Harvard Catalyst Profiles

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Shideh Kazerounian, Ph.D.


I am an instructor in the Department of Medicine at BWH. My focus is on the role of tumor-associated fibroblasts and fibroblast-like synoviocytes in mediating the signaling pathways involved in inflammation in cancer and RA. I will also work on patient-derived organoids as a platform for RA target validation.

As a senior postdoctoral fellow and an Instructor in Dr. Hanna Gazda’s laboratory in the Division of Genetics and Genomics, Boston Children’s Hospital, my focus was on the effect of ribosomal protein mutations on the development of soft tissue sarcoma. We identified three cases of soft tissue sarcomas in our mouse model of DBA (Kazerounian et al, 2016, Journal of Cancer), which allowed me to study the underlying mechanism for cancer development in patients with DBA. My research interests also included identifying the genetic causes and molecular pathogenesis of Diamond-Blackfan anemia (DBA) with a goal to identify new targets for developing new therapies.

My Ph.D. project was focused on investigating the molecular mechanism of Paraneoplastic Pemphigus autoimmune disease. I demonstrated that sera from patients with Paraneoplastic Pemphigus contained antibodies against linker regions of periplakin and envoplakin. In continuation of my studies, I also identified a new nuclear protein, periphilin, which interacted with periplakin linker region in keratinocytes. Recent studies have shown that periphilin also has a role in developing Parkinson's disease.

During my postdoctoral training, I demonstrated that spleen tyrosine kinase (Syk) was important for enhancing the VEGFR-2 signaling pathways by up-regulating the phosphorylation of Y-1175 in a positive feed-back loop. This work led to the novel discovery of the cross-talk between the thrombospondin-1 (TSP-1) anti-angiogenic and the VEGF-A pro-angiogenic signaling pathways through Syk. These findings also developed new insights into the complexity of the mechanism of angiogenic switch and suggested the possible role of Syk as a mediator of tumor progression.

My future goal is to establish an interdisciplinary collaboration with investigators in academia and industry to optimize novel therapeutic approaches for cancer immunotherapy.

I am open to start new collaborations with investigators in the field of signal transduction pathway and cancer biology.
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Funded by the NIH National Center for Advancing Translational Sciences through its Clinical and Translational Science Awards Program, grant number UL1TR002541.