AI Article Synopsis
- Researchers developed a mouse model (ApoE/ArKO) lacking apolipoprotein E and aromatase to study breast cancer in the context of metabolic syndrome, as these patients often have worse outcomes.
- In experiments, ApoE/ArKO mice with implanted breast cancer cells showed significantly more tumor growth compared to wild-type mice, with notable differences in factors like insulin-like growth factor binding protein-5, though metastasis rates were lower in these mice.
- This new mouse model is valuable for exploring how metabolic syndrome influences breast cancer biology and may lead to a better understanding of treatment outcomes.
Article Abstract
Background/aim: Patients with breast cancer and metabolic syndrome have poorer outcomes. We aimed to develop and characterise an apolipoprotein E-null/aromatase knockout (ApoE/ArKO) mouse model of breast cancer with metabolic syndrome to aid research of the mechanisms behind poor prognosis.
Materials And Methods: Wild-type, ApoE and ApoE/ArKO mice were orthotopically implanted with EO771 murine breast cancer cells. Tumour growth was monitored and tumours investigated for pathological features such as cancer-associated adipocytes, hypoxia and cancer cell proliferation.
Results: Tumours from ApoE/ArKO mice were significantly more proliferative than those from wild-type mice (p=0.003), and exhibited reduced expression of insulin-like growth factor binding protein-5 (p=0.002). However, ApoE/ArKO mice also had a reduced rate of metastasis compared to wild-type and ApoE mice. Tumour hypoxia and the number of cancer-associated adipocytes did not differ.
Conclusion: The ApoE/ArKO model with EO771 breast cancer provides a novel mouse model to investigate the effects of metabolic syndrome on aspects of breast tumour biology.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6199598 | PMC |
| http://dx.doi.org/10.21873/invivo.11348 | DOI Listing |
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