Professor, Laboratory Medicine, UCSF School of Medicine
Pathology
Dr. Scott C. Kogan, MD
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Dr. Scott C. Kogan is an expert in the field of Pathology. He attended University of California San Francisco School of Medicine. University of California San Francisco School of Medicine is a top medical college. University of California San Francisco School of Medicine has a rank of 3 in research and a 3 in primary care Scott Kogan is a published doctor and has 92 publications published. The lastest was: 'The PEBP2betaMYH11 fusion created by Inv(16)(p13;q22) in myeloid leukemia impairs neutrophil maturation and contributes to granulocytic dysplasia.' Doctor Scott C. Kogan, MD is registered with Medicare and accepts Medicare payments.
Publications
- Functional evidence implicating chromosome 7q22 haploinsufficiency in myelodysplastic Syndrome pathogenesis.
- Cooperative loss of RAS feedback regulation drives Myeloid leukemogenesis.
- Preclinical efficacy of MEK inhibition in Nras mutant Acute myeloid leukemia.
- MLL3 Is a Haploinsufficient 7q Tumor Suppressor in Acute Myeloid Leukemia.
- Crenolanib is a selective type I pan-FLT3 inhibitor.
- PML-RARα co-operates with Sox4 in Acute myeloid leukemia development in mice.
- Initially disadvantaged, TEL-AML1 cells expand and initiate Leukemia in response to irradiation and cooperating mutations.
- Sustained MEK inhibition abrogates Myeloproliferative disease in Nf1 mutant mice.
- Genetically Mediated Nf1 Loss in Mice Promotes Diverse Radiation-Induced Tumors Modeling Second Malignant Neoplasms.
- Control of the senescence-associated secretory phenotype by NF-{kappa}B promotes senescence and enhances chemosensitivity.
- PML-RARα enhances constitutive autophagic activity through inhibiting the Akt/mTOR pathway.
- RNAi screen identifies Brd4 as a therapeutic target in Acute myeloid leukaemia.
- An integrated approach to dissecting oncogene addiction implicates a Myb-coordinated self-renewal program as essential for Leukemia maintenance.
- A rapid and scalable system for studying gene function in mice using conditional RNA interference.
- Hematopoiesis and leukemogenesis in mice expressing oncogenic NrasG12D from the endogenous locus.
- Treatment with 5-azacytidine accelerates Acute promyelocytic leukemia leukemogenesis in a transgenic mouse model.
- Dose-dependent effects of focal fractionated irradiation on secondary malignant neoplasms in Nf1 mutant mice.
- Gain of MYC underlies recurrent trisomy of the MYC chromosome in Acute promyelocytic leukemia.
- PML-RAR{alpha} and Dnmt3a1 cooperate in vivo to promote Acute promyelocytic leukemia.
- p53 loss promotes Acute myeloid leukemia by enabling aberrant self-renewal.
- Use of chromosome engineering to model a segmental deletion of chromosome band 7q22 found in Myeloid malignancies.
- Medicine. Poisonous contacts.
- Mutant Ikzf1, KrasG12D, and Notch1 cooperate in T lineage leukemogenesis and modulate responses to targeted agents.
- Mouse models of human AML accurately predict chemotherapy response.
- Curing APL: differentiation or destruction?
- mTORC1 promotes survival through translational control of Mcl-1.
- PPARgamma-active triterpenoid CDDO enhances ATRA-induced differentiation in APL.
- Haploinsufficiency of EGR1, a candidate gene in the del(5q), leads to the development of Myeloid disorders.
- Beta common receptor inactivation attenuates Myeloproliferative disease in Nf1 mutant mice.
- CCAAT/enhancer binding proteins alpha and epsilon cooperate with all-trans retinoic acid in therapy but differ in their antileukemic activities.
- Determinants of sensitivity and resistance to rapamycin-chemotherapy drug combinations in vivo.
- Loss of p53 impedes the antileukemic response to BCR-ABL inhibition.
- Increased CCAAT enhancer-binding protein epsilon (C/EBPepsilon) expression and premature apoptosis in Myeloid cells expressing Gfi-1 N382S mutant associated with sever...
- Forced retinoic acid receptor alpha homodimers prime mice for APL-like Leukemia.
- Induction of tumor arrest and differentiation with prolonged survival by intermittent hypoxia in a mouse model of Acute myeloid leukemia.
- Cbf beta-SMMHC induces distinct abnormal myeloid progenitors able to develop Acute myeloid leukemia.
- Role of O6-alkylguanine-DNA alkyltransferase in protecting against 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU)-induced long-term toxicities.
- Therapy-induced malignant neoplasms in Nf1 mutant mice.
- HOXB6 overexpression in murine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem cell expansion and Acute myeloid leukemia in ...
- Somatic inactivation of Nf1 in hematopoietic cells results in a progressive Myeloproliferative disorder.
- Mouse models of human cancers (part 3).
- Somatic activation of oncogenic Kras in hematopoietic cells initiates a rapidly fatal Myeloproliferative disorder.
- Recurring chromosomal abnormalities in leukemia in PML-RARA transgenic mice identify cooperating events and genetic pathways to Acute promyelocytic leukemia.
- Cooperation of cytokine signaling with chimeric transcription factors in leukemogenesis: PML-retinoic acid receptor alpha blocks growth factor-mediated differentiation.
