W Michael Kuehl

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint Multiple myeloma: evolving genetic events and host interactions
    W Michael Kuehl
    Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda Naval Hospital, Maryland 20889 5105, USA
    Nat Rev Cancer 2:175-87. 2002
  2. doi request reprint Modeling multiple myeloma by AID-dependent conditional activation of MYC
    W Michael Kuehl
    Genetics Branch, National Cancer Institute, Bethesda, MD 20889, USA
    Cancer Cell 13:85-7. 2008
  3. pmc Classical and/or alternative NF-kappaB pathway activation in multiple myeloma
    Yulia N Demchenko
    Genetics Branch, National Cancer Institute, Bethesda, MD, USA
    Blood 115:3541-52. 2010
  4. pmc A mechanistic rationale for MEK inhibitor therapy in myeloma based on blockade of MAF oncogene expression
    Christina M Annunziata
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, 10 Center Dr, Bethesda, MD 20892 1374, USA
    Blood 117:2396-404. 2011
  5. pmc Molecular pathogenesis of multiple myeloma and its premalignant precursor
    W Michael Kuehl
    Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA
    J Clin Invest 122:3456-63. 2012
  6. pmc A der(8)t(8;11) chromosome in the Karpas-620 myeloma cell line expresses only cyclin D1: yet both cyclin D1 and MYC are repositioned in close proximity to the 3'IGH enhancer
    Amel Dib
    Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20889 5101, USA
    DNA Repair (Amst) 8:330-5. 2009
  7. pmc Secondary genomic rearrangements involving immunoglobulin or MYC loci show similar prevalences in hyperdiploid and nonhyperdiploid myeloma tumors
    Ana Gabrea
    Genetics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA
    Genes Chromosomes Cancer 47:573-90. 2008
  8. pmc Frequent engagement of the classical and alternative NF-kappaB pathways by diverse genetic abnormalities in multiple myeloma
    Christina M Annunziata
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
    Cancer Cell 12:115-30. 2007
  9. pmc Pathogenesis of monoclonal gammopathy of undetermined significance and progression to multiple myeloma
    Adriana Zingone
    Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20889 5105, USA
    Semin Hematol 48:4-12. 2011
  10. doi request reprint Molecular and biologic markers of progression in monoclonal gammopathy of undetermined significance to multiple myeloma
    Sham Mailankody
    Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Leuk Lymphoma 51:2159-70. 2010

