1. TET2 Mutations Affect Non-CpG Island DNA Methylation at Enhancers and Transcription Factor-Binding Sites in Chronic Myelomonocytic Leukemia.

    Cancer Research 75(14):2833 (2015) PMID 25972343 PMCID PMC4506197

    TET2 enzymatically converts 5-methylcytosine to 5-hydroxymethylcytosine as well as other covalently modified cytosines and its mutations are common in myeloid leukemia. However, the exact mechanism and the extent to which TET2 mutations affect DNA methylation remain in question. Here, we report ...
  2. Phase I study of azacitidine and oxaliplatin in patients with advanced cancers that have relapsed or are refractory to any platinum therapy.

    Clinical Epigenetics 7(1):29 (2015) PMID 25806091 PMCID PMC4371799

    Demethylation process is necessary for the expression of various factors involved in chemotherapy cytotoxicity or resistance. Platinum-resistant cells may have reduced expression of the copper/platinum transporter CTR1. We hypothesized that azacitidine and oxaliplatin combination therapy may res...
  3. TET1 is a maintenance DNA demethylase that prevents methylation spreading in differentiated cells.

    Nucleic Acids Research 42(11):6956 (2014) PMID 24875481 PMCID PMC4066785

    TET1 is a 5-methylcytosine dioxygenase and its DNA demethylating activity has been implicated in pluripotency and reprogramming. However, the precise role of TET1 in DNA methylation regulation outside of developmental reprogramming is still unclear. Here, we show that overexpression of the TET1 ...
  4. TET1 is a maintenance DNA demethylase that prevents methylation spreading in differentiated cells.

    Nucleic Acids Research 42(11):6956 (2014) PMID 24875481 PMCID PMC4066785

    TET1 is a 5-methylcytosine dioxygenase and its DNA demethylating activity has been implicated in pluripotency and reprogramming. However, the precise role of TET1 in DNA methylation regulation outside of developmental reprogramming is still unclear. Here, we show that overexpression of the TET1 ...
  5. Age-related epigenetic drift in the pathogenesis of MDS and AML.

    Genome Research 24(4):580 (2014) PMID 24414704 PMCID PMC3975058

    The myelodysplastic syndrome (MDS) is a clonal hematologic disorder that frequently evolves to acute myeloid leukemia (AML). Its pathogenesis remains unclear, but mutations in epigenetic modifiers are common and the disease often responds to DNA methylation inhibitors. We analyzed DNA methylatio...
  6. Age-related epigenetic drift in the pathogenesis of MDS and AML.

    Genome Research 24(4):580 (2014) PMID 24414704 PMCID PMC3975058

    The myelodysplastic syndrome (MDS) is a clonal hematologic disorder that frequently evolves to acute myeloid leukemia (AML). Its pathogenesis remains unclear, but mutations in epigenetic modifiers are common and the disease often responds to DNA methylation inhibitors. We analyzed DNA methylatio...
  7. Epigenetic reprogramming of HOXC10 in endocrine-resistant breast cancer.

    Science Translational Medicine 6(229):229ra41 (2014) PMID 24670685 PMCID PMC4277862

    Resistance to aromatase inhibitors (AIs) is a major clinical problem in the treatment of estrogen receptor (ER)-positive breast cancer. In two breast cancer cell line models of AI resistance, we identified widespread DNA hyper- and hypomethylation, with enrichment for promoter hypermethylation o...
  8. Epigenetic reprogramming of HOXC10 in endocrine-resistant breast cancer.

    Science Translational Medicine 6(229):229ra41 (2014) PMID 24670685 PMCID PMC4277862

    Resistance to aromatase inhibitors (AIs) is a major clinical problem in the treatment of estrogen receptor (ER)-positive breast cancer. In two breast cancer cell line models of AI resistance, we identified widespread DNA hyper- and hypomethylation, with enrichment for promoter hypermethylation o...
  9. Epigenetic reprogramming of HOXC10 in endocrine-resistant breast cancer.

    Science Translational Medicine 6(229):229ra41 (2014) PMID 24670685 PMCID PMC4277862

    Resistance to aromatase inhibitors (AIs) is a major clinical problem in the treatment of estrogen receptor (ER)-positive breast cancer. In two breast cancer cell line models of AI resistance, we identified widespread DNA hyper- and hypomethylation, with enrichment for promoter hypermethylation o...
  10. Epigenetic reprogramming of HOXC10 in endocrine-resistant breast cancer.

