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One area of focus is on evolution’s solution to a challenging problem: how can bones, which are rigid and incapable of interstitial growth, increase their size while providing skeletal support to a growing animal? For most of the skeleton, the answer is by re-enacting the evolutionary transition from a cartilaginous to a bony skeleton. We focus most of our research on mutations in rats and mice (naturally-occurring, knock-outs, and knock-ins) that block bone resorption to identify genes and signaling pathways required for normal cell differentiation and for the complex interactions of bone, cartilage, blood vessels, and marrow that control the transition from cartilage to bone during growth. We have identified genes that impact several of the constituent tissues simultaneously, pointing the way to common regulatory pathways. We bring a range of histopathologic, genetic, and molecular techniques to study these questions, including digital imaging, microarray expression profiling, cell and tissue culture, and in situ hybridization.
We are actively engaged in many collaborations with scientists in laboratories from around North America and in Europe.
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Our lab continues the work of Sandy C. Marks, Jr., DDS, PhD, for more on Sandy, follow this link:
http://www.umassmed.edu/cellbio/sandymarks.aspx
Download a memorial booklet comprised of contributions from colleagues, and friends worldwide. (PDF 2.3 MB)
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55 Lake Avenue North Worcester, MA 01655