The "bad cholesterol" binds to LDL receptors in the liver, the organ
in charge of degrading it and excreting it from the organism as bile.
"Cancer cells need lipids to grow. They can make their own lipids or get
more from the host because these cells grow so fast," explains Lehner.
"The tumor signals to the liver: 'I need more cholesterol for growth'
and the liver is reprogrammed to secrete those lipids."
One of the key factors for this process are proteins we all have
that, in larger quantities, may cause a decrease in the amount of LDL
receptors to excrete the cholesterol. The tumor affects these proteins
to reduce clearance of cholesterol from the blood, leaving the LDL for
cancer to feed off of it.
These findings led Lehner and Hoefler to an interesting hypothesis:
minimizing the liver's production of LDL would deprive a tumor from its
constant supply and therefore reduce its possibility of growth. Their
experiments in pre-clinical models proved to be successful, confirming
lower tumor development with the regulation of the proteins that affect
production of VLDL (precursors of LDL) and uptake of LDL by receptors
from the liver. The next step for Lehner and his team will be to test existing
medications that would help in limiting the production of cholesterol on
patients undergoing cancer treatment, adding them to their current
therapies.
"There are medications approved that we can test", says Lehner. "They
were not developed for cancer, they were manufactured for people with
hypercholesterolemia (chronic condition where patients have very high
level of cholesterol in their blood), but it will be interesting for us to test them with cancer patients and see if there is improvement."
No comments:
Post a Comment