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With regard to tumor progression, targeted expression of YB-1 in the mammary gland under the WAP promoter leads to the development of tumors; 100% of mice develop invasive carcinomas within 52 months [ 14].
The female mice develop invasive mammary gland tumors by 16 weeks of age [ 8].
C3(1)-SV40 T-antigen transgenic mice develop invasive mammary carcinomas independently of hormone supplementation or pregnancy, with a 15% incidence of lung metastasis.
Chfr knockout mice develop invasive lymphomas and solid tumors (lung, liver, gastrointestinal) after 40 weeks and have an increased susceptibility to chemical carcinogenesis [ 20].
Nf2 F/F ;Trp53 F/F ;Cdkn2a */* mice develop invasive mesotheliomas after intrathoracic Ad5-Cre injection due to loss of Nf2 and p53 in the mesothelial lining (Jongsma et al, 2008).
This model can be seen a gold standard for pancreatic cancer treatment, as it recapitulates many of the clinical features of the human disease including its poor response to gemcitabine (and most other cytotoxic chemotherapy agents), and mice develop invasive and metastatic disease.
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In our colony, disease progression in these mice was modestly delayed (by a few weeks) as compared to what was reported by Wang et al, [4](Table 3), the PBCre4×Ptenflox/flox mice developed invasive carcinomas and adenocarcinomas at a time when the ARR2PBCreER(T2)×Ptenfl/fl mice treated with OHT at 2 wks of age, were starting to develop microinvasive carcinomas.
Heterozygous Tp53 R270H/+ Nkx3.1-Cre mice developed invasive CaP by 30 weeks of age, with incomplete penetrance.
Sixty percent of the double mutant mice developed invasive Müllerian and mammary carcinomas.
Interestingly, long-lived TRF1/p53 double null mice spontaneously develop invasive and genomically unstable squamous cell carcinomas (Martinez et al., 2009).
However, when p53 is additionally targeted by deletion or mutation, mice rapidly develop invasive adenocarcinoma with a median latency of between 120 and 180 days (Hingorani et al, 2005) and we have previously found that p53 mutation, but not loss, could drive metastasis in this model (Morton et al, 2010b).
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mice develop extensive
mice develop high
mice develop glaucoma-like
mice develop local
mice develop severe
mice develop pituitary
mice develop spontaneous
mice develop progressive
mice develop renal
mice develop hepatic
mice develop significant
mice develop thymic
mice develop systemic
mice develop α-synuclein-dependent
mice develop mild
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