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The bcr-abl oncogene, present in 95% of patients with chronic myelogenous leukemia (CML), has been implicated as the cause of this disease. A compound, designed to inhibit the Abl protein tyrosine kinase, was evaluated for its effects on cells containing the Bcr-Abl fusion protein. Cellular proliferation and tumor formation by Bcr-Abl-expressing cells were specifically inhibited by this compound. In colony-forming assays of peripheral blood or bone marrow from patients with CML, there was a 98% decrease in the number of bcr-abl colonies formed but no inhibition of normal colony formation. This compound may be useful in the treatment of bcr-abl-positive leukemias.


24.HOW CAN I FIND MORE INFORMATION?

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Copyright © 1996, 1997 MPD Research Center
Most recent revision Saturday, December 20, 1997

GIF89a#! NETSCAPE2.0!,#U+U+++++UUUUUUUUՀUժUUUUUUUUU+UU+U+U+U+U+UUUUUUUUUUUUUUUUUUUՀUUUUUUUժUUUUUUUUUUUUUUUUU+U+++++UUUUUUUUՀUժՀUՀՀՀՀՀUU+U+++++UUUUUUUUՀUժժUժժժժ UUՀժ+U+Հ+ժ+++UUUՀUժUUUUՀժՀUՀժժUՀժUՀժU+U+++++UUUUUUUUՀUժUU𠠤zH*\ȰCF,oÁ+8ƍ =aEQX#ʏ!WrfJ1id9SK6}d)͝_4yT%OPqB$IŽ1fܸV-zKٳhӒ !,#/3:H///15(158::-5:=?JS?Xhv?WfvWu////$/////)///5DS/5DScq3RbpRpo//'/////.///8ER8R`o7Q_n}Qn}m////)////16//1=JW/=JVcp<Vbo|Uo|tn////,////6=//5BO[/BO[huAZgtZts///.////;E//:GT`/GS`myF_ly_yeEuϋ/xzH*\ȰCF,oÁ+8ƍ =aEQX#ʏ!WrfJ1id9SK6}d)͝_4yT%OPqB$IŽ1fܸV-zKٳhӒ !,#U+U+++++UUUUUUUUՀUժUUUUUUUUU+UU+U+U+U+U+UUUUUUUUUUUUUUUUUUUՀUUUUUUUժUUUUUUUUUUUUUUUUU+U+++++UUUUUUUUՀUժՀUՀՀՀՀՀUU+U+++++UUUUUUUUՀUժժUժժժժ UUՀժ+U+Հ+ժ+++UUUՀUժUUUUՀժՀUՀժժUՀժUՀժU+U+++++UUUUUUUUՀUժUU𠠤zH*\ȰCF,oÁ+8ƍ =aEQX#ʏ!WrfJ1id9SK6}d)͝_4yT%OPqB$IŽ1fܸV-zKٳhӒ !This GIF file was assembled with GIF Construction Set from: Alchemy Mindworks Inc. P.O. Box 500 Beeton, Ontario L0G 1A0 CANADA. This comment block will not appear in files created with a registered version of GIF Construction Set! GIFCONnb1.0  Clipboard  new02.gif  Clipboard; MPD-NET.CML-FAQ: Myeloproliferative Disorders

MPD-NET.CML-FAQ

Frequently Asked Questions About Chronic Myelogenous Leukemia

Maintained By: Joyce Niblack JNiblack@aol.com
FAX No. (602)-443-1154

MPD-NET CML-FAQ TEAM

Dave Benway (team leader)
Joyce Niblack (team leader)
Reg Clift. PhD
Richard Bolson
Alexandre Azevedo, MD

DISCLAIMER

Statements contained herein are of a general nature and should not be construed as personal advice in lieu of recommendations by your physician or other relevant professional consultant

INDEX

1.WHAT IS CML?

CML is shorthand for chronic myeloid, chronic myelocytic or chronic myelogenous leukemia (also known as chronic granulocytic leukemia or cgl) CML is a form of leukemia which affects the cells which make granulocytes (the polymorphs that eat bacteria) and the platelets (the little cells which help the blood to clot). In its early stages it produces an increase in the numbers of granulocytes and platelets but these cells still function normally and the patient may have no symptoms. This situation may continue for 3 or 4 years (known as chronic phase) and the disease may be unsuspected with the diagnosis made incidentally in the course of an insurance examination or a pre-anesthetic work-up. However, eventually the nature of the disease changes and CML starts to behave like other leukemias. These changes are called transformation and are often slight to start with (accelerated phase), but within 6 months or so usually progress to the full-blown leukemic picture (blast phase). Survival from the development of blast phase is usually measured in months. CML is one of the myeloproliferative disorders.


