Hello. Very interesting indeed. A picture of cysts would help surely, but do you know whether cells in the center of the cysts are undifferentiated and maybe still proliferative ? Do you have signs of basal detachment in certain epidermal areas which may reveal altered integrins engagement in cell adhesion, and an explanation for their sequestration in cysts ?

The multi-formed micro-cysts in the p53 -/- mouse skin after DMBA/ IR genotoxic stress is composed of differentiated cells and the center is completely empty.  As you mentioned above, cyst-wall cells have the altered expression pattern of integerin (especially ITGA6). Anyway, cyst formation is considered to be the process of discarding process of DNA-damaged senescent cells.  

The question is very interesting, I am not sure, if I can bring about the answer but hope my discussion will provide clues and the refs. will be of help.

I think the initial response to a genotoxic signal are the events that follow DNA damage, such as DNA repair, apoptosis or growth arrest, proliferation and differentiation as a rescue mechanism. The formation of cysts, may be the initial response to it, as these are formed when plutripotent stem cells are stimulated and form progentor basal cell lineages, which form the cysts with the abilty to differentiate (following initial proliferation) like the basal cells of the regular epidermis. Apoptosis of sun burn cells, found in the basal layers, following UV, and Epidermal differentiation are important for cells to remove their toxic substances, as the normal cornified squames are dead cells which remove toxic substance such involucrin, loricrin etc, besides forming mechanical barrier reqd for protection.

Many cell signalling molecules involved in epidermal proliferation, differentiation and apoptosis, all play their roles in response to stress or DNA damage. Some of the interplay occur between oncogenes and transcription factors, such Notch, Ets 1, p63 isoforms. All of these processes proliferation and differentiation and apoptosis are impaired in the processes of genotoxicty that in stages leads to cancer, by initation, promotion, progression and metastasis as the cells lose their differentiating capacity and gain a high proliferative index as more and more mutations are acquired with time and with more genotoxicity. Some ref below may be of help.

http://www.nature.com/cdd/journal/v16/n2/full/cdd2008147a.html

http://bio.biologists.org/content/2/12/1336.full

http://www.pnas.org/content/97/25/13473.full

Thank you for your precise comment, Dr Tahmina C Islam. As you explained, the differentiation is regarded to be one of the machineries to prevent accumulated DNA damage leading to carcinogenesis. As differentiation goes on, the cell-to-cell interaction might trigger cell-competition-like system to discard the "potentially dangerous" cells to maintain the tissue homeostasis.     

I would be looking at keratin 14 and 5 expression within and external to cysts.