Melanocytic Nevus or Melanoma, Gene Determines Mole, as Benign tumor, exists in almost every adults’ skin. It has been long known that the mutation of BRAF gene can cause the growth of mole. But why the moles stop growing is still unknown. Recently, researchers at University of Pennsylvania have found that a gene called CDKN2B (encodes p15 protein) is the key factor for a mole been stuck in a non-proliferation, non-growing state. This gene leads to the possibility that there’s only one step away from Melanocytic Nevus to Melanoma. Nevi and melanomas both originate in the skin melanocytes. Scientists have discovered a decade ago, the mutation of BRAF gene may lead to overgrowth of melanocytes, just like opening the valve of melanin growth, leading to the growth of nausea nevi and melanoma. But different from melanoma, when the melanocytic nevi in the skin accumulation reaches a certain size (typically a few millimeters in diameter), the cells stop growing. But here’s the question: why they are they the same BRAF mutation, mole inside melanoma cell proliferation can be limited, but the Melanoma can not? Todd W. Ridky MD is one of the researchers in this studies. He and his colleagues compared the normal melanocytic nevi and melanoma cells from ordinary. As a result, they found that the concentrations of a mole protein in Melanocytes is 140 times higher than those in the Melanoma cells. p15 is a protein associated with tumor transplantation, that can block some cell division, acting as a brake in the process of tumor formation. Nevus cells derived from this model would have been under normal circumstances and will not develop into melanoma cells, but if the corresponding gene p15 protein was knocked out, the canceration would occur. At the same time, they also found that if the BRAF mutant protein activity increases, it is possible to cause the cells to secrete a signaling molecule TGF-β(a cellular growth factor). The high concentration of p15 has great significance in the maintenance of a benign mole. p15 has a similar protein, p16, and they both play a role in cell growth inhibition. But the researchers proved that p15 has its own unique features to limit the excessive proliferation of melanocytic nevi. In-depth research on p15 can help us understand the formation of the growth of melanoma and nevi history. Skin cancer-related diseases will increasing as the exposure to ultraviolet light increases. Therefore, the melanoma cell related research will always have a very important practical significance.
Mole, as Benign tumor, exists in almost every adults’ skin. It has been long known that the mutation of BRAF gene can cause the growth of mole. But why the moles stop growing is still unknown. Recently, researchers at University of Pennsylvania have found that a gene called CDKN2B (encodes p15 protein) is the key factor for a mole been stuck in a non-proliferation, non-growing state. This gene leads to the possibility that there’s only one step away from Melanocytic Nevus to Melanoma.
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Melanocytic Nevus or Melanoma, Gene DeterminesMole, as Benign
tumor, exists in almost every adults skin. It has been long known
that themutation o B!"# gene can cause the growth o mole. But why
the moles sto$ growing is stillunknown. !ecently, researchers at
%niversity o &ennsylvania have ound that a gene called'D(N)B
*encodes $+, $rotein- is the key actor or a mole been stuck in a
non.$rolieration,non.growing state. /his gene leads to the
$ossibility that theres only one ste$ away romMelanocytic Nevus to
Melanoma.Neviand melanomas both originate in the skin melanocytes.
0cientists have discovered adecade ago, the mutation o B!"# gene
may lead to overgrowth o melanocytes, 1ust likeo$ening the valve o
melanin growth, leading to the growth o nausea neviand melanoma.But
dierent rom melanoma, when the melanocytic nevi in the skin
accumulation reaches acertain si2e *ty$ically a ew millimeters in
diameter-, the cells sto$ growing. But heres the3uestion4 why they
are they the same B!"# mutation, mole inside melanoma cell
$rolierationcan be limited, but the Melanoma can not5/odd 6. !idky
MD is one o the researchers in this studies. 7e and his colleagues
com$aredthe normal melanocytic nevi and melanoma cells rom
ordinary. "s a result, they ound thatthe concentrations o a mole
$rotein in Melanocytes is +89 times higher than those in
theMelanoma cells. $+, is a $rotein associated with tumor
trans$lantation, that can block somecell division, acting as a
brake in the $rocess o tumor ormation. Nevus cells derived rom
thismodel wouldhavebeenundernormal circumstancesandwill not
develo$intomelanomacells, but i
thecorres$ondinggene$+,$roteinwasknockedout,
thecancerationwouldoccur. "t the same time,theyalso oundthatithe
B!"# mutant $roteinactivity increases, itis$ossible to cause the
cells to secrete a signaling molecule /G#.:*a cellular growth
actor-./he high concentration o $+, has great signiicance in the
maintenance o a benign mole.$+, hasasimilar $rotein,$+;, and they
both $lay arolein cellgrowth inhibition. But theresearchers $roved
that $+, has its own uni3ue eatures to limit the excessive
$rolieration omelanocytic nevi. In.de$th research on $+, can hel$
us understand the ormation o the growth o melanomaand nevihistory.
0kin cancer.related diseases willincreasing as the ex$osure to
ultravioletlight increases. /hereore, themelanomacell
relatedresearchwill always haveaveryim$ortant $ractical
signiicance.
