Cancer progression requires mechanisms that sustain proliferative signaling, avoid growth control mechanisms, and evade immune surveillance. During my graduate work, I studied mechano-transduction pathways important for cancer development. As a postdoctoral fellow, I discovered cell types that coordinate stem cell proliferation and tissue repair in a cancer-resistant flatworm, Schmidtea mediterranea. I now want to study signaling mechanisms differentially regulated in planaria compared to humans in order to identify potential targets for therapeutic intervention.

The immediate goal of this proposal is to apply my background in stem cell biology and signal transduction mechanisms to understan...

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Cancer progression requires mechanisms that sustain proliferative signaling, avoid growth control mechanisms, and evade immune surveillance. During my graduate work, I studied mechano-transduction pathways important for cancer development. As a postdoctoral fellow, I discovered cell types that coordinate stem cell proliferation and tissue repair in a cancer-resistant flatworm, Schmidtea mediterranea. I now want to study signaling mechanisms differentially regulated in planaria compared to humans in order to identify potential targets for therapeutic intervention.

The immediate goal of this proposal is to apply my background in stem cell biology and signal transduction mechanisms to understand how Wnt-dependent gene regulatory networks and immune cell interactions with stem cells modulate cancer stem cell proliferation and immune clearance of solid tumors. During regeneration, planaria activate signaling pathways commonly associated with cancer. However, after genotoxic stress, Wnt-dependent signaling inhibits wound-induced stem cell proliferation.

In the first project, I will identify Wnt-dependent gene regulatory networks that inhibit stem cell expansion and determine if they can be exploited to inhibit Wnt-driven tumors like colorectal cancer. In the second project, I will study a subset of planarian macrophages activated after replicative stress and that share traits with tumor associated macrophages. I will identify molecules required for recognition of damaged stem cells and target them to improve immune infiltration of pancreatic cancer.

Baylor College of Medicine is an ideal place to establish my laboratory and develop the proposed projects. Collaborations within the Duncan Cancer Center and STaR Center will accelerate completion of my aims and catalyze future research. Long-term, this research will broaden our understanding of cancer stem cell proliferation, detection, and clearance and will open new avenues for treatment.

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