Collaborators

Detail Information

Publications21

  1. ncbi request reprint Multiple myeloma: evolving genetic events and host interactions
    W Michael Kuehl
    Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda Naval Hospital, Maryland 20889 5105, USA
    Nat Rev Cancer 2:175-87. 2002
    ..What causes full-blown myeloma? And can our molecular understanding of this common haematological malignancy be used to develop effective preventive and treatment strategies?..
  2. doi request reprint Modeling multiple myeloma by AID-dependent conditional activation of MYC
    W Michael Kuehl
    Genetics Branch, National Cancer Institute, Bethesda, MD 20889, USA
    Cancer Cell 13:85-7. 2008
    ..Although much remains to be done to fully characterize this model, this approach is likely to impact the creation of sporadic models for other kinds of germinal center B cell tumors...
  3. pmc Classical and/or alternative NF-kappaB pathway activation in multiple myeloma
    Yulia N Demchenko
    Genetics Branch, National Cancer Institute, Bethesda, MD, USA
    Blood 115:3541-52. 2010
    ..Our results suggest that MM tumors can achieve increased autonomy from the bone marrow microenvironment by mutations that activate either NF-kappaB pathway...
  4. pmc A mechanistic rationale for MEK inhibitor therapy in myeloma based on blockade of MAF oncogene expression
    Christina M Annunziata
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, 10 Center Dr, Bethesda, MD 20892 1374, USA
    Blood 117:2396-404. 2011
    ..The data presented herein demonstrate that the MEK-ERK pathway regulates MAF transcription, providing molecular rationale for clinical evaluation of MEK inhibitors in MAF-expressing myeloma...
  5. pmc Molecular pathogenesis of multiple myeloma and its premalignant precursor
    W Michael Kuehl
    Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA
    J Clin Invest 122:3456-63. 2012
    ..Here we review the current understanding of myeloma pathogenesis and insight into new therapeutic strategies provided by animal models and genetic screens...
  6. pmc A der(8)t(8;11) chromosome in the Karpas-620 myeloma cell line expresses only cyclin D1: yet both cyclin D1 and MYC are repositioned in close proximity to the 3'IGH enhancer
    Amel Dib
    Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20889 5101, USA
    DNA Repair (Amst) 8:330-5. 2009
    ..The secondary translocation that dysregulated MYC resulted in extensive regions from both donor chromosomes being transmitted to both derivative chromosomes, suggesting a defect in DNA recombination or repair in the myeloma tumor cell...
  7. pmc Secondary genomic rearrangements involving immunoglobulin or MYC loci show similar prevalences in hyperdiploid and nonhyperdiploid myeloma tumors
    Ana Gabrea
    Genetics Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA
    Genes Chromosomes Cancer 47:573-90. 2008
    ..We conclude that IG light chain and MYC rearrangements, as well as secondary IGH rearrangements, make similar contributions to the progression of both HRD and NHRD MM tumors...
  8. pmc Frequent engagement of the classical and alternative NF-kappaB pathways by diverse genetic abnormalities in multiple myeloma
    Christina M Annunziata
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
    Cancer Cell 12:115-30. 2007
    ..These data demonstrate that addiction to the NF-kappaB pathway is frequent in myeloma and suggest that IKKbeta inhibitors hold promise for the treatment of this disease...
  9. pmc Pathogenesis of monoclonal gammopathy of undetermined significance and progression to multiple myeloma
    Adriana Zingone
    Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20889 5105, USA
    Semin Hematol 48:4-12. 2011
    ..However, two models based on clinical laboratory tests indicate that it is possible to stratify MGUS tumors into groups that have average rates of progression as low as 0.26% per year and as high as 12% per year...
  10. doi request reprint Molecular and biologic markers of progression in monoclonal gammopathy of undetermined significance to multiple myeloma
    Sham Mailankody
    Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Leuk Lymphoma 51:2159-70. 2010
    ..A better understanding of the pathogenesis will allow us to define the biological high-risk precursor disease and, ultimately, to develop early intervention strategies designed to delay and prevent full-blown MM...
  11. pmc A critical role for the NFkB pathway in multiple myeloma
    Yulia N Demchenko
    Genetics Branch, National Cancer Institute, Bethesda, MD, USA
    Oncotarget 1:59-68. 2010
    ..Given the strong dependence of MGUS and MM tumors on NFkB pathway activation, inhibition by a combination of targeting extrinsic signaling plus both NFkB pathways appears to be an attractive therapeutic approach in MM tumors...
  12. ncbi request reprint Overexpression of c-maf is a frequent oncogenic event in multiple myeloma that promotes proliferation and pathological interactions with bone marrow stroma
    Elaine M Hurt
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Cancer Cell 5:191-9. 2004
    ..The frequent overexpression of c-maf in myeloma makes it an attractive target for therapeutic intervention...
  13. pmc Aberrant immunoglobulin class switch recombination and switch translocations in activated B cell-like diffuse large B cell lymphoma
    Georg Lenz
    Metabolism Branch, Division of Cancer Treatment and Diagnosis, National Cancer Institute NCI, National Institutes of Health NIH, Bethesda, MD 20892, USA
    J Exp Med 204:633-43. 2007
    ..Accordingly, aberrant switch recombination was responsible for translocations in ABC DLBCLs involving BCL6, MYC, and a novel translocation partner, SPIB...
  14. ncbi request reprint Critical roles for immunoglobulin translocations and cyclin D dysregulation in multiple myeloma
    P Leif Bergsagel
    Weill Medical College of Cornell University, New York, NY 10021, USA
    Immunol Rev 194:96-104. 2003
    ..We speculate that ectopic cyclin D1 expression without t(11;14) is dependent on tumor-specific interaction with bone marrow stromal cells...
  15. ncbi request reprint Genetics and cytogenetics of multiple myeloma: a workshop report
    Rafael Fonseca
    Division of Hematology, Mayo Clinic, Rochester, Minnesota, USA
    Cancer Res 64:1546-58. 2004
    ..Areas in need of further study were identified. The study of the genetic aberrations will likely form the platform for targeted therapy for the disease...
  16. ncbi request reprint Waldenström macroglobulinemia neoplastic cells lack immunoglobulin heavy chain locus translocations but have frequent 6q deletions
    Roelandt F J Schop
    Department of Hematology and Internal Medicine and the Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN 55905, USA
    Blood 100:2996-3001. 2002
    ..However, WM tumor cells, which appear to be diploid or near diploid, often have deletions of 6q21...
  17. ncbi request reprint Molecular pathogenesis and a consequent classification of multiple myeloma
    P Leif Bergsagel
    Comprehensive Cancer Center, Division of Hematology Oncology, Mayo Clinic, Scottsdale, AZ 85259, USA
    J Clin Oncol 23:6333-8. 2005
    ....
  18. ncbi request reprint Advances in biology of multiple myeloma: clinical applications
    Teru Hideshima
    Jerome Lipper Multiple Myeloma Center, Department of Medical Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA
    Blood 104:607-18. 2004
    ....
  19. pmc CKS1B, overexpressed in aggressive disease, regulates multiple myeloma growth and survival through SKP2- and p27Kip1-dependent and -independent mechanisms
    Fenghuang Zhan
    Donna D and Donald M Lambert Laboratory of Myeloma Genetics at the Myeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, 4301 W Markham Street, Little Rock, AR 72205, USA
    Blood 109:4995-5001. 2007
    ....
  20. pmc Cyclin D dysregulation: an early and unifying pathogenic event in multiple myeloma
    P Leif Bergsagel
    Mayo Clinic Scottsdale, Comprehensive Cancer Center and Division of Hematology Oncology, Scottsdale, AZ, USA
    Blood 106:296-303. 2005
    ..However, despite subsequent progression events, these groups have differing gene expression profiles and also significant differences in the prevalence of bone disease, frequency at relapse, and progression to extramedullary tumor...
  21. ncbi request reprint The enigma of ectopic expression of FGFR3 in multiple myeloma: a critical initiating event or just a target for mutational activation during tumor progression
    Marta Chesi
    Weill Medical College of Cornell University, New York, USA
    Curr Opin Hematol 9:288-93. 2002
    ..However, it remains to be proven if and how dysregulation of FGFR3 or MMSET mediates an early oncogenic process in multiple myeloma...