The High Cost of Drugs

[Joe]

Nothing new to most of us..But an interesting article<

Regards
Joe

[gdpawel]

I would think that the major obstacle in controlling high cancer drug prices is the widespread inappropriate use of the drugs. As the increasing numbers and types of cancer drugs are developed, oncologists become more and more likely to misuse them in their practice. There is seldom a "standard" therapy which has been proven to be superior to any other therapy. What may work for one, may not work for another.

And the newer "targeted" therapeutics provide mostly small benefit to patients. Each of these new targeted drugs are not for everybody. Even when the disease is the same type, different patients' tumors respond differently to the same agents. These "smart" drugs do not work for everyone.

The needed change in the "war on cancer" will not be on the types of expensive drugs being developed, but on the understanding of all the drugs that are already out there. The system is overloaded with drugs (hundreds of them) and underloaded with the wisdom and expertise for using them.

Cancer chemotherapy could save more lives if pre-testing were incorporated into clinical medicine. The respected cancer journals are publishing articles that identify safer and more effective treatment regimens, yet few oncologists are incorporating these synergistic methods into their clinical practice. Cancer patients often suffer through chemotherapy sessions that do not integrate all possibilities.

It is impossible to design a single chemotherapy protocol that is effective against all types of cancer. The oncologist might need to administer several chemotherapy drugs at varying doses because tumor cells express survival factors with a wide degree of individual cell variability. The objective of pre-testing is to provide the patient with more options to discuss with their oncologist and to bring about multimodality approaches to improve the probability of a successful outcome.

It is highly desirable to know what drugs are effective against your particular cancer cells before these toxic agents are systemically administered into your body. Having a good tumor-drug match not only would improve survival rates, it would be cost-effective, and the high cost of the newer cancer therapies reinforces the necessity of choosing the right therapy the first time around.

Pre-testing on fresh specimens of cancer cells to determine the optimal combination of chemotherapy drugs could be more beneficial for many cancer patients. A failed attempt at chemotherapy is detrimental to the physical and emotional well being of patients, is financially burdensome, and may preclude further effective therapies. Patients, physicians and insurance carriers are all calling for predictive tests that allow for rational and cost-effective use of chemotherapeutic drugs.

[Sandy in Silicon Valley]

Dear Mr. Pawelski,

I completely agree - there are many, many cancer treatments available now, but only a very few ways of determining which txs are likely to be effective against which dxs!

I think this may be the next frontier in cancer diagnostics and treatments. There's a test, still needing refinements & expanded applicability, as I undertand it, called OncDX - which, when it works as it is intended, can predict which treatment is most likely to be effective against which cancer sub-type.

Within the breast cancer community, I've recently read that there are at least 6 subspecies of bc, and perhaps 130+ different specific cancers that fall in those subcategories. HER2neu+++ is, indeed, just one way of differentiating some breast cancers from others - it may be a fairly broad-stroke differentiation. At least, for me, I believe that when my metastasized disease was dx'd and px'd as HER2neu+++ (with the odds having been about 1:4 - not a small percentage, really!), it was a provident new opportunity to try a new drug's effectiveness against my very aggressive, insidious disease.

And it has worked, with and without synergistic chemo tx! Except in my brain, which is why I'm now on Tykerb as well, which I'm hoping will be equally effective as Herceptin, but also able to traverse the BBB. For me, this is no small progress - that the pathology test (which was not available in 1992, when I was first dx'd with Stage II bc) could determine my HER2neu protein over-expression, and that Herceptin has worked so well at slowing down/ killing off bcmets cells in my body.

I look forward to a day when EVERY patient dx'd with cancer, will be able to have their pathology include tests for which of the currently available treatments will be most likely to effectively stop/slow the cancer's progression.

I'm also very sorry to read (on your website) that your wife died of ovarian cancer. I commend you for staying on this list and providing your perceptions.

The difficulty, currently, of getting regular dx tests to catch ovarian cancer in its early stages, when it might be more successfully treatable, and its often asymptomatic presentation, have frightened me so much that, 5 years after my initial dx and tx for bc, learning that I carry a genetic mutation that predisposes me to bc and a variety of other cancers, including ovarian, I had a prophylactic oopherectomy. Then, when my bc recurrence was dx'd 5 years after that, the pathology indicated that the bcmets were no longer hormone-receptive...

Warm regards,
Sandy in Silicon Valley

[AlaskaAngel]

From Lani, on the main forum today:

http://her2support.org/vbulletin/showthread.php?t=30524

[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.