Esther Jane, PhD

Research Assistant Professor


Esther Jane

Contact

412-692-6580

Biography

Esther Jane, PhD, graduated from Madurai Kamaraj University in India. She did her post doctoral training in Case Western Reserve University in Cleveland, Ohio, on the molecular mechanisms underlying regulation of homeotic gene expression during Drosophila development.

Before joining the University of Pittsburgh Department of Neurological Surgery, she worked in the Pittsburgh Development Center in studying the cell biology of human embryonic stem cells before and after differentiation towards neuronal lineage.

Dr. Jane is currently working on a project examining compounds that inhibit the function of individual kinases using diverse panel of malignant glioma cell lines.

Specialized Areas of Interest

Mode of action of multi-target tyrosine kinase inhibitors in glioma cells.

Professional Organization Membership

American Association For Cancer Research

Education & Training

BSc, Zoology, Sarah Tucker College, 1983
MSc, Zoology, The American College, 1986
PhD, Biology, The Madurai Kamaraj University, 1992

Selected Publications

Jane EP, Premkumar DR, Cavaleri JM, Sutera PA, Rajasekar T, Pollack IF. Dinaciclib, a Cyclin-Dependent Kinase Inhibitor Promotes Proteasomal Degradation of Mcl-1 and Enhances ABT-737-Mediated Cell Death in Malignant Human Glioma Cell Lines. J Pharmacol Exp Ther 356(2):354-65, 2016.

Foster KA, Jane EP, Premkumar DR, Morales A, Pollack IF. NVP-BKM120 potentiates apoptosis in tumor necrosis factor-related apoptosis-inducing ligand-resistant glioma cell lines via upregulation of Noxa and death receptor 5. Int J Oncol 47(2):506-16, 2015.

Premkumar DR, Jane EP, Pollack IF. Cucurbitacin-I inhibits Aurora kinase A, Aurora kinase B and survivin, induces defects in cell cycle progression and promotes ABT-737-induced cell death in a caspase-independent manner in malignant human glioma cells. Cancer Biol Ther 16(2):233-43, 2015.

Foster KA, Jane EP, Premkumar DR, Morales A, Pollack IF. Co-administration of ABT-737 and SAHA induces apoptosis, mediated by Noxa upregulation, Bax activation and mitochondrial dysfunction in PTEN-intact malignant human glioma cell lines. J Neurooncol 120(3):459-72, 2014.

Jane EP, Premkumar DR, Morales A, Foster KA, Pollack IF. Inhibition of phosphatidylinositol 3-kinase/AKT signaling by NVP-BKM120 promotes ABT-737-induced toxicity in a caspase-dependent manner through mitochondrial dysfunction and DNA damage response in established and primary cultured glioblastoma cells. J Pharmacol Exp Ther 350(1):22-35, 2014.

Premkumar DR, Jane EP, Foster KA, Pollack IF. Survivin inhibitor YM-155 sensitizes tumor necrosis factor- related apoptosis-inducing ligand-resistant glioma cells to apoptosis through Mcl-1 downregulation and by engaging the mitochondrial death pathway. J Pharmacol Exp Ther 346(2):201-10, 2013.

Jane EP, Premkumar DR, DiDomenico JD, Hu B, Cheng SY, Pollack IF. YM-155 potentiates the effect of ABT-737 in malignant human glioma cells via survivin and Mcl-1 downregulation in an EGFR-dependent context. Mol Cancer Ther 12(3):326-38, 2013.

Premkumar DR, Jane EP, DiDomenico JD, Vukmer NA, Agostino NR, Pollack IF. ABT-737 synergizes with bortezomib to induce apoptosis, mediated by Bid cleavage, Bax activation, and mitochondrial dysfunction in an Akt-dependent context in malignant human glioma cell lines. J Pharmacol Exp Ther 341(3):859-72, 2012.

Premkumar DR, Jane EP, Agostino NR, DiDomenico JD, Pollack IF. Bortezomib-induced sensitization of malignant human glioma cells to vorinostat-induced apoptosis depends on reactive oxygen species production, mitochondrial dysfunction, Noxa upregulation, Mcl-1 cleavage, and DNA damage. Mol Carcinog 52(2):118-33, 2013.

Jane EP, Premkumar DR, Pollack IF. Bortezomib sensitizes malignant human glioma cells to TRAIL, mediated by inhibition of the NF-{kappa}B signaling pathway. Mol Cancer Ther 10(1):198-208, 2011.

A complete list of Dr. Jane's publications can be reviewed through the National Library of Medicine's publication database.

Research Activities

The prognosis for malignant glioma, the most common brain tumor, is still poor, underscoring the need to develop novel treatment strategies. Because glioma cells commonly exhibit genomic alterations involving genes that regulate cell-cycle control, there is a strong rationale for examining the potential efficacy of strategies to counteract this process. Researchers are examining the antiproliferative effects of the cyclin-dependent kinase inhibitor in malignant human glioma cell lines, with intact, deleted, or mutated p53 or phosphatase and tensin homolog on chromosome 10; intact or deleted or p14ARF or wild-type or amplified epidermal growth factor receptor.