From: Testicular cancer in mice: interplay between stem cells and endocrine insults
1 | Disrupted spermatogenesis, increased inflammation, giant cells with vacuolated cytoplasm (GCNIS) were observed in big sized testes with increased vascularity |
2 | Increased expression of OCT-4. Despite atrophied appearance of the testes with loss of seminiferous tubules, increased numbers of OCT-4 positive (both nuclear and cytoplasmic) cells were observed. This was associated with reduced expression of spermatogonial marker c-KIT and MVH |
3 | Testicular cancer cells had high proliferative potential as evident by increased expression of PCNA and Ki-67 and proliferation occurred in a Sertoli cells independent manner since SOX9 expression was affected by DES treatment |
4 | Global hypomethylation was evident due to low or reduced expression of 5-methyl cytosine and altered expression of DNMTs |
5 | Disrupted expression of chromatin modulator NP95 and tumor suppressor p53 [13], PTEN and Meg3 |
6 | Increased expression of growth promoting imprinted gene Igf2 and Dlk-1 |
7 | Down regulation of cyclin dependent kinase inhibitor p57KIP2 |
8 | Reduced expression of H19 and Meg3 which negatively affects cell proliferation |
9 | Increased expression of CD166, a marker for cancer stem cells. CD166 positive CSCs appeared to be shedding from surface into the peritoneal cavity |
10 | The tumor-like growth was associated with increased Erβ and FSHR3 |