Alan S. Jonason

TL;DR: Skin appears to possess a p53-dependent 'guardian-of-the-tissue' response to DNA damage which aborts precancerous cells, and if this response is reduced in a single cell by a prior p53 mutation, sunburn can select for clonal expansion of the p 53-mutated cell into the AK.

TL;DR: It is concluded that, in addition to being a tumorigenic mutagen, sunlight acts as a tumor promoter by favoring the clonal expansion of p53-mutated cells, which results in normal individuals carrying a substantial burden of keratinocytes predisposed to cancer.

TL;DR: Skin appears to possess a p53-dependent "cellular proofreading" response to DNA damage in which precancerous cells self-destruct, if this response is reduced in a single cell by a prior p53 mutation, sunburn can thereafter select for clonal expansion of the p 53-mutated cell into an actinic keratosis.

TL;DR: A human IgG1 monoclonal antibody, MAb 5261 that specifically binds to human, rodent and primate CXCL13 with an affinity of approximately 5 nM and is capable of neutralizing the activity of CxCL13 from these various species in in vitro functional assays is developed.

TL;DR: It is shown that blocking SEMA4D enhances immune infiltration into tumor and increases antitumor activity in synergy with other immunomodulatory therapies, and the combination of anti-SEMA 4D antibody with antibody to CTLA-4 acts synergistically to promote complete tumor rejection and survival.