2.WHAT ARE THE SYMPTOMS?

Patients often have nonspecific symptoms such as fatigue, weakness, loss of appetite or weight loss, or are diagnosed from blood studies done for other reasons. When patients are first seen, the spleen is usually moderately enlarged which can cause epigastric distress and a sense of fullness. Minor lymphadenopathy (minor problems with the lymph nodes) can occur but this is much less evident than in CLL. Hemostatis is rarely impaired until late, after "blastic transformation" develops or after therapy or the evolution of the disease leads to thrombocytopenia (low platelet counts). In patients who develop thrombocytosis (platelets greater than 1,000,000), homeostatic problems may be secondary to inadequate platelet function.


3. HOW IS CML DIAGNOSED?

CML is generally considered in patients with an elevation in blood granulocyte concentration if the explanations of infection and inflammation aren't likely. The differential diagnosis includes the other myeloproliferative disorders, myelofibrosis, polycythemia vera, other causes of leukocytosis (inflammation or infection). The presence of enlarged spleen, the characteristic blood picture, bone marrow aspirate, leukocyte alkaline phosphatase test and the presence of the Philadelphia (Ph) chromosome help in differentiation.


4.WHAT ARE THE LABORATORY FINDINGS IN DIAGNOSIS?

Granulocyte count of more than 30,000 (normal 4 - 8,000) with the cells maturing in an orderly fashion. Platelet count more than 400,000 (normal 150 - 350,000). The marrow is packed with large numbers of mature and maturing granulocytes. When the chromosomes of these cells are examined by cytogenetic tests, a particular type of deformed chromosome is discovered. This is known as the Philadelphia chromosome (Ph chromosome) and its presence is diagnostic of CML (although very rarely it can be found in other types of leukemia). However, a small percentage of CML patients are Ph negative. Unless the Ph chromosome or the BCR/ABL product can be detected, the correct diagnosis is not CML, and the patient has a different type of MPD.


5. WHAT IS THE PHILADELPHIA CHROMOSOME, BCR-ABL?

BCR-ABL stands for the name given to an abnormal gene that is the result of a fusion of material from 2 chromosomes (22 and 9). In fact, this has everything to do with CML and the Philadelphia chromosome. This Philadelphia (PH) chromosome is an abnormal chromosome that results from an exchange of material (DNA) between the normal chromosomes 22 and 9. It is present in over 90% of CML cases. In chromosome 9, there is a gene called c-abl (from "Abelson"). A break occurs beside this gene, and it is translocated to a place in chromosome 22, called bcr (breakpoint cluster region). What happens then is the fusion of these two pieces of DNA, that gives rise to a fusion gene (bcr-abl). This fusion gene is involved in the pathogenesis of CML and possibly other leukemias (e.g. ALL). Also, it serves as a molecular marker of PH-positive cells, and is currently screened by PCR in the post-BMT period. Very interestingly, bcr-abl might prove useful as a target for specific treatment with antibodies directed to it. That, if feasible, would permit us to attack only the leukemic cells, sparing normal tissues from the damage caused by chemotherapy (which is not selective for leukemic tissue).


6.WHAT ARE THE TREATMENT OPTIONS FOR CML?

For many years the only treatment was palliation with the drug busulfan (also known as myleran). This treatment reduces the number of white GIF89aPkei3gKfDx_hxʠ\3_/mCf3"#$(%K#Á>=ţB- \] =^"i( `B!%ărvI!=ȸI@J-PРSߎXBl]v- {9,DD[oO# 4@eBU3U$tØ@ %@s7;Dx KR#V %@C PB? cW8 IV3H-!dgl CLhU &NVU<Ͽ /([aOlŀ$& H489zK3OVjU@EXR_+p!fP~@1n$(F\Ƌ)\av RJ "!P?828n%EhpcS)Bd#~0P>8 pЦGκKoZXt+\/@9- ЃsQ#8ED@dRPa\ FRΩ)J<-7ՠ 4(0GEͤCw<@vq.1Qd帙o2.ʀ f6ؠrvKSF7 <`+@/xIKZao(GgF_J^JڂdLJ<"MNK"oQ9Q(1 $f7@G;=% tP2 ԙڔ"PĈ@@mXi`@'D!)i Ep!^PؔƩrQ;ǜq 5T@ ZQQRW@ g܈u0b|@  WP̰ͩBY \9 !2}J