We are interested in understanding mechanisms of tumor progression and metastasis in gynecological cancers. Emphasis is on  consequences of contextual alterations in signaling due to stress.

Major methodologies used include: Animal models of ovarian cancer metastasis, cell line and patient derived primary cellular strategies, transcriptomics ( RNA seq), kinome, proteomic approaches and therapeutic strategies ( antibody and small molecule)

Current Research Projects

Metastasis Projects

Late-stage ovarian cancer is marked by poor patient survival due to metastatic spread in the peritoneal cavity. Malignant ascites in the peritoneal cavity of ovarian cancer patients, harbor tumor cells that exhibit survival capabilities and adaptations to a variety of stress responses required for metastasis. Our ongoing efforts are focused on defining key signals that support stress adaptations, particularly hypoxia and anchorage independent survival during metastasis .

  1. Mechanism of cellular adaptation to anchorage independent survival and the role of Sox2 and Sox2 targets in anoikis resistance in ovarian cancer ( NIH R01CA230628)
  2. Mechanisms of tumor angiogenesis in advanced ovarian cancers: Role of Inhibins, activins and hypoxia driven pathways in advanced ovarian cancer (NIH R01CA219495)

Regulation of ligand availability and receptor biology projects

These projects utilize a combination of biochemical and molecular tools  to address the overarching question of how cells fine tune response to ligands. Emphasis is on post-translational modifications of receptors and the impact on receptor-ligand interactions. (NIH R01CA219495)

  1. Role of part time proteoglycans such as betaglycan in modulating signaling and cancer.
  2. Impact of Endoglin/CD105 in signaling and angiogenesis.
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