New Discoveries in Cancer and Heart Disease


Why We Undertook this Research

Until now, the underlying mechanism of atherosclerotic vascular disease has remained elusive. How do pathogenic lipids trigger an inflammatory response? How do atherosclerotic arteries become calcified?

Proof of Concept

An important finding in our laboratory is that sera from different cancer patients (30 are documented to date) and normal donors have widely varying abilities to promote or inhibit MCED.  We believe that patient-specific circulating pro-angiogenic (or anti-MCED) factors have clinical implications.

We are not certain yet if a single inhibitory factor, multiple inhibitory factors, or some combination of inhibitory and stimulatory factors are involved.  In principle, this would be a fairly straightforward project for a well-equipped bio-pharmaceutical laboratory.  It should be possible for such a lab to perform various types of chromatography/separation of serum studies and then to enrich for and purify the precise factors involved.  Once the MCED promoters and/or inhibitors have been identified and isolated, pharmaceuticals that either mimic, enhance, or abrogate their activity can be developed. 

Meanwhile, in our own lab, expanded studies are underway in 60 additional samples of sera from patients with diagnosed cardiovascular disease.   Larger studies with an academic institutional collaborator will then follow.

“MCED explains why blood cholesterol and other lipid levels do not reliably correlate with coronary artery disease.”

“MCED explains why anti-angiogenic cancer treatment increases the risk of cardiovascular disease.”

“MCED explains why glioblastoma (the most common primary brain tumor) patients who have favorable responses to bevacizumab (Avastin) develop early calcifications in the tumor bed while glioblastoma patients with poor responses to bevacizumab do not develop calcifications.”