Yogen Saunthararajah

Summary

Affiliation: Cleveland Clinic Foundation
Country: USA

Publications

  1. pmc High cytidine deaminase expression in the liver provides sanctuary for cancer cells from decitabine treatment effects
    Quteba Ebrahem
    Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA
    Oncotarget 3:1137-45. 2012
  2. pmc CpG methylation patterns and decitabine treatment response in acute myeloid leukemia cells and normal hematopoietic precursors
    S Negrotto
    Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Leukemia 26:244-54. 2012
  3. pmc p53-Independent, normal stem cell sparing epigenetic differentiation therapy for myeloid and other malignancies
    Yogen Saunthararajah
    Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Semin Oncol 39:97-108. 2012
  4. pmc S110, a novel decitabine dinucleotide, increases fetal hemoglobin levels in baboons (P. anubis)
    Donald Lavelle
    Department of Medicine, University of Illinois at Chicago, 840 S, Wood St, Chicago, Illinois 60612 7323, USA
    J Transl Med 8:92. 2010
  5. pmc Epigenetic regulation by decitabine of melanoma differentiation in vitro and in vivo
    Oscar Alcazar
    Taussig Cancer Institute, Cleveland Clinic Foundation, Cleveland, OH, USA
    Int J Cancer 131:18-29. 2012
  6. doi request reprint Ribosomal S6 kinase and AKT phosphorylation as pharmacodynamic biomarkers in patients with myelodysplastic syndrome treated with RAD001
    Anjali S Advani
    Department of Hematologic Oncology and Blood Disorders, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH Electronic address
    Clin Lymphoma Myeloma Leuk 14:172-177.e1. 2014
  7. pmc Increased CDA expression/activity in males contributes to decreased cytidine analog half-life and likely contributes to worse outcomes with 5-azacytidine or decitabine therapy
    Reda Z Mahfouz
    Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Clin Cancer Res 19:938-48. 2013
  8. pmc Noncytotoxic differentiation treatment of renal cell cancer
    Soledad Negrotto
    Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, Ohio, USA
    Cancer Res 71:1431-41. 2011
  9. pmc Decitabine maintains hematopoietic precursor self-renewal by preventing repression of stem cell genes by a differentiation-inducing stimulus
    Zhenbo Hu
    Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA
    Mol Cancer Ther 9:1536-43. 2010
  10. doi request reprint Expression of phosphorylated signal transducer and activator of transcription 5 is associated with an increased risk of death in acute myeloid leukemia
    Anna Brady
    Hematologic Oncology and Blood Disorders, Cleveland Clinic Taussig Cancer Institute, Cleveland, OH 44195, USA
    Eur J Haematol 89:288-93. 2012

