292:
234:
336:
344:
630:
situations it may be the preferred myelosuppressive agent due to its relative lack of leukemogenic effects and hence the relative lack of potential for secondary haematologic malignancies to result from treatment. IRIS, an international study that compared interferon/cytarabine combination and the first of these new drugs imatinib, with long-term follow up, demonstrated the clear superiority of tyrosine-kinase-targeted inhibition over existing treatments.
167:(TKIs) which have led to dramatically improved long-term survival rates since 2001. These drugs have revolutionized treatment of this disease and allow most patients to have a good quality of life when compared to the former chemotherapy drugs. In Western countries, CML accounts for 15–25% of all adult leukemias and 14% of leukemias overall (including the pediatric population, where CML is less common).
3095:
328:
447:. Drug treatment will usually stop this progression if early. One of the drivers of the progression from chronic phase through acceleration and blast crisis is the acquisition of new chromosomal abnormalities (in addition to the Philadelphia chromosome). Some patients may already be in the accelerated phase or blast crisis by the time they are diagnosed.
456:
how early the disease was diagnosed as well as the therapies used. In the absence of treatment, the disease progresses to an accelerated phase. Precise patient staging based on clinical markers and personal genomic profile will likely prove beneficial in the assessment of disease history with respect to progression risk.
646:(FDA) in 2001. Imatinib was found to inhibit the progression of CML in the majority of patients (65–75%) sufficiently to achieve regrowth of their normal bone marrow stem cell population (a cytogenetic response) with stable proportions of maturing white blood cells. Because some leukemic cells (as evaluated by
709:, administered subcutaneously (under the skin) in patients who had failed with imatinib and exhibited T315I kinase domain mutation. This is a study which is ongoing through 2014. In September 2012, the FDA approved omacetaxine for the treatment of CML in the case of resistance to other chemotherapeutic agents.
311:, causing genomic instability and making the cell more susceptible to developing further genetic abnormalities. The action of the BCR-ABL protein is the pathophysiologic cause of chronic myelogenous leukemia. With improved understanding of the nature of the BCR-ABL protein and its action as a tyrosine kinase,
455:
Approximately 85% of patients with CML are in the chronic phase at the time of diagnosis. During this phase, patients are usually asymptomatic or have only mild symptoms of fatigue, left side pain, joint and/or hip pain, or abdominal fullness. The duration of chronic phase is variable and depends on
689:
While capable of producing significantly improved responses compared with the action of imatinib, neither dasatinib nor nilotinib could overcome drug resistance caused by one particular mutation found to occur in the structure of BCR-ABL1 known as the T315I mutation (in other words, where the 315th
224:
CML is more common in males than in females (male to female ratio of 1.4:1) and appears more commonly in the elderly with a median age at diagnosis of 65 years. Exposure to ionising radiation appears to be a risk factor, based on a 50 fold higher incidence of CML in
Hiroshima and Nagasaki nuclear
780:
The
American Cancer Society estimates that in 2014, about 5,980 new cases of chronic myeloid leukemia were diagnosed, and about 810 people died of the disease. This means that a little over 10% of all newly diagnosed leukemia cases will be chronic myeloid leukemia. The average risk of a person
535:
The patient is considered to be in the accelerated phase if any of the above are present. The accelerated phase is significant because it signals that the disease is progressing and transformation to blast crisis is imminent. Drug treatment often becomes less effective in the advanced stages.
379:
is often performed as part of the evaluation for CML, and CML is diagnosed by cytogenetics that detects the translocation t(9;22)(q34;q11.2) which involves the ABL1 gene in chromosome 9 and the BCR gene in chromosome 22. As a result of this translocation, the chromosome looks smaller than its
629:
translocation. Despite the move to replacing cytotoxic antineoplastics (standard anticancer drugs) with tyrosine kinase inhibitors sometimes hydroxyurea is still used to counteract the high leukocyte counts encountered during treatment with tyrosine kinase inhibitors like imatinib; in these
712:
Independently, ARIAD pharmaceuticals, adapting the chemical structures from first and second-generation TK inhibitors, arrived at a new pan-BCR-ABL1 inhibitor which showed (for the first time) efficacy against T315I, as well as all other known mutations of the oncoprotein. The drug,
662:, blocks several further oncogenic proteins, in addition to more potent inhibition of the BCR-ABL protein, and was approved in 2007, by the U.S. Food and Drug Administration (FDA) to treat CML in people who were either resistant to or intolerant of imatinib. A second TK inhibitor,
674:
received US FDA and EU European
Medicines Agency approval on 4 September 2012, and 27 March 2013, respectively for the treatment of adults with Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML) with resistance, or intolerance to prior therapy.
758:
A 2011 followup of 832 patients using imatinib who achieved a stable cytogenetic response found an overall survival rate of 95.2% after 8 years, which is similar to the rate in the general population. Fewer than 1% of patients died because of leukemia progression.
507:
Additional clonal chromosomal abnormalities in
Philadelphia (Ph) chromosome-positive (Ph+) cells at diagnosis, including so-called major route abnormalities (a second Ph chromosome, trisomy 8, isochromosome 17q, trisomy 19), complex karyotype, and abnormalities of
2032:
Monestime S, Al
Sagheer T, Tadros M. Asciminib (Scemblix): A third-line treatment option for chronic myeloid leukemia in chronic phase with or without T315I mutation. Am J Health Syst Pharm. 2023 Jan 5;80(2):36-43. doi: 10.1093/ajhp/zxac286. PMID:
581:
treatment. Due to the high median age of patients with CML it is relatively rare for CML to be seen in pregnant women, despite this, however, chronic myelogenous leukemia can be treated with relative safety at any time during pregnancy with the
472:. The WHO criteria are perhaps most widely used, and define the accelerated phase by the presence of ≥1 of the following haematological/cytogenetic criteria or provisional criteria concerning response to tyrosine kinase inhibitor (TKI) therapy
717:, gained FDA approval in December 2012 for treatment of patients with resistant or intolerant CML. Just as with second-generation TK inhibitors, early approval is being sought to extend the use of ponatinib to newly diagnosed CML also.
