HIGH CHOLESTEROL CAN INCREASE YOUR CANCER RISK
According to some studies it is said that suggest individuals who take cholesterol-lowering drugs may have a reduced risk of cancer, and, conversely that individuals with the highest levels of cholesterol seem to have an elevated risk of cancer.
However, until now genetic evidence directly linking cholesterol and malignancy has been lacking.
Cholesterol is a fat-like substance supplied in foods and made in cells throughout the body. Too much cholesterol is bad for the heart and vascular system. It is typically measured as serum cholesterol by routine blood test.
Unlike serum cholesterol that is bound to proteins, however, cholesterol also hides inside cells. While locked inside cell membranes before it is eventually exported, cholesterol has an impact on cell growth and survival. A gene, known as ABCA1, is at the crossroads of the process that shuttles intracellular cholesterol outbound.
However, until now genetic evidence directly linking cholesterol and malignancy has been lacking.
Cholesterol is a fat-like substance supplied in foods and made in cells throughout the body. Too much cholesterol is bad for the heart and vascular system. It is typically measured as serum cholesterol by routine blood test.
Unlike serum cholesterol that is bound to proteins, however, cholesterol also hides inside cells. While locked inside cell membranes before it is eventually exported, cholesterol has an impact on cell growth and survival. A gene, known as ABCA1, is at the crossroads of the process that shuttles intracellular cholesterol outbound.
Several years ago while conducting unrelated experiments some researchers first noticed the importance of ABCA1. At that time, they identified a network of approximately 100 so-called "cooperation response genes" that mediate the action of cancer genes. ABCA1 was found among these genes and is frequently turned off in presence of other mutant cancer genes. The researchers found that defective cholesterol exportation appears to be a key component in a variety of cancers.
The proper function of ABCA1, in fact, is critical for sensing of cell stress. If ABCA1 function is lost in cancer cells, cholesterol is allowed to build up in the cells' mitochondria, or energy centers, making their membranes more rigid.
This in turn inhibits the function of cell-death triggers that normally become activated in response to cell stresses, as for example cancer gene activation. Therefore, when functioning properly ABCA1 has anti-cancer activity - in the sense that by keeping mitochondrial cholesterol low it protects the functioning of cellular stress response systems and acts as a barrier to tumor formation and progression.
The researchers demonstrated that some of the relatively rare ABCA1 mutations found in human colon cancers by other investigators disabled the gene's ability to export cholesterol. And by re-establishing the cholesterol export function in human colon cancer cells, they inhibited the cells' ability to grow as cancers when grafted onto mice.
This study, therefore, is the first to directly show how ABCA1 loss-of-function and cholesterol may play a role in cancer.
The proper function of ABCA1, in fact, is critical for sensing of cell stress. If ABCA1 function is lost in cancer cells, cholesterol is allowed to build up in the cells' mitochondria, or energy centers, making their membranes more rigid.
This in turn inhibits the function of cell-death triggers that normally become activated in response to cell stresses, as for example cancer gene activation. Therefore, when functioning properly ABCA1 has anti-cancer activity - in the sense that by keeping mitochondrial cholesterol low it protects the functioning of cellular stress response systems and acts as a barrier to tumor formation and progression.
The researchers demonstrated that some of the relatively rare ABCA1 mutations found in human colon cancers by other investigators disabled the gene's ability to export cholesterol. And by re-establishing the cholesterol export function in human colon cancer cells, they inhibited the cells' ability to grow as cancers when grafted onto mice.
This study, therefore, is the first to directly show how ABCA1 loss-of-function and cholesterol may play a role in cancer.
Millions of people take cholesterol-lowering drugs or statins, as prescribed by physicians. The drugs work by blocking the action of key enzymes in the liver, which synthesizes cholesterol. Clinical trials also are evaluating statins as a tool against cancer, and some previous studies suggest that when used in combination with chemotherapy, statins might make chemotherapy more effective by sensitizing certain cancer cells to chemotherapy-induced cell death.
Doctors do not know the appropriate statin dose for cancer prevention or treatment of cancer-related conditions. Side effects cannot be ignored either, and little research has distinguished between the responses among people who take statins.
The link between cholesterol and cancer is clear, but it's premature to say that statins are the answer, according to the researchers.
Doctors do not know the appropriate statin dose for cancer prevention or treatment of cancer-related conditions. Side effects cannot be ignored either, and little research has distinguished between the responses among people who take statins.
The link between cholesterol and cancer is clear, but it's premature to say that statins are the answer, according to the researchers.
Labels: ABCA1, cancer, chemotherapy, Cholesterol, Colon cancer, genes, heart, statins, vascular disease
posted by G S Iyer at 9:04 AM
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