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Loretta Lau

Researcher at Boston Children's Hospital

Publications -  58
Citations -  5153

Loretta Lau is an academic researcher from Boston Children's Hospital. The author has contributed to research in topics: Biology & Medicine. The author has an hindex of 23, co-authored 44 publications receiving 3519 citations. Previous affiliations of Loretta Lau include University of Sydney & Royal Children's Hospital.

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Pan-cancer analysis of whole genomes

Peter J. Campbell, +1332 more
- 06 Feb 2020 - 
TL;DR: The flagship paper of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium describes the generation of the integrative analyses of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types, the structures for international data sharing and standardized analyses, and the main scientific findings from across the consortium studies.
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Whole-genome landscapes of major melanoma subtypes

Nicholas K. Hayward, +62 more
- 03 May 2017 - 
TL;DR: Analysis of whole-genome sequences from cutaneous, acral and mucosal subtypes of melanoma reveals diverse carcinogenic processes across its subtypes, some unrelated to sun exposure, and extends potential involvement of the non-coding genome in its pathogenesis.
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Whole-genome landscape of pancreatic neuroendocrine tumours

Aldo Scarpa, +129 more
- 02 Mar 2017 - 
TL;DR: In this paper, the authors performed whole-genome sequencing of 102 primary pancreatic neuroendocrine tumours and defined the genomic events that characterize their pathogenesis, including a deficiency in G:C,>T:A base excision repair due to inactivation of MUTYH, which encodes a DNA glycosylase.
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Epigenomic alterations define lethal CIMP-positive ependymomas of infancy

Stephen C. Mack, +88 more
- 27 Feb 2014 - 
TL;DR: It is concluded that epigenetic modifiers are the first rational therapeutic candidates for this deadly malignancy, which is epigenetically deregulated but genetically bland.
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HDM2 antagonist Nutlin-3 disrupts p73-HDM2 binding and enhances p73 function.

TL;DR: Results provide the first evidence that Nutlin-3 disrupts endogenous p73–HDM2 interaction and enhances the stability and proapoptotic activities of p73 and thus, provides a rationale for the use of Nutin-3 in the large number of human tumors in which p53 is inactivated.