TY  - JOUR
TI  - MMTV-neu mice deficient in STAT1 are susceptible to develop ovarian teratomas
AU  - Hannesdóttir, Lára
AU  - Daschil, Nina
AU  - Philipp, Sonja
AU  - Tymoszuk, Piotr
AU  - Müller-Holzner, Elisabeth
AU  - Klima, Günter
AU  - Verdorfer, Irmgard
AU  - Doppler, Wolfgang
T2  - The International Journal of Developmental Biology
AB  - Signal transducer and activator of transcription 1 (STAT1) serves in the protection of the organism against pathogens and other harmful insults. It is implicated in innate immune response, immunosurveillance, tumor-suppression, and the response to genotoxic as well as oxidative stress. We report here that 9 of 140 examined STAT1 deficient mouse mammary tumor virus-neu (MMTV-neu) mice developed differentiated ovarian teratomas, which histologically resemble benign dermatoid cysts. Conventional karyotyping revealed diploidy without structural rearrangements of the chromosomes. STAT1 proficient MMTV-neu mice with the same genetic background (FVB/N), and STAT1 deficient C57BL/6 mice failed to develop this type of tumor. This indicates that STAT1 deficiency promotes teratoma formation and this depends on MMTV-neu expression and/or the genetic background. Since ovarian teratomas are considered to develop as a consequence of alterations in the maturation of oocytes and follicular cells, we compared the ovaries from non-tumor bearing STAT1 deficient and proficient MMTV-neu mice. No detectable alterations in the number and proportion of the different follicular developmental stages were detected, implying the absence of non-redundant functions of STAT1 in normal folliculogenesis, as well as in follicular atresia. However, strong staining for STAT1 was detectable in granulosa and theca cells. These results point to a role for STAT1 in protecting from teratoma formation in a later step of tumorigenesis, e.g. by inducing apoptosis and eliminating premature or aberrantly formed follicles which have the potential to transform into teratomas. 
PY  - 2012
DO  - 10.1387/ijdb.113397lh
VL  - 56
IS  - 4
SP  - 279
EP  - 283
J2  - Int. J. Dev. Biol.
LA  - en
SN  - 0214-6282
SN  - 1696-3547
UR  - https://ijdb.ehu.eus/article/113397lh
Y2  - 2024/11/21/22:23:21
ER  -