Moles are found on the body of almost all individuals. However, they stay in no-growth and non-cancerous state because of a tumor suppressor protein called p15.
The study – complete details of which have been published in the journal Cancer Discovery -- was conducted by the researchers at the Perelman School of Medicine, Penn University. It was long known that a mutation in the BRAF gene triggers moles to start growing, however, the researchers in the past were not sure what stopped moles from growing further.
"The BRAF mutation that stimulates the initial growth of moles also stimulates the production of a tumor suppressor protein, p15, which ultimately acts as a powerful brake on further cell division," said senior author Todd W. Ridky, in a statement.
During the study, Ridky and his colleagues prepared skin grafts containing human mole cell deficit of the p15 suppressor protein. The graft had all other mutations that were known to be important for the development of melanoma. The research team transplanted the grafted tissue in mice and discovered that the depleted p15 cells develop into melanoma.
"The model tissues are medically relevant because they used the naturally occurring human mole cells in the 3-dimensional environment of living skin, which allows detailed functional studies - the field hasn't had an experimental system like this before," said Andrew McNeal, the lead study author.
The mole cells used during the study were derived from the benign moles of the patients. The team compared the mole cells against the normal melanocytes and discovered that the former had 140 times more p15 than the normal melanocyte skin cells. The researchers thus concluded that p15 is essential to keep moles in benign condition and that the removal of the protein would lead to transition of benign moles to melanoma.