564:
The only curative treatment for CML is a bone marrow transplant or an allogeneic stem cell transplant. Other than this there are four major mainstays of treatment in CML: treatment with tyrosine kinase inhibitors, myelosuppressive or
650:) persist in nearly all patients, the treatment has to be continued indefinitely. Since the advent of imatinib, CML has become the first cancer in which a standard medical treatment may give to the patient a normal life expectancy.
403:
CML, or cases of suspected CML in which the
Philadelphia chromosome cannot be detected. Many such patients in fact have complex chromosomal abnormalities that mask the (9;22) translocation, or have evidence of the translocation by
1296:"Proposals and rationale for revision of the World Health Organization diagnostic criteria for polycythemia vera, essential thrombocythemia, and primary myelofibrosis: recommendations from an ad hoc international expert panel"
319:) that specifically inhibit the activity of the BCR-ABL protein have been developed. These tyrosine kinase inhibitors can induce complete remissions in CML, confirming the central importance of bcr-abl as the cause of CML.
781:
getting this disease is 1 in 588. The disease is more common in men than women, and more common in whites than
African-Americans. The average age at diagnosis is 64 years, and this disease is rarely seen in children.
666:, was approved by the FDA for the same indication. In 2010, nilotinib and dasatinib were also approved for first-line therapy, making three drugs in this class available for treatment of newly diagnosed CML. In 2012,
2245:
2230:
849:"Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980-2015: a systematic analysis for the Global Burden of Disease Study 2015"
755:
With the use of tyrosine kinase inhibitors, survival rates have improved dramatically. A 2006 follow-up of 553 patients using imatinib (Gleevec) found an overall survival rate of 89% after five years.
2177:
800:"Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015"
303:
subunit. The BCR-ABL transcript is continuously active and does not require activation by other cellular messaging proteins. In turn, BCR-ABL activates a cascade of proteins that control the
2045:"Effect of a p210 multipeptide vaccine associated with imatinib or interferon in patients with chronic myeloid leukaemia and persistent residual disease: a multicentre observational trial"
190:
may put pressure on the stomach causing a loss of appetite and resulting weight loss. It may also present with mild fever and night sweats due to an elevated basal level of metabolism.
412:
in spite of normal routine karyotyping. The small subset of patients without detectable molecular evidence of BCR-ABL1 fusion may be better classified as having an undifferentiated
1845:
724:(Scemblix), the first TK inhibitor specifically targeting the ABL1 myristoyl pocket (STAMP) via allosteric binding, as a third-line option for patients with chronic-phase-CML.
48:
2970:
178:
Most patients (~90%) are diagnosed during the chronic stage which is most often asymptomatic. In these cases, it may be diagnosed incidentally with an elevated
431:
CML is often divided into three phases based on clinical characteristics and laboratory findings. In the absence of intervention, CML typically begins in the
2260:
670:
joined the class of novel agents in the inhibition of the BCR-ABL protein and was approved in South Korea for people resistant to or intolerant of imatinib.
464:
Criteria for diagnosing transition into the accelerated phase are somewhat variable; the most widely used criteria are those put forward by investigators at
2189:
2450:
798:
Vos T, Allen C, Arora M, Barber RM, Bhutta ZA, Brown A, et al. (GBD 2015 Disease and Injury
Incidence and Prevalence Collaborators) (October 2016).
2891:
2601:
2554:
2455:
847:
Wang H, Naghavi M, Allen C, Barber RM, Bhutta ZA, Carter A, et al. (GBD 2015 Mortality and Causes of Death
Collaborators) (October 2016).
1960:"Homoharringtonine (Omacetaxine Mepesuccinate) in Treating Patients With Chronic Myeloid Leukemia (CML) With the T315I BCR-ABL Gene Mutation"
1871:
Jabbour E, Cortes JE, Giles FJ, O'Brien S, Kantarjian HM (June 2007). "Current and emerging treatment options in chronic myeloid leukemia".
752:
Before the advent of tyrosine kinase inhibitors, the median survival time for CML patients had been about 3–5 years from time of diagnosis.
2379:
2345:
2750:
2460:
413:
1418:
1401:
970:
658:
To overcome imatinib resistance and to increase responsiveness to TK inhibitors, four novel agents were later developed. The first,
17:
548:, with rapid progression and short survival. Blast crisis is diagnosed if any of the following are present in a patient with CML:
2871:
1924:
Kimura S, Ashihara E, Maekawa T (October 2006). "New tyrosine kinase inhibitors in the treatment of chronic myeloid leukemia".
1242:"Clinical features at diagnosis in 430 patients with chronic myeloid leukaemia seen at a referral centre over a 16-year period"
705:
released results of an open-label Phase 2/3 study (CGX-635-CML-202) that investigated the use of a non BCR-ABL targeted agent
2527:
2350:
1699:
3036:
2886:
347:
A small, hypolobated megakaryocyte (center of field) in a bone marrow aspirate, characteristic of chronic myeloid leukemia.
1846:"FDA approves Novartis Scemblix (asciminib), with novel mechanism of action for the treatment of chronic myeloid leukemia"
272:
on chromosome 9. This abnormal "fusion" gene generates a protein of p210 or sometimes p185 weight (p210 is short for 210
175:
The way CML presents depends on the stage of the disease at diagnosis as it has been known to skip stages in some cases.
249:. This chromosomal abnormality is so named because it was first discovered and described in 1960 by two scientists from
276:
protein, a shorthand used for characterizing proteins based solely on size). Because abl carries a domain that can add
3115:
1566:
Karbasian
Esfahani M, Morris EL, Dutcher JP, Wiernik PH (May 2006). "Blastic phase of chronic myelogenous leukemia".
982:
622:
405:
389:
60:
2611:
2372:
625:
drugs that specifically target BCR-ABL, the constitutively activated tyrosine kinase fusion protein caused by the
2876:
2787:
2616:
610:
1441:
Sokal JE, Baccarani M, Russo D, Tura S (January 1988). "Staging and prognosis in chronic myelogenous leukemia".
