Talk:Chronic myelogenous leukemia

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WikiProject Medicine / Hematology-oncology (Rated B-class, High-importance)
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Does this article now need a reference and link to Bosutinib, possibly under the "Treatment-resistant CML" section? (talk) 10:05, 10 October 2015 (UTC)

Yes, the link to bosutinib has been added. — Preceding unsigned comment added by (talk) 02:05, 5 July 2016 (UTC)


"Long-term exposure to benzene may also contribute.[citation needed]" If someone wants to put this back in the article, find a reference. (talk) 00:11, 6 November 2009 (UTC)

"There was some evidence of an increased risk of AML and CLL. The meta-analysis indicated a lack of association between benzene exposure and the risk of CML." —Preceding unsigned comment added by Mizi mtl (talkcontribs) 06:15, 10 July 2010 (UTC)


where did chronic myeloid leukemia originate? from india?

In Japan. No, seriously, do you mean the origin of the malignant cells, or the origin of the term?
The cells come from the bone marrow. The term was probably coined in the 19th century in Germany. JFW | T@lk 21:05, 7 Apr 2005 (UTC)

can it harm the baby if you are pregnant[edit]

Why are you asking? If this concerns yourself you should be asking your doctor. JFW | T@lk 07:47, 15 November 2005 (UTC)

HSCT since imatinib[edit]

doi:10.1111/j.1365-2141.2007.06582.x - imatinib has markedly reduced need for bone marrow transplant in CML. JFW | T@lk 22:56, 2 May 2007 (UTC)


should say somewhere that also called CGL. chronic granulocytic leukemia.

  • Done. There seems to be a rather brief article on CGL in Wikipedia - I've suggested it should be merged with this article since it seems pointless to have two different articles dealing with the same illness. Jammycaketin (talk) 13:13, 12 December 2008 (UTC)


Lancet review today doi:10.1016/S0140-6736(07)61165-9 JFW | T@lk 15:05, 27 July 2007 (UTC)

Also an excellent review in the "How I treat..." section of Blood recently: PMID 17626839. And a very important study on drug treatment (e.g. imatinib and sons) vs. transplantation also came out in the past month in Blood: PMID 17317858. We should work these in. This article has been on my improvement list for a long time, but I haven't got around to it yet. Maybe we should start? It's about 50% of the way to being a very solid article. MastCell Talk 17:13, 27 July 2007 (UTC)

You fire the first salvo. After your golden touch to the AML article I trust this one is in good hands. JFW | T@lk 10:37, 31 July 2007 (UTC)

The J Clin Invest has a theme issue about Ph. May be useful. Here JFW | T@lk 20:38, 2 August 2007 (UTC)

References for drug trials[edit]

This is my humble opinion, but we shouldn't use commercial pharmaceutical company websites as references for any drug trials. First of all, FDA labeling prevents them from saying anything. Secondly, they're really meant for investors rather than anyone trying to understand this disease. I'll look up some primary research and fix the references on those trials. BTW, the commercial websites could be put in the additional reading section. OrangeMarlin Talk• Contributions 00:06, 8 September 2007 (UTC)

Agree; the treatment section sounds fairly self-promoting, as if it were pulled from - or written by - someone with a vested interest in that form of treatment. Secondly, although Wikipedia is often American-heavy, the articles *are* intended and used by international readers; hence, whether something is FDA-approved or not is not vital information. Anyone who has access to the treatment itself has access to better resources for whether it is nationally approved. Glacialfury (talk) 14:10, 23 September 2009 (UTC)


bcr-abl is only the first step in a cascade of oncogenesis. It seems PP2A plays a role, and PP2A inhibitors are doing interesting things doi:10.1172/JCI31095 JFW | T@lk 14:46, 10 September 2007 (UTC)


  • Genes are written in small letters like "abl" and not "ABL"
  • The gene transcripts or proteins are written in cabitals; eg: "abl" gene transcript is called "ABL"
  • I made the necessary correction long back but someone reverted it.
  • Thus, this article contains gross conventional mistakes.
  • Please discuss and correct.

sarindam7 (talk) 11:14, 13 April 2008 (UTC)

The New England Journal of Medicine uses caps for the name of the protein, eg BCR-ABL, and caps in italics for the name of the gene, eg BCR-ABL. But they use lower-case italics for mouse genes, and they sometimes use lower case for human genes, eg ras. What style book are you using? --Nbauman (talk) 00:10, 4 July 2009 (UTC)

The symptoms of thrombocytopenia[edit]

