S C Kogan

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc Gain of MYC underlies recurrent trisomy of the MYC chromosome in acute promyelocytic leukemia
    Letetia Jones
    Helen Diller Family Comprehensive Cancer Center and Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA 94143, USA
    J Exp Med 207:2581-94. 2010
  2. ncbi request reprint Mouse models of acute promyelocytic leukemia
    S C Kogan
    Department of Laboratory Medicine and Comprehensive Cancer Center, University of California, San Francisco, Room S 864, 513 Parnassus Avenue, San Francisco, CA 94143 0100, USA
    Curr Top Microbiol Immunol 313:3-29. 2007
  3. doi request reprint Curing APL: differentiation or destruction?
    Scott C Kogan
    Department of Laboratory Medicine and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94143, USA
    Cancer Cell 15:7-8. 2009
  4. pmc BCL-2 cooperates with promyelocytic leukemia retinoic acid receptor alpha chimeric protein (PMLRARalpha) to block neutrophil differentiation and initiate acute leukemia
    S C Kogan
    Department of Laboratory Medicine, University of California at San Francisco, San Francisco, California 94143, USA
    J Exp Med 193:531-43. 2001
  5. ncbi request reprint Acute promyelocytic leukemia: a view from a mouse
    S C Kogan
    Department of Laboratory Medicine, University of California San Francisco, San Francisco, CA 94143 0128, USA
    Blood Cells Mol Dis 26:620-5. 2000
  6. ncbi request reprint Mouse intestinal goblet cells expressing SV40 T antigen directed by the MUC2 mucin gene promoter undergo apoptosis upon migration to the villi
    J R Gum
    Department of Veterans Affairs Medical Center, 4150 Clement Street, San Francisco, California 94121, USA
    Cancer Res 61:3472-9. 2001
  7. pmc Cooperation of cytokine signaling with chimeric transcription factors in leukemogenesis: PML-retinoic acid receptor alpha blocks growth factor-mediated differentiation
    Vernon T Phan
    Department of Laboratory Medicine and Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California 94143, USA
    Mol Cell Biol 23:4573-85. 2003
  8. ncbi request reprint CCAAT/Enhancer binding proteins repress the leukemic phenotype of acute myeloid leukemia
    Bao Tran H Truong
    Comprehensive Cancer Center and Department of Laboratory Medicine, University of California, San Francisco 94143 0128, USA
    Blood 101:1141-8. 2003
  9. ncbi request reprint Bethesda proposals for classification of nonlymphoid hematopoietic neoplasms in mice
    Scott C Kogan
    Comprehensive Cancer Center and Department of Laboratory Medicine, University of California, San Francisco, 94143, USA
    Blood 100:238-45. 2002
  10. pmc Dose-dependent effects of focal fractionated irradiation on secondary malignant neoplasms in Nf1 mutant mice
    Jean L Nakamura
    Department of Radiation Oncology, University of California, San Francisco, California 94158, USA
    Cancer Res 71:106-15. 2011

Collaborators

Detail Information

Publications39

  1. pmc Gain of MYC underlies recurrent trisomy of the MYC chromosome in acute promyelocytic leukemia
    Letetia Jones
    Helen Diller Family Comprehensive Cancer Center and Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA 94143, USA
    J Exp Med 207:2581-94. 2010
    ..In addition, we found that human myeloid leukemias with trisomy 8 have increased MYC. These data show that gain of MYC can contribute to the pathogenic effect of the most common trisomy of human AML...
  2. ncbi request reprint Mouse models of acute promyelocytic leukemia
    S C Kogan
    Department of Laboratory Medicine and Comprehensive Cancer Center, University of California, San Francisco, Room S 864, 513 Parnassus Avenue, San Francisco, CA 94143 0100, USA
    Curr Top Microbiol Immunol 313:3-29. 2007
    ..Furthermore, preclinical studies utilizing these mice have advanced therapy for myeloid leukemia...
  3. doi request reprint Curing APL: differentiation or destruction?
    Scott C Kogan
    Department of Laboratory Medicine and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94143, USA
    Cancer Cell 15:7-8. 2009
    ..Targeted destruction of the PML-RARalpha oncoprotein appears key to eliminating the cells from which relapse can arise...
