1. Results of phase 2 randomized study of low-dose decitabine with or without valproic acid in patients with myelodysplastic syndrome and acute myelogenous leukemia.

    Cancer 121(4):556 (2015) PMID 25336333

    Hypomethylating agents have demonstrated activity in patients with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Preclinical and single-arm trials have suggested that adding histone deacetylase (HDAC) inhibitors may synergize the epigenetic modulation of hypomethylating agents...
  2. Results of phase 2 randomized study of low-dose decitabine with or without valproic acid in patients with myelodysplastic syndrome and acute myelogenous leukemia.

    Cancer 121(4):556 (2015) PMID 25336333

    Hypomethylating agents have demonstrated activity in patients with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Preclinical and single-arm trials have suggested that adding histone deacetylase (HDAC) inhibitors may synergize the epigenetic modulation of hypomethylating agents...
  3. Results of phase 2 randomized study of low-dose decitabine with or without valproic acid in patients with myelodysplastic syndrome and acute myelogenous leukemia.

    Cancer 121(4):556 (2015) PMID 25336333

    Hypomethylating agents have demonstrated activity in patients with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Preclinical and single-arm trials have suggested that adding histone deacetylase (HDAC) inhibitors may synergize the epigenetic modulation of hypomethylating agents...
  4. Results of phase 2 randomized study of low-dose decitabine with or without valproic acid in patients with myelodysplastic syndrome and acute myelogenous leukemia.

    Cancer 121(4):556 (2015) PMID 25336333 PMCID PMC4320000

    Hypomethylating agents have demonstrated activity in patients with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Preclinical and single-arm trials have suggested that adding histone deacetylase (HDAC) inhibitors may synergize the epigenetic modulation of hypomethylating agents...
  5. A phase 1 clinical trial of vorinostat in combination with decitabine in patients with acute myeloid leukaemia or myelodysplastic syndrome.

    British Journal of Haematology 167(2):185 (2014) PMID 25040094

    Patients with acute myeloid leukaemia (AML) or myelodysplastic syndrome (MDS) may respond to treatment with epigenetic-modifying agents. Histone deacetylase inhibitors may synergize with hypomethylating agents. This phase 1 dose-escalation study was designed to determine the maximum tolerated do...
  6. A recombinant reporter system for monitoring reactivation of an endogenously DNA hypermethylated gene.

    Cancer Research 74(14):3834 (2014) PMID 24876104 PMCID PMC4103012

    Reversing abnormal gene silencing in cancer cells due to DNA hypermethylation of promoter CpG islands may offer new cancer prevention or therapeutic approaches. Moreover, such approaches may be broadly applicable to enhance the efficacy of radiotherapy, chemotherapy, or immunotherapy. Here, we d...
  7. A recombinant reporter system for monitoring reactivation of an endogenously DNA hypermethylated gene.

    Cancer Research 74(14):3834 (2014) PMID 24876104 PMCID PMC4103012

    Reversing abnormal gene silencing in cancer cells due to DNA hypermethylation of promoter CpG islands may offer new cancer prevention or therapeutic approaches. Moreover, such approaches may be broadly applicable to enhance the efficacy of radiotherapy, chemotherapy, or immunotherapy. Here, we d...
  8. A recombinant reporter system for monitoring reactivation of an endogenously DNA hypermethylated gene.

    Cancer Research 74(14):3834 (2014) PMID 24876104 PMCID PMC4103012

    Reversing abnormal gene silencing in cancer cells due to DNA hypermethylation of promoter CpG islands may offer new cancer prevention or therapeutic approaches. Moreover, such approaches may be broadly applicable to enhance the efficacy of radiotherapy, chemotherapy, or immunotherapy. Here, we d...
  9. Aging and epigenetic drift: a vicious cycle.

    Journal of Clinical Investigation 124(1):24 (2014) PMID 24382386 PMCID PMC3871228

    The term epigenetics refers to stable patterns of gene expression that are seen during differentiation or X chromosome inactivation and are not dependent on dynamic changes in coding DNA. These gene expression states are encoded in the epigenome - a collection of marks on DNA or on histone tails...
  10. Aging and epigenetic drift: a vicious cycle.

    Journal of Clinical Investigation 124(1):24 (2014) PMID 24382386 PMCID PMC3871228

    The term epigenetics refers to stable patterns of gene expression that are seen during differentiation or X chromosome inactivation and are not dependent on dynamic changes in coding DNA. These gene expression states are encoded in the epigenome - a collection of marks on DNA or on histone tails...
  11. Aging and epigenetic drift: a vicious cycle.

