Wilms tumour articles from across Nature Portfolio

The genetic and epigenetic predisposition of bilateral Wilms tumour remains to be investigated. Here, the authors perform multiomics analysis and identify the predominant genetic and epigenetic events associated with bilateral Wilms tumour predisposition.

Treatment of diffuse anaplastic Wilms tumours (DAWT) remains a challenge. Here, the authors perform multi-omic analysis and identify a desert-like DAWT subtype accounting for one third of DAWT cases and suggest treating them with HDAC and/or WEE1 inhibitors.

Here, the authors describe the history of the efforts to expand knowledge of Wilms tumour biology, genetics, embryonal origin and associated syndromic and familial conditions, and to clinically apply prognostic biomarkers and development of preclinical models.

Wilms tumour is the most common renal malignancy of childhood. Here, the authors review the genetic landscape of Wilms tumour and discuss how precision medicine guided by genomic information might lead to new therapeutic approaches and improve patient survival.

Elizabeth Perlman and colleagues use genome-wide sequencing, RNA expression, DNA copy number and methylation analyses to characterize the genomic landscape of Wilms tumors. Their integrated analyses implicate two major classes of genetic changes in Wilms tumors that preserve the progenitor state and/or interrupt normal kidney development.

Nazneen Rahman, Geert Kops and colleagues report the identification of biallelic loss-of-function mutations in TRIP13 in six individuals with Wilms tumor who presented with features of mosaic variegated aneuploidy. They show that TRIP13-mutant cells show spindle assembly checkpoint defects and suggest that mechanisms leading to aneuploidy may contribute directly to increased cancer risk.

A new study provides a comprehensive catalogue of the genetic changes in Wilms tumour. Understanding the interplay between genetic and epigenetic aberrations during tumorigenesis and clonal evolution is fundamental to enabling prediction of who is at risk and which tumours will relapse when so many are curable.

A paper inCellshows that partial reprogramming of somatic cells induces epithelial tumorigenesis.