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Wolter J. Mooi
Researcher at VU University Medical Center
Publications - 144
Citations - 14399
Wolter J. Mooi is an academic researcher from VU University Medical Center. The author has contributed to research in topics: Melanoma & Survival rate. The author has an hindex of 50, co-authored 144 publications receiving 13403 citations. Previous affiliations of Wolter J. Mooi include VU University Amsterdam & Erasmus University Rotterdam.
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Journal ArticleDOI
BRAFE600-associated senescence-like cell cycle arrest of human naevi
Chrysiis Michaloglou,Liesbeth C.W. Vredeveld,Maria S. Soengas,Christophe Denoyelle,Thomas Kuilman,Chantal M.A.M. van der Horst,Donne Majoor,Jerry W. Shay,Wolter J. Mooi,Daniel S. Peeper +9 more
TL;DR: It is shown that sustained BRAFV600E expression in human melanocytes induces cell cycle arrest, which is accompanied by the induction of both p16INK4a and senescence-associated acidic β-galactosidase (SA-β-Gal) activity, a commonly usedsenescence marker.
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The essence of senescence
TL;DR: The various features of cellular senescence are reviewed and their contribution to tumor suppression is discussed and the power and limitations of the biomarkers currently used to identify senescent cells in vitro and in vivo are highlighted.
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Oncogene-Induced Senescence Relayed by an Interleukin-Dependent Inflammatory Network
Thomas Kuilman,Chrysiis Michaloglou,Liesbeth C.W. Vredeveld,Sirith Douma,Remco van Doorn,Christophe Desmet,Lucien A. Aarden,Wolter J. Mooi,Daniel S. Peeper +8 more
TL;DR: A model is proposed in which the context-dependent cytostatic and promitogenic functions of specific interleukins contribute to connect senescence with an inflammatory phenotype and cancer.
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Neu-protein overexpression in breast cancer. Association with comedo-type ductal carcinoma in situ and limited prognostic value in stage II breast cancer.
van de Vijver Mj,Johannes L. Peterse,Wolter J. Mooi,P. Wisman,Lomans J,Otilia Dalesio,Roel Nusse +6 more
TL;DR: It is concluded that neu overexpression may be an early step in the development of a distinct histologic type of carcinoma of the breast, but it could find no association of overeexpression with lymph-node status or tumor recurrence.
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Loss of p16Ink4a confers susceptibility to metastatic melanoma in mice.
TL;DR: The results show that, in the mouse, Ink4a is a tumour-suppressor gene that, when lost, can recapitulate the tumour predisposition seen in humans.