1345:"Combined Population Dynamics and Entropy Modelling Supports Patient Stratification in Chronic Myeloid Leukemia"
1050:
Faderl S, Talpaz M, Estrov Z, Kantarjian HM (August 1999). "Chronic myelogenous leukemia: biology and therapy".
772:
CML accounts for 8% of all leukaemias in the UK, and around 680 people were diagnosed with the disease in 2011.
2960:
2152:
148:) and their precursors is found; characteristic increase in basophils is clinically relevant. It is a type of
2728:
2589:
2487:
3068:
3003:
2465:
2011:
1989:
1985:
1806:"Multicenter independent assessment of outcomes in chronic myeloid leukemia patients treated with imatinib"
1519:"The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia"
643:
264:
In this translocation, parts of two chromosomes (the 9th and 22nd) switch places. As a result, part of the
3053:
2834:
2770:
2718:
2706:
2477:
2445:
2365:
465:
225:
bombing survivors. The rate of CML in these individuals seems to peak about 10 years after the exposure.
149:
1804:
Gambacorti-Passerini C, Antolini L, Mahon FX, Guilhot F, Deininger M, Fava C, et al. (April 2011).
291:
3085:
2965:
2780:
2732:
2103:
Druker BJ, Guilhot F, O'Brien SG, Gathmann I, Kantarjian H, Gattermann N, et al. (December 2006).
1639:
Shapira T, Pereg D, Lishner M (September 2008). "How I treat acute and chronic leukemia in pregnancy".
523:
Haematological resistance (or failure to achieve a complete haematological response d) to the first TKI
254:
250:
208:
phase in which the symptoms are most likely fever, bone pain and an increase in bone marrow fibrosis.
2671:
2392:
2340:
469:
393:
242:
164:
153:
1885:
2856:
2822:
2522:
2271:
1723:
1400:
Kantarjian HM, Dixon D, Keating MJ, Talpaz M, Walters RS, McCredie KB, Freireich EJ (April 1988).
2549:
2185:
1613:
1343:
Brehme M, Koschmieder S, Montazeri M, Copland M, Oehler VG, Radich JP, et al. (April 2016).
626:
258:
246:
157:
56:
1750:
936:
900:
3026:
2812:
2696:
2661:
2579:
2512:
2435:
2044:
1880:
1201:"Classification, diagnosis and management of myeloproliferative disorders in the JAK2V617F era"
621:
were used as treatments of CML in the chronic phase, but since the 2000s have been replaced by
381:
300:
2311:
1751:"Imatinib therapy for patients with chronic myelogenous leukemia: are patients living longer?"
526:
Any haematological, cytogenetic, or molecular indications of resistance to two sequential TKIs
481:
Persistent or increasing high white blood cell count (> 10 × 10/L), unresponsive to therapy
419:
CML must be distinguished from a leukemoid reaction, which can have a similar appearance on a
193:
Some (<10%) are diagnosed during the accelerated stage which most often presents bleeding,
3063:
2336:
2357:
1517:
Arber DA, Orazi A, Hasserjian R, Thiele J, Borowitz MJ, Le Beau MM, et al. (May 2016).
1294:
Tefferi A, Thiele J, Orazi A, Kvasnicka HM, Barbui T, Hanson CA, et al. (August 2007).
1063:
335:
2985:
2975:
2881:
1356:
1148:
352:
233:
1959:
8:
2249:
2043:
Bocchia M, Gentili S, Abruzzese E, Fanelli A, Iuliano F, Tabilio A, et al. (2005).
1360:
1258:
1241:
1152:
2930:
2844:
2265:
2134:
2085:
1906:
1783:
1591:
1548:
1499:
1377:
1344:
1325:
1271:
1172:
1121:
1075:
1024:
999:
873:
848:
824:
799:
578:
376:
372:
183:
2254:
2063:
1680:
1109:
864:
815:
2980:
2935:
2282:
2126:
2077:
1941:
1898:
1827:
1775:
1695:
1691:
1656:
1583:
1540:
1491:
1450:
1423:
1382:
1317:
1263:
1222:
1176:
1164:
1113:
1067:
1029:
978:
878:
829:
201:. In these patients fevers are most commonly the result of opportunistic infections.
68:
2138:
2089:
1910:
1595:
1552:
1275:
1217:
1200:
1079:
182:
count on a routine laboratory test. It can also present with symptoms indicative of
2116:
2067:
2059:
1933:
1890:
1817:
1787:
1765:
1648:
1575:
1530:
1503:
1481:
1413:
1372:
1364:
1329:
1307:
1253:
1212:
1156:
1125:
1105:
1059:
1019:
1011:
868:
860:
819:
811:
586:
495:
312:
179:
113:
2322:
529:
Occurrence of two or more mutations in the BCR-ABL1 fusion gene during TKI therapy
380:
homologue chromosome, and this appearance is known as the Philadelphia chromosome
343:
3099:
3041:
2276:
2105:"Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia"
1770:
1535:
1518:
1312:
1295:
488:
371:
are almost universally increased; this feature may help differentiate CML from a
281:
1937:
1722:
Besa EC, Buehler B, Markman M, Sacher RA (27 December 2013). Krishnan K (ed.).
1687:
1675:
1652:
1612:
Besa EC, Buehler B, Markman M, Sacher RA (27 December 2013). Krishnan K (ed.).
1486:
1469:
1419:
10.1002/1097-0142(19880401)61:7<1441::AID-CNCR2820610727>3.0.CO;2-C
935:
Besa EC, Buehler B, Markman M, Sacher RA (27 December 2013). Krishnan K (ed.).
899:
Besa EC, Buehler B, Markman M, Sacher RA (27 December 2013). Krishnan K (ed.).
598:
545:
444:
205:
2287:
2239:
1579:
1096:
Hehlmann R, Hochhaus A, Baccarani M (July 2007). "Chronic myeloid leukaemia".
681:(Scemblix) was approved for medical use in the United States in October 2021.
