James Fleming

TL;DR: It is shown that H2AX function is essential for mammalian DNA repair and genomic stability, and not required for NHEJ per se.

TL;DR: It is shown that pro-B lymphomas in mice deficient for both p53 and nonhomologous end-joining (NHEJ) contain complicons that coamplify c-myc and IgH sequences, suggesting a general model for oncogenic complicon formation.

TL;DR: Artemis appears to be required for a subset of NHEJ reactions that require end processing, most notably in prevention of translocations and telomeric fusions, and may also suppress genomic instability in humans.

TL;DR: It is reported that aged granulocyte-macrophage colony stimulating factor-deficient mice develop a systemic lupus erythematosis (SLE)-like disorder associated with the impaired phagocytosis of apoptotic cells, demonstrating that the interplay of infectious agents with cytokine-mediated regulation of immune homeostasis is a critical determinant of cancer susceptibility.

TL;DR: The view that loss of a single lig4 allele results in NHEJ activity being sufficiently reduced to engender chromosomal aberrations that drive non-lymphoid tumorigenesis is supported.