The study which was published online in the journal Cancer Discovery found that both moles and melanomas originate from melanin-producing cells (melanocytes) within the skin. Researchers found that lower level of protein called p15 may promote growth of moles into melanoma. The findings also revealed what keeps typical moles stop in their usual non-cancerous, no-growth state.
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Scientists have known for years that a mutation in the cell growth gene called BRAF makes them start growing, but until now did not understand why they stopped. "The BRAF mutation that stimulates the initial growth of moles also stimulates the production of a tumour suppressor protein, p15, which ultimately acts as a powerful brake on further cell division," said study senior author Todd Ridky, assistant professor at Perelman School of Medicine at the University of Pennsylvania in the US.
"It is this cell division that ultimately allows the transition from a normal mole into melanoma. When mole cells lose the p15 brake, cells can start dividing again and can progress into cancer," Ridky noted.
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The researchers studied mole cells isolated directly from normal benign moles removed from patients, and compared them to melanocytes isolated from normal (non-mole) skin. The mole melanocytes had 140 times more p15 than the normal skin melanocytes.
Comparing cells from melanoma patients that had originated from previously benign moles, the researchers found generally high p15 levels in the mole tissue, and very low or undetectable p15 in the melanomas. This suggested that p15 is important for holding regular moles in a benign state, and that any subsequent loss of p15 would promote the transition to melanoma.