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Yes!
Over the last seven years, the New York Times has been on this topic like white on rice, as Dr. Brian Klepper, Director of the Center for Practical Health Reform, described it in a recent posting on The Doctor Weighs In blog.
While the Harvard/Michigan study documented what happen before the new Medicare law, a survey by Dr. Neil Love, "Patterns of Care," showed results that the Medicare reforms still were not working. It was still an impossible conflict of interest.
With the lastest New York Times articles exploring the deep financial conflicts in oncology drug prescribing, Dr. Klepper stated, even though Medicare has limited the profits of oncologists who prescribe drugs, Medicare's total cancer care expenditures keep rising because oncologists have found new treatments and procedures to bill for. And the rules guiding Medicare reimbursement for cancer and drug rebates are complex, resulting in patients often receiving more costly drugs.
The government wasn't reducing payment for cancer care under the new Medicare bill. They were simply reducing overpayment for chemotherapy drugs, and paying cancer specialists the same as other physicians. The government can't afford to overpay for drugs, in an era where ALL these new drugs are being introduced, which are fantastically expensive.
Although the new Medicare bill tried to curtail the Chemotherapy Concession, private insurers still go along with it. What needs to be done is to remove the profit incentive from the choice of drug treatments. Medical oncologists should be taken out of the retail pharmacy business and let their expertise as doctors prevail.
In regards to the first link article, aside from the financial incentives working here, there are marked differences between these two drugs.
Cells are the most basic structure of the body. Cells make up tissues, and tissues make up organs, such as the lungs or liver. Each cell is surrounded by a membrane, a thin layer that separates the outside of the cell from the inside.
For a cell to perform necessary functions for the body and respond to its surroundings, it needs to communicate with other cells in the body. Communication occurs through chemical messages in a process called signal transduction. The purpose of these signals is to tell the cell what to do, such as when to grow, divide into two new cells, and die.
Targeted cancer therapies use drugs that block the growth and spread of cancer by interfering with specific molecules involved in carcinogenesis (the process by which normal cells become cancer cells) and tumor growth. By focusing on molecular and cellular changes that are specific to cancer, targeted cancer therapies may be more effective than current treatments and less harmful to normal cells (although some have their own insidious side effects).
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. But, is something more elemental going on? Does the drug even enter the cell? Once entered, does it immediately get metabolized or pumped out, or does it accumulate?
Cell culture assays with "functional profiling" are able to measure the response of tumor cells to drug exposure. Following this exposure, it measures both cell metabolism and cell morphology. The effect of drugs on the whole cell, resulting in a cellular response to the drug, measuring the interaction of the entire genome. The variety of metabolic and apoptotic measurements are used to determine if the specific drug was successful at killing the patient's cancer cells.
Results from these assays can show that some clones of tumor cells don't accumulate the drug. These cells won't get killed by it. But you wouldn't pick this up with an assay which only measured the kinases themselves. A "functional profiling" assay measures the net effect of everything which goes on. Are the cells ultimately killed, or aren't they?
Each of these new targeted drugs are not for everybody (just like conventional cancer drugs are not for everybody). Even when the disease is the same type, different patients' tumor respond differently to the same agents. As the saying goes, "don't throw out the baby with the bath water." If a drug works extremely well for only 10% of cancer patients, identify which 10%. If one drug or another is working for "some" people (not average populations), then obviously there are others out there who would also benefit.
The methods of cancer medicine during the last thirty some years are coming to haunt the "one-size-fits-all" establishment. Technologies, developed over the last twenty years by private researchers, hold the 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.
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