511:
Any new clonal chromosomal abnormality in Ph+ cells that occurs during therapy
331:
Chronic myeloid leukemia in a 4 years old female. Peripheral blood (MGG stain)
128:
and the accumulation of these cells in the blood. CML is a clonal bone marrow
3109:
2636:
2568:
1470:"The World Health Organization (WHO) classification of the myeloid neoplasms"
702:
698:
residue). Two approaches were developed to the treatment of CML as a result:
566:
544:
Blast crisis is the final phase in the evolution of CML, and behaves like an
339:
Peripheral blood (MGG stain): marked leukocytosis with granulocyte left shift
1160:
653:
2951:
2940:
2130:
2081:
1945:
1902:
1831:
1779:
1660:
1587:
1544:
1495:
1386:
1321:
1226:
1168:
1117:
1071:
1033:
882:
833:
570:
443:. Blast crisis is the terminal phase of CML and clinically behaves like an
385:
1822:
1805:
1454:
1427:
1267:
241:
CML was the first cancer to be linked to a clear genetic abnormality, the
2920:
2406:
2306:
2121:
2104:
733:
706:
606:
574:
416:, as their clinical course tends to be different from patients with CML.
356:
133:
125:
73:
1803:
1402:"Characteristics of accelerated disease in chronic myelogenous leukemia"
268:("breakpoint cluster region") gene from chromosome 22 is fused with the
1894:
695:
614:
602:
420:
368:
308:
304:
198:
141:
137:
2222:
2072:
1565:
1368:
237:
Diagram showing the translocation found in the Philadelphia chromosome
2424:
2317:
1015:
721:
714:
691:
678:
671:
667:
663:
659:
360:
277:
186:
and the resulting left upper quadrant pain this causes. The enlarged
129:
307:, speeding up cell division. Moreover, the BCR-ABL protein inhibits
2909:
2650:
2501:
2014:(Press release). US Food and Drug Administration. September 4, 2012
639:
583:
364:
316:
269:
265:
194:
145:
117:
77:
1000:"Discovery of the Philadelphia chromosome: a personal perspective"
2759:
2685:
2388:
1342:
618:
121:
2102:
1674:
Kufe DW; Pollack RE; Weichselbaum RR; et al., eds. (2003).
1673:
2866:
2415:
2400:
2234:
2012:"FDA approves new orphan drug for chronic myelogenous leukemia"
741:
647:
409:
187:
2042:
484:
Persistent or increasing splenomegaly, unresponsive to therapy
2801:
2387:
2178:"What are the key statistics about chronic myeloid leukemia?"
1870:
1205:
Hematology. American Society of Hematology. Education Program
435:
phase, and over the course of several years progresses to an
41:
Chronic myeloid leukemia, chronic granulocytic leukemia (CGL)
2971:
Adult type of generalized eruption of cutaneous mastocytosis
1399:
1139:
Rowley JD (June 2013). "Genetics. A story of swapped ends".
1049:
47:
1293:
720:
In October 2021, the Food and Drug Administration approved
1799:
1797:
1516:
740:
p210 fusion protein in patients with stable disease, with
1614:"Chronic Myelogenous Leukemia Treatment & Management"
1095:
654:
Dasatinib, nilotinib, radotinib, bosutinib, and asciminib
555:
The presence of an extramedullary proliferation of blasts
273:
216:
In most cases, no obvious cause for CML can be isolated.
120:
characterized by the increased and unregulated growth of
1721:
1611:
977:(3rd ed.). Singapore: Wiley-Blackwell. p. 76.
934:
898:
504:
10–19% blasts in the peripheral blood and/or bone marrow
1986:"FDA approves Synribo for chronic myelogenous leukemia"
1794:
1440:
327:
1676:"Tyrosine Kinase Inhibitors: Targeting Considerations"
1467:
846:
3083:
1923:
388:, and the involved genes BCR-ABL1 can be detected by
2212:
1468:
Vardiman JW, Harris NL, Brunning RD (October 2002).
937:"Chronic Myelogenous Leukemia Clinical Presentation"
642:(marketed as Gleevec or Glivec), approved by the US
384:. Thus, this abnormality can be detected by routine
1638:
1239:
797:
1679:
163:CML is largely treated with targeted drugs called
1240:Savage DG, Szydlo RM, Goldman JM (January 1997).
3107:
2892:Refractory cytopenia with multilineage dysplasia
288:fusion gene product is also a tyrosine kinase.
2555:Accelerated phase chronic myelogenous leukemia
1667:
295:Diagram showing the cells CML can develop from
2373:
968:
299:The fused BCR-ABL protein interacts with the
204:Some patients are initially diagnosed in the
2153:"Chronic myeloid leukaemia (CML) statistics"
1978:
1748:
1045:
1043:
132:disorder in which a proliferation of mature
2036:
491:(> 1000 × 10/L), unresponsive to therapy
414:myelodysplastic/myeloproliferative disorder
2380:
2366:
1917:
1194:
1192:
1190:
1188:
1186:
1091:
1089:
732:In 2005, encouraging but mixed results of
684:
552:>20% blasts in the blood or bone marrow
46:
2120:
2071:
1884:
1821:
1769:
1534:
1485:
1417:
1376:
1311:
1257:
1216:
1040:
1023:
872:
823:
791:
638:The first of this new class of drugs was
359:of all types, typically including mature
351:CML is often suspected on the basis of a
1810:Journal of the National Cancer Institute
971:"Chapter 7 Chronic myelogenous leukemia"
964:
962:
960:
958:
840:
342:
334:
326:
290:
232:
2872:Refractory anemia with excess of blasts
1864:
1632:
1607:
1605:
1198:
1183:
1086:
1064:10.7326/0003-4819-131-3-199908030-00008
501:≥ 20% basophils in the peripheral blood
498:(< 100 × 10/L), unrelated to therapy
14:
3108:
2337:Chronic Myelogenous Leukemia Treatment
1289:
1287:
1285:
1138:
997:
930:
928:
926:
924:
922:
2361:
2351:Merck Manual of Diagnosis and Therapy
1568:Current Treatment Options in Oncology
1004:The Journal of Clinical Investigation
955:
894:
892:
170:
3037:Acute panmyelosis with myelofibrosis
2887:Paroxysmal nocturnal haemoglobinuria
1926:Current Pharmaceutical Biotechnology
1749:DeAngelo DJ, Ritz J (January 2004).
