Research on leukemias were always allowed to advance fundamental knowledge in cancer. Is an once again the case with second generation targeted molecules available this year to treat chronic myeloid leukemia. "Mauricette Michallet lack neither enthusiasm nor experience. The hematologist of hôpital Edouard-Herriot in Lyon, the fight against this scourge is to take a step with the arrival of a new generation of "smart" molecules selectively removing the diseased cells. "We now have a wide range of solutions enabling us to support effectively the disease", announces the Lyon physician.
In fact, the results presented at the recent Congress of the American Society of Hematology (ASH) in Orlando, Florida, contain good news and bad news. Positive side, the pharmacy industry continue to discover molecules targeted, able to identify the tumor cells circulating in the blood. Reverse of the Medal, the first cases of resistance to these innovative therapies appear in treated patients. Outcome of the race apparently endless: must be a blow to advance on the enemy. But, little by little, the cancer began to have a therapeutic arsenal of molecules adapted to each type of cancer. These multi purpose: identify tumor cells by"the ends".
Imatinib, the molecule apparition Novartis features in 2001 (Glivec), was one of the pioneers of this family. "This was a revolution." "We have seen patients with chronic myeloid leukemia regained taste for life and an almost normal activity," reported Mauricette Michallet.
The CMA is a serious and rare disease (600 new cases per year in France). It is due to a well identified non-hereditary chromosome anomaly: the Philadelphia chromosome. It results in an overproduction of white blood cells in the bone marrow, the plant for the production of blood cells: red, white cells and platelets. "It's like a runaway of the chain of production of lymphocytes", said Dr. Michallet.
This accumulation of white blood cells become immortal translates into intense fatigue. Without treatment, the disease progresses to a fatal outcome in three phases (chronic, accelerated, and acute). For a long time therapies were limited to the bone marrow transplant (risky and made difficult by the lack of compatible donors) and interferon-alpha (causing heavy side effects). The first clinical trials of Imatinib started in 1998. In 2002, his arrival on the market has revolutionized the support of the disease. But the first cases of therapeutic escape emerged quickly. "We have identified the gene a large number of mutations responsible for these resistances", adds the Professor François Guilhot, hematologist at the CHU of Poitiers.
In fact, this problem is recurring in oncology. It was therefore more or less expected by therapists. As of 2002, Bristol-Myers Squibb laboratory was launched on a different track: a molecule which blocks the intracellular signals and acts on most of the listed mutations: dasatinib. In the United States, this multi-focused (trade name Sprycel) molecule has received a certification procedure ultrafast ("fast track") on the part of the Agency for the approval of drugs (Food and Drug Administration). "This was very quickly." The first evidence of activity has been discovered in 2001, the first patient was treated in 2003 and a communication has been published in "Science" in July 2004. "The green light from the FDA was obtained in June 2006," said Dr. Francis Lee, discoverer of dasatinib at the research centre of BMS in Princeton in the United States. In Europe, a cohort of patients included in a clinical trial launched in 2003 was handled by this molecule. "It is a good solution for patients resistant to existing treatments, but effectiveness depends on the mutation affecting each individual," reports Martin Müller, researcher at the University of Heidelberg in Germany who coordinated clinical trials German.
BMS is not the only industry in the running in this race to the target molecules. Orlando, Novartis introduced the successor of Gleevec (nilotinib called Tasigna) and Merck announced his arrival in the camp of the producers of the tyrosine kinase inhibitors. This novelty (Aurora phase 1/2) is effective on a mutation that eludes to other molecules (T 3151). Only disadvantage, the almost miraculous treatments reach the huge price levels: 134 EUR per day in the case of dasatinib and an amount equivalent to other molecules.
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