Collaborators

Detail Information

Publications26

  1. pmc High cytidine deaminase expression in the liver provides sanctuary for cancer cells from decitabine treatment effects
    Quteba Ebrahem
    Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA
    Oncotarget 3:1137-45. 2012
    ..This protection can be reversed without increasing myelotoxicity by combining tetrahydrouridine with a lower dose of decitabine...
  2. pmc CpG methylation patterns and decitabine treatment response in acute myeloid leukemia cells and normal hematopoietic precursors
    S Negrotto
    Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Leukemia 26:244-54. 2012
    ....
  3. pmc p53-Independent, normal stem cell sparing epigenetic differentiation therapy for myeloid and other malignancies
    Yogen Saunthararajah
    Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Semin Oncol 39:97-108. 2012
    ..Decitabine or 5-azacytidine dose and schedule can be rationalized to emphasize this mechanism of action, as an alternative or complement to conventional apoptosis-based oncotherapy...
  4. pmc S110, a novel decitabine dinucleotide, increases fetal hemoglobin levels in baboons (P. anubis)
    Donald Lavelle
    Department of Medicine, University of Illinois at Chicago, 840 S, Wood St, Chicago, Illinois 60612 7323, USA
    J Transl Med 8:92. 2010
    ..In these experiments the effect of S110 on HbF levels in baboons and its ability to reduce DNA methylation of the γ-globin gene promoter in vivo were evaluated...
  5. pmc Epigenetic regulation by decitabine of melanoma differentiation in vitro and in vivo
    Oscar Alcazar
    Taussig Cancer Institute, Cleveland Clinic Foundation, Cleveland, OH, USA
    Int J Cancer 131:18-29. 2012
    ..Modification of decitabine dose, schedule and formulation for differentiation rather than cytotoxic objectives inhibits the growth of melanoma cells in vitro and in vivo...
  6. doi request reprint Ribosomal S6 kinase and AKT phosphorylation as pharmacodynamic biomarkers in patients with myelodysplastic syndrome treated with RAD001
    Anjali S Advani
    Department of Hematologic Oncology and Blood Disorders, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH Electronic address
    Clin Lymphoma Myeloma Leuk 14:172-177.e1. 2014
    ....
  7. pmc Increased CDA expression/activity in males contributes to decreased cytidine analog half-life and likely contributes to worse outcomes with 5-azacytidine or decitabine therapy
    Reda Z Mahfouz
    Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH 44195, USA
    Clin Cancer Res 19:938-48. 2013
    ..Hence, genetic factors that decrease the half-lives of these drugs could impact efficacy. Documentation of such impact, and elucidation of underlying mechanisms, could lead to improved clinical application...
  8. pmc Noncytotoxic differentiation treatment of renal cell cancer
    Soledad Negrotto
    Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, Ohio, USA
    Cancer Res 71:1431-41. 2011
    ..The distinctive mechanism of action of a dose and schedule of DAC designed for noncytotoxic depletion of DNMT1 suggests a potential role in treating RCC...
  9. pmc Decitabine maintains hematopoietic precursor self-renewal by preventing repression of stem cell genes by a differentiation-inducing stimulus
    Zhenbo Hu
    Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA
    Mol Cancer Ther 9:1536-43. 2010
    ..Using decitabine to deplete DNMT1 after this early repression phase does not impair progressive differentiation...
  10. doi request reprint Expression of phosphorylated signal transducer and activator of transcription 5 is associated with an increased risk of death in acute myeloid leukemia
    Anna Brady
    Hematologic Oncology and Blood Disorders, Cleveland Clinic Taussig Cancer Institute, Cleveland, OH 44195, USA
    Eur J Haematol 89:288-93. 2012
    ..Constitutive activation of STAT5 (by phosphorylation) has been identified in a number of malignancies, including acute myeloid leukemia (AML)...
  11. doi request reprint Race and intensity of post-remission therapy in acute myeloid leukemia
    Anna K Brady
    Department of Hematologic Oncology and Blood Disorders, Cleveland Clinic Taussig Cancer Institute, Cleveland, OH, USA
    Leuk Res 35:346-50. 2011
    ..In many cancers, including AML, blacks have poorer overall survival. We investigated whether differences in post-remission therapy (PRT) were a contributing factor...
  12. ncbi request reprint Differential effects of low-dose decitabine on immune effector and suppressor responses in melanoma-bearing mice
    Pierre L Triozzi
    Taussig Cancer Institute, R40, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA
    Cancer Immunol Immunother 61:1441-50. 2012
    ..Effects on host immune effector and suppressor responses have not been well characterized...
  13. ncbi request reprint Monosomy 3 by FISH in uveal melanoma: variability in techniques and results
    Mary Aronow
    Cole Eye Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA
    Surv Ophthalmol 57:463-73. 2012
    ..FISH is a widely available, versatile technology, and when performed optimally has the potential to be a valuable tool for determining the prognosis of uveal melanoma...
  14. ncbi request reprint Key clinical observations after 5-azacytidine and decitabine treatment of myelodysplastic syndromes suggest practical solutions for better outcomes
    Yogen Saunthararajah