1715:
1602:
518:Provisional response-to-TKI criteria
459:
2109:The New England Journal of Medicine
1282:
1259:10.1046/j.1365-2141.1997.d01-1982.x
919:
477:Haematological/cytogenetic criteria
24:
2658:
889:
623:Bcr-Abl tyrosine-kinase inhibitors
592:
399:Controversy exists over so-called
228:
25:
3127:
2346:Chronic Myelocytic Leukemia (CML)
2208:
767:
426:
390:fluorescent in situ hybridization
152:associated with a characteristic
61:fluorescent in situ hybridization
3093:
2612:Juvenile myelomonocytic leukemia
775:
450:
2877:Chromosome 5q deletion syndrome
2788:Acute megakaryoblastic leukemia
2617:Chronic myelomonocytic leukemia
2528:Myeloid dendritic cell leukemia
2170:
2145:
2096:
2026:
2004:
1952:
1838:
1742:
1559:
1510:
1461:
1434:
1393:
1336:
1233:
1218:10.1182/asheducation-2006.1.240
762:
539:
280:groups to tyrosine residues (a
219:
2961:Diffuse cutaneous mastocytosis
1724:"Chronic Myelogenous Leukemia"
1246:British Journal of Haematology
1132:
991:
901:"Chronic Myelogenous Leukemia"
727:
13:
1:
2729:Chronic eosinophilic leukemia
2488:Chronic neutrophilic leukemia
2064:10.1016/S0140-6736(05)17945-8
1110:10.1016/S0140-6736(07)61165-9
969:Provan D, Gribben JG (2010).
865:10.1016/s0140-6736(16)31012-1
816:10.1016/S0140-6736(16)31678-6
784:
690:amino acid is mutated from a
301:interleukin 3beta(c) receptor
3069:Biphenotypic acute leukaemia
3004:Xanthelasmoidal mastocytosis
1990:Food and Drug Administration
1771:10.1158/1078-0432.CCR-1218-3
1682:Holland-Frei Cancer Medicine
1536:10.1182/blood-2016-03-643544
1313:10.1182/blood-2007-04-083501
747:
644:Food and Drug Administration
559:
322:
102:Chronic myelogenous leukemia
33:Chronic myelogenous leukemia
7:
2446:Acute myeloblastic leukemia
1052:Annals of Internal Medicine
633:
569:therapy (to counteract the
468:, by Sokal et al., and the
466:M.D. Anderson Cancer Center
150:myeloproliferative neoplasm
10:
3132:
2966:Erythrodermic mastocytosis
2781:Essential thrombocythaemia
2733:Hypereosinophilic syndrome
2341:National Cancer Institute
1938:10.2174/138920106778521532
1653:10.1016/j.blre.2008.03.006
1487:10.1182/blood-2002-04-1199
439:phase and ultimately to a
255:University of Pennsylvania
253:, US: Peter Nowell of the
251:Philadelphia, Pennsylvania
165:tyrosine-kinase inhibitors
3050:
3023:
3016:
2994:
2949:
2917:
2908:
2853:
2831:
2809:
2800:
2767:
2758:
2749:
2715:
2693:
2684:
2649:
2629:
2598:
2576:
2567:
2536:
2509:
2500:
2474:
2432:
2423:
2414:
2399:
2393:haematological malignancy
2297:
2216:
1580:10.1007/s11864-006-0012-y
998:Nowell PC (August 2007).
573:during early treatment),
470:World Health Organization
243:chromosomal translocation
154:chromosomal translocation
91:
83:
67:
54:
45:
37:
32:
3116:Chronic myeloid leukemia
1758:Clinical Cancer Research
355:, which shows increased
315:(the first of which was
257:and David Hungerford of
211:
110:chronic myeloid leukemia
18:Chronic myeloid leukemia
2550:Philadelphia chromosome
2186:American Cancer Society
1161:10.1126/science.1241318
736:were reported with the
685:Treatment-resistant CML
627:Philadelphia chromosome
382:chromosomal abnormality
259:Fox Chase Cancer Center
247:Philadelphia chromosome
158:Philadelphia chromosome
57:Philadelphia chromosome
1690:book) (6th ed.).
1443:Seminars in Hematology
348:
340:
332:
296:
238:
3064:Primary myelofibrosis
2996:Systemic mastocytosis
2941:Systemic mastocytosis
346:
338:
330:
294:
236:
112:, is a cancer of the
2986:Solitary mastocytoma
2976:Urticaria pigmentosa
2882:Sideroblastic anemia
2354:Professional Edition
2122:10.1056/NEJMoa062867
1988:(Press release). US
975:Molecular Hematology
859:(10053): 1459–1544.
810:(10053): 1545–1602.
353:complete blood count
1823:10.1093/jnci/djr060
1361:2016NatSR...624057B
1153:2013Sci...340.1412R
2931:Mast cell leukemia
2845:Polycythaemia vera
2823:Erythroleukemia/M6
2707:Acute eosinophilic
2298:External resources
2192:on 9 February 2015
2157:Cancer Research UK
1992:. October 26, 2012
1895:10.1002/cncr.22661
1728:Medscape Reference
1618:Medscape Reference
1349:Scientific Reports
1199:Tefferi A (2006).
