Ruth Wild

TL;DR: These data show that common, low-penetrance susceptibility alleles predispose to colorectal neoplasia, and suggest that susceptibility to CRC is mediated through development of adenomas.

TL;DR: These data provide the first evidence for the existence of common, low-penetrance susceptibility to a hematological malignancy and new insights into disease causation in CLL.

TL;DR: The combined analysis of 206 families provides direct evidence for Mendelian predisposition to CLL and evidence for the location of disease loci.

TL;DR: Observations provide evidence that familial CLL is essentially indistinguishable from sporadic CLL, favoring a genetic basis to disease development in general rather than a simple environmental etiology.

TL;DR: It is suggested that this Cockayne‐like phenotype with thrombocytopenia and nephrotic syndrome may be a novel DNA repair disorder, and it is proposed that further investigation of other affected families may help identify the causative genetic defect.