One of the questions I often get is if colon cancer has traveled to the liver is it then liver cancer or is it still colon cancer.
The answer is very easy. It is still colon cancer but the consequences of it being in the liver or any other organ are getting more and more important.
The scientists call it the tumor environment. We have known for years from animal experiments that if we take a tumor from its original site and put it into the liver or lung, the tumor changes its sensitivity to drugs significantly not because the tumor changed but because the environment is important to whether the tumor can grow or even metastasize. Only in recent years have we gained much better understanding about the interactions between the tumor and its environment.
For example, we know that tumor blood vessel formation is induced by the environment. The host of the patient plays an important role in the way tumors can grow and the way the tumor responds to chemotherapy. The tumor can take advantage of the environment for nutrition or blood supply, for example.
It is our job to take advantage of the tumor’s advantage.
What do I mean? We know, for example, the liver has everything the tumor needs– food and oxygen. One of the driving pathways of growth in the tumor is the EGFR pathway. In the clinic we have seen when Erbitux is combined with chemotherapy there is a higher response rates for tumors in the liver than tumors outside the liver.
Patients with liver- limited disease are being looked at to be able to convert them to resectability and a chance of cure. Particularly in these patients we need to get the treatment right because it can make a difference between death and life. We are seeing an increasing number of patients who present with metastatic disease in liver and lung which we were able to cure.
We will do even better in the future because of new, more effective drugs, but we will also know what drugs are more likely to work. All our new trials use drugs which are targeted to specific markers present only in the tumor. We need to test tumors to see if this specific marker is in the tumor to be treated.
It is an exciting time for new treatments and hopefully curing more and more patients with metastatic disease.
October 29, 2009 at 7:50 am, Banma said:
Let’s say a patient has metastatic colon cancer limited to the liver. The tumor is wild-type KRAS, the patient has neoadjuvant chemotherapy (say Folfox) with an EGFR inhibitor (say cetuximab) and responds very well. The liver is then successfully resected and the patient has the same adjuvant chemo.
Does this scenario suggest anything about the likelihood of recurrence? You mention that the EGFR pathway is important in the tumor environment of the liver; is it also important in microscopic disease?
October 29, 2009 at 10:31 am, Heinz-Josef Lenzq said:
very good question. we dont know N0147 the adjuvant trial for colon cancer is still ongoing but will help us to understand the role of erbitux in the adjuvant……but convinced that resection of metastatic disease is not the same adjuvant therapy as resected of primary tumor since in the first case tumors metastatsized and are more aggressive.
November 06, 2009 at 2:27 am, Anon said:
If the patient has stage 3b adenocarcinoma of the colon, post hemicolectomy, with 4 out of 28 lymphnodes resected, and wild type of KRAS mutation, then would it be beneficial to add Cetuximab to the regime of capacetabine and oxaliplatine?