- A model of APL with FLT3 mutation is responsive to retinoic acid and a receptor tyrosine kinase inhibitor, SU11657.
- CCAAT/Enhancer binding proteins repress the leukemic phenotype of Acute myeloid leukemia.
- Recurring chromosomal abnormalities in leukemia in PML-RARA transgenic mice parallel human Acute promyelocytic leukemia.
- Environment, genetics and idiopathic Parkinson''s Disease.
- Genetic basis of Hemophilia A.
- Characteristics of consumer terminology for health information retrieval.
- Problems and challenges in patient information retrieval: a descriptive study.
- Donor myocardial infarction impairs the therapeutic potential of bone marrow cells by an interleukin-1-mediated inflammatory response.
- Patient and clinician vocabulary: how different are they?
- The protective effect of KCNMB1 E65K against hypertension is restricted to blood pressure treatment with beta-blockade.
- Genitourinary malformations associated with agenesis of the corpus callosum.
- Images in clinical medicine. Indinavir crystalluria.
- Amino acid substitutions in conserved domains of factor VIII and related proteins: study of patients with mild and moderately severe Hemophilia A.
- An improved method for prenatal diagnosis of genetic diseases by analysis of amplified DNA sequences. Application to Hemophilia A.
- Mutations of factor VIII cleavage sites in Hemophilia A.
- Functional dissection and sequence of yeast HAP1 activator.
- Mutations and a polymorphism in the factor VIII gene discovered by denaturing gradient gel electrophoresis.
- PML-RARA-targeted DNA vaccine induces protective immunity in a mouse model of Leukemia.
- BCL-2 and mutant NRAS interact physically and functionally in a mouse model of progressive myelodysplasia.
- Inhibition of apoptosis by the retinoblastoma gene product.
- Opinion: how patients have benefited from mouse models of Acute promyelocytic leukaemia.
- Hematopoietic stem cell quiescence is maintained by compound contributions of the retinoblastoma gene family.
- In vivo activation of cAMP signaling induces growth arrest and differentiation in Acute promyelocytic leukemia.
- Acute promyelocytic leukemia: from treatment to genetics and back.
- The role of p53 in suppression of KSHV cyclin-induced lymphomagenesis.
- Acute promyelocytic leukemia: a view from a mouse.
- A PMLRARA transgene results in a retinoid-deficient phenotype associated with enhanced susceptibility to skin tumorigenesis.
- A sumoylation site in PML/RARA is essential for leukemic transformation.
- A PMLRARalpha transgene initiates murine Acute promyelocytic leukemia.
- Mouse models of Acute promyelocytic leukemia.
- Retinoic acid and arsenic synergize to eradicate leukemic cells in a mouse model of Acute promyelocytic leukemia.
- Mouse intestinal goblet cells expressing SV40 T antigen directed by the MUC2 mucin gene promoter undergo apoptosis upon migration to the villi.
- New evidence supporting megakaryocyte-erythrocyte potential of flk2/flt3+ multipotent hematopoietic progenitors.
- Retroviral integration at the Epi1 locus cooperates with Nf1 gene loss in the progression to Acute myeloid leukemia.
- Survival signalling by Akt and eIF4E in oncogenesis and cancer therapy.
- Leukemia with distinct phenotypes in transgenic mice expressing PML/RAR alpha, PLZF/RAR alpha or NPM/RAR alpha.
- The PEBP2betaMYH11 fusion created by Inv(16)(p13;q22) in myeloid Leukemia impairs neutrophil maturation and contributes to granulocytic dysplasia.
- BCL-2 cooperates with promyelocytic leukemia retinoic acid receptor alpha chimeric protein (PMLRARalpha) to block neutrophil differentiation and initiate Acute leukemia.
- Leukemia initiated by PMLRARalpha: the PML domain plays a critical role while retinoic acid-mediated transactivation is dispensable.
- Bethesda proposals for classification of lymphoid neoplasms in mice.
- Bethesda proposals for classification of nonlymphoid hematopoietic neoplasms in mice.
- Conditional MLL-CBP targets GMP and models therapy-related Myeloproliferative disease.
- Trp53 loss during in vitro selection contributes to acquired Ara-C resistance in Acute myeloid leukemia.
- Haploinsufficiency of Runx1/AML1 promotes Myeloid features and leukaemogenesis in BXH2 mice.
- Dual treatment with FLT3 inhibitor SU11657 and doxorubicin increases survival of leukemic mice.
- Survival and tumorigenesis in O6-methylguanine DNA methyltransferase-deficient mice following cyclophosphamide exposure.
- Response and resistance to MEK inhibition in leukaemias initiated by hyperactive Ras.
Schools
University of California At San Francisco
University Ca Sf School Of Med
Conditions Treated
- Acute Leukemia
- Anemia
- Antiphospholipid Syndrome (APS)
- Chronic Myeloid Leukemia (CML)
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Doctors Specialties
- Hematology
- Hematopathology
- Pathology
Accepted Insurances
Education
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UCSF -
University of California San Francisco School of Medicine
Hospital
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San Francisco General Hospital and Trauma Center -
UCSF Medical Center
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1932141884 |
| Last Name Of The Provider | KOGAN |
| First Name Of The Provider | SCOTT |
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