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It is well known that long-term high cholesterol levels are associated with increased breast cancer risk and worse outcomes for most cancers, but this connection is not fully understood by scientists
Now a research team led by the Cancer Institute of Duke University has determined the working mechanism, describing how breast cancer cells use cholesterol to develop stress resistance, so that they will not die because they migrate from the original tumor site
Dr.
Based on early laboratory research, MacDonnell and his colleagues focused on the relationship between high cholesterol and estrogen-positive breast and gynecological cancers
But there is a paradox in estrogen-negative breast cancer
In current studies using cancer cell lines and mouse models, researchers at Duke University have found that migrating cancer cells can engulf cholesterol in response to stress
But in the theme of "what-doesn't-kill-you-makes-you-stronger", those cells that survived have a super power that enables them to resist iron sagging.
This process seems to apply not only to Er-negative breast cancer cells, but also to other types of tumors, including melanoma
MacDonnell said: "Unlocking this approach highlights new methods that may be useful for the treatment of advanced disease
Original search:
1 Dysregulated cholesterol homeostasis results in resistance to 2 ferroptosis and increased cancer cell metastasis