今日の臨床サポート

慢性骨髄性白血病

著者: 川口辰哉 熊本大学 血液・膠原病・感染症内科学分野

監修: 木崎昌弘 埼玉医科大学総合医療センター

著者校正/監修レビュー済:2017/11/30
患者向け説明資料

概要・推奨   

疾患のポイント:
  1. 慢性骨髄性白血病(CML)は、BCR-ABL1融合遺伝子を特徴とする多能性造血幹細胞異常に基づく骨髄増殖性腫瘍の1つであり、顆粒球系細胞の異常増殖を特徴とする。
  1. 慢性骨髄性白血病(CML)は年間10万人あたり1~2人の頻度で、50~60歳代をピークに、やや男性に多く発症する。
  1. BCR-ABL1融合遺伝子は、分子量210kDaのp210 BCR-ABL1を産生する。CMLでは、このBCR-ABL1が恒常的にチロシンキナーゼ活性を有するために細胞の異常増殖が生ずる。
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  1. 慢性期CMLでは、末梢血および骨髄で各分化段階の顆粒球系細胞の増加、好中球アルカリホスファターゼ(NAP)低値、血清ビタミンB12の高値などを認める。確定診断には、G-バンド法による染色体検査でt(9;22)転座(Ph染色体)を証明するか、FISH法あるいはRT-PCR法によりBCR-ABL1キメラ遺伝子を検出する。
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  1. BCR-ABL1キメラ遺伝子:
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  1. BCR-ABL1変異解析のタイミングおよび変異に基づく治療選択:
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  1. 慢性骨髄性白血病(CML)の診断はフィラデルフィア(Ph)染色体(t[9;22]転座)あるいはBCR-ABL1融合遺伝子が証明されれば確定する。
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薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
川口辰哉 : 特に申告事項無し[2021年]
監修:木崎昌弘 : 講演料(ブリストル・マイヤーズスクイブ,ヤンセンファーマ,ノバルティスファーマ,セルジーン,MSD,小野薬品,武田薬品,大日本住友製薬),研究費・助成金など(武田薬品),奨学(奨励)寄付など(協和キリン,中外製薬,武田薬品,小野薬品,第一三共)[2021年]

病態・疫学・診察

疾患情報  
  1. 慢性骨髄性白血病(CML)は、BCR-ABL1融合遺伝子を特徴とする多能性造血幹細胞異常に基づく骨髄増殖性腫瘍の1つであり、顆粒球系細胞の異常増殖を特徴とする。
  1. 慢性骨髄性白血病(CML)は年間10万人あたり1~2人の頻度で、50~60歳代をピークに、やや男性に多く発症する。
  1. 多能性造血幹細胞異常に基づく骨髄増殖性腫瘍の1つであり、顆粒球系細胞の異常増殖を特徴とする。
  1. t(9;22)転座(フィラデルフィア[Ph]染色体)あるいはBCR-ABL1融合遺伝子が証明されれば診断が確定する。
  1. 未治療だと4~5年の慢性期から移行期を経て急性白血病化し(急性転化期)、死に至る。
  1. BCR-ABL1蛋白の恒常的チロシンキナーゼ活性化が腫瘍化と関連し、その選択的阻害薬(チロシンキナーゼ阻害薬、TKI)であるイマチニブが有効である。
  1. イマチニブは長期予後を著しく改善した(10年生存率が83.3%)[1]
  1. イマチニブより強力な第2世代TKI(ニロチニブ、ダサチニブ)の登場により、さらなる予後改善が期待されている[2][3]。 エビデンス 
  1. CML治療に用いられるTKIの種類と特徴:<図表>
問診・診察のポイント  
  1. 原因は不明であるが、一部は放射線被ばくとの関連が指摘されている。