    Journal of Clinical Investigation 124(1):24 (2014) PMID 24382386 PMCID PMC3871228

    The term epigenetics refers to stable patterns of gene expression that are seen during differentiation or X chromosome inactivation and are not dependent on dynamic changes in coding DNA. These gene expression states are encoded in the epigenome - a collection of marks on DNA or on histone tails...
  12. Impact of decitabine on immunohistochemistry expression of the putative tumor suppressor genes FHIT, WWOX, FUS1 and PTEN in clinical tumor samples.

    Clinical Epigenetics 6(1):13 (2014) PMID 25024751 PMCID PMC4094901

    Since tumor suppressor gene function may be lost through hypermethylation, we assessed whether the demethylating agent decitabine could increase tumor suppressor gene expression clinically. For fragile histidine triad (FHIT), WW domain-containing oxidoreductase (WWOX), fused in sarcoma-1 (FUS1) ...
  13. Aging and epigenetic drift: a vicious cycle.

    Journal of Clinical Investigation 124(1):24 (2014) PMID 24382386 PMCID PMC3871228

    The term epigenetics refers to stable patterns of gene expression that are seen during differentiation or X chromosome inactivation and are not dependent on dynamic changes in coding DNA. These gene expression states are encoded in the epigenome - a collection of marks on DNA or on histone tails...
  14. Impact of decitabine on immunohistochemistry expression of the putative tumor suppressor genes FHIT, WWOX, FUS1 and PTEN in clinical tumor samples.

    Clinical Epigenetics 6(1):13 (2014) PMID 25024751 PMCID PMC4094901

    Since tumor suppressor gene function may be lost through hypermethylation, we assessed whether the demethylating agent decitabine could increase tumor suppressor gene expression clinically. For fragile histidine triad (FHIT), WW domain-containing oxidoreductase (WWOX), fused in sarcoma-1 (FUS1) ...
  15. Decitabine impact on the endocytosis regulator RhoA, the folate carriers RFC1 and FOLR1, and the glucose transporter GLUT4 in human tumors.

    Clinical Epigenetics 6(1):2 (2014) PMID 24401732 PMCID PMC3895853

    In 31 solid tumor patients treated with the demethylating agent decitabine, we performed tumor biopsies before and after the first cycle of decitabine and used immunohistochemistry (IHC) to assess whether decitabine increased expression of various membrane transporters. Resistance to chemotherap...
  16. Decitabine impact on the endocytosis regulator RhoA, the folate carriers RFC1 and FOLR1, and the glucose transporter GLUT4 in human tumors.

    Clinical Epigenetics 6(1):2 (2014) PMID 24401732 PMCID PMC3895853

    In 31 solid tumor patients treated with the demethylating agent decitabine, we performed tumor biopsies before and after the first cycle of decitabine and used immunohistochemistry (IHC) to assess whether decitabine increased expression of various membrane transporters. Resistance to chemotherap...
  17. β-Thalassemia due to intronic LINE-1 insertion in the β-globin gene (HBB): molecular mechanisms underlying reduced transcript levels of the β-globin(L1) allele.

    Human Mutation 34(10):1361 (2013) PMID 23878091

    We describe the molecular etiology of β(+)-thalassemia that is caused by the insertion of the full-length transposable element LINE-1 (L1) into the intron-2 of the β-globin gene (HBB). The transcript level of the affected β-globin gene was severely reduced. The remaining transcripts consisted of...
  18. A blueprint for an international cancer epigenome consortium. A report from the AACR Cancer Epigenome Task Force.

    Cancer Research 72(24):6319 (2012) PMID 23188507

  19. DNA methylation as a clinical marker in oncology.

    Journal of Clinical Oncology 30(20):2566 (2012) PMID 22564986

  20. DNA demethylation-dependent AR recruitment and GATA factors drive Rhox5 homeobox gene transcription in the epididymis.

    Molecular Endocrinology 26(4):538 (2012) PMID 22322598 PMCID PMC3327359

    Mammalian male fertility depends on the epididymis, a highly segmented organ that promotes sperm maturation and protects sperm from oxidative damage. Remarkably little is known about how gene expression is controlled in the epididymis. A candidate to regulate genes crucial for epididymal functio...