  4. pmc BCL-2 cooperates with promyelocytic leukemia retinoic acid receptor alpha chimeric protein (PMLRARalpha) to block neutrophil differentiation and initiate acute leukemia
    S C Kogan
    Department of Laboratory Medicine, University of California at San Francisco, San Francisco, California 94143, USA
    J Exp Med 193:531-43. 2001
    ..Our results indicate that genetic changes that inhibit apoptosis can cooperate with PMLRARalpha to initiate APL...
  5. ncbi request reprint Acute promyelocytic leukemia: a view from a mouse
    S C Kogan
    Department of Laboratory Medicine, University of California San Francisco, San Francisco, CA 94143 0128, USA
    Blood Cells Mol Dis 26:620-5. 2000
    ..Molecularly targeted therapies that either restore maturation or abrogate growth autonomy represent a hope for improving survival of patients with other subtypes of AML...
  6. ncbi request reprint Mouse intestinal goblet cells expressing SV40 T antigen directed by the MUC2 mucin gene promoter undergo apoptosis upon migration to the villi
    J R Gum
    Department of Veterans Affairs Medical Center, 4150 Clement Street, San Francisco, California 94121, USA
    Cancer Res 61:3472-9. 2001
    ..These experiments demonstrate that apoptosis effectively blocks inappropriate goblet cell proliferation in the intestine, supporting its proposed role as an antineoplastic mechanism...
  7. pmc Cooperation of cytokine signaling with chimeric transcription factors in leukemogenesis: PML-retinoic acid receptor alpha blocks growth factor-mediated differentiation
    Vernon T Phan
    Department of Laboratory Medicine and Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California 94143, USA
    Mol Cell Biol 23:4573-85. 2003
    ..This combination can be potently leukemogenic, but the particular manner in which these types of mutations interact determines the ability of such combinations to generate acute myeloid leukemia...
  8. ncbi request reprint CCAAT/Enhancer binding proteins repress the leukemic phenotype of acute myeloid leukemia
    Bao Tran H Truong
    Comprehensive Cancer Center and Department of Laboratory Medicine, University of California, San Francisco 94143 0128, USA
    Blood 101:1141-8. 2003
    ..Our results support the hypothesis that induction of C/EBP activity is a critical effect of tRA in APL. Furthermore, our findings suggest that targeted modulation of C/EBP activities could provide a new approach to therapy of AML...
  9. ncbi request reprint Bethesda proposals for classification of nonlymphoid hematopoietic neoplasms in mice
    Scott C Kogan
    Comprehensive Cancer Center and Department of Laboratory Medicine, University of California, San Francisco, 94143, USA
    Blood 100:238-45. 2002
    ..This classification will be of particular value to investigators seeking to develop, use, and communicate about mouse models of human hematopoietic neoplasms...
  10. pmc Dose-dependent effects of focal fractionated irradiation on secondary malignant neoplasms in Nf1 mutant mice
    Jean L Nakamura
    Department of Radiation Oncology, University of California, San Francisco, California 94158, USA
    Cancer Res 71:106-15. 2011
    ..This technique for administering focal fractionated irradiation will facilitate mechanistic and translational studies of SMNs...
  11. ncbi request reprint HOXB6 overexpression in murine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem cell expansion and acute myeloid leukemia in vivo
    Neal A Fischbach
    Department of Medicine, Veterans Affairs Medical Center, San Francisco, CA 94121, USA
    Blood 105:1456-66. 2005
    ..These biologic effects of HOXB6 were largely dependent on DNA binding but independent of direct interaction with PBX1...
  12. ncbi request reprint A model of APL with FLT3 mutation is responsive to retinoic acid and a receptor tyrosine kinase inhibitor, SU11657
    Jastinder Sohal
    Comprehensive Cancer Center and the Department of Laboratory Medicine, University of California, San Francisco, 94143, USA
    Blood 101:3188-97. 2003
    ..Our findings also indicate that APL patients with FLT3 mutations may benefit from combination therapy with all-trans retinoic acid plus an FLT3 inhibitor...
