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Table 1 Various features of T2GCT observed in mice neonatally exposed to DES

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