regulation of Bim by FoxO3A mediates hepatocyte lipoapoptosis
    Fernando J Barreyro
    Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA
    J Biol Chem 282:27141-54. 2007
    ..In conclusion, saturated FFA stimulate protein phosphatase 2A activity, which activates FoxO3a, inducing expression of the intracellular death mediator Bim...
  46. ncbi Primary sclerosing cholangitis and cholangiocarcinoma
    Konstantinos N Lazaridis
    Division of Gastroenterology and Hepatology, Center for Basic Research in Digestive Diseases, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
    Semin Liver Dis 26:42-51. 2006
    ..Future studies should emphasize deciphering the sequence of events that transform the inflammatory changes of the biliary tree to cancer. Only then will chemoprevention, early diagnosis, and therapy of CCA in patients with PSC improve...
  47. ncbi Free fatty acids promote hepatic lipotoxicity by stimulating TNF-alpha expression via a lysosomal pathway
    Ariel E Feldstein
    Department of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Hepatology 40:185-94. 2004
    ..quot; In conclusion, these data support a lipotoxic model of FFA-mediated lysosomal destabilization...
  48. ncbi Interleukin-6 contributes to Mcl-1 up-regulation and TRAIL resistance via an Akt-signaling pathway in cholangiocarcinoma cells
    Shogo Kobayashi
    Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
    Gastroenterology 128:2054-65. 2005
    ..The present study evaluated the possibility that IL-6 signaling contributes to Mcl-1 up-regulation in cholangiocarcinoma...
  49. ncbi Vascular complications after orthotopic liver transplantation after neoadjuvant therapy for hilar cholangiocarcinoma
    Hendrik T J Mantel
    William J von Liebig Transplant Center, Department of Radiology, Mayo Clinic Rochester and Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Liver Transpl 13:1372-81. 2007
    ..Liver transplantation with neoadjuvant therapy is associated with far higher rates of late arterial and portal venous complications, but these complications do not adversely affect patient and graft survival...
  50. ncbi Trail induces cell migration and invasion in apoptosis-resistant cholangiocarcinoma cells
    Norihisa Ishimura
    Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905, USA
    Am J Physiol Gastrointest Liver Physiol 290:G129-36. 2006
    ..These data demonstrate that TRAIL promotes cell migration and invasion via a NF-kappaB-dependent pathway in human cholangiocarcinoma cell lines, an observation that has a potential negative implication for TRAIL in cancer therapy...
  51. ncbi TNF-alpha-mediated lysosomal permeabilization is FAN and caspase 8/Bid dependent
    Nate Werneburg
    Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905, USA
    Am J Physiol Gastrointest Liver Physiol 287:G436-43. 2004
    ..In conclusion, these studies suggest FAN is upstream of caspase-8/Bid in a signaling cascade culminating in lysosomal permeabilization...
  52. ncbi Nitric oxide inhibits apoptosis downstream of cytochrome C release by nitrosylating caspase 9
    Natalie J Torok
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota 55905, USA
    Cancer Res 62:1648-53. 2002
    ..In conclusion, NO inhibits apoptosis downstream of cytochrome c release by directly blocking caspase 9 activation...
  53. ncbi Death receptor 5 internalization is required for lysosomal permeabilization by TRAIL in malignant liver cell lines
    Yuko Akazawa
    Miles and Shirley Fiterman Center for Digestive Diseases, Division of Gastroenterology and Hepatology, College of Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA
    Gastroenterology 136:2365-2376.e1-7. 2009
    ..Our aims were to determine which TRAIL receptor, death receptor (DR) 4 or DR5, mediates lysosomal permeabilization and assess whether receptor endocytosis followed by trafficking to lysosomes contributes in this process...
  54. ncbi A multivariable model using advanced cytologic methods for the evaluation of indeterminate pancreatobiliary strictures
    Emily G Barr Fritcher
    Department of Laboratory Medicine and Pathology, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA
    Gastroenterology 136:2180-6. 2009
    ..The goal of this study was to retrospectively compare the performance of RC, DIA, and FISH on clinical brushing specimens...
