Health,Stem Cells, and Technology

Sunday, June 19, 2016

Clinical Trial to Begin Targeting Vasculogenic Mimicry:

Tumors have been known for many years to grow their own blood supply, and this mechanism became a target for many cancer therapeutics (Folkman, 1971). In 1999, Dr. Andrew Maniotis, Ph.D., a colleague of Folkman at Harvard Medical School who had moved to the University of Iowa, discovered a different means by which tumors can supply themselves blood and nutrients. The mechansim was named vasculogenic mimicry (VM) because the extracellular matrix and microenvironment surrounding the tumor had transformed into an architecture that included channels resembling the vasculature (Maniotis et al, 1999).

 This year a company launched a phase I trial to evaluate the safety of CVM-1118 in people with a variety of untreatable cancers and to assess its effectiveness. The new drug CVM-1118 curbs the activity of Nodal, a gene that drives vasculogenic mimicry by making cancer cells more like stem cells. While this new therapeutic strategy uses the advantage of knocking down one important pathway in the development of VM, cancer is a biological entity, and as such, usually has a variety of adaptive strategies available to circumvent this "one pathway disruption" caused by CVM-1118. Many other "one molecule for one pathway" strategies to treat cancer have failed in the past. We'll know soon whether CVM-1118 joins the ranks of the many drugs that do little or nothing to treat cancer.

References:

Judah Folkman (1971) Tumor Angiogenesis: Therapeutic Implications. N Engl J Med 1971; 285:1182-1186November 18, 1971DOI: 10.1056/NEJM197111182852108

Maniotis AJ1, Folberg R, Hess A, Seftor EA, Gardner LM, Pe'er J, Trent JM, Meltzer PS, Hendrix MJ. (1999) Vascular channel formation by human melanoma cells in vivo and in vitro: vasculogenic mimicry. Am J Pathol. 1999 Sep;155(3):739-52.

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