  13. pmc The PEBP2betaMYH11 fusion created by Inv(16)(p13;q22) in myeloid leukemia impairs neutrophil maturation and contributes to granulocytic dysplasia
    S C Kogan
    G W Hooper Foundation, University of California, San Francisco, CA 94143 0552, USA
    Proc Natl Acad Sci U S A 95:11863-8. 1998
    ..These results show that PEBP2betaMYH11 can impair neutrophil development and provide evidence that alterations of Pebp2 can contribute to the genesis of myelodysplasia...
  14. pmc Somatic activation of oncogenic Kras in hematopoietic cells initiates a rapidly fatal myeloproliferative disorder
    Benjamin S Braun
    Department of Pediatrics, University of California, San Francisco, CA 94143, USA
    Proc Natl Acad Sci U S A 101:597-602. 2004
    ..Oncogenic RAS is sufficient to initiate myeloid leukemogenesis in mice, and this provides an in vivo system for biologic and preclinical studies...
  15. pmc Use of chromosome engineering to model a segmental deletion of chromosome band 7q22 found in myeloid malignancies
    Jasmine C Y Wong
    Department of Pediatrics, University of California, San Francisco, CA 94143, USA
    Blood 115:4524-32. 2010
    ....
  16. ncbi request reprint Therapy-induced malignant neoplasms in Nf1 mutant mice
    Richard C Chao
    Department of Pediatrics, University of California, San Francisco, San Francisco, California 94143, USA
    Cancer Cell 8:337-48. 2005
    ..Nf1(+/-) mice provide a tractable model for investigating the pathogenesis of common mutagen-induced cancers and for testing preventive strategies...
  17. ncbi request reprint Somatic inactivation of Nf1 in hematopoietic cells results in a progressive myeloproliferative disorder
    Doan T Le
    Department of Pediatrics, University of California, San Francisco, 513 Parnassus Ave, HSE 302, San Francisco, CA 94143, USA
    Blood 103:4243-50. 2004
    ..These Mx1-Cre, Nf1(flox/flox) mice establish a tractable experimental model for testing therapeutics and for identifying mutations that cooperate with hyperactive Ras in myeloid leukemogenesis...
  18. pmc PML-RAR{alpha} and Dnmt3a1 cooperate in vivo to promote acute promyelocytic leukemia
    Deepa Subramanyam
    Institute for Regeneration Medicine, University of California, San Francisco, California 94143, USA
    Cancer Res 70:8792-801. 2010
    ..Our findings show a cooperation between the PML-RARĪ± oncogene and the Dnmt3a1 enzyme in vivo and that Dnmt levels can be rate limiting in APL progression...
  19. pmc Dual treatment with FLT3 inhibitor SU11657 and doxorubicin increases survival of leukemic mice
    Brian D Lee
    Department of Laboratory Medicine, UCSF, San Francisco, CA 94143, USA
    Leuk Res 31:1131-4. 2007
    ..003) when compared to controls. Neither agent alone or in combination increased survival of control mice. These results suggest that the use of targeted therapeutics can overcome resistance to traditional chemotherapies in AML...
  20. pmc Beta common receptor inactivation attenuates myeloproliferative disease in Nf1 mutant mice
    Andrew Kim
    Department of Pediatrics, University of California San Francisco, USA
    Blood 109:1687-91. 2007
    ..Whereas inhibiting GM-CSF signaling may be of therapeutic benefit in JMML, our data also demonstrate aberrant proliferation of Nf1-/-myeloid progenitors that is independent of signaling through the GM-CSF receptor...
  21. pmc CCAAT/enhancer binding proteins alpha and epsilon cooperate with all-trans retinoic acid in therapy but differ in their antileukemic activities
    Young Jin Lee
    Dept of Laboratory Medicine, Box 0134, 513 Parnassus Ave, San Francisco, CA 94143, USA
    Blood 108:2416-9. 2006
    ..We also show that forced expression of C/EBPalpha or C/EBPepsilon in combination with ATRA treatment has a synergistic effect on survival of leukemic mice compared with either therapy alone...
  22. ncbi request reprint PPARgamma-active triterpenoid CDDO enhances ATRA-induced differentiation in APL
    Yoko Tabe
    Section of Molecular Hematology and Therapy, Department of Stem Cell Transplantation and Cellular Therapy, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
    Cancer Biol Ther 6:1967-77. 2007
    ..In summary, these results provide rationale for the combined targeting of RAR and PPARgamma nuclear receptors in the therapy of APL...
