Proc Natl Acad Sci U S A. 2019 Oct 7. pii: 201906120. doi:10.1073/pnas.1906120116

Leeman JE, Li Y, Bell A, Hussain SS, Majumdar R, Rong-Mullins X, Blecua P, Damerla R, Narang H, Ravindran PT, Lee NY, Riaz N, Powell SN, Higginson DS.

Human papillomavirus 16 promotes microhomology-mediated end-joining.

[[!31591214 desc="“Compared to HPV-negative HNSCC genomes, HPV+ cases demonstrated a marked increase in the proportion of deletions with flanking microhomology, a signature associated with a backup, error-prone double-strand break repair pathway known as microhomology-mediated end-joining (MMEJ). Then, using 3 different methodologies to comprehensively profile double-strand break repair pathways in isogenic paired cell lines, we demonstrate that the HPV16 E7 oncoprotein suppresses canonical nonhomologous end-joining (NHEJ) and promotes error-prone MMEJ, providing a mechanistic rationale for the clinical radiosensitivity of these cancers.”"]]