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@ARTICLE{Polubothu:600684,
author = {Polubothu, Satyamaanasa and Bender, Nicole and Muthiah,
Siobhan and Zecchin, Davide and Demetriou, Charalambos and
Martin, Sara Barberan and Malhotra, Sony and Travnickova,
Jana and Zeng, Zhiqiang and Böhm, Markus and Barbarot,
Sebastien and Cottrell, Catherine and Davies, Olivia and
Baselga, Eulalia and Burrows, Nigel P. and Carmignac,
Virginie and Diaz, Joey Santiago and Fink, Christine and
Haenssle, Holger A. and Happle, Rudolf and Harland, Mark and
Majerowski, Jacquelyn and Vabres, Pierre and Vincent, Marie
and Newton-Bishop, Julia A. and Bishop, D. Tim and Siegel,
Dawn and Patton, E. Elizabeth and Topf, Maya and Rajan, Neil
and Drolet, Beth and Kinsler, Veronica A.},
title = {{PTPN}11 {M}osaicism {C}auses a {S}pectrum of {P}igmentary
and {V}ascular {N}eurocutaneous {D}isorders and
{P}redisposes to {M}elanoma},
journal = {The journal of investigative dermatology},
volume = {143},
number = {6},
issn = {0022-202X},
address = {Amsterdam},
publisher = {Elsevier},
reportid = {PUBDB-2023-08102},
pages = {1042 - 1051.e3},
year = {2023},
abstract = {Phakomatosis pigmentovascularis is a diagnosis that denotes
the coexistence of pigmentary and vascular birthmarks of
specific types, accompanied by variable multisystem
involvement, including CNS disease, asymmetrical growth, and
a predisposition to malignancy. Using a tight phenotypic
group and high-depth next-generation sequencing of affected
tissues, we discover here clonal mosaic variants in gene
PTPN11 encoding SHP2 phosphatase as a cause of phakomatosis
pigmentovascularis type III or spilorosea. Within an
individual, the same variant is found in distinct pigmentary
and vascular birthmarks and is undetectable in blood. We go
on to show that the same variants can cause either the
pigmentary or vascular phenotypes alone, and drive melanoma
development within pigmentary lesions. Protein structure
modeling highlights that although variants lead to loss of
function at the level of the phosphatase domain, resultant
conformational changes promote longer ligand binding. In
vitro modeling of the missense variants confirms downstream
MAPK pathway overactivation and widespread disruption of
human endothelial cell angiogenesis. Importantly, patients
with PTPN11 mosaicism theoretically risk passing on the
variant to their children as the germline RASopathy Noonan
syndrome with lentigines. These findings improve our
understanding of the pathogenesis and biology of nevus
spilus and capillary malformation syndromes, paving the way
for better clinical management.},
cin = {CSSB-LIV/UKE-MT},
ddc = {610},
cid = {$I:(DE-H253)CSSB-LIV_UKE-MT-20220525$},
pnm = {899 - ohne Topic (POF4-899) / ZF-MEL-CHEMBIO - Chemical
Biology in Zebrafish: Drug-Leads and New Targets in the
Melanocyte Lineage and Melanoma (648489)},
pid = {G:(DE-HGF)POF4-899 / G:(EU-Grant)648489},
experiment = {EXP:(DE-MLZ)NOSPEC-20140101},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:36566878},
UT = {WOS:001010699700001},
doi = {10.1016/j.jid.2022.09.661},
url = {https://bib-pubdb1.desy.de/record/600684},
}