[gdpawel]

Sandy

I hope soon that they'll be able to have a genomic test for ovarian cancer (like Oncotype DX and MammaPrint for breast cancer, Lung Metagene Predictor for lung cancer, and DiagnoCure for colon cancer) to help find out if a cancer patient is "low" risk or "high" risk at having a recurrence if treated with surgery alone. If they are at "low" risk, they do not need to be unnecessarily exposed to toxic chemotherapy cocktails. If the test finds a patient to be at "high" risk, it is possible to design a treatment protocol from fresh "live" cancer tissues that have the best opportunity of being successful.

There is a campaign aloft by surgeons to encourage other surgeons to obtain and analyze fresh "live" tissues for both cell culture and molecular testing, and to brow best their medical oncologists to look at the results of these assays very carefully in the context of other known prognostic factors and choose agents based on patient profiles.

What needs to be done is to sort out what's the best profile in terms of which patients benefit from this drug or that drug. Can they be combined? What's the proper way to work with these new drugs? If a drug works extremely well for a certain percentage of cancer patients, identify which ones. If one drug or another is working for some people (not average populations) then obviously there are others out there who would also benefit.

Every cancer patient should have his/her own unique chemotherapy trial based on consultation of pathogenic profiles and drug sensitivity testing data. Having some foreknowledge of a given agent's expected result before its administration would benefit the "individual" patient (personalized cancer medicine). The oncologist should take advantage of all the "tools"available to him/her to treat a patient.

Your point about Herceptin and Tykerb is well taken. Monoclonal antibodies like Herceptin and Erbitux are "large" 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.

Exciting results have come from studies of "multitargeted" tyrosine kinase inhibitors, "small" molecules that act on multiple receptors in the cancerous cells, like Tykerb and Sutent. Tykerb is one of the first oral agents with the potential to compete directly with the IV drugs which is both a high-volume and high-revenue part of office-based practices. Early use of Tykerb will likely be limited to patients whose breast cancer is refractory to Herceptin. In the longer term, it could perhaps find a place to replace Herceptin's use.

Everyone is scared to death (and rightly so) at what is going to happen to the healthcare economic system with the introduction of these increasingly expensive new drugs that benefit only a small percentage of patients who receive them. It should be in the FDA's interest in saving the healthcare system perhaps billions of dollars a year (and thereby the healthcare system itself) by ensuring that expensive treatments are used appropriately. It should serve their interest in using currently available genetic and cell culture technologies to improve the effectiveness of existing drugs and save lives today by administering the right drug to the right patient at the right time.