  55. ncbi Sorafenib inhibits signal transducer and activator of transcription-3 signaling in cholangiocarcinoma cells by activating the phosphatase shatterproof 2
    Boris R A Blechacz
    Division of Gastroenterology and Hepatology, Miles and Shirley Fiterman Center for Digestive Diseases, College of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    Hepatology 50:1861-70. 2009
    ..CONCLUSION: Sorafenib accelerates STAT3 dephosphorylation by stimulating phosphatase SHP2 activity, sensitizes CCA cells to TRAIL-mediated apoptosis, and is therapeutic in a syngeneic rat, orthotopic CCA model that mimics human disease...
  56. ncbi Preliminary experience with liver transplantation in selected patients with unresectable hilar cholangiocarcinoma
    Ziad Hassoun
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, 200 First Street SW, Rochester, MN 55905, USA
    Surg Oncol Clin N Am 11:909-21. 2002
    ..This finding confirms the importance of the staging laparotomy as an essential component of the protocol...
  57. ncbi TRAIL mediates liver injury by the innate immune system in the bile duct-ligated mouse
    Alisan Kahraman
    Miles and Shirley Fitterman Center for Digestive Diseases, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN 55905, USA
    Hepatology 47:1317-30. 2008
    ..Conclusion: These observations support a pivotal role for TRAIL in cholestatic liver injury mediated by NK 1.1-positive NK/NKT cells...
  58. ncbi Bile acids induce cyclooxygenase-2 expression via the epidermal growth factor receptor in a human cholangiocarcinoma cell line
    Jung-Hwan Yoon
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota 55905, USA
    Gastroenterology 122:985-93. 2002
    ..CONCLUSIONS: The results show that EGFR is activated by bile acids and functions to induce COX-2 expression by an MAPK cascade. This induction of COX-2 may participate in the genesis and progression of cholangiocarcinomas...
  59. ncbi Treatment of hepatocellular carcinoma
    Ziad Hassoun
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota 55905, USA
    Clin Gastroenterol Hepatol 1:10-8. 2003
  60. ncbi The relationship between apoptosis and non-alcoholic fatty liver disease: an evolutionary cornerstone turned pathogenic
    A Canbay
    Division of Gastroenterology and Hepatology, Department of Medicine, University Hospital Essen, University of Duisburg Essen, Essen, Germany
    Z Gastroenterol 43:211-7. 2005
    ....
  61. ncbi Apoptosis: a mechanism of acute and chronic liver injury
    M E Guicciardi
    Mayo Clinic College of Medicine, 200 First St SW, Rochester, Minnesota 55905, USA
    Gut 54:1024-33. 2005
  62. ncbi Liver transplantation for malignant disease
    G J Gores
    Division of Gastroenterology and Internal Medicine, Mayo Clinic, Rochester, Minnesota
    Gastroenterol Clin North Am 22:285-99. 1993
    ....
  63. ncbi Diagnostic role of serum CA 19-9 for cholangiocarcinoma in patients with primary sclerosing cholangitis
    J C Nichols
    Division of Gastroenterology and Internal Medicine, Mayo Clinic, Rochester, Minnesota 55905
    Mayo Clin Proc 68:874-9. 1993
    ..The measurement of serum concentrations of CA 19-9 is a promising test for detecting cholangiocarcinoma in patients with PSC...
  64. ncbi Clinical Trial of the Pan-Caspase Inhibitor, IDN-6556, in Human Liver Preservation Injury
    E S Baskin Bey
    William J von Liebig Transplant Center, Mayo Clinic College of Medicine, Rochester, Minnesota, USA
    Am J Transplant 7:218-25. 2007
    ..However, larger studies are required to confirm these observations...
  65. ncbi Bile acid-mediated hepatocyte apoptosis and cholestatic liver disease
    M E Guicciardi
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, MN 55905, USA
    Dig Liver Dis 34:387-92. 2002
  66. ncbi Review article: the modern diagnosis and therapy of cholangiocarcinoma
    H Malhi
    Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Aliment Pharmacol Ther 23:1287-96. 2006
    ..Patients with unresectable cholangiocarcinoma or pre-existing primary sclerosing cholangitis should be considered for liver transplantation with neoadjuvant chemoirradiation, in specialized centres...
