Hi Pedro,

I was previously in the lab that originally generated the PyMT mouse model. A far as I know no one as systematically sequenced or look for CNV changes in that model. It was always assume that since tumors develop fairly quickly in that model, no other genetic changes are required for tumorigenesis (depending on mouse strain, it develops as quickly as 5-6 weeks!).

Hi Richard,

Thanks for the answer!

I'm curious about this because I see some CD8 T cells infiltrating the tumours and was wondering if they are somehow involved in immune control of the tumour growth (which would depend on them recognising mutated antigens). But, as you say, I wouldn't be surprised if such a rapidly developing cancer would be devoid of any additional mutations.

Dear Pedro,

I am currently working with the MMTV-PyMT model in the FVB/n background. The immune system will play definitely a critical role in the growth and progression of these tumors, as it is known in the literature that already at the initial stages that leukocytes infiltrate the tumor mass. As for the human disease counterpart, MMTV-PyMT initially express quite high levels of both ER and PR, that is over time lost while positivity for HER2 is acquired.

Good luck! :)

Matteo

Hi Matteo,

I've found some data showing how CD4 T cells play a pro-tumor role (at least in the FVB background) but I was curious about CD8 T cells. Interesting about the ER, PR HER2 dynamics - wondering how much of that is due to deregulated gene expression/epigenetics or accumulation of mutations.

Greetings from the East Coast of Sweden.

Pedro