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Preparing a will or trust not only ensures that your assets are distributed according to your wishes, but it also leaves behind a legacy by supporting causes that you care about.
Learn how the Colorectal Cancer Alliance is advocating for the passage of the Nancy Gardner Sewell Multi-Cancer Early Detection Act (HR 2407), a bipartisan bill that ensures immediate Medicare coverage for life-saving cancer detection tests once approved by the FDA.
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Learn about The Cancer Promise initiative and how political candidates can pledge to support cancer research, prevention, and care policies. Make your voice heard this election.
The BRAF gene is present in all the cells in our bodies. A BRAF mutation (a change or damage to the gene) is found in about 10% of colorectal cancer patients. If your biomarker tests show an abnormal BRAF mutation, treatments that target abnormal BRAF genes may be helpful. BRAF inhibitors are drugs that can turn off and stop mutated BRAF activity.
When colorectal cancer spreads, it can cause high or low levels of certain chemicals in the blood. Carcinoembryonic antigen, also called CEA, is a protein that may be elevated in colorectal cancer patients. High CEA levels can indicate your cancer has recurred or has spread beyond the colon. CEA is also sometimes higher in those who smoke or women who are pregnant. It may take additional testing to confirm the results of your CEA testing.
Our bodies have a gene that produces the dihydropyrimidine dehydrogenase enzyme, which helps break down certain medications in the liver. If there is mutation in the gene, your body will not produce enough of the dihydropyrimidine dehydrogenase enzyme. This condition is called dihydropyrimidine dehydrogenase deficiency (DPD).
Having DPD can cause fluorouracil-based chemotherapy drugs (which are commonly used in colon cancer treatment) to build up in your body and cause severely toxic reactions.
The HER2 protein is a receptor, which is a microscopic “spike” that sticks out on the surface of almost all the cells in our body. Sometimes there is an abnormality in the cell and multiple HER2 genes are produced, which is called amplification. When the HER2 gene is amplified, it produces excess receptors on the cell surface; this is called overexpression. Overexpression drives uncontrolled growth of the cells, which is how a cancer tumor forms.
KRAS biomarkers are members of the RAS family of genes that include NRAS and HRAS. A normal KRAS gene teams up with a group of proteins as an “on/off” switch to monitor cell growth. An abnormal mutation in the KRAS gene happens early in the development of cancer. Approximately 40-45% of colorectal cancer patients have a KRAS mutation in their tumor. Patients with mutated or unknown KRAS status should receive chemotherapy including FOLFOX, CAPOX, or FOLFIRI with or without bevacizumab.
NRAS is a member of the RAS family of genes that include KRAS and HRAS. A normal NRAS gene teams up with a group of proteins as an “on/off” switch to monitor cell growth. This abnormality is known as a driver mutation because it causes the switch to be locked in the “on” position and drives uncontrolled cell growth, leading a cancer tumor to form. NRAS mutations are found in about 5% of colorectal cancer patients. Patients with NRAS-mutated colorectal cancer should receive chemotherapy (some examples are FOLFOX, CAPOX, and FOLFIRI), with or without Bevacizumab (an antibody that inhibits the growth of blood vessels and oxygen supply in the tumor).
PIK3CA is a gene that is involved in several different processes in cell growth. A PIK3CA mutation is a driver mutation that drives the growth of cells. It exists in many types of cancer and in 10-20% of colorectal cancers. Patients with PIK3CA-mutated colorectal cancer should receive standard chemotherapy. There is at least one drug being used successfully in PIK3CA-mutated breast cancer and it has opened up clinical trials for other PIK3CA-mutated solid tumors, including colorectal cancer.