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Types of Cancer > Leukemia > Chronic Myelogenous Leukemia (CML) > Overview
Chronic Myeloid Leukemia (CML): The Basics
Carolyn Vachani, RN, MSN, AOCN
Affiliation:
Abramson Cancer Center of the University of Pennsylvania
Last Modified: September 22, 2007
This article is a more specific discussion of CML. Please be sure to read Leukemia: The Basics first, so you have a basic understanding of leukemia.
The discovery of CML
CML is a chronic blood cancer that starts with a defect in two chromosomes and results in an overgrowth of white blood cells. Each person has 23 chromosomes, which contain DNA and a person's genetic makeup (genes). While CML has been recognized since the late 1800's, it was the discovery of the Philadelphia chromosome in 1960 that changed the face of CML.
Drs. Peter Nowell and David Hungerford, two Philadelphia researchers, were experimenting with cells from various types of leukemia when one noticed a smaller-than-normal chromosome number 22 on the cancer cells of 2 individuals with CML. With the far less sophisticated techniques of the time, they were unable to tell what happened to the material missing from the small chromosome.
Nowell and Hungerford published their research in 1960, describing the abnormality that had then been found in 9 out of 10 CML patients they studied. The findings were confirmed by a group in the United Kingdom, and the abnormality was subsequently named the Philadelphia Chromosome, for the city in which it was discovered. Nowell and Hungerford had demonstrated that this genetic change was required for the development of CML a novel and often unaccepted concept at that time.
It would be 1972 before another researcher; Janet Rowley, MD, would discover the missing piece of chromosome number 22 attached to chromosome number 9, thereby identifying the first known chromosomal translocation. The 9;22 translocation is found on the leukemic cells of more than 95% of patients with CML. As the field of genetics grew, it was discovered that the gene abl (pronounced “able”), normally located on chromosome 9, had attached itself to the gene bcr (pronounced “b-c-r”) on chromosome 22. The bcr-abl gene causes the cell to release an abnormal protein (called tyrosine kinase), resulting in too many stem cells developing into white blood cells, leaving a shortage of other cell types. This genetic change to bcr-abl occurs during a person's lifetime and is not passed on to future generations or inherited from parents.
You may wonder why all of this is important. Well, these discoveries led to the development of a drug, called Gleevec, which changed the lives of people with CML, which we will discuss later.
The facts about CML
CML accounts for about 15% of all leukemia cases in the United States, with an estimated 4,570 new cases to be diagnosed in 2007. The Leukemia & Lymphoma Society estimates that over 21,500 people are living with CML. It can occur at any age, but most often occurs in people over age 50. Only 10% of people diagnosed with CML are under the age of 20.