941:Medscape Reference
905:Medscape Reference
615:interferon alfa 2b
579:interferon alfa-2b
377:bone marrow biopsy
373:leukemoid reaction
349:
341:
333:
313:targeted therapies
297:
239:
184:hepatosplenomegaly
171:Signs and symptoms
116:. It is a form of
3081:
3080:
3077:
3076:
3012:
3011:
2981:Mast cell sarcoma
2936:Mast cell sarcoma
2904:
2903:
2900:
2899:
2867:Refractory anemia
2796:
2795:
2745:
2744:
2741:
2740:
2680:
2679:
2645:
2644:
2625:
2624:
2563:
2562:
2496:
2495:
2332:
2331:
1966:(database record)
1964:ClinicalTrial.gov
1701:978-1-55009-213-4
1692:Hamilton, Ontario
1369:10.1038/srep24057
640:imatinib mesylate
611:alkylating agents
460:Accelerated phase
114:white blood cells
108:), also known as
99:
98:
27:Medical condition
16:(Redirected from
3123:
3098:
3097:
3096:
3089:
3057:
3030:
3021:
3020:
3017:Multiple/unknown
2997:
2954:
2924:
2915:
2914:
2860:
2838:
2816:
2807:
2806:
2774:
2765:
2764:
2756:
2755:
2722:
2700:
2691:
2690:
2672:Acute basophilic
2665:
2656:
2655:
2605:
2583:
2574:
2573:
2543:
2516:
2507:
2506:
2481:
2439:
2430:
2429:
2421:
2420:
2412:
2411:
2382:
2375:
2368:
2359:
2358:
2214:
2213:
2202:
2201:
2199:
2197:
2188:. Archived from
2174:
2168:
2167:
2165:
2163:
2149:
2143:
2142:
2124:
2100:
2094:
2093:
2075:
2058:(9460): 657–62.
2049:
2040:
2034:
2030:
2024:
2023:
2021:
2019:
2008:
2002:
2001:
1999:
1997:
1982:
1976:
1975:
1973:
1971:
1956:
1950:
1949:
1921:
1915:
1914:
1888:
1868:
1862:
1861:
1859:
1857:
1842:
1836:
1835:
1825:
1801:
1792:
1791:
1773:
1755:
1746:
1740:
1739:
1737:
1735:
1719:
1713:
1712:
1710:
1708:
1685:
1671:
1665:
1664:
1636:
1630:
1629:
1627:
1625:
1609:
1600:
1599:
1563:
1557:
1556:
1538:
1529:(20): 2391–405.
1514:
1508:
1507:
1489:
1465:
1459:
1458:
1438:
1432:
1431:
1421:
1397:
1391:
1390:
1380:
1340:
1334:
1333:
1315:
1291:
1280:
1279:
1261:
1237:
1231:
1230:
1220:
1196:
1181:
1180:
1147:(6139): 1412–3.
1136:
1130:
1129:
1104:(9584): 342–50.
1093:
1084:
1083:
1047:
1038:
1037:
1027:
1016:10.1172/JCI31771
995:
989:
988:
966:
953:
952:
950:
948:
932:
917:
916:
914:
912:
896:
887:
886:
876:
844:
838:
837:
827:
795:
744:as an adjuvant.
587:interferon-alpha
496:thrombocytopenia
392:, as well as by
180:white blood cell
50:
30:
29:
21:
3131:
3130:
3126:
3125:
3124:
3122:
3121:
3120:
3106:
3105:
3104:
3094:
3092:
3084:
3082:
3073:
3051:
3046:
3042:Myeloid sarcoma
3024:
3008:
2995:
2990:
2950:
2945:
2918:
2896:
2854:
2849:
2832:
2827:
2810:
2792:
2768:
2737:
2716:
2711:
2694:
2676:
2659:
2641:
2621:
2599:
2594:
2577:
2559:
2537:
2532:
2510:
2492:
2475:
2470:
2433:
2404:
2395:
2386:
2333:
2328:
2327:
2293:
2292:
2225:
2211:
2206:
2205:
2195:
2193:
2176:
2175:
2171:
2161:
2159:
2151:
2150:
2146:
2115:(23): 2408–17.
2101:
2097:
2047:
2041:
2037:
2031:
2027:
2017:
2015:
2010:
2009:
2005:
1995:
1993:
1984:
1983:
1979:
1969:
1967:
1958:
1957:
1953:
1922:
1918:
1886:10.1.1.605.7683
1879:(11): 2171–81.
1869:
1865:
1855:
1853:
1852:(Press release)
1844:
1843:
1839:
1802:
1795:
1764:(1 Pt 1): 1–3.
1753:
1747:
1743:
1733:
1731:
1720:
1716:
1706:
1704:
1702:
1694:: B.C. Decker.
1672:
1668:
1637:
1633:
1623:
1621:
1610:
1603:
1564:
1560:
1515:
1511:
1480:(7): 2292–302.
1466:
1462:
1439:
1435:
1398:
1394:
1341:
1337:
1292:
1283:
1238:
1234:
1197:
1184:
1137:
1133:
1094:
1087:
1048:
1041:
996:
992:
985:
967:
956:
946:
944:
933:
920:
910:
908:
897:
890:
845:
841:
796:
792:
787:
778:
770:
765:
750:
730:
687:
656:
636:
599:antimetabolites
595:
562:
542:
462:
453:
429:
325:
282:tyrosine kinase
231:
229:Pathophysiology
222:
214:
173:
28:
23:
22:
15:
12:
11:
5:
3129:
3119:
3118:
3103:
3102:
3079:
3078:
3075:
3074:
3072:
3071:
3066:
3060:
3058:
3048:
3047:
3045:
3044:
3039:
3033:
3031:
3018:
3014:
3013:
3010:
3009:
3007:
3006:
3000:
2998:
2992:
2991:
2989:
2988:
2983:
2978:
2973:
2968:
2963:
2957:
2955:
2947:
2946:
2944:
2943:
2938:
2933:
2927:
2925:
2912:
2906:
2905:
2902:
2901:
2898:
2897:
2895:
2894:
2889:
2884:
2879:
2874:
2869:
2863:
2861:
2851:
2850:
2848:
2847:
2841:
2839:
2829:
2828:
2826:
2825:
2819:
2817:
2804:
2798:
2797:
2794:
2793:
2791:
2790:
2784:
2783:
2777:
2775:
2762:
2753:
2747:
2746:
2743:
2742:
2739:
2738:
2736:
2735:
2725:
2723:
2713:
2712:
2710:
2709:
2703:
2701:
2688:
2682:
2681:
2678:
2677:
2675:
2674:
2668:
2666:
2653:
2647:
2646:
2643:
2642:
2640:
2639:
2633:
2631:
2627:
2626:
2623:
2622:
2620:
2619:
2614:
2608:
2606:
2596:
2595:
2593:
2592:
2586:
2584:
2571:
2565:
2564:
2561:
2560:
2558:
2557:
2552:
2546:
2544:
2534:
2533:
2531:
2530:
2525:
2519:
2517:
2504:
2498:
2497:
2494:
2493:
2491:
2490:
2484:
2482:
2472:
2471:
2469:
2468:
2463:
2458:
2453:
2448:
2442:
2440:
2427:
2418:
2409:
2397:
2396:
2385:
2384:
2377:
2370:
2362:
2356:
2355:
2343:
2330:
2329:
2326:
2325:
2314:
2302:
2301:
2299:
2295:
2294:
2291:
2290:
2279:
2268:
2257:
2242:
2226:
2221:
2220:
2218:
2217:Classification
2210:
2209:External links
2207:
2204:
2203:
2169:
2144:
2095:
2035:
2025:
2003:
1977:
1951:
1916:
1863:
1837:
1793:
1741:
1714:
1700:
1688:NCBI bookshelf
1666:
1631:
1601:
1558:
1509:
1460:
1433:
1392:
1335:
1281:
1232:
1182:
1131:
1085:
1039:
990:
983:
954:
918:
888:
839:
789:
788:
786:
783:
777:
774:
769:
768:United Kingdom
766:
764:
761:
749:
746:
729:
726:
694:residue to an
686:
683:
655:
652:
635:
632:
594:
591:
561:
558:
557:
556:
553:
546:acute leukemia
541:
538:
533:
532:
531:
530:
527:
524:
514:
513:
512:
509:
505:
502:
499:
492:
489:thrombocytosis
485:
482:
461:
458:
452:
449:
445:acute leukemia
428:
427:Classification
425:
324:
321:
230:
227:
221:
218:
213:
210:
172:
169:
97:
96:
93:
89:
88:
87:298,000 (2015)
85:
81:
80:
71:
65:
64:
52:
51:
43:
42:
39:
35:
34:
26:
9:
6:
4:
3:
2:
3128:
3117:
3114:
3113:
3111:
3101:
3091:
3090:
3087:
3070:
3067:
3065:
3062:
3061:
3059:
3056:
3055:
3049:
3043:
3040:
3038:
3035:
3034:
3032:
3029:
3028:
3022:
3019:
3015:
3005:
3002:
3001:
2999:
2993:
2987:
2984:
2982:
2979:
2977:
2974:
2972:
2969:
2967:
2964:
2962:
2959:
2958:
2956:
2953:
2948:
2942:
2939:
2937:
2934:
2932:
2929:
2928:
2926:
2923:
2922:
2916:
2913:
2911:
2907:
2893:
2890:
2888:
2885:
2883:
2880:
2878:
2875:
2873:
2870:
2868:
2865:
2864:
2862:
2859:
2858:
2852:
2846:
2843:
2842:
2840:
2837:
2836:
2830:
2824:
2821:
2820:
2818:
2815:
2814:
2808:
2805:
2803:
2799:
2789:
2786:
2785:
2782:
2779:
2778:
2776:
2773:
2772:
2766:
2763:
2761:
2757:
2754:
2752:
2748:
2734:
2730:
2727:
2726:
2724:
2721:
2720:
2714:
2708:
2705:
2704:
2702:
2699:
2698:
2692:
2689:
2687:
2683:
2673:
2670:
2669:
2667:
2664:
2663:
2657:
2654:
2652:
2648:
2638:
2637:Histiocytosis
2635:
2634:
2632:
2628:
2618:
2615:
2613:
2610:
2609:
2607:
2604:
2603:
2597:
2591:
2588:
2587:
2585:
2582:
2581:
2575:
2572:
2570:
2569:Myelomonocyte
2566:
2556:
2553:
2551:
2548:
2547:
2545:
2542:
2541:
2535:
2529:
2526:
2524:
2521:
2520:
2518:
2515:
2514:
2508:
2505:
2503:
2499:
2489:
2486:
2485:
2483:
2480:
2479:
2473:
2467:
2464:
2462:
2459:
2457:
2454:
2452:
2449:
2447:
2444:
2443:
2441:
2438:
2437:
2431:
2428:
2426:
2422:
2419:
2417:
2413:
2410:
2408:
2402:
2398:
2394:
2390:
2383:
2378:
2376:
2371:
2369:
2364:
2363:
2360:
2353:
2352:
2347:
2344:
2342:
2338:
2335:
2334:
2324:
2320:
2319:
2315:
2313:
2309:
2308:
2304:
2303:
2300:
2296:
2289:
2285:
2284:
2280:
2278:
2274:
2273:
2269:
2267:
2263:
2262:
2258:
2256:
2252:
2251:
2247:
2243:
2241:
2237:
2236:
2232:
2228:
2227:
2224:
2219:
2215:
2191:
2187:
2183:
2179:
2173:
2158:
2154:
2148:
2140:
2136:
2132:
2128:
2123:
2118:
2114:
2110:
2106:
2099:
2091:
2087:
2083:
2079:
2074:
2069:
2065:
2061:
2057:
2053:
2046:
2039:
2029:
2013:
2007:
1991:
1987:
1981:
1965:
1961:
1955:
1947:
1943:
1939:
1935:
1931:
1927:
1920:
1912:
1908:
1904:
1900:
1896:
1892:
1887:
1882:
1878:
1874:
1867:
1851:
1847:
1841:
1833:
1829:
1824:
1819:
1816:(7): 553–61.
1815:
1811:
1807:
1800:
1798:
1789:
1785:
1781:
1777:
1772:
1767:
1763:
1759:
1752:
1745:
1729:
1725:
1718:
1703:
1697:
1693:
1689:
1684:
1683:
1677:
1670:
1662:
1658:
1654:
1650:
1647:(5): 247–59.
1646:
1642:
1641:Blood Reviews
1635:
1619:
1615:
1608:
1606:
1597:
1593:
1589:
1585:
1581:
1577:
1574:(3): 189–99.
1573:
1569:
1562:
1554:
1550:
1546:
1542:
1537:
1532:
1528:
1524:
1520:
1513:
1505:
1501:
1497:
1493:
1488:
1483:
1479:
1475:
1471:
1464:
1456:
1452:
1448:
1444:
1437:
1429:
1425:
1420:
1415:
1412:(7): 1441–6.
