Bo R. Rueda, Ph.D.

       
Associate Director, Vincent Center for Reproductive Biology, Massachusetts 
	General Hospital
Director, Clinical Fellows Research Program, Vincent Obstetrics & Gyncology 
	Service,	Massachusetts General Hospital 
Associate Professor, Dept. of Obstetrics, Gynecology & Reproductive Biology, 
	Harvard,	Harvard Medical School
Affiliated Faculty, Harvard Stem Cell Institute


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Brief Overview of Rueda Lab Research 

Identification and functional characterization of gynecologic cancer stem cells.
Recent experiments conducted by our group in collaboration with Drs. Rosemary Foster and Dr. David Scadden (Harvard Stem Cell Institute) provide evidence to support the concept that both human endometrial and ovarian cancers contain a rare subpopulation of tumor-initiating cells, which have stem/progenitor like properties. We are actively optimizing strategies to better isolate these rare cells, define their stem like properties, determine how they are regulated, how their local environment may influence them, whether they are resistant to current radiation or chemotherapy and ultimately how we may target them.

Molecular interrogation of gynecologic tumors.
In collaboration with Drs. Darrell Borger and A. John Iafrate of the Translational Research Laboratory (MGH Cancer Center), we have been actively developing strategies for real-time identification of novel cell signaling pathways that contribute to malignant transformation, the pathology of the disease and/or chemoresistance and recurrence in gynecologic cancers. Once identified, we are actively testing new biologics and determining their efficacy in primary ovarian and/or endometrial tumor explant models and in short-term patient cell cultures derived from primary ovarian and/or endometrial tumors.

Delineating the contribution of novel genomic mutations to the pathology of gynecologic cancers.
We are currently conducting array CGH analysis of a large cohort of endometrial and ovarian gynecologic cancer samples with annotated clinical information in an attempt to detect novel mediators of malignant transformation and tumor growth, and expression with clinical response.

Defining the functional significance of mediators of cell proliferation and/or differentiation in ovarian and uterine biology.
We continue to focus effort into gaining a better overall understanding of steroid and growth factor induced cell proliferation. More recently, we have been identifying and characterizing Cables 1 interacting proteins to determine their functional significance in the regulation of the cell cycle, cell proliferation, differentiation and/or apoptosis. Moreover, we are assessing whether the biochemical interactions involving Cables 1 and the corresponding functional components are altered in the presence or absence of steroids and/or growth factors.

Identification of novel modulators in the pathogenesis of endometriosis.
Endometriosis is a polygenic disease with complex multifactorial etiologies affecting reproductive-aged women. Although this disorder is commonly treated in clinical practice, the mechanisms by which ectopic endometrium is disseminated and proliferates, is not completely understood. There are a number of different factors, which have been implicated in either the genesis or the propagation of endometriosis. They include but are not limited to prostaglandins, cytokines, growth factors, chemokines, cell adhesion molecules and steroid hormones. It is, however, difficult to investigate the functional role of these factors without adequate in vivo model systems. Dr. Styer and Dr. Rueda are continuing to develop mouse models which have been manipulated to ‘mimic’ the human disease in order that they may study the effect of specific factors on the growth of ectopic endometrium. The mouse model was chosen to incorporate the power of mouse genetics. Using mutant mouse strains that are devoid or over express one or more of the factors described above they should be able to delineate their cause an effect relationships with the pathogenesis of the disease. Using this strategy in tandem with gene and protein analysis Dr. Styer and Dr. Rueda hope to gain a better understanding of the underlying mechanisms of endometriosis. This information will also serve to develop more effective alternative treatment modalities.