The most frequently observed platelet abnormality in newly diagnosed CML patients is thrombocytosis rather than thrombocytopenia. Because most of the patients are diagnosed in chronic phase rather than accelerated phase. In current edition, it is misleading.Steelshark (talk) 12:38, 18 June 2008 (UTC)steelshark

I'm trying to find an explanation about thrombocytosis associated with CML but to no avail. It's counterintuitive since CML is a Granulocyte-monocyte abnormality. Linuxo (talk) 15:03, 3 June 2018 (UTC)

My son has CML...[edit]

My son has CML...I dont understand why Wiki hasnt mentioned the drug he has been taking for 5 years to keep him it a lack of research? The drug is called come Wik?


I'm not sure as I have never heard of it. I am willing to do some research on the drug tommorrow as time permits and will include in the article if valid third party sources are found to provide useful information. B.s.n. R.N.contribs 10:03, 19 September 2009 (UTC)

Is there a cure?[edit]

Is there a complete cure for this disease?

No, at least not as of now. My spouse was diagnosed with CML seven years ago. As explained to me by an oncologist at Dana-Farber (Boston, MA), the Philadelphia chromosome positive cells are not homogeneous in their response to current medications and, in fact, have a very pronounced biphasic response. Imatinib is very effective for eliminating the vast majority of the population, but a small percentage of resistant cells survive. The conventional thinking is that discontinuation of therapy will result in relapse of the disease, and may also increase the risk for progression to accelerated phase. Obviously, a controlled experiment cannot be performed for ethical reasons. However, the possibility of a complete cure is a very hot topic for researchers. My understanding is that the resistant cells have properties similar to those of undifferentiated fetal stem cells. Your question points to an interesting topic that remains unaddressed on Wikipedia to my knowledge: the existence of distinct subsets of tumor cells in this and other neoplasms that are highly resistant to chemotherapy. SteveKatz123 (talk) 16:06, 29 June 2010 (UTC)

Nilotinib (Tasigna) versus Imatinib (Gleevec) as initial therapy for CML[edit]

The article mentions that dasatinib (Sprycell) and nilotinib (Tasigna) are currently approved to treat CML when imatinib (Gleevec) therapy fails. The article specifically mentions a trial to compare dasatinib with imatinib as initial therapy in newly diagnosed cases. There is no similar mention of a trial of nilotinib.

Last week, the New England Journal of Medicine published the initial results from an international, multi-center study of nilotinib versus imatinib in newly diagnosed patients. 846 new patients were randomly assigned to the two drugs. At 12 months, twice as many of the patients treated with nilotinib have achieved a major molecular response. Also, the patients taking nilotinib have a significant improvement in the time to progression to accelerated phase or blast crisis. The article is: Saglio, et. al., NILOTINIB VERSUS IMATINIB FOR NEWLY DIAGNOSED CHRONIC MYELOID LEUKEMIA, NEJM 2010; 362:2251-2259. I think this new information is worth including. SteveKatz123 (talk) 16:37, 29 June 2010 (UTC)


An anon posted this at the main Leukemia page:

This DNA mutation takes place with a crossover between cromosome 9 and 22,also known as the Philadelphia chromosome, specifically gene 34 and 11. During this cross over the ABL1 gene located on chromosome 9 is fused with the BCR gene on 22. This new gene, BCR-ABL, encodes an unregulated, cytoplasm-targeted tyrosine kinase that allows the cells to proliferate without being regulated by cytokines. This, in turn, allows the cell to become cancerous.

IMO it's too detailed for that article, but perhaps it would be useful here. WhatamIdoing (talk) 05:05, 22 October 2010 (UTC)


I have a question about the statement "The only well-described risk factor for CML is exposure to ionizing radiation." If I am understanding this correctly, wouldn't the Philadelpha translocation chromosome be a risk factor (present in 95% of CML cases), or does risk factor imply non-congenital? On a side note, I wanted to mention that I found pathophysiology section to be very well written and informative. Vokesk (talk) 16:16, 7 July 2012 (UTC)

Diagnosis phases[edit]

Approximately 85% of patients with CML are in the chronic phase at the time of diagnosis. The reference to this claim is cited as 5 which is about prediction qualities of JAK2. I have found no mention of the diagnosis phase. Am I missing anything or is the information unreferenced? — Preceding unsigned comment added by (talk) 15:04, 13 May 2014 (UTC)


doi:10.1016/S0140-6736(13)62120-0 Lancet JFW | T@lk 15:35, 12 April 2015 (UTC)