    1Hematologic Malignancies and Blood Disorders, Cleveland Clinic, Cleveland, OH and
    Hematology Am Soc Hematol Educ Program 2013:511-21. 2013
    ....
  15. doi request reprint A phase 2 trial of combination therapy with thalidomide, arsenic trioxide, dexamethasone, and ascorbic acid (TADA) in patients with overlap myelodysplastic/myeloproliferative neoplasms (MDS/MPN) or primary myelofibrosis (PMF)
    Nelli Bejanyan
    Leukemia Program, Department of Hematologic Oncology and Blood Disorders, Cleveland Clinic Taussig Cancer Institute, Cleveland, Ohio, USA
    Cancer 118:3968-76. 2012
    ..In this phase 2 study, the authors combined multiple active agents (thalidomide, arsenic trioxide, dexamethasone, and ascorbic acid [TADA]) to treat patients with these disorders...
  16. ncbi request reprint Chromosome 3 status in uveal melanoma: a comparison of fluorescence in situ hybridization and single-nucleotide polymorphism array
    Arun D Singh
    Department of Ophthalmic Oncology, Cole Eye Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA
    Invest Ophthalmol Vis Sci 53:3331-9. 2012
    ..To compare fluorescence in situ hybridization (FISH) using a centromeric probe for chromosome 3 (CEP3) and 3p26 locus-specific probe with single-nucleotide polymorphism array (SNP-A) analysis in the detection of high-risk uveal melanoma...
  17. pmc AML cells are differentially sensitive to chemotherapy treatment in a human xenograft model
    Mark Wunderlich
    Division of Experimental Hematology, University of Cincinnati College of Medicine, Cincinnati, OH, USA
    Blood 121:e90-7. 2013
    ..Overall, the data show that this model system is useful for the evaluation of novel chemotherapies in combination with standard induction therapy...
  18. pmc Aberrant DNA methylation is a dominant mechanism in MDS progression to AML
    Ying Jiang
    Experimental Hematology and Hematopoiesis Section, Taussig Cancer Center, Cleveland Clinic, OH 44195, USA
    Blood 113:1315-25. 2009
    ..However, the ubiquity, extent, and correlation with disease progression suggest that aberrant DNA methylation is the dominant mechanism for TSG silencing and clonal variation in MDS evolution to AML...
  19. pmc RUNX1 regulates corepressor interactions of PU.1
    Zhenbo Hu
    Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA
    Blood 117:6498-508. 2011
    ..1 and mutated or translocated RUNX1. RUNX1 deficiency is associated with persistent corepressor interaction with PU.1. Thus, inhibiting HDAC can partly compensate for the functional consequences of RUNX1 deficiency...
  20. doi request reprint A Phase 1 study of imatinib mesylate in combination with cytarabine and daunorubicin for c-kit positive relapsed acute myeloid leukemia
    Anjali S Advani
    Department of Hematologic Oncology and Blood Disorders, Cleveland Clinic, Taussig Cancer Institute, Cleveland, OH 44195, USA
    Leuk Res 34:1622-6. 2010
    ..The maximum tolerated dose of IM was 300 mg. The dose-limiting toxicity was Grade 3-4 hepatic toxicity. The CR/CRp rate was 57%. Cytotoxic therapy that includes IM for relapsed AML is well-tolerated and effective...
  21. pmc Sex differences in the incidence of chronic myeloid leukemia
    Tomas Radivoyevitch
    Department of Epidemiology and Biostatistics, School of Medicine, Case Western Reserve University, Cleveland, OH, 44106, USA
    Radiat Environ Biophys 53:55-63. 2014
    ..Comprehensive mathematical models of CML could lead to a better understanding of the role of HSCs in CML and other preleukemias that can progress to acute leukemia...
  22. ncbi request reprint Risk for developing myelodysplastic syndromes in prostate cancer patients definitively treated with radiation
    Sudipto Mukherjee
    Affiliations of authors Leukemia Program SM, RVT, AAA, YS, KP, SH, JPM, BJB, MK, MAS, Department of Radiation Oncology CAR, JPC, MA W, and Department of Solid Tumor Oncology RD, Cleveland Clinic Taussig Cancer Institute, Cleveland, OH Levine Cancer Institute, Carolinas HealthCare System, Charlotte, NC EC Glickman Urological and Kidney Institute, Cleveland Clinic, Cleveland, OH EAK
    J Natl Cancer Inst 106:djt462. 2014
    ..Exposure to ionizing radiation has been linked to myelodysplastic syndromes (MDS); it is not clear whether therapeutic radiation doses used for prostate cancer pose an increased MDS risk...
  23. pmc SF3B1 haploinsufficiency leads to formation of ring sideroblasts in myelodysplastic syndromes
    Valeria Visconte
    Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, OH, USA
    Blood 120:3173-86. 2012
    ..In conclusion, we report the first experimental evidence of the association between SF3B1 and RS phenotype. Our data suggest that SF3B1 haploinsufficiency leads to RS formation...
  24. doi request reprint Circulating tumor cells in uveal melanoma
    Virginia Torres
    Taussig Cancer Institute, Cleveland Clinic Foundation, Ohio, USA
    Future Oncol 7:101-9. 2011
    ..However, more research on the biology of uveal melanoma as well as improvements upon the current technologies are needed...
  25. pmc Somatic SETBP1 mutations in myeloid malignancies
    Hideki Makishima
    Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, Ohio, USA
    Nat Genet 45:942-6. 2013
    ..Somatic mutations of SETBP1 seem to cause gain of function, are associated with myeloid leukemic transformation and convey poor prognosis in myelodysplastic syndromes (MDS) and CMML. ..