I am not sure where you are being treated but I hope it is at a specialist haematology centre?
CMML is a myeloproliferative disorder see list below. First of all it seems that a small number of patients with MPD's have a rearrangement of the platelet derived growth factor receptor - PDGFR- for CMML this is PDGFRb through TEL-PDGFRb
CMML patients with this particular rearrangement responded to treatment with imatinib.... see published articles below.
The MPDs - include
chronic myelomonocytic leukemia (CMML),
systemic mast cell disease (SMCD),
polycythemia vera (PV),
essential thrombocythemia (ET),
chronic eosinophilic leukemia (CEL),
primary myelofibrosis (PMF)......
However the list now excludes CML because of the importance of the BCR-ABL translocation for diagnosis and treatment with imatinib and other TKI's.
I suggest as a first step you might register for the online forum at
http://www.mpninfo.org/register.html
MPN-NET/MPN Education Foundation:
www.mpninfo.org
MPD's are classified as MPN's -MyeloProliferative Neoplasms.
I have done some very brief searches re: CMML and current therapy and it seems that stem cell transplant is recommended in those who are eligible (i.e age plus fitness level and whether you can locate a donor)-
However, there are some published articles that show CMML with the particular rearrangement outlined above- or with the
ETV6-PDGFRB fusion gene do respond to imatinib (Glivec).
I have copied some snippets and links from the articles...
I hope this is of some help.
Best wishes,
Sandy
"Some "empiric use of imatinib in CEL and CMML led to significant clinical benefit and the discovery of the role of rearrangements of the platelet derived growth factor receptor - ...
PDGFRb (beta)........for CMML."
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http://www.ncbi.nlm.nih.gov/pubmed/12181402
Response to imatinib mesylate in patients with chronic myeloproliferative diseases with rearrangements of the platelet-derived growth factor receptor beta.
Apperley JF, Gardembas M, Melo JV, Russell-Jones R, Bain BJ, Baxter EJ, Chase A, Chessells JM, Colombat M, Dearden CE, Dimitrijevic S, Mahon FX, Marin D, Nikolova Z, Olavarria E, Silberman S, Schultheis B, Cross NC, Goldman JM.
Department of Haematology, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom. j.apperley@ic.ac.uk
Abstract
BACKGROUND:
A small proportion of patients with chronic myeloproliferative diseases have constitutive activation of the gene for platelet-derived growth factor receptor beta (PDGFRB), which encodes a receptor tyrosine kinase.
The gene is located on chromosome 5q33, and the activation is usually caused by a t(5;12)(q33;p13) translocation associated with an ETV6-PDGFRB fusion gene.
METHODS:
We treated four patients who had chronic myeloproliferative diseases and chromosomal translocations involving 5q33 with imatinib mesylate (400 mg daily). Three of the four patients presented with leukocytosis and eosinophilia; their leukemia cells carried the ETV6-PDGFRB fusion gene. The fourth patient had leukocytosis, eosinophilia, and a t(5;12) translocation involving PDGFRB ....
CONCLUSIONS:
Imatinib mesylate induces durable responses in patients with chronic myeloproliferative diseases associated with activation of PDGFRB.
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Durable responses to imatinib in patients with PDGFRB fusion gene-positive and BCR-ABL-negative chronic myeloproliferative disorders.
David M, Cross NC, Burgstaller S, Chase A, Curtis C, Dang R, Gardembas M, Goldman JM, Grand F, Hughes G, Huguet F, Lavender L, McArthur GA, Mahon FX, Massimini G, Melo J, Rousselot P, Russell-Jones RJ, Seymour JF, Smith G, Stark A, Waghorn K, Nikolova Z, Apperley JF.
Source
Department of Haematology, University of Pecs, Pecs, Hungary.
Abstract
Fusion genes derived from the platelet-derived growth factor receptor beta (PDGFRB) or alpha (PDGFRA) play an important role in the pathogenesis of BCR-ABL-negative chronic myeloproliferative disorders (CMPDs).
http://www.ncbi.nlm.nih.gov/pubmed/16960151