Research Topics
| S C KoganSummaryAffiliation: University of California Country: USA Publications
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Publications
Bethesda proposals for classification of nonlymphoid hematopoietic neoplasms in miceScott 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...
BCL-2 cooperates with promyelocytic leukemia retinoic acid receptor alpha chimeric protein (PMLRARalpha) to block neutrophil differentiation and initiate acute leukemiaS 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...- Acute promyelocytic leukemia: a view from a mouseS 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... - The PEBP2betaMYH11 fusion created by Inv(16)(p13;q22) in myeloid leukemia impairs neutrophil maturation and contributes to granulocytic dysplasiaS 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... - Mouse intestinal goblet cells expressing SV40 T antigen directed by the MUC2 mucin gene promoter undergo apoptosis upon migration to the villiJ 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... 
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...- Dose-dependent effects of focal fractionated irradiation on secondary malignant neoplasms in Nf1 mutant miceJean 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... - HOXB6 overexpression in murine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem cell expansion and acute myeloid leukemia in vivoNeal 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... - Cooperation of cytokine signaling with chimeric transcription factors in leukemogenesis: PML-retinoic acid receptor alpha blocks growth factor-mediated differentiationVernon 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... - CCAAT/Enhancer binding proteins repress the leukemic phenotype of acute myeloid leukemiaBao 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... - A model of APL with FLT3 mutation is responsive to retinoic acid and a receptor tyrosine kinase inhibitor, SU11657Jastinder 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... - Mouse models of acute promyelocytic leukemiaS 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... - Somatic activation of oncogenic Kras in hematopoietic cells initiates a rapidly fatal myeloproliferative disorderBenjamin 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... - Use of chromosome engineering to model a segmental deletion of chromosome band 7q22 found in myeloid malignanciesJasmine C Y Wong
Department of Pediatrics, University of California, San Francisco, CA 94143, USA
Blood 115:4524-32. 2010.... - Therapy-induced malignant neoplasms in Nf1 mutant miceRichard 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... - PML-RAR{alpha} and Dnmt3a1 cooperate in vivo to promote acute promyelocytic leukemiaDeepa 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... - Somatic inactivation of Nf1 in hematopoietic cells results in a progressive myeloproliferative disorderDoan 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... - CCAAT/enhancer binding proteins alpha and epsilon cooperate with all-trans retinoic acid in therapy but differ in their antileukemic activitiesYoung 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... - Beta common receptor inactivation attenuates myeloproliferative disease in Nf1 mutant miceAndrew 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... - Dual treatment with FLT3 inhibitor SU11657 and doxorubicin increases survival of leukemic miceBrian 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... - Haploinsufficiency of EGR1, a candidate gene in the del(5q), leads to the development of myeloid disordersJohn 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... - Recurring chromosomal abnormalities in leukemia in PML-RARA transgenic mice parallel human acute promyelocytic leukemiaMichelle 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... - Recurring chromosomal abnormalities in leukemia in PML-RARA transgenic mice identify cooperating events and genetic pathways to acute promyelocytic leukemiaMichelle 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... - Cbf beta-SMMHC induces distinct abnormal myeloid progenitors able to develop acute myeloid leukemiaYa 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... - Haploinsufficiency of Runx1/AML1 promotes myeloid features and leukaemogenesis in BXH2 miceNamiko 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... - Increased CCAAT enhancer-binding protein epsilon (C/EBPepsilon) expression and premature apoptosis in myeloid cells expressing Gfi-1 N382S mutant associated with severe congenital neutropeniaDazhong Zhuang
Department of Biological Sciences, University of Toledo, Toledo, Ohio 43606, USA
J Biol Chem 281:10745-51. 2006.... - 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 - Conditional MLL-CBP targets GMP and models therapy-related myeloproliferative diseaseJing 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... - Role of O6-alkylguanine-DNA alkyltransferase in protecting against 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU)-induced long-term toxicitiesRyan 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... - Survival and tumorigenesis in O6-methylguanine DNA methyltransferase-deficient mice following cyclophosphamide exposureRamamoorthy 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... - PPARgamma-active triterpenoid CDDO enhances ATRA-induced differentiation in APLYoko 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... - Induction of tumor arrest and differentiation with prolonged survival by intermittent hypoxia in a mouse model of acute myeloid leukemiaWei 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... - Bethesda proposals for classification of lymphoid neoplasms in miceHerbert 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... - Determinants of sensitivity and resistance to rapamycin-chemotherapy drug combinations in vivoHans 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... - Forced retinoic acid receptor alpha homodimers prime mice for APL-like leukemiaThomas 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... - Loss of p53 impedes the antileukemic response to BCR-ABL inhibitionHans 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... - Trp53 loss during in vitro selection contributes to acquired Ara-C resistance in acute myeloid leukemiaBin 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..CONCLUSIONS: These data indicate that Trp53 loss-of-function could partly explain the acquisition of AML chemoresistance, and suggest that PFTalpha could be useful in treatment of relapsed AML...