Recurrent somatic mutation of FAT1 in multiple human cancers leads to aberrant Wnt activation
Luc G. T. Morris,Andrew Kaufman,Yongxing Gong,Deepa Ramaswami,Logan A. Walsh,Sevin Turcan,Stephanie Eng,Kasthuri Kannan,Yilong Zou,Luke Peng,Victoria E. Banuchi,P. Paty,Zhaoshi Zeng,Efsevia Vakiani,David B. Solit,Bhuvanesh Singh,Ian Ganly,Linda M. Liau,Timothy C. Cloughesy,Paul S. Mischel,Ingo K. Mellinghoff,Timothy A. Chan +21 more
TLDR
Recurrent somatic mutations of the Drosophila melanogaster tumor suppressor–related gene FAT1 in glioblastoma, colorectal cancer, and head and neck cancer strongly point to FAT1 as a tumor suppressing gene driving loss of chromosome 4q35, a prevalent region of deletion in cancer.Abstract:
Aberrant Wnt signaling can drive cancer development. In many cancer types, the genetic basis of Wnt pathway activation remains incompletely understood. Here, we report recurrent somatic mutations of the Drosophila melanogaster tumor suppressor-related gene FAT1 in glioblastoma (20.5%), colorectal cancer (7.7%), and head and neck cancer (6.7%). FAT1 encodes a cadherin-like protein, which we found is able to potently suppress cancer cell growth in vitro and in vivo by binding β-catenin and antagonizing its nuclear localization. Inactivation of FAT1 via mutation therefore promotes Wnt signaling and tumorigenesis and affects patient survival. Taken together, these data strongly point to FAT1 as a tumor suppressor gene driving loss of chromosome 4q35, a prevalent region of deletion in cancer. Loss of FAT1 function is a frequent event during oncogenesis. These findings address two outstanding issues in cancer biology: the basis of Wnt activation in non-colorectal tumors and the identity of a 4q35 tumor suppressor.read more
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Novel Developments in the Molecular Genetic Basis of Oral Squamous Cell Carcinoma (OSCC)
TL;DR: This chapter will focus on the most important and common molecular genetic alterations at the genomic, epigenetic, and transcriptomic levels and study changes in tumor suppressor genes, oncogenes, gene expression, epigenetically and genomic instability, mitochondrial DNA (mtDNA) mutations, noncoding RNA, and loss of heterozygosity (LOH) in OSCC.
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TL;DR: The latest evidence linking genetic alterations and the Hippo pathway in HNSCC is summarized, with the aim of contributing to the continued development of precision medicine.
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Stephen T. Sherry,Minghong Ward,Michael Kholodov,Jonathan Baker,Lon Phan,Elizabeth M. Smigielski,Karl Sirotkin +6 more
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Integrated genomic analyses of ovarian carcinoma
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TL;DR: It is reported that high-grade serous ovarian cancer is characterized by TP53 mutations in almost all tumours (96%); low prevalence but statistically recurrent somatic mutations in nine further genes including NF1, BRCA1,BRCA2, RB1 and CDK12; 113 significant focal DNA copy number aberrations; and promoter methylation events involving 168 genes.
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