 "A single cell shines new light on how cancers develop")
It was just a tiny speck, a single cell that researchers had marked with a fluorescent green dye. But it was the very first cell of what would grow to be a melanoma, the deadliest form of skin cancer. Never before had researchers captured a cancer so early.
The cell was not a cancer yet. But its state was surprising: It was a cell that had reverted to an embryonic form, when it could have developed into any cell type. As it began to divide, cancer genes took over and the single primitive cell barreled forward into a massive tumour.
Those were the findings of Leonard Zon of Boston Children's Hospital, Charles K Kaufman, and their colleagues, in a study published recently in the journal Science that offers new insight into how cancers may develop. The researchers stumbled on that first cell of a melanoma when they set out to solve a puzzle that has baffled cancer investigators: Why do many cells that have cancer genes never turn cancerous?
The work was in fish that had been given human genes, but the investigators found the same genetic programmes in human melanomas, indicating that they too started when a cell reverted to an embryonic state. Much more study is needed, but researchers say the result can help them understand why melanomas and possibly other cancers form, and potentially prevent them. And it may provide a way to stop melanomas from growing back after they have been cut down by new targeted drugs.
"It's a significant advance in the field," said Ze'ev Ronai, the scientific director of La Jolla Sanford Burnham Prebys Medical Discovery Institute, a nonprofit research centre. Ronai was not involved in the study.
The prevailing idea about the development of a cancer is that genes randomly mutate in a healthy cell, perhaps from sun exposure, perhaps from simple bad luck. The mutated genes drive aberrant cell growth, and the growing mass of cells accumulates more and more mutations that drive it to grow faster and spread until, finally, a cancer is formed.
Yet researchers keep finding cancer genes in perfectly normal, healthy cells that never turn malignant. These are genes that take the brakes off cell growth and are considered essential drivers of tumour growth.
Human skin cells are exemplars of the effect. In one study, Peter Campbell and his colleagues at Cambridge University looked for 74 cancer genes in normal skin cells. In many they saw the same pattern of mutations as is found in skin cancers. But since these cells were not cancerous, they realised something must be missing. What, besides powerful cancer genes, is needed to make a cancer?
Moles also show the effect. "One of the things we've known about moles is that the vast majority never will become melanomas," said Keith T Flaherty, a melanoma expert at Massachusetts General Hospital who was not associated with the new study. "The odds are against it." Yet almost every mole contains one of two potent gene mutations that are characteristic of melanomas, BRAF or NRAS, he added, and a third also harbour another notorious cancer gene, P53. New targeted drugs that block BRAF can slow melanoma growth.
"More and more data suggest that just having mutations is not sufficient to cause cancer," said Kornelia Polyak, a breast cancer researcher at the Dana-Farber Cancer Institute, who was not associated with the new study. "You need the right context."
©2016 The New York Times News Service
The cell was not a cancer yet. But its state was surprising: It was a cell that had reverted to an embryonic form, when it could have developed into any cell type. As it began to divide, cancer genes took over and the single primitive cell barreled forward into a massive tumour.
Those were the findings of Leonard Zon of Boston Children's Hospital, Charles K Kaufman, and their colleagues, in a study published recently in the journal Science that offers new insight into how cancers may develop. The researchers stumbled on that first cell of a melanoma when they set out to solve a puzzle that has baffled cancer investigators: Why do many cells that have cancer genes never turn cancerous?
The work was in fish that had been given human genes, but the investigators found the same genetic programmes in human melanomas, indicating that they too started when a cell reverted to an embryonic state. Much more study is needed, but researchers say the result can help them understand why melanomas and possibly other cancers form, and potentially prevent them. And it may provide a way to stop melanomas from growing back after they have been cut down by new targeted drugs.
"It's a significant advance in the field," said Ze'ev Ronai, the scientific director of La Jolla Sanford Burnham Prebys Medical Discovery Institute, a nonprofit research centre. Ronai was not involved in the study.
The prevailing idea about the development of a cancer is that genes randomly mutate in a healthy cell, perhaps from sun exposure, perhaps from simple bad luck. The mutated genes drive aberrant cell growth, and the growing mass of cells accumulates more and more mutations that drive it to grow faster and spread until, finally, a cancer is formed.
Yet researchers keep finding cancer genes in perfectly normal, healthy cells that never turn malignant. These are genes that take the brakes off cell growth and are considered essential drivers of tumour growth.
Human skin cells are exemplars of the effect. In one study, Peter Campbell and his colleagues at Cambridge University looked for 74 cancer genes in normal skin cells. In many they saw the same pattern of mutations as is found in skin cancers. But since these cells were not cancerous, they realised something must be missing. What, besides powerful cancer genes, is needed to make a cancer?
Moles also show the effect. "One of the things we've known about moles is that the vast majority never will become melanomas," said Keith T Flaherty, a melanoma expert at Massachusetts General Hospital who was not associated with the new study. "The odds are against it." Yet almost every mole contains one of two potent gene mutations that are characteristic of melanomas, BRAF or NRAS, he added, and a third also harbour another notorious cancer gene, P53. New targeted drugs that block BRAF can slow melanoma growth.
"More and more data suggest that just having mutations is not sufficient to cause cancer," said Kornelia Polyak, a breast cancer researcher at the Dana-Farber Cancer Institute, who was not associated with the new study. "You need the right context."
©2016 The New York Times News Service