Significance of deeper molecular responses in patients with chronic myeloid leukemia in early chronic phase treated with tyrosine kinase inhibitors
Most patients with chronic myeloid leukemia (CML) in chronic phase (CP) treated with tyrosine kinase inhibitors (TKI) achieve complete cytogenetic response (CCyR). An increasing number of patients also achieve deep molecular responses (MR). We determined the frequency and significance of deep MR aft...
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| Published in | American journal of hematology Vol. 88; no. 12; pp. 1024 - 1029 |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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United States
Wiley Subscription Services, Inc
01.12.2013
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| Abstract | Most patients with chronic myeloid leukemia (CML) in chronic phase (CP) treated with tyrosine kinase inhibitors (TKI) achieve complete cytogenetic response (CCyR). An increasing number of patients also achieve deep molecular responses (MR). We determined the frequency and significance of deep MR after TKI therapy for CML in CP. MR included: major molecular response (MMR), MR4, MR4.5, and undetectable transcripts (UND), i.e., BCR‐ABL/ABL of ≤0.1, ≤0.01, ≤0.0032%, and undetectable transcripts, respectively. Four hundred eighty‐three patients received imatinib 400 mg/day (IM400, 71, July 2000 to April 2001), imatinib 800 mg/day (IM800, 204, June 2001 to July 2005), nilotinib (106, July 2005 to date), or dasatinib (102, November 2005 to date). UND rates at 36 months were 18.1, 30.6, 29.2, and 28.6%, respectively. Patients achieving UND have superior transformation‐free survival (TFS) and overall survival (OS) versus those obtaining ≤MMR, but not other MR levels. At the 18‐ and 24‐month landmark analysis, patients achieving UND have no advantage in TFS and OS compared to those achieving a lesser degree of MR. Among patients achieving MR4.5, those who maintain it for ≥2 years (susMR4·5) have no additional benefit in TFS or OS. Most patients with early CP CML receiving TKI achieve MMR. BCR‐ABL transcripts become undetectable in a significant fraction of them. Deeper MR at 18 or 24 months are not associated with a benefit in TFS or OS. Furthermore, achieving susMR4·5 does not appear to further reduce the risk of transformation or death. Am. J. Hematol. 88:1024–1029, 2013. © 2013 Wiley Periodicals, Inc. |
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| AbstractList | Most patients with chronic myeloid leukemia (CML) in chronic phase (CP) treated with tyrosine kinase inhibitors (TKI) achieve complete cytogenetic response (CCyR). An increasing number of patients also achieve deep molecular responses (MR). We determined the frequency and significance of deep MR after TKI therapy for CML in CP. MR included: major molecular response (MMR), MR4, MR4.5, and undetectable transcripts (UND), i.e., BCR-ABL/ABL of ≤0.1, ≤0.01, ≤0.0032%, and undetectable transcripts, respectively. Four hundred eighty-three patients received imatinib 400 mg/day (IM400, 71, July 2000 to April 2001), imatinib 800 mg/day (IM800, 204, June 2001 to July 2005), nilotinib (106, July 2005 to date), or dasatinib (102, November 2005 to date). UND rates at 36 months were 18.1, 30.6, 29.2, and 28.6%, respectively. Patients achieving UND have superior transformation-free survival (TFS) and overall survival (OS) versus those obtaining ≤MMR, but not other MR levels. At the 18- and 24-month landmark analysis, patients achieving UND have no advantage in TFS and OS compared to those achieving a lesser degree of MR. Among patients achieving MR4.5, those who maintain it for ≥2 years (susMR4·5) have no additional benefit in TFS or OS. Most patients with early CP CML receiving TKI achieve MMR. BCR-ABL transcripts become undetectable in a significant fraction of them. Deeper MR at 18 or 24 months are not associated with a benefit in TFS or OS. Furthermore, achieving susMR4·5 does not appear to further reduce the risk of transformation or death.Most patients with chronic myeloid leukemia (CML) in chronic phase (CP) treated with tyrosine kinase inhibitors (TKI) achieve complete cytogenetic response (CCyR). An increasing number of patients also achieve deep molecular responses (MR). We determined the frequency and significance of deep MR after TKI therapy for CML in CP. MR included: major molecular response (MMR), MR4, MR4.5, and undetectable transcripts (UND), i.e., BCR-ABL/ABL of ≤0.1, ≤0.01, ≤0.0032%, and undetectable transcripts, respectively. Four hundred eighty-three patients received imatinib 400 mg/day (IM400, 71, July 2000 to April 2001), imatinib 800 mg/day (IM800, 204, June 2001 to July 2005), nilotinib (106, July 2005 to date), or dasatinib (102, November 2005 to date). UND rates at 36 months were 18.1, 30.6, 29.2, and 28.6%, respectively. Patients achieving UND have superior transformation-free survival (TFS) and overall survival (OS) versus those obtaining ≤MMR, but not other MR levels. At the 18- and 24-month landmark analysis, patients achieving UND have no advantage in TFS and OS compared to those achieving a lesser degree of MR. Among patients achieving MR4.5, those who maintain it for ≥2 years (susMR4·5) have no additional benefit in TFS or OS. Most patients with early CP CML receiving TKI achieve MMR. BCR-ABL transcripts become undetectable in a significant fraction of them. Deeper MR at 18 or 24 months are not associated with a benefit in TFS or OS. Furthermore, achieving susMR4·5 does not appear to further reduce the risk of transformation or death. Most patients with chronic myeloid leukemia (CML) in chronic phase (CP) treated with tyrosine kinase inhibitors (TKI) achieve complete cytogenetic response (CCyR). An increasing number of patients also achieve deep molecular responses (MR). We determined the frequency and significance of deep MR after TKI therapy for CML in CP. MR included: major molecular response (MMR), MR4, MR4.5, and undetectable transcripts (UND), i.e., BCR-ABL/ABL of ≤0.1, ≤0.01, ≤0.0032%, and undetectable transcripts, respectively. Four hundred eighty-three patients received imatinib 400 mg/day (IM400, 71, July 2000 to April 2001), imatinib 800 mg/day (IM800, 204, June 2001 to July 2005), nilotinib (106, July 2005 to date), or dasatinib (102, November 2005 to date). UND rates at 36 months were 18.1, 30.6, 29.2, and 28.6%, respectively. Patients achieving UND have superior transformation-free survival (TFS) and overall survival (OS) versus those obtaining ≤MMR, but not other MR levels. At the 18- and 24-month landmark analysis, patients achieving UND have no advantage in TFS and OS compared to those achieving a lesser degree of MR. Among patients achieving MR4.5, those who maintain it for ≥2 years (susMR4·5) have no additional benefit in TFS or OS. Most patients with early CP CML receiving TKI achieve MMR. BCR-ABL transcripts become undetectable in a significant fraction of them. Deeper MR at 18 or 24 months are not associated with a benefit in TFS or OS. Furthermore, achieving susMR4·5 does not appear to further reduce the risk of transformation or death. Am. J. Hematol. 88:1024-1029, 2013. © 2013 Wiley Periodicals, Inc. [PUBLICATION ABSTRACT] Most patients with chronic myeloid leukemia (CML) in chronic phase (CP) treated with tyrosine kinase inhibitors (TKI) achieve complete cytogenetic response (CCyR). An increasing number of patients also achieve deep molecular responses (MR). We determined the frequency and significance of deep MR after TKI therapy for CML in CP. MR included: major molecular response (MMR), MR4, MR