1. Erk Negative Feedback Control Enables Pre-B Cell Transformation and Represents a Therapeutic Target in Acute Lymphoblastic Leukemia.

    Cancer Cell 28(1):114 (2015) PMID 26073130

    Studying mechanisms of malignant transformation of human pre-B cells, we found that acute activation of oncogenes induced immediate cell death in the vast majority of cells. Few surviving pre-B cell clones had acquired permissiveness to oncogenic signaling by strong activation of negative feedba...
  2. drexplorer: A tool to explore dose-response relationships and drug-drug interactions.

    PMID 25600946 PMCID PMC4426846

    Nonlinear dose-response models are primary tools for estimating the potency [e.g. half-maximum inhibitory concentration (IC) known as IC50] of anti-cancer drugs. We present drexplorer software, which enables biologists to evaluate replicate reproducibility, detect outlier data points, fit differ...
  3. Development of a robust classifier for quality control of reverse-phase protein arrays.

    PMID 25380958 PMCID PMC4375399

    High-throughput reverse-phase protein array (RPPA) technology allows for the parallel measurement of protein expression levels in approximately 1000 samples. However, the many steps required in the complex protocol (sample lysate preparation, slide printing, hybridization, washing and amplified ...
  4. Loss of TRIM62 Expression Is an Independent Adverse Prognostic Factor in Acute Myeloid Leukemia.

    Clinical Lymphoma Myeloma and Leukemia 15(2):115 (2015) PMID 25248926

    Tripartite motif (TRIM)-62 is a putative tumor suppressor gene whose role in leukemia is unknown. We evaluated the effect of TRIM62 protein expression in patients with acute myeloid leukemia (AML). We used reverse-phase protein array methodology to determine TRIM62 levels in leukemia-enriched pr...
  5. Loss of TRIM62 Expression Is an Independent Adverse Prognostic Factor in Acute Myeloid Leukemia.

    Clinical Lymphoma Myeloma and Leukemia 15(2):115 (2015) PMID 25248926

    Tripartite motif (TRIM)-62 is a putative tumor suppressor gene whose role in leukemia is unknown. We evaluated the effect of TRIM62 protein expression in patients with acute myeloid leukemia (AML). We used reverse-phase protein array methodology to determine TRIM62 levels in leukemia-enriched pr...
  6. Loss of TRIM62 Expression Is an Independent Adverse Prognostic Factor in Acute Myeloid Leukemia.

    Clinical Lymphoma Myeloma and Leukemia 15(2):115 (2015) PMID 25248926

    Tripartite motif (TRIM)-62 is a putative tumor suppressor gene whose role in leukemia is unknown. We evaluated the effect of TRIM62 protein expression in patients with acute myeloid leukemia (AML). We used reverse-phase protein array methodology to determine TRIM62 levels in leukemia-enriched pr...
  7. The protein phosphatase 2A regulatory subunit B55α is a modulator of signaling and microRNA expression in acute myeloid leukemia cells.

    Biochimica et Biophysica Acta 1843(9):1969 (2014) PMID 24858343 PMCID PMC4165504

    We recently discovered that the protein phosphatase 2A (PP2A) B55α subunit (PPP2R2A) is under-expressed in primary blast cells and is unfavorable for remission duration in AML patients. In this study, reverse phase protein analysis (RPPA) of 230 proteins in 511 AML patient samples revealed a str...
  8. The protein phosphatase 2A regulatory subunit B55α is a modulator of signaling and microRNA expression in acute myeloid leukemia cells.

    Biochimica et Biophysica Acta 1843(9):1969 (2014) PMID 24858343 PMCID PMC4165504

    We recently discovered that the protein phosphatase 2A (PP2A) B55α subunit (PPP2R2A) is under-expressed in primary blast cells and is unfavorable for remission duration in AML patients. In this study, reverse phase protein analysis (RPPA) of 230 proteins in 511 AML patient samples revealed a str...
  9. VEGF/VEGFR-2 upregulates EZH2 expression in lung adenocarcinoma cells and EZH2 depletion enhances the response to platinum-based and VEGFR-2-targeted therapy.

    Clinical Cancer Research 20(14):3849 (2014) PMID 24850841 PMCID PMC4190586

    To investigate the mechanisms of regulation and role associated with enhancer of zeste homolog 2 (EZH2) expression in lung cancer cells. We investigated the mechanisms of EZH2 expression associated with the VEGF/VEGFR-2 pathway. Furthermore, we sought to determine the role of EZH2 in response of...
  10. VEGF/VEGFR-2 upregulates EZH2 expression in lung adenocarcinoma cells and EZH2 depletion enhances the response to platinum-based and VEGFR-2-targeted therapy.

