What Your Genes Say About Your Cancer
Posted on July 22, 2013
After her recent trip to the American Society for Clinical Oncology (ASCO) Conference, we sat down with Dr. Laura Porter to hear more about the latest news in genetics and CRC.
What is the Cancer Genome Atlas (TCGA)?
Did you know that doctors are now able to predict which treatments will work for you just by looking at your genes? And they’re getting better and better at it every day, thanks to the Cancer Genome Atlas (TCGA).
The Cancer Genome Atlas Project was started in 2006 by the National Cancer Institute and Human Genome Research Institute. The goal is to map out all the genetic mutations in 20 different types of cancer – including colorectal.
By comparing samples of normal tissue with samples of cancer tissue taken from the same patient, researchers can find changes specific to that particular cancer. And thanks to the TCGA, by looking at many samples from many different patients, researchers can connect specific genetic changes with specific outcomes.
In short, in the near future, colorectal cancer will be treated based on specific biomarkers or genetic mutations – increasing survival outcomes and decreasing side effects.
Cancer Treatment: One Size Does Not Fit All
Genetic analysis of the tumor and the TCGA project appear to be paving the way for better use of the treatments that we currently have and the development of future drugs.
Thanks to the TCGA, the days of personalized medicine – based on the genetic profile of your tumor – is not just a dream anymore. Here are some other exciting breakthroughs that we heard about during ASCO:
- Researchers would like to use genetic mutations or the genetic profile of your tumor as biomarkers in the future to determine who will respond to which drug. This applies mainly to biologics not chemotherapy, for example KRAS wild type, non-mutated will respond to EGFR inhibitors such as Vectibix and Erbitux but KRAS mutants will not.
- Researchers have recently discovered more KRAS mutations along with other mutations in the same pathway which may affect a person’s response to Erbitux or Vectibix. Initially it was thought that there were only two KRAS mutations.
- The genetic mutations in tumors are heterogeneous, meaning they are not the same and can vary by the different sites of the metastases, even within the same organ and within the same tumor. This difference can cause resistance to treatment. Tumors can even become more resistant during treatment by acquiring new mutations. To overcome this resistance, researchers are looking at using multiple drugs or biologics against different targets based on a person’s genetic profile while being careful to monitor the toxicity.
- Tumor DNA is different from normal cellular DNA. The mutations are highly specific for pre-cancerous and cancerous cells. These mutations can be found in the blood stream, which researchers are now using to develop a blood test that will quantify the tumor burden, or the total mass of tumors present in an individual, based on circulating tumor DNA, also called cell free DNA.
- 15% of all colorectal cancers are hereditary, and of these most of the mutations are not known. The familial syndromes or hereditary colon cancers such as Lynch Syndrome and FAP are passed down through chromosomes via large chromosomal mutations. The remaining 85% are not passed down through the family but are sporadic. Many small genetic mutations, or point mutations, are being identified that may account for the disease and may eventually be a biomarker using circulating tumor DNA.
- All patients with CRC should be tested for Lynch Syndrome, it should be as routine as BRAC testing in breast cancer. It is also important to note that the BRAC mutation causes an increased incidence of colon cancer.
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