  23. ncbi request reprint Recurring chromosomal abnormalities in leukemia in PML-RARA transgenic mice identify cooperating events and genetic pathways to acute promyelocytic leukemia
    Michelle M Le Beau
    Section of Hematology Oncology, University of Chicago, 5841 S Maryland Ave, MC2115, Chicago, IL 60637, USA
    Blood 102:1072-4. 2003
    ..Our results demonstrate that different cooperating events may generate leukemia via different pathways...
  24. ncbi request reprint Haploinsufficiency of Runx1/AML1 promotes myeloid features and leukaemogenesis in BXH2 mice
    Namiko Yamashita
    Institute of Molecular and Cell Biology, Singapore
    Br J Haematol 131:495-507. 2005
    ..In conclusion, the BXH2-Runx1+/- system is a promising mouse model to investigate the mechanism of leukaemogenesis in FPD/AML...
  25. ncbi request reprint Cbf beta-SMMHC induces distinct abnormal myeloid progenitors able to develop acute myeloid leukemia
    Ya Huei Kuo
    Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
    Cancer Cell 9:57-68. 2006
    ..These data show that a leukemia oncoprotein can inhibit differentiation and proliferation while not affecting the maintenance of long-term HSCs...
  26. ncbi request reprint Induction of tumor arrest and differentiation with prolonged survival by intermittent hypoxia in a mouse model of acute myeloid leukemia
    Wei Liu
    Department of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis of Ministry of Education of China, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine
    Blood 107:698-707. 2006
    ..Additional investigations may uncover ways to mimic the differentiative effects of hypoxia in a manner that will benefit human patients with AML...
  27. ncbi request reprint Recurring chromosomal abnormalities in leukemia in PML-RARA transgenic mice parallel human acute promyelocytic leukemia
    Michelle M Le Beau
    Section of Hematology Oncology, University of Chicago, Illinois 60637, USA
    Blood 99:2985-91. 2002
    ..Thus, our results suggest that PML-RARA-initiated murine leukemia is associated with a defined spectrum of genetic changes, and that these secondary mutations recapitulate, in part, the cytogenetic abnormalities found in human APL...
  28. pmc Haploinsufficiency of EGR1, a candidate gene in the del(5q), leads to the development of myeloid disorders
    John M Joslin
    Section of Hematology Oncology and the Cancer Research Center, University of Chicago, IL 60637, USA
    Blood 110:719-26. 2007
    ..Our data suggest that haploinsufficiency for Egr1 plays a role in murine leukemogenesis, and in the development of AML/MDS characterized by abnormalities of chromosome 5...
  29. pmc Survival and tumorigenesis in O6-methylguanine DNA methyltransferase-deficient mice following cyclophosphamide exposure
    Ramamoorthy Nagasubramanian
    Department of Pediatrics, University of Chicago, 5841 S Maryland Avenue, Chicago, IL 60637, USA
    Mutagenesis 23:341-6. 2008
    ..9 x 10(6)). These data indicate that MGMT deficiency does not protect against long-term toxicity or mutagenicity from CP and appears to attenuate the occurrence of CP-induced tumours in an Nf1+/- background...
  30. ncbi request reprint Bethesda proposals for classification of lymphoid neoplasms in mice
    Herbert C Morse
    Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 0760, USA
    Blood 100:246-58. 2002
    ..The classification should facilitate communications about mouse models of human lymphoid diseases...
  31. ncbi request reprint Determinants of sensitivity and resistance to rapamycin-chemotherapy drug combinations in vivo
    Hans Guido Wendel
    Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA
    Cancer Res 66:7639-46. 2006
    ..Understanding these genotype-response relationships in human tumors will be important for the effective use of rapamycin or other compounds targeting the PI(3)K pathway in the clinic...
  32. pmc Loss of p53 impedes the antileukemic response to BCR-ABL inhibition
    Hans Guido Wendel
    Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA
    Proc Natl Acad Sci U S A 103:7444-9. 2006
    ..Our results identify p53 as a determinant of the response to oncogene inhibition and suggest one way in which resistance to targeted therapy can emerge during the course of tumor evolution...