    Clinical Cancer Research 20(14):3849 (2014) PMID 24850841 PMCID PMC4190586

    To investigate the mechanisms of regulation and role associated with enhancer of zeste homolog 2 (EZH2) expression in lung cancer cells. We investigated the mechanisms of EZH2 expression associated with the VEGF/VEGFR-2 pathway. Furthermore, we sought to determine the role of EZH2 in response of...
  11. Transcriptomic architecture of the adjacent airway field cancerization in non-small cell lung cancer.

    JNCI Journal of the National Cancer Institute 106(3):dju004 (2014) PMID 24563515 PMCID PMC3982778

    Earlier work identified specific tumor-promoting abnormalities that are shared between lung cancers and adjacent normal bronchial epithelia. We sought to characterize the yet unknown global molecular and adjacent airway field cancerization (FC) in early-stage non-small cell lung cancer (NSCLC). ...
  12. Transcriptomic architecture of the adjacent airway field cancerization in non-small cell lung cancer.

    JNCI Journal of the National Cancer Institute 106(3):dju004 (2014) PMID 24563515 PMCID PMC3982778

    Earlier work identified specific tumor-promoting abnormalities that are shared between lung cancers and adjacent normal bronchial epithelia. We sought to characterize the yet unknown global molecular and adjacent airway field cancerization (FC) in early-stage non-small cell lung cancer (NSCLC). ...
  13. Synergistic targeting of AML stem/progenitor cells with IAP antagonist birinapant and demethylating agents.

    JNCI Journal of the National Cancer Institute 106(2):djt440 (2014) PMID 24526787 PMCID PMC3952202

    Acute myeloid leukemia (AML) therapy has limited long-term efficacy because patients frequently develop disease relapse because of the inability of standard chemotherapeutic agents to target AML stem/progenitor cells. Here, we identify deregulated apoptotic components in AML stem/progenitor cell...
  14. Synergistic targeting of AML stem/progenitor cells with IAP antagonist birinapant and demethylating agents.

    JNCI Journal of the National Cancer Institute 106(2):djt440 (2014) PMID 24526787 PMCID PMC3952202

    Acute myeloid leukemia (AML) therapy has limited long-term efficacy because patients frequently develop disease relapse because of the inability of standard chemotherapeutic agents to target AML stem/progenitor cells. Here, we identify deregulated apoptotic components in AML stem/progenitor cell...
  15. Synergistic targeting of AML stem/progenitor cells with IAP antagonist birinapant and demethylating agents.

    JNCI Journal of the National Cancer Institute 106(2):djt440 (2014) PMID 24526787 PMCID PMC3952202

    Acute myeloid leukemia (AML) therapy has limited long-term efficacy because patients frequently develop disease relapse because of the inability of standard chemotherapeutic agents to target AML stem/progenitor cells. Here, we identify deregulated apoptotic components in AML stem/progenitor cell...
  16. Synergistic targeting of AML stem/progenitor cells with IAP antagonist birinapant and demethylating agents.

    JNCI Journal of the National Cancer Institute 106(2):djt440 (2014) PMID 24526787 PMCID PMC3952202

    Acute myeloid leukemia (AML) therapy has limited long-term efficacy because patients frequently develop disease relapse because of the inability of standard chemotherapeutic agents to target AML stem/progenitor cells. Here, we identify deregulated apoptotic components in AML stem/progenitor cell...
  17. Genes suppressed by DNA methylation in non-small cell lung cancer reveal the epigenetics of epithelial-mesenchymal transition.

    BMC Genomics 15:1079 (2014) PMID 25486910

    DNA methylation is associated with aberrant gene expression in cancer, and has been shown to correlate with therapeutic response and disease prognosis in some types of cancer. We sought to investigate the biological significance of DNA methylation in lung cancer. We integrated the gene expressio...
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  18. Genes suppressed by DNA methylation in non-small cell lung cancer reveal the epigenetics of epithelial-mesenchymal transition.

    BMC Genomics 15:1079 (2014) PMID 25486910 PMCID PMC4298954

    DNA methylation is associated with aberrant gene expression in cancer, and has been shown to correlate with therapeutic response and disease prognosis in some types of cancer. We sought to investigate the biological significance of DNA methylation in lung cancer. We integrated the gene expressio...
  19. Genes suppressed by DNA methylation in non-small cell lung cancer reveal the epigenetics of epithelial-mesenchymal transition.

    BMC Genomics 15:1079 (2014) PMID 25486910 PMCID PMC4298954

    DNA methylation is associated with aberrant gene expression in cancer, and has been shown to correlate with therapeutic response and disease prognosis in some types of cancer. We sought to investigate the biological significance of DNA methylation in lung cancer. We integrated the gene expressio...
  20. Genes suppressed by DNA methylation in non-small cell lung cancer reveal the epigenetics of epithelial-mesenchymal transition.

    BMC Genomics 15:1079 (2014) PMID 25486910

    DNA methylation is associated with aberrant gene expression in cancer, and has been shown to correlate with therapeutic response and disease prognosis in some types of cancer. We sought to investigate the biological significance of DNA methylation in lung cancer. We integrated the gene expressio...
    PDF not found