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文献 

著者: Andreas Hochhaus, Richard A Larson, François Guilhot, Jerald P Radich, Susan Branford, Timothy P Hughes, Michele Baccarani, Michael W Deininger, Francisco Cervantes, Satoko Fujihara, Christine-Elke Ortmann, Hans D Menssen, Hagop Kantarjian, Stephen G O'Brien, Brian J Druker, IRIS Investigators
雑誌名: N Engl J Med. 2017 Mar 9;376(10):917-927. doi: 10.1056/NEJMoa1609324.
Abstract/Text BACKGROUND: Imatinib, a selective BCR-ABL1 kinase inhibitor, improved the prognosis for patients with chronic myeloid leukemia (CML). We conducted efficacy and safety analyses on the basis of more than 10 years of follow-up in patients with CML who were treated with imatinib as initial therapy.
METHODS: In this open-label, multicenter trial with crossover design, we randomly assigned patients with newly diagnosed CML in the chronic phase to receive either imatinib or interferon alfa plus cytarabine. Long-term analyses included overall survival, response to treatment, and serious adverse events.
RESULTS: The median follow-up was 10.9 years. Given the high rate of crossover among patients who had been randomly assigned to receive interferon alfa plus cytarabine (65.6%) and the short duration of therapy before crossover in these patients (median, 0.8 years), the current analyses focused on patients who had been randomly assigned to receive imatinib. Among the patients in the imatinib group, the estimated overall survival rate at 10 years was 83.3%. Approximately half the patients (48.3%) who had been randomly assigned to imatinib completed study treatment with imatinib, and 82.8% had a complete cytogenetic response. Serious adverse events that were considered by the investigators to be related to imatinib were uncommon and most frequently occurred during the first year of treatment.
CONCLUSIONS: Almost 11 years of follow-up showed that the efficacy of imatinib persisted over time and that long-term administration of imatinib was not associated with unacceptable cumulative or late toxic effects. (Funded by Novartis Pharmaceuticals; IRIS ClinicalTrials.gov numbers, NCT00006343 and NCT00333840 .).

PMID 28273028  N Engl J Med. 2017 Mar 9;376(10):917-927. doi: 10.1056/・・・
著者: Hagop Kantarjian, Neil P Shah, Andreas Hochhaus, Jorge Cortes, Sandip Shah, Manuel Ayala, Beatriz Moiraghi, Zhixiang Shen, Jiri Mayer, Ricardo Pasquini, Hirohisa Nakamae, Françoise Huguet, Concepción Boqué, Charles Chuah, Eric Bleickardt, M Brigid Bradley-Garelik, Chao Zhu, Ted Szatrowski, David Shapiro, Michele Baccarani
雑誌名: N Engl J Med. 2010 Jun 17;362(24):2260-70. doi: 10.1056/NEJMoa1002315. Epub 2010 Jun 5.
Abstract/Text BACKGROUND: Treatment with dasatinib, a highly potent BCR-ABL kinase inhibitor, has resulted in high rates of complete cytogenetic response and progression-free survival among patients with chronic myeloid leukemia (CML) in the chronic phase, after failure of imatinib treatment. We assessed the efficacy and safety of dasatinib, as compared with imatinib, for the first-line treatment of chronic-phase CML.
METHODS: In a multinational study, 519 patients with newly diagnosed chronic-phase CML were randomly assigned to receive dasatinib at a dose of 100 mg once daily (259 patients) or imatinib at a dose of 400 mg once daily (260 patients). The primary end point was complete cytogenetic response by 12 months, confirmed on two consecutive assessments at least 28 days apart. Secondary end points, including major molecular response, were tested at a significance level of 0.0001 to adjust for multiple comparisons.
RESULTS: After a minimum follow-up of 12 months, the rate of confirmed complete cytogenetic response was higher with dasatinib than with imatinib (77% vs. 66%, P=0.007), as was the rate of complete cytogenetic response observed on at least one assessment (83% vs. 72%, P=0.001). The rate of major molecular response was higher with dasatinib than with imatinib (46% vs. 28%, P<0.0001), and responses were achieved in a shorter time with dasatinib (P<0.0001). Progression to the accelerated or blastic phase of CML occurred in 5 patients who were receiving dasatinib (1.9%) and in 9 patients who were receiving imatinib (3.5%). The safety profiles of the two treatments were similar.
CONCLUSIONS: Dasatinib, administered once daily, as compared with imatinib, administered once daily, induced significantly higher and faster rates of complete cytogenetic response and major molecular response. Since achieving complete cytogenetic response within 12 months has been associated with better long-term, progression-free survival, dasatinib may improve the long-term outcomes among patients with newly diagnosed chronic-phase CML. (ClinicalTrials.gov number, NCT00481247.)

2010 Massachusetts Medical Society
PMID 20525995  N Engl J Med. 2010 Jun 17;362(24):2260-70. doi: 10.1056・・・
著者: Giuseppe Saglio, Dong-Wook Kim, Surapol Issaragrisil, Philipp le Coutre, Gabriel Etienne, Clarisse Lobo, Ricardo Pasquini, Richard E Clark, Andreas Hochhaus, Timothy P Hughes, Neil Gallagher, Albert Hoenekopp, Mei Dong, Ariful Haque, Richard A Larson, Hagop M Kantarjian, ENESTnd Investigators
雑誌名: N Engl J Med. 2010 Jun 17;362(24):2251-9. doi: 10.1056/NEJMoa0912614. Epub 2010 Jun 5.
Abstract/Text BACKGROUND: Nilotinib has been shown to be a more potent inhibitor of BCR-ABL than imatinib. We evaluated the efficacy and safety of nilotinib, as compared with imatinib, in patients with newly diagnosed Philadelphia chromosome-positive chronic myeloid leukemia (CML) in the chronic phase.
METHODS: In this phase 3, randomized, open-label, multicenter study, we assigned 846 patients with chronic-phase Philadelphia chromosome-positive CML in a 1:1:1 ratio to receive nilotinib (at a dose of either 300 mg or 400 mg twice daily) or imatinib (at a dose of 400 mg once daily). The primary end point was the rate of major molecular response at 12 months.
RESULTS: At 12 months, the rates of major molecular response for nilotinib (44% for the 300-mg dose and 43% for the 400-mg dose) were nearly twice that for imatinib (22%) (P<0.001 for both comparisons). The rates of complete cytogenetic response by 12 months were significantly higher for nilotinib (80% for the 300-mg dose and 78% for the 400-mg dose) than for imatinib (65%) (P<0.001 for both comparisons). Patients receiving either the 300-mg dose or the 400-mg dose of nilotinib twice daily had a significant improvement in the time to progression to the accelerated phase or blast crisis, as compared with those receiving imatinib (P=0.01 and P=0.004, respectively). No patient with progression to the accelerated phase or blast crisis had a major molecular response. Gastrointestinal and fluid-retention events were more frequent among patients receiving imatinib, whereas dermatologic events and headache were more frequent in those receiving nilotinib. Discontinuations due to aminotransferase and bilirubin elevations were low in all three study groups.
CONCLUSIONS: Nilotinib at a dose of either 300 mg or 400 mg twice daily was superior to imatinib in patients with newly diagnosed chronic-phase Philadelphia chromosome-positive CML. (ClinicalTrials.gov number, NCT00471497.)

2010 Massachusetts Medical Society
PMID 20525993  N Engl J Med. 2010 Jun 17;362(24):2251-9. doi: 10.1056/・・・
著者:
雑誌名: J Natl Cancer Inst. 1997 Nov 5;89(21):1616-20.
Abstract/Text BACKGROUND: Several randomized clinical trials in chronic myeloid leukemia (CML) have reported better patient survival with interferon alfa (IFN alpha) than with standard chemotherapeutic agents, such as busulfan or hydroxyurea. However, the size and persistence of this survival benefit is uncertain. Our aim was to assess these reliably, both overall and in particular patient subgroups.
METHODS: We collaborated in a worldwide overview of all clinical trials in which patients with CML were randomly assigned to receive either IFN alpha as the main drug or standard chemotherapy. Trials were identified by electronic and hand searching of the medical literature and databases and by personal contact. Individual patient data were available for each of 1554 patients who had been randomly assigned to treatment in seven trials (German, Italian, British, French, Japanese, and "Benelux"). Intention-to-treat stratified logrank survival analyses were performed, reporting two-sided P values.
RESULTS: Almost all of the patients in these trials had disease with the Philadelphia chromosome abnormality. Among those who did, the regimens that involved IFN alpha produced a statistically significantly better survival than those involving either hydroxyurea (P = .001) or busulfan (P = .00007) alone. The 5-year survival rates were 57% with IFN alpha and 42% with chemotherapy, with an absolute difference of 15% (standard deviation = 3%; P<.00001). There were no trials or subgroups of patients in which the treatment difference was statistically significantly different from the average.
CONCLUSION: For patients with Philadelphia chromosome-positive chronic myeloid leukemia, the inclusion of IFN alpha in the therapeutic regimen produced substantially better 5-year survival than standard chemotherapy alone.

PMID 9362160  J Natl Cancer Inst. 1997 Nov 5;89(21):1616-20.
著者: Brian J Druker, François Guilhot, Stephen G O'Brien, Insa Gathmann, Hagop Kantarjian, Norbert Gattermann, Michael W N Deininger, Richard T Silver, John M Goldman, Richard M Stone, Francisco Cervantes, Andreas Hochhaus, Bayard L Powell, Janice L Gabrilove, Philippe Rousselot, Josy Reiffers, Jan J Cornelissen, Timothy Hughes, Hermine Agis, Thomas Fischer, Gregor Verhoef, John Shepherd, Giuseppe Saglio, Alois Gratwohl, Johan L Nielsen, Jerald P Radich, Bengt Simonsson, Kerry Taylor, Michele Baccarani, Charlene So, Laurie Letvak, Richard A Larson, IRIS Investigators
雑誌名: N Engl J Med. 2006 Dec 7;355(23):2408-17. doi: 10.1056/NEJMoa062867.
Abstract/Text BACKGROUND: The cause of chronic myeloid leukemia (CML) is a constitutively active BCR-ABL tyrosine kinase. Imatinib inhibits this kinase, and in a short-term study was superior to interferon alfa plus cytarabine for newly diagnosed CML in the chronic phase. For 5 years, we followed patients with CML who received imatinib as initial therapy.
METHODS: We randomly assigned 553 patients to receive imatinib and 553 to receive interferon alfa plus cytarabine and then evaluated them for overall and event-free survival; progression to accelerated-phase CML or blast crisis; hematologic, cytogenetic, and molecular responses; and adverse events.
RESULTS: The median follow-up was 60 months. Kaplan-Meier estimates of cumulative best rates of complete cytogenetic response among patients receiving imatinib were 69% by 12 months and 87% by 60 months. An estimated 7% of patients progressed to accelerated-phase CML or blast crisis, and the estimated overall survival of patients who received imatinib as initial therapy was 89% at 60 months. Patients who had a complete cytogenetic response or in whom levels of BCR-ABL transcripts had fallen by at least 3 log had a significantly lower risk of disease progression than did patients without a complete cytogenetic response (P<0.001). Grade 3 or 4 adverse events diminished over time, and there was no clinically significant change in the profile of adverse events.
CONCLUSIONS: After 5 years of follow-up, continuous treatment of chronic-phase CML with imatinib as initial therapy was found to induce durable responses in a high proportion of patients. (ClinicalTrials.gov number, NCT00006343 [ClinicalTrials.gov].)

Copyright 2006 Massachusetts Medical Society.
PMID 17151364  N Engl J Med. 2006 Dec 7;355(23):2408-17. doi: 10.1056/・・・
著者: Michele Baccarani, Jorge Cortes, Fabrizio Pane, Dietger Niederwieser, Giuseppe Saglio, Jane Apperley, Francisco Cervantes, Michael Deininger, Alois Gratwohl, François Guilhot, Andreas Hochhaus, Mary Horowitz, Timothy Hughes, Hagop Kantarjian, Richard Larson, Jerald Radich, Bengt Simonsson, Richard T Silver, John Goldman, Rudiger Hehlmann, European LeukemiaNet
雑誌名: J Clin Oncol. 2009 Dec 10;27(35):6041-51. doi: 10.1200/JCO.2009.25.0779. Epub 2009 Nov 2.
Abstract/Text PURPOSE: To review and update the European LeukemiaNet (ELN) recommendations for the management of chronic myeloid leukemia with imatinib and second-generation tyrosine kinase inhibitors (TKIs), including monitoring, response definition, and first- and second-line therapy.
METHODS: These recommendations are based on a critical and comprehensive review of the relevant papers up to February 2009 and the results of four consensus conferences held by the panel of experts appointed by ELN in 2008.
RESULTS: Cytogenetic monitoring was required at 3, 6, 12, and 18 months. Molecular monitoring was required every 3 months. On the basis of the degree and the timing of hematologic, cytogenetic, and molecular results, the response to first-line imatinib was defined as optimal, suboptimal, or failure, and the response to second-generation TKIs was defined as suboptimal or failure.
CONCLUSION: Initial treatment was confirmed as imatinib 400 mg daily. Imatinib should be continued indefinitely in optimal responders. Suboptimal responders may continue on imatinb, at the same or higher dose, or may be eligible for investigational therapy with second-generation TKIs. In instances of imatinib failure, second-generation TKIs are recommended, followed by allogeneic hematopoietic stem-cell transplantation only in instances of failure and, sometimes, suboptimal response, depending on transplantation risk.

PMID 19884523  J Clin Oncol. 2009 Dec 10;27(35):6041-51. doi: 10.1200/・・・
著者: David Marin, Dragana Milojkovic, Eduardo Olavarria, Jamshid S Khorashad, Hugues de Lavallade, Alistair G Reid, Letizia Foroni, Katayoun Rezvani, Marco Bua, Francesco Dazzi, Jiri Pavlu, Matthias Klammer, Jaspal S Kaeda, John M Goldman, Jane F Apperley
雑誌名: Blood. 2008 Dec 1;112(12):4437-44. doi: 10.1182/blood-2008-06-162388. Epub 2008 Aug 20.
Abstract/Text The majority of patients with chronic myeloid leukemia in chronic phase gain substantial benefit from imatinib but some fail to respond or lose their initial response. In 2006, the European LeukemiaNet published recommendations designed to help identify patients responding poorly to imatinib. Patients were evaluated at 3, 6, 12, and 18 months and some were classified as "failure" or "suboptimal responders." We analyzed outcomes for 224 patients with chronic myeloid leukemia in chronic phase treated in a single institution to validate these recommendations. Patients were followed for a median of 46.1 months. At each time point, patients classified as "failure" showed significantly worse survival, progression-free survival, and cytogenetic response than other patients; for example, based on the assessment at 12 months, the 5-year survival was 87.1% versus 95.1% (P = .02), progression-free survival 76.% versus 90% (P = .002), and complete cytogenetic response rate 26.7% versus 94.1% (P < .001). Similarly, the criteria for "suboptimal response" at 6 and 12 months identified patients destined to fare badly, although criteria at 18 months were less useful. The predictive value of some other individual criteria varied. In general, the LeukemiaNet criteria have useful predictive value, but a case could now be made for combining the categories "failure" and "suboptimal response."

PMID 18716134  Blood. 2008 Dec 1;112(12):4437-44. doi: 10.1182/blood-2・・・
著者: Timothy P Hughes, Andreas Hochhaus, Susan Branford, Martin C Müller, Jaspal S Kaeda, Letizia Foroni, Brian J Druker, François Guilhot, Richard A Larson, Stephen G O'Brien, Marc S Rudoltz, Manisha Mone, Elisabeth Wehrle, Vijay Modur, John M Goldman, Jerald P Radich, IRIS investigators
雑誌名: Blood. 2010 Nov 11;116(19):3758-65. doi: 10.1182/blood-2010-03-273979. Epub 2010 Aug 2.
Abstract/Text This study examines the prognostic significance of early molecular response using an expanded dataset in chronic myeloid leukemia patients enrolled in the International Randomized Study of Interferon and STI571 (IRIS). Serial molecular studies demonstrate decreases in BCR-ABL transcripts over time. Analyses of event-free survival (EFS) and time to progression to accelerated phase/blast crisis (AP/BC) at 7 years were based on molecular responses using the international scale (IS) at 6-, 12-, and 18-month landmarks. Patients with BCR-ABL transcripts > 10% at 6 months and > 1% at 12 months had inferior EFS and higher rate of progression to AP/BC compared with all other molecular response groups. Conversely, patients who achieved major molecular response [MMR: BCR-ABL (IS) ≤ 0.1%] by 18 months enjoyed remarkably durable responses, with no progression to AP/BC and 95% EFS at 7 years. The probability of loss of complete cytogenetic response by 7 years was only 3% for patients in MMR at 18 months versus 26% for patients with complete cytogenetic response but not MMR (P < .001). This study shows a strong association between the degree to which BCR-ABL transcript numbers are reduced by therapy and long-term clinical outcome, supporting the use of time-dependent molecular measures to determine optimal response to therapy. This study is registered at www.clinicaltrials.gov as NCT00006343.

PMID 20679528  Blood. 2010 Nov 11;116(19):3758-65. doi: 10.1182/blood-・・・

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