  67. ncbi The bile acid taurochenodeoxycholate activates a phosphatidylinositol 3-kinase-dependent survival signaling cascade
    C Rust
    Division of Gastroenterology and Hepatology, Department of Oncology, Mayo Clinic, Rochester, Minnesota 55905, USA
    J Biol Chem 275:20210-6. 2000
    ..Collectively, these data suggest that some hydrophobic bile acids such as TCDC activate PI3K-dependent survival pathways, which prevent their otherwise inherent toxicity...
  68. ncbi Cryptosporidium parvum activates nuclear factor kappaB in biliary epithelia preventing epithelial cell apoptosis
    X M Chen
    Center for Basic Research in Digestive Diseases, Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic and Foundation, Rochester, Minnesota 55905, USA
    Gastroenterology 120:1774-83. 2001
    ....
  69. ncbi Proteasome inhibition-induces endoplasmic reticulum dysfunction and cell death of human cholangiocarcinoma cells
    Yucel Ustundag
    Mayo Clinic College of Medicine, 200 First Street SW, Rochester, Minnesota 55905, USA
    World J Gastroenterol 13:851-7. 2007
    ..To determine if proteasome inhibition induces apoptosis in human cholangiocarcinoma cells, and if so, to elucidate the cellular mechanisms...
  70. ncbi Liver transplantation for cholangiocarcinoma
    Charles B Rosen
    Division of Transplantation Surgery, Mayo Clinic, Rochester, MN 55905, USA
    Transpl Int 23:692-7. 2010
    ....
  71. ncbi A smac mimetic reduces TNF related apoptosis inducing ligand (TRAIL)-induced invasion and metastasis of cholangiocarcinoma cells
    Christian D Fingas
    Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA
    Hepatology 52:550-61. 2010
    ..These data support the emerging concept that IAPs are prometastatic and represent targets for antimetastatic therapies...
  72. ncbi CHOP and AP-1 cooperatively mediate PUMA expression during lipoapoptosis
    Sophie C Cazanave
    Division of Gastroenterology and Hepatology, College of Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA
    Am J Physiol Gastrointest Liver Physiol 299:G236-43. 2010
    ..Finally, loss of function studies suggest that both transcription factors are necessary for maximal PUMA induction. Collectively, these data suggest that CHOP and AP-1 cooperatively mediate PUMA induction during hepatocyte lipoapoptosis...
  73. ncbi A novel endoscopic approach to brachytherapy in the management of Hilar cholangiocarcinoma
    Dia T Simmons
    Department of Medicine, Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
    Am J Gastroenterol 101:1792-6. 2006
    ..Unlike NBTs, stents can potentially be placed in bilateral ductal systems to accommodate dual brachytherapy catheters when indicated...
  74. ncbi Long-term probability of and mortality from de novo malignancy after liver transplantation
    Kymberly D S Watt
    Division of Gastroenterology and Hepatology, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA
    Gastroenterology 137:2010-7. 2009
    ..We analyzed a multicenter, prospectively obtained database to assess the probabilities of and risk factors for de novo malignancies in patients after liver transplantation...
  75. ncbi The lysosomal-mitochondrial axis in free fatty acid-induced hepatic lipotoxicity
    Zhengzheng Li
    Department of Cell Biology, Cleveland Clinic, Cleveland, OH 44195, USA
    Hepatology 47:1495-503. 2008
    ..Our data further suggest this process is dependent on lysosomal disruption and activation of cathepsin B...
  76. ncbi Liver transplantation for perihilar cholangiocarcinoma after aggressive neoadjuvant therapy: a new paradigm for liver and biliary malignancies?
    Julie K Heimbach
    William J von Liebig Transplant Center, Mayo Clinic College of Medicine, Rochester, Minn 55905, USA
    Surgery 140:331-4. 2006
  77. ncbi Emerging drugs for hepatocellular carcinoma
    Lewis R Roberts
    Mayo Clinic College of Medicine, Miles and Shirley Fiterman Center for Digestive Diseases, 200 First Street SW, Rochester, MN 55905, USA
    Expert Opin Emerg Drugs 11:469-87. 2006
    ....
  78. ncbi Treatment options for hepatobiliary and pancreatic cancer
    Steven R Alberts
    Division of Medical Oncology, College of Medicine, Mayo Clinic, Rochester, MN 55905, USA
    Mayo Clin Proc 82:628-37. 2007
    ..For pancreatic cancer, surgery, radiation, and systemic therapy all have potential roles. This review provides an updated summary of diagnosis and assessment together with treatment options for this group of cancers...
  79. ncbi Our new president--Nicholas F. LaRusso, MD
    Konstantinos N Lazaridis
    Center for Basic Research in Digestive Disease, Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
    Gastroenterology 132:2005-11. 2007
  80. ncbi MicroRNA-21 is overexpressed in human cholangiocarcinoma and regulates programmed cell death 4 and tissue inhibitor of metalloproteinase 3
    Florin M Selaru
    Division of Gastroenterology and Hepatology, Department of Medicine, Johns Hopkins University, Baltimore, MD 21287, USA
    Hepatology 49:1595-601. 2009
    ..Conclusions: MiR-21 is overexpressed in human CCAs. Furthermore, miR-21 may be oncogenic, at least in part, by inhibiting PDCD4 and TIMP3. Finally, these data suggest that TIMP3 is a candidate tumor suppressor gene in the biliary tree...
  81. ncbi Tumor necrosis factor-related apoptosis-inducing ligand activates a lysosomal pathway of apoptosis that is regulated by Bcl-2 proteins
    Nathan W Werneburg
    Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
    J Biol Chem 282:28960-70. 2007
    ..Collectively, these data suggest that TRAIL can trigger an apoptotic pathway that involves JNK-dependent activation of Bim, which in turn induces Bax-mediated permeabilization of lysosomes...
  82. ncbi Effect of local anesthetic on neuronal cytoplasmic calcium and plasma membrane lysis (necrosis) in a cell culture model
    Michael E Johnson
    Anesthesiology Department, Division of Gastroenterology and Hepatology, Mayo Clinic and Foundation, 200 Southwest First Street, Rochester, MN 55905, USA
    Anesthesiology 97:1466-76. 2002
    ....
  83. ncbi Predictors of disease recurrence following neoadjuvant chemoradiotherapy and liver transplantation for unresectable perihilar cholangiocarcinoma
    Julie K Heimbach
    William J von Liebig Transplant Center, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Transplantation 82:1703-7. 2006
    ..We reviewed our experience with the aim to identify clinicopathological predictors of disease recurrence...
  84. ncbi Apoptotic cell death and function of cryopreserved porcine hepatocytes in a bioartificial liver
    Takakazu Matsushita
    Division of Transplantation Surgery, Mayo Clinic, Rochester, MN 55905, USA
    Cell Transplant 12:109-21. 2003
    ..These data demonstrate that inhibition of apoptosis also preserves cell function...
  85. ncbi Transplantation for hilar cholangiocarcinoma
    Julie K Heimbach
    William J von Liebig Transplant Center, Mayo Clinic College of Medicine, Rochester, MN, USA
    Liver Transpl 10:S65-8. 2004
    ..4. Survival following liver transplantation for unresectable, perihilar CCAs, mass lesion if present <3 cm, is greater than 80% at 5 years. 5. Patients with intrahepatic CCAs are not eligible for liver transplantation...
  86. ncbi A comparison of routine cytology and fluorescence in situ hybridization for the detection of malignant bile duct strictures
    Benjamin R Kipp
    Department of Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA
    Am J Gastroenterol 99:1675-81. 2004
    ..FISH may improve the clinical management of patients who are being evaluated for malignancy in bile duct strictures...
  87. ncbi COX-2 inhibits Fas-mediated apoptosis in cholangiocarcinoma cells
    Ugochukwu C Nzeako
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, 200 First Street SW, Rochester, MN 55905, USA
    Hepatology 35:552-9. 2002
    ..Pharmacologic inhibition of COX-2 may be useful in augmenting Fas-mediated apoptosis of cholangiocarcinoma cells...
  88. ncbi A prospective comparison of digital image analysis and routine cytology for the identification of malignancy in biliary tract strictures
    Todd H Baron
    Division of Gastroenterology, Mayo Clinic, Rochester, Minnesota 55905, USA
    Clin Gastroenterol Hepatol 2:214-9. 2004
    ..Digital image analysis (DIA) allows quantification of nuclear DNA content and may help distinguish benign and malignant strictures of the biliary tract...
  89. ncbi Synthetic Smac/DIABLO peptides enhance the effects of chemotherapeutic agents by binding XIAP and cIAP1 in situ
    Christina R Arnt
    Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Graduate School, Rochester, Minnesota 55905, USA
    J Biol Chem 277:44236-43. 2002
    ..These studies demonstrate that inhibition of IAP proteins can modulate the efficacy of antineoplastic agents...
  90. ncbi Bile acids up-regulate death receptor 5/TRAIL-receptor 2 expression via a c-Jun N-terminal kinase-dependent pathway involving Sp1
    Hajime Higuchi
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota 55905, USA
    J Biol Chem 279:51-60. 2004
    ..Finally, point mutations of the Sp1 binding site attenuated promoter activity. In conclusion, Sp1 is a bile acid-responsive transcription factor that mediates DR5/TRAIL-R2 gene expression downstream of JNK...
  91. ncbi p16INK4a promoter mutations are frequent in primary sclerosing cholangitis (PSC) and PSC-associated cholangiocarcinoma
    Makiko Taniai
    Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota 55905, USA
    Gastroenterology 123:1090-8. 2002
    ..Because p16(INK4a) inactivation has been implicated in cholangiocarcinoma, our aims were to examine PSC cholangiocytes for p16(INK4a) gene mutations...
  92. ncbi Pilot study to assess patient outcomes following endoscopic application of photodynamic therapy for advanced cholangiocarcinoma
    Gavin C Harewood
    Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA
    J Gastroenterol Hepatol 20:415-20. 2005
    ..The aim of this pilot study was to assess the outcome in patients with non-resectable cholangiocarcinoma following endoscopic application of PDT directly into the biliary tract...
  93. ncbi Neuroimaging in hepatic encephalopathy
    Charmaine A Stewart
    Division of Gastroenterology, Mayo Clinic, 200 First Street, Southwest, Rochester, Minnesota 55905, USA
    Clin Gastroenterol Hepatol 3:197-207. 2005
    ..In this review, we have provided an outline of the understood mechanisms of HE and the associated findings on neuroimaging...
  94. ncbi Interleukin 6 upregulates myeloid cell leukemia-1 expression through a STAT3 pathway in cholangiocarcinoma cells
    Hajime Isomoto
    Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Hepatology 42:1329-38. 2005
    ..In conclusion, we have directly demonstrated a STAT3 regulatory element in the Mcl-1 promoter. Downregulation of Mcl-1 transcription by inhibiting this cascade is a potential strategy for the treatment of this cancer...
  95. ncbi Inducible nitric oxide synthase up-regulates Notch-1 in mouse cholangiocytes: implications for carcinogenesis
    Norihisa Ishimura
    Division of Gastroenterology and Hepatology, Mayo Clinic, College of Medicine, Rochester, Minnesota 55905, USA
    Gastroenterology 128:1354-68. 2005
    ..Because cholangiocarcinomas arise in a background of inflammation and express the inflammatory mediator inducible nitric oxide synthase (iNOS), we aimed to determine whether iNOS expression alters Notch expression and signaling...
  96. ncbi "Will all liver transplantation patients eventually die from cancer?"
    William Sanchez
    Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55901, USA
    J Hepatol 44:13-8. 2006
  97. ncbi Mortality and hospital utilization for hepatocellular carcinoma in the United States
    W Ray Kim
    Division of Gastroenterology and Hepatology and Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA
    Gastroenterology 129:486-93. 2005
    ..Hospital service utilization was estimated based on length of stay, total hospitalization charges, and principal procedures...
  98. ncbi mir-29 regulates Mcl-1 protein expression and apoptosis
    J L Mott
    Division of Gastroenterology and Hepatology, Miles and Shirley Fiterman Center for Digestive Diseases, Mayo Clinic College of Medicine, Rochester, MN, USA
    Oncogene 26:6133-40. 2007
    ..Thus mir-29 is an endogenous regulator of Mcl-1 protein expression, and thereby, apoptosis...
  99. ncbi Death by association: BH3 domain-only proteins and liver injury
    E S Baskin-Bey
    Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Am J Physiol Gastrointest Liver Physiol 289:G987-90. 2005
    ....
  100. ncbi TRAIL resistance results in cancer progression: a TRAIL to perdition?
    H Malhi
    Division of Gastroenterology and Hepatology, Miles and Shirley Fiterman Center in Digestive Diseases, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    Oncogene 25:7333-5. 2006
    ..A paradigm emerges from this information, that chemotherapy, targeting NF-kappaB, cFLIP, or antiapoptotic proteins of the Bcl-2 family, in combination with TRAIL maybe more rational than TRAIL therapy alone...
  101. ncbi Ursodeoxycholic acid 'mechanisms of action and clinical use in hepatobiliary disorders'
    K N Lazaridis
    Division of Gastroenterology and Hepatology, Mayo Clinic and Foundation, 55905, USA
    J Hepatol 35:134-46. 2001
    ....

Research Grants20

  1. MECHANISMS OF LIVER CELL INJURY
    Gregory J Gores; Fiscal Year: 2010
    ..The results of these studies are germane to mechanisms of liver injury in the common syndrome of nonalcoholic fatty liver disease, and have the potential to identify new therapeutic strategies for this liver disease. ..
  2. Organelle Dysfunction and Apoptosis in Liver Epithelia
    Gregory Gores; Fiscal Year: 2009
    ..Lysosome disruption results in the release of toxic compounds into the cell culminating in cell demise. The results of these studies are germane both to mechanisms of liver injury and the use of TRAIL as a chemotherapeutic agent. ..
  3. Mechanisms of Carcinogenesis in Biliary Epithelia
    Gregory J Gores; Fiscal Year: 2010
    ..The information emanating from these studies may potentially help identify therapeutic strategies for the treatment and/or chemoprevention of cholangiocarcinoma. ..
  4. Organelle Dysfunction and Apoptosis in Liver Epithelia
    Gregory J Gores; Fiscal Year: 2010
    ..Lysosome disruption results in the release of toxic compounds into the cell culminating in cell demise. The results of these studies are germane both to mechanisms of liver injury and the use of TRAIL as a chemotherapeutic agent. ..
  5. Mechanisms of Carcinogenesis in Biliary Epithelia
    Gregory Gores; Fiscal Year: 2007
    ..The information emanating from these studies may potentially help identify therapeutic strategies for the treatment and/or chemoprevention of cholangiocarcinoma. ..
  6. Organelle Dysfunction and Apoptosis in Liver Epithelia
    Gregory Gores; Fiscal Year: 2007
    ..The significance of the information generated is that it will provide a framework for the potential development of novel therapeutic strategies effective in attenuating human liver injury. ..
  7. Mechanisms of Carcinogenesis in Biliary Epithelia
    Gregory Gores; Fiscal Year: 2005
    ..Successful completion of these proposed studies has the potential for development of new strategies to prevent and treat malignant human liver diseases. ..
  8. MECHANISMS OF LIVER CELL INJURY
    Gregory Gores; Fiscal Year: 2007
    ..The significance of the information generated is that it will help provide a framework for the potential development of novel therapeutic strategies effective in attenuating cholestatic liver injury. ..
  9. MECHANISMS OF LIVER CELL INJURY
    Gregory J Gores; Fiscal Year: 2010
    ..The results of these studies are germane to mechanisms of liver injury in the common syndrome of nonalcoholic fatty liver disease, and have the potential to identify new therapeutic strategies for this liver disease. ..