Knowledge Base

Colon Cancer

A 58 years old man whose daughter was just married…

The patient was taken to the emergency unit due to acute bowel blockage (ileus). During the operation surgeons found a large tumor in his colon, which they removed. Unfortunately, the tumor already had spread to the liver. This second tumor was also very large and was already attached to the muscle separating the abdominal cavity and the chest (diaphragm). The only hope was that a well-chosen combination of chemotherapy and targeted therapy could shrink the tumor well enough to become separated from the diaphragm.

The onco-team was in a difficult situation, if they choose a wrong therapy the tumor in the liver grows larger until the next CT control two months later. This would mean that the last chance to cure this patient would be lost. Two targeted drugs were available as registered first line therapies, both had around 50-60% chance to be effective. It could be that both, neither of the two or only one of them is the right choice.

In colon cancer the tumor growth is due to the overstimulation of the molecule called EGFR receptor in around 25% of cases. Normally, the body can regulate how many colon cells we have by activating this receptor on the cell surface. However, in these tumors the hormone like molecules are produced by the tumor cells themselves. This way the tumor cell can stimulate itself. In the other 75% of colon cancers mutations in other genes cause “short circuit” in growth signals. If we want find out who are the patients who benefit from drugs, which target the EGFR molecules we have to exclude other gene mutations. These gene mutations should be targeted with other targeted therapies mainly in clinical development programs.

Routinely, the most common gene mutation, the KRAS is tested in all colon cancer patients. KRAS mutation is present in 35-40% of colon cancers.

In this patient, KRAS was tested in the local laboratory, but did not have any mutations. Therefore, EGFR targeted therapy was an option but still, there was a 50% risk that other than KRAS may have mutations EGFR therapy may fail. This is why, the oncologist first thought that it is safer to use angiogenesis inhibitor which has milder side effects and similar chance to be active.

The daughter of the patient was just married and he was building a new house for the couple. His son-in-law found Oncompass™ on the internet and asked for a more comprehensive testing.

There are several other genes, e.g. NRAS, BRAF, PIK3CA, HER-2, MET etc., which can be mutated in colon cancer in 5-10% of cases. Oncompass™ excluded the mutation of several other genes in addition to KRAS. If there is no mutation in a gene it is called “wild type” which is actually the normal type (commonly found in “the wild”). When none of the potentially faulty genes have mutation, the tumor is “super wild type”. These tumors are the ones in which EGFR is over stimulated by its own ligand and can be stopped by anti-EGFR targeted drugs.

In this tumor we did not found mutations in the alternative cancer genes, the tumor was super wild type therefore the Oncompass™ suggested anti-EGFR therapy. After receiving the Oncompass™ Report, the oncologists chose an anti-EGFR therapy for this patient. After two months treatment, the tumor in the liver started to shrink dramatically and six month later the remaining small tumor was surgically removed and the patient became tumor free.

Oncompass™ can find additional targets in both KRAS wild type and KRAS mutant colon cancers. For KRAS mutant patients we can help to find targeted therapies in clinical trials.

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