Aggressive treatment for end-stage cancer gives false hope

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Aggressive treatment for end-stage cancer gives false hope

Posted Jun 8th 2006 9:20PM by Jacki Donaldson
Filed under: Chemotherapy, All Cancers, Daily news

At the same Atlanta meeting of the American Society of Clinical Oncology where the breast cancer drug Tykerb was touted as perhaps the next wonder drug, findings were also released concerning chemotherapy and end-stage cancer. It seems that many patients in the last weeks and days of their lives are receiving chemotherapy -- when it is clear that there is no hope for survival. Perhaps patients don't want to give up and so they choose to fight to the very end. I think I would be hard-pressed to throw in the towel if a doctor thought I might benefit from continued treatment. Miracles do happen.

Doctors may be part of the problem, though, according to researchers. Patients don't want to give up -- and neither do doctors. But cancer specialists report that overly aggressive treatment gives false hope and puts people though unnecessary suffering and costly ordeals when hospice would be a more effective route. The purpose of hospice -- to help people die with dignity and in comfort -- is ineffective, however, when it's not used to its full potential. A large review of Medicare records showed in 1999 that nearly 12 percent of cancer patients died after receiving chemotherapy in the last two weeks of life. This was up from 1993 -- 10 percent -- and is probably higher today. These individuals could have been peacefully preparing for death and instead were suffering through the trials of harsh treatment.

The solution -- that must be implemented by doctors -- is a willingness to accept that there is a time to stop followed by an honest conversation with the patient whose cancer has spread widely and is incurable.

Another study presented at this Atlanta meeting revealed that some patients are not being offered newer treatments that might truly save their lives. New lung cancer treatments have extended survival from 20 percent at one year to 50 percent, for example. Yet only 11 percent of doctors in one Wisconsin study would refer such patients for treatment.

It would be nice to know for sure that one life is about to end, regardless of treatment, and to know that another might be saved because of treatment. And maybe one day -- when treating cancer is an exact science -- this will be a reality.

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Reader Comments

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1. I wish, that doctors has good education

Posted at 9:58AM on Jun 9th 2006 by StylerS

2. I believe greater utilization of the various assay tests holds a key to solving some of the problems confronting a healthcare system that is seeking ways to best allocate available resources while accomplishing the critical task of matching individual patients with the treatments most likely to benefit them.

Some of these assays sometimes provide benefit to patients who have failed traditional therapies, many of which do not work for everyone, often have unwanted side effects, and most are extremely expensive. Most oncology practices are not treating with single-agent, but with combinations of chemotherapy drugs. This further exasterbates the problem.

One example is the Her2/neu. It can reasonably pick out the estimated 20% of breast cancer women at risk for recurrence, saving the other 80% of cancer patients the added expense, suffering and even death from having to take chemotherapy. Oncotype DX and EGFRx amplification/mutation have been proven in clinical decisions regarding treatment selection.

Since studies show that only 25-30% of patients do respond to chemotherapy that is available to them, there should be due consideration to looking at laboratory-based mechanisms for improving the match between tumors and an ever-increasing number of partially effective and very expensive drug therapies.

Posted at 3:00PM on Jun 10th 2006 by Gregory D. Pawelski

3. The new EGFRx (TM) Assay

The "targets" that the new "smart drugs" go after can be located on the "inside" or "outside" of a cancer cell. The most common targets on the outside are receptors, proteins that help relay chemical messages. And many targets on the inside are enzymes, proteins that help speed up chemical reactions in the body.

According to Chemical & Engineering News, targeted "small-molecule" therapies ruled at the annual ASCO meeting of oncologists. The most exciting results shown came from studies of multitargeted tyrosine kinase inhibitors, small molecules that act on multiple receptors in the cancerous cells, like Tykerb and Sutent. The trend IS away from the monoclonals to the small molecules, a trend which EGFRx (TM) may be able to hasten.

The new EGFRx (TM) assay will test drugs like Iressa, Tarceva, Sutent and possibly Nexavar, because of being small molecules. The monoclonal antibodies like Herceptin and Erbitux are "enormous" molecules. These very large molecules don't have a convenient way of getting access to the large majority of cells. Plus, there is multicellular resistance, the drugs affecting only the cells on the outside may not kill these cells if they are in contact with cells on the inside, which are protected from the drug. The cells may pass small molecules back and forth.

This may be why angiogenesis drugs may be a problem also (resistance). Some of these drugs work on anti-angiogenesis (starving tumors by shutting off their blood flow). However, tumors can acquire a blood supply by "three" different mechanisms: angiogenesis, co-option of existing blood vessels, and vasculogenic mimicry. "All" must be inhibited to consistently starve tumors of oxygen. Instead of growing new blood vessels, tumor cells can just grow along existing blood vessels, thus creating resistance to the drug.

Co-option (tumor cells growing along existing blood vessels) cannot be stopped with drugs that inhibit new blood vessel formation. Vasculogenic mimicry (some types of cancers form channels that carry blood but are not actual blood vessels) cannot be stopped with drugs that inhibit new blood vessel formation. The realization that starving tumors by shutting off their blood flow requires that "all three" mechanisms be addressed.

Drugs like Avastin (although a monoclonal antibody) can be tested with EGFRx (TM) because the target of Avastin is not the cells themselves, but rather a hormone (VEGF) secreted by the tumor cells. The Avastin complexes with free VEGF and blocks its action. The EGFRx (TM) test can discriminate between the activity of different targeted drugs and identify situations in which it is advantageous to combine the targeted drugs with other types of cancer drugs. All the more reason to "test the tumor first."

Posted at 4:57PM on Jun 20th 2006 by Gregory D. Pawelski



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