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Why don't all moles progress to melanoma?

ess and gets rid of excess incoming amino acids, giving the ER a chance to catch up. If that doesn't work, the UPR causes the cell to destroy itself in a process called apoptosis.

"Traditionally, the ER's role was considered to be limited to protein folding or protein modification," Soengas says. "But scientists like Randal Kaufman, a U-M professor of biological chemistry and co-author on our paper, have found that the ER can sense changes in glucose, nutrients, oxygen levels and other aspects of cellular physiology associated with diseases like diabetes and Alzheimer's disease."

"In our study, we found that the ER senses the activity of certain oncogenes in the melanocyte and triggers a response that prevents the malignant transformation of these cells," Soengas adds.

According to Soengas, the tumor suppressive mechanism induced by the ER in melanocytes with these cancer-causing mutations is premature senescence ?a form of "suspended animation" that stops the cell cycle and keeps cells from dividing, but doesn't kill them.

"The cells are held in check ?they don't die, but they don't proliferate either," Soengas explains. "In the case of moles, melanocytes can stay this way for 20 to 40 years or even your whole life. For most of us, just holding cells in an arrested state is sufficient to prevent the development of cancer. That's why so many people have moles, but few have melanoma."

In the study, U-M scientists found that the tumor suppressive response in melanocytes varied depending on the type of oncogene being expressed in the cell.

"We found that some oncogenes activated the endoplasmic reticulum, while other oncogenes didn't," Soengas says.

In a previous study, Soengas and colleagues found that certain oncogenes use a different senescence mechanism, which doesn't activate the ER, to block the transformation of melanocytes. Both these mechanisms work in addition to or independent from other well-
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Source:University of Michigan Health System


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