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TGFBeta inhibition in Prostate to Bone Metastasis
Tuesday 23rd July 2013, 4pm, Pearson Lecture Theatre
Bone metastasis is common in prostate cancer progression. In bone, prostate cancer cells derive factors necessary for progression by manipulating bone forming osteoblasts and bone resorbing osteoclasts, resulting in areas of excessive osteogenesis and osteolysis, respectively. Transforming growth factor beta (TGFBeta) is a key factor in the progression of bone metastases. Therapeutic inhibition of TGFBeta however, presents a dilemma since it can have differential effects on various cell types in the tumor-bone microenvironment. In the current study, we have utilized an integrated approach using mathematical and in vivo models to test the impact of TGFBeta inhibition on prostate to bone metastases. We developed an agent-based mathematical model where the interactions between key cell types and their role on the evolutionary dynamics of the tumor can be studied.
I used to be a particle physicist and then turned into a modeler of biological complexity at University College London’s brilliant CoMPLEX program. Finally I decided to focus on modeling aneuploidy in cancer for my PhD. I'm currently in my first Postdoc at Moffitt working with David Basanta and the Lynch Lab. We are modeling Prostate Bone Metastasis at the interphase between mathematics, biology and the clinic. We deal with complex systems and emergent behaviors because we find they have the potential to investigate counter intuitive ideas and results. I have artistic tendencies, which is a nice way of saying my logic is somewhat fuzzy. I also strive to find the fun side of things, as it helps maintain my balance while doing research into such a serious disease. I look forward to meeting and collaborating with all sorts of people, as I think we all have important things to contribute to the advancement of humanity, and that by working together we can really make a difference in the world.
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