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Chronic myelogenous leukemia

Chronic myelogenous leukemia (or CML) is a form of chronic leukemia characterised by increased production of myeloid cells in the bone marrow. It is a type of myeloproliferative disease associated with a characteristic chromosomal translocation termed the Philadelphia chromosome. It is traditionally treated with chemotherapy, interferon and bone marrow transplantation, although a specific inhibitor (imatinib mesylate) has radically changed the management. more...

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Signs and symptoms

Patients are often asymptomatic at diagnosis, presenting incidentally with an elevated white blood count on a routine laboratory test. Symptoms may include: malaise, low grade fever, increased susceptibility to infections, anemia and thrombocytopenia with resultant bruising (although an increased platelet count, thrombocytosis, may be a feature). Splenomegaly may also be seen.

The disease may remain dormant for years, but a proportion proceed to accelerated phase (in which the diseases progresses rapidly) or overt blast crisis, which has the symptoms and risks of acute myelogenous leukemia (AML).

Diagnosis

CML is often suspected on the basis on the full blood count, which shows increased granulocytes of all types (including basophils). When the index of suspicion is high, a bone marrow biopsy is required to distinguish CML from other diseases that feature the same symptoms.

Ultimately, CML is diagnosed by detecting the Philadelphia chromosome (a translocation between the 9th and 22nd chromosome leading to an aberrant protein that drives cell division). This translocation leads to bcr-abl fusion and activation of protein tyrosine kinase cascade.

Disease activity can be determined on the basis of the bone marrow examination, cytogenetics and by quantitative PCR.

Pathophysiology

CML was the first malignancy to be linked to a clear genetic abnormality, the chromosomal translocation named Philadelphia chromosome, in 1960. The fusion of two genes on chromosomes 9 and 22, termed abl and bcr respectively, leads to a protein that propels mitosis and causes genomic instability (leading to further mutations).

CML progresses to accelerated phase, and then blast crisis, when additional genetic abnormalities speed up the rate at which new malignant cells are produced in the bone marrow. A second Philadelphia chromosome may appear, as well as deletions of (parts of) chromosomes.

Epidemiology

CML occurs in all age groups, but most commonly in the middle-aged and elderly. Its annual incidence is about 1 per million.

Treatment

Chronic phase

Chronic phase CML is treated with imatinib (marketed as Gleevec or Glivec; previously known as STI-571). In the past, hydroxyurea, alkylating agents (e.g. cytarabine), interferon alfa 2b and steroids were used, but this has been replaced by imatinib. Imatinib is a new agent which specifically targets the abnormality caused by the Philadelphia chromosome. It is better tolerated and more effective than previous therapies. Bone marrow transplants were also used as initial treatment for CML before imatinib and can be curative. In patients who fail to achieve a cytogenetic remission with imatinib or who relapse while on imatinib, a bone marrow transplant should be considered.

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Stopping a killer with interferon? - chronic myelogenous leukemia
From Science News, 4/26/86 by Joanne Silberner

Stopping a killer with interferon?

By name alone, chronic myelogenous leukemia (CML) might not sound as serious as acute leukemia. But CML moves quickly from chronic to fatal, generally killing its victims within three-and-a-half years after diagnosis, regardless of chemotherapy. In an effort to halt that progression, researchers at the M.D. Anderson Hospital in Houston have treated patients with a genetically engineered form of interferon. While it is too early to tell if the treatment reverses the disease, it did normalize in the April 24 NEW ENGLAND JOURNAL OF MEDICINE.

The researchers, led by Moshe Talpaz and Jordan Gutterman, treated 17 patients. In the 13 responders, who have been on the therapy for up to 15 months, blood cell counts returned to normal. Side effects were relatively minor. "We just don't know the impact on survival yet," says Gutterman. "But that you can use a natural substance to get the blood counts and [genetics] normal is exciting."

More than 90 percent of CML cases are marked by a jump of genetic material from one chromosome to another; in six of the 13 responders, cells with the abnormality disappeared (though in one of these patients it returned after the paper had gone to press).

"That's very impressive," comments Ken Foon, a cancer researcher at the University of Michigan in Ann Arbor. "Whether that will translate into a cure or prolonged survival I don't know, but we can't do that with [conventional] drugs." Ezre Raze, head of the CML program at Roswell Park Memorial Institute in Buffalo, N.Y., says it is not known yet if the genetic abnormality is a cause of CML. "If it is," she says, "then getting rid of it should eradicate the disease." But if the change is a result rather than a cause, normalizing it won't help. "I think only time will tell," she says.

COPYRIGHT 1986 Science Service, Inc.
COPYRIGHT 2004 Gale Group

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