    Science Translational Medicine 6(229):229ra41 (2014) PMID 24670685

    Resistance to aromatase inhibitors (AIs) is a major clinical problem in the treatment of estrogen receptor (ER)-positive breast cancer. In two breast cancer cell line models of AI resistance, we identified widespread DNA hyper- and hypomethylation, with enrichment for promoter hypermethylation o...
  11. Epigenetic reprogramming of HOXC10 in endocrine-resistant breast cancer.

    Science Translational Medicine 6(229):229ra41 (2014) PMID 24670685

    Resistance to aromatase inhibitors (AIs) is a major clinical problem in the treatment of estrogen receptor (ER)-positive breast cancer. In two breast cancer cell line models of AI resistance, we identified widespread DNA hyper- and hypomethylation, with enrichment for promoter hypermethylation o...
  12. Fusobacterium in colonic flora and molecular features of colorectal carcinoma.

    Cancer Research 74(5):1311 (2014) PMID 24385213

    Fusobacterium species are part of the gut microbiome in humans. Recent studies have identified overrepresentation of Fusobacterium in colorectal cancer tissues, but it is not yet clear whether this is pathogenic or simply an epiphenomenon. In this study, we evaluated the relationship between Fus...
  13. Fusobacterium in colonic flora and molecular features of colorectal carcinoma.

    Cancer Research 74(5):1311 (2014) PMID 24385213 PMCID PMC4396185

    Fusobacterium species are part of the gut microbiome in humans. Recent studies have identified overrepresentation of Fusobacterium in colorectal cancer tissues, but it is not yet clear whether this is pathogenic or simply an epiphenomenon. In this study, we evaluated the relationship between Fus...
  14. Colorectal carcinomas with CpG island methylator phenotype 1 frequently contain mutations in chromatin regulators.

    Gastroenterology 146(2):530 (2014) PMID 24211491 PMCID PMC3918446

    Subgroups of colorectal carcinomas (CRCs) characterized by DNA methylation anomalies are termed CpG island methylator phenotype (CIMP)1, CIMP2, or CIMP-negative. The pathogenesis of CIMP1 colorectal carcinomas, and their effects on patients' prognoses and responses to treatment, differ from thos...
  15. Colorectal carcinomas with CpG island methylator phenotype 1 frequently contain mutations in chromatin regulators.

    Gastroenterology 146(2):530 (2014) PMID 24211491 PMCID PMC3918446

    Subgroups of colorectal carcinomas (CRCs) characterized by DNA methylation anomalies are termed CpG island methylator phenotype (CIMP)1, CIMP2, or CIMP-negative. The pathogenesis of CIMP1 colorectal carcinomas, and their effects on patients' prognoses and responses to treatment, differ from thos...
  16. Colorectal Carcinomas With CpG Island Methylator Phenotype 1 Frequently Contain Mutations in Chromatin Regulators

    Gastroenterology 146(2):530 (2014)

    Background & Aims Subgroups of colorectal carcinomas (CRCs) characterized by DNA methylation anomalies are termed CpG island methylator phenotype (CIMP)1, CIMP2, or CIMP-negative. The pathogenesis of CIMP1 colorectal carcinomas, and their effects on patients' prognoses and re...
  17. Colorectal carcinomas with CpG island methylator phenotype 1 frequently contain mutations in chromatin regulators.

    Gastroenterology 146(2):530 (2014) PMID 24211491 PMCID PMC3918446

    Subgroups of colorectal carcinomas (CRCs) characterized by DNA methylation anomalies are termed CpG island methylator phenotype (CIMP)1, CIMP2, or CIMP-negative. The pathogenesis of CIMP1 colorectal carcinomas, and their effects on patients' prognoses and responses to treatment, differ from thos...
  18. TET1 is a maintenance DNA demethylase that prevents methylation spreading in differentiated cells.

    Nucleic Acids Research 42(11):6956 (2014) PMID 24875481 PMCID PMC4066785

    TET1 is a 5-methylcytosine dioxygenase and its DNA demethylating activity has been implicated in pluripotency and reprogramming. However, the precise role of TET1 in DNA methylation regulation outside of developmental reprogramming is still unclear. Here, we show that overexpression of the TET1 ...
  19. 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) ...
  20. 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) ...