1411:
1407:
1403:
1396:
1388:
1384:
1379:
1374:
1370:
1366:
1362:
1358:
1354:
1350:
1346:
1339:
1331:
1327:
1323:
1319:
1314:
1309:
1306:(4): 1092–7.
1305:
1301:
1297:
1290:
1288:
1286:
1277:
1273:
1269:
1265:
1260:
1255:
1251:
1247:
1243:
1236:
1228:
1224:
1219:
1214:
1210:
1206:
1202:
1195:
1193:
1191:
1189:
1187:
1178:
1174:
1170:
1166:
1162:
1158:
1154:
1150:
1146:
1142:
1135:
1127:
1123:
1119:
1115:
1111:
1107:
1103:
1099:
1092:
1090:
1081:
1077:
1073:
1069:
1065:
1061:
1058:(3): 207–19.
1057:
1053:
1046:
1044:
1035:
1031:
1026:
1021:
1017:
1013:
1010:(8): 2033–5.
1009:
1005:
1001:
994:
986:
984:9781444318548
980:
976:
972:
965:
963:
961:
959:
942:
938:
931:
929:
927:
925:
923:
906:
902:
895:
893:
884:
880:
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2016:. Retrieved
2006:
1994:. Retrieved
1980:
1968:. Retrieved
1963:
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1932:(5): 371–9.
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357:granulocytes
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134:granulocytes
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2921:Mastocytoma
2307:MedlinePlus
2018:October 27,
1996:October 27,
1970:October 27,
1707:October 27,
734:vaccination
728:Vaccination
707:omacetaxine
607:hydroxyurea
575:splenectomy
494:Persistent
487:Persistent
437:accelerated
421:blood smear
401:Ph-negative
369:eosinophils
156:called the
142:eosinophils
138:neutrophils
126:bone marrow
74:Haematology
59:as seen by
38:Other names
2405:and other
2339:at the US
2283:DiseasesDB
2182:cancer.org
2162:28 October
2073:2108/41872
1856:29 October
785:References
696:isoleucine
603:cytarabine
309:DNA repair
305:cell cycle
199:ecchymosis
2425:Myelocyte
2391:-related
2318:eMedicine
2196:6 January
2033:36197958.
1881:CiteSeerX
1734:3 January
1624:4 January
1355:: 24057.
1211:: 240–5.
1177:206550237
947:3 January
911:3 January
748:Prognosis
722:asciminib
715:ponatinib
703:Chemgenex
701:In 2007,
692:threonine
679:Asciminib
672:Bosutinib
668:radotinib
664:nilotinib
660:dasatinib
560:Treatment
365:Basophils
323:Diagnosis
278:phosphate
195:petechiae
146:basophils
130:stem cell
84:Frequency
69:Specialty
3110:Category
3100:Medicine
2910:CFU-Mast
2651:CFU-Baso
2502:Monocyte
2139:21772851
2131:17151364
2090:26816784
2082:15721470
1946:17076652
1911:46509746
1903:17431887
1850:Novartis
1832:21422402
1780:14734443
1661:18472198
1596:21092684
1588:16615875
1553:18338178
1545:27069254
1496:12239137
1387:27048866
1322:17488875
1276:41243342
1227:17124067
1169:23788787
1118:17662883
1080:46260906
1072:10428738
1034:17671636
883:27733281
834:27733282
738:BCR/ABL1
634:Imatinib
619:steroids
584:cytokine
317:imatinib
270:ABL gene
118:leukemia
78:oncology
2760:CFU-Meg
2686:CFU-Eos
2523:AMoL/M5
2389:Myeloid
2323:med/371
2277:D015464
2266:M9875/3
1788:1761631
1730:. WebMD
1620:. WebMD
1504:9413654
1455:3279515
1428:3162181
1378:4822142
1357:Bibcode
1330:7086172
1268:9012696
1149:Bibcode
1141:Science
1126:1420863
1025:1934591
943:. WebMD
907:. WebMD
874:5388903
825:5055577
601:(e.g.,
433:chronic
286:bcr-abl
284:), the
122:myeloid
63:(FISH).
3086:Portal
2466:APL/M3
2416:CFU-GM
2401:CFU-GM
2312:000570
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742:GM-CSF
648:RT-PCR
617:, and
508:3q26.2
410:RT-PCR
188:spleen
92:Deaths
2802:CFU-E
2630:Other
2602:MD-MP
2261:ICD-O
2255:205.1
2240:C92.1
2135:S2CID
2086:S2CID
2048:(PDF)
1907:S2CID
1784:S2CID
1754:(PDF)
1592:S2CID
1549:S2CID
1523:Blood
1500:S2CID
1474:Blood
1326:S2CID
1300:Blood
1272:S2CID
1173:S2CID
1122:S2CID
1076:S2CID
212:Cause
206:blast
2288:2659
2272:MeSH
2250:9-CM
2198:2015
2164:2014
2127:PMID
2078:PMID
2020:2012
1998:2012
1972:2012
1942:PMID
1899:PMID
1858:2021
1828:PMID
1776:PMID
1736:2014
1709:2012
1696:ISBN
1657:PMID
1626:2014
1584:PMID
1541:PMID
1492:PMID
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1424:PMID
1383:PMID
1318:PMID
1264:PMID
1223:PMID
1209:2006
1165:PMID
1114:PMID
1068:PMID
1030:PMID
979:ISBN
949:2014
913:2014
879:PMID
830:PMID
577:and
406:FISH
375:. A
367:and
197:and
144:and
76:and
55:The
3027:AML
2813:AML
2751:MEP
2697:AML
2662:AML
2580:AML
2540:CML
2513:AML
2436:AML
2348:at
2246:ICD
2231:ICD
2117:doi
2113:355
2068:hdl
2060:doi
2056:365
1934:doi
1891:doi
1877:109
1818:doi
1814:103
1766:doi
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1373:PMC
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1102:370
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1020:PMC
1012:doi
1008:117
869:PMC
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857:388
820:PMC
812:doi
808:388
609:),
408:or
394:PCR
274:kDa
266:BCR
106:CML
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