  33. ncbi request reprint Trp53 loss during in vitro selection contributes to acquired Ara-C resistance in acute myeloid leukemia
    Bin Yin
    University of Minnesota Cancer Center, Department of Genetics, Cell Biology and Development, University of Minnesota, Minneapolis, MN 55455, USA
    Exp Hematol 34:631-41. 2006
    ..We have attempted to investigate genetic mechanisms causing resistance to Ara-C [1-beta-D-arabinofuranosyl-cytosine (cytarabine)], one mainstay in AML chemotherapy for decades...
  34. ncbi request reprint Increased CCAAT enhancer-binding protein epsilon (C/EBPepsilon) expression and premature apoptosis in myeloid cells expressing Gfi-1 N382S mutant associated with severe congenital neutropenia
    Dazhong Zhuang
    Department of Biological Sciences, University of Toledo, Toledo, Ohio 43606, USA
    J Biol Chem 281:10745-51. 2006
    ....
  35. ncbi request reprint Forced retinoic acid receptor alpha homodimers prime mice for APL-like leukemia
    Thomas Sternsdorf
    Gene Expression Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA
    Cancer Cell 9:81-94. 2006
    ..These results demonstrate that the dimerization interface of RARalpha fusion partners is a critical element in APL pathogenesis while pointing to other features of PML for enhancing penetrance and progression...
  36. ncbi request reprint Role of O6-alkylguanine-DNA alkyltransferase in protecting against 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU)-induced long-term toxicities
    Ryan J Hansen
    Committee on Cancer Biology, The University of Chicago, Chicago, IL 60637, USA
    J Pharmacol Exp Ther 315:1247-55. 2005
    ..In contrast, liver and kidney toxicity was only observed in mice treated with BCNU (50 mg/kg). These results suggest that O6-benzylguanine enhances long-term pulmonary toxicity associated with BCNU in mice...
  37. pmc Conditional MLL-CBP targets GMP and models therapy-related myeloproliferative disease
    Jing Wang
    Department of Pathology and Medicine, Howard Hughes Medical Institute, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
    EMBO J 24:368-81. 2005
    ..This model of MLL-CBP therapy-related myeloproliferative disease demonstrates the selectivity of this MLL fusion for GMP cells and its ability to initiate leukemogenesis in conjunction with cooperating mutations...
  38. ncbi request reprint Mouse models of human cancers (part 3)
    Alexander D Borowsky
    Center for Comparative Medicine, University of California Davis, 95615, USA
    Comp Med 54:258-70. 2004

Research Grants8

  1. Molecular Mechanisms of Leukemogenesis by PMLRAR alpha
    Scott Kogan; Fiscal Year: 2002
    ..This work will aid the development of new molecularly-targeted treatments for these malignancies. ..
  2. Molecular Mechanisms of Leukemogenesis by PMLRAR alpha
    Scott Kogan; Fiscal Year: 2003
    ..This work will aid the development of new molecularly-targeted treatments for these malignancies. ..
  3. Molecular Mechanisms of Leukemogenesis by PMLRAR alpha
    Scott Kogan; Fiscal Year: 2004
    ..This work will aid the development of new molecularly-targeted treatments for these malignancies. ..
  4. Molecular Mechanisms of Leukemogenesis by PMLRAR alpha
    Scott Kogan; Fiscal Year: 2005
    ..This work will aid the development of new molecularly-targeted treatments for these malignancies. ..
  5. Molecular Mechanisms of Leukemogenesis by PMLRAR alpha
    Scott Kogan; Fiscal Year: 2009
    ..The results of the proposed studies should help us to understand acute myeloid leukemia and thereby should aid the development of new treatments for leukemias and other cancers. ..
  6. Molecular Mechanisms of Leukemogenesis by PMLRAR alpha
    Scott C Kogan; Fiscal Year: 2010
    ..The results of the proposed studies should help us to understand acute myeloid leukemia and thereby should aid the development of new treatments for leukemias and other cancers. ..
  7. PATHOGENESIS AND THERAPY OF ACUTE PROMYELOCYTIC LEUKEMIA
    Scott Kogan; Fiscal Year: 2003
    ....
  8. Molecular Mechanisms of Leukemogenesis by PMLRAR alpha
    Scott Kogan; Fiscal Year: 2006
    ..This work will aid the development of new molecularly-targeted treatments for these malignancies. ..