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The phenotype of 4L C* mouse model mimics some neuronopathic variants of human Gaucher disease.
Whether the mouse model mimics the human model in this regard is unclear.
Thus, this mouse model mimics for the first time the situation in human erbB2-positive breast tumors, in which amplification of erbB2 has been observed.
Collectively, these data demonstrate that the osteolytic bone microenvironment in our mouse model mimics the bone microenvironment in human breast cancer but not that of other metastatic microenvironments (i.e., lung and brain metastases).
It is notable that the renal changes are caused by hyperglycaemia instead of direct effects of the EGF-R transgene, and thus the E1-DN mouse model mimics human diabetes with poor glycaemic control.
Inducing an earlier onset of breast cancer can increase the likelihood of women developing ER-negative tumors (Benz 2008; Vetto et al. 2009), including HER2-positive breast cancer, which this mouse model mimics.
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Over the past decade, many laboratories tried to develop a mouse model mimicking human nephrotic syndrome (Table 1).
Recently, it was also reported that inhibition of the kit ligand/cKit axis attenuates metastasis in the mouse model, mimicking BC relapse after radiotherapy [ 49].
We developed a mouse model mimicking human BRCA1-deficient breast cancer to gain insight into the molecular progression of BRCA1-deficient tumors and to test putative therapies [ 12].
In a mouse model mimicking inflammation, infection and oestrogen deficiency, i.e. various conditions predisposing to bone loss, the net effect of IFN-γ was pro-resorptive 5.
In the lung, miRNA profiles were significantly changed in the experimental mouse model mimicking acute and chronic human asthma [ 5, 6].
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