Skin Cancer Linked to Mutated Collagen VII

Researchers have found that a peptide fragment derived from the protein collagen VII, a normal component of skin cells, is linked to the development and spread of squamous cell skin cancer.

Investigators at Stanford University School of Medicine (Palo Alto, CA, USA) worked with skin cancer cells obtained from children that expressed different mutations in the gene that codes for collagen VII. This type of mutation underlies the blistering skin disorder recessive dystrophic epidermolysis bullosa (RDEB). Victims of this disorder are particularly at risk of developing skin cancer.

A study published in the March 18, 2005, issue of Science revealed that after transplantation in mice, cancer cells totally lacking collagen VII did not spread whereas those retaining a specific collagen VII fragment (the amino-terminal noncollagenous domain NC1) formed malignant tumors. Treatment with antibodies that neutralized collagen VII prevented the cancer from spreading but did not kill the cancer cells.

Senior author Dr. Paul Khavari, professor of dermatology at Stanford University School of Medicine said, "I can imagine a drug that blocks the collagen VII fragment being used preemptively to prevent skin cancer from spreading in people who are highly susceptible, such as children with RDEB or people who are chronically immune suppressed due to organ transplantation.”



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