James E. Cleaver

TL;DR: Patients with xeroderma pigmentosum develop fatal skin cancers when exposed to sunlight, and so the failure of DNA repair in the skin must be related to carcinogenesis.

TL;DR: Comparison of cellular responses associated with photoenhanced repair and nucleotide excision (“dark”) repair indicated that light‐mediated correction of UV damage was an important factor in cell survival, and a general dependence of photoproduct induction and D37 values on cell size and shape was indicated.

TL;DR: Nucleotide-excision repair diseases exhibit cancer, complex developmental disorders and neurodegeneration, and complex clinical phenotypes might result from unanticipated effects on other genes and proteins.

TL;DR: The bifunctional role of Notch in human cancer thus emphasizes the context dependency of signaling outcomes and suggests that targeted inhibition of the Notch pathway may induce squamous epithelial malignancies.

TL;DR: The mapping of mutations in recently solved protein structures has begun to clarify the links between the molecular defects and phenotypes, but the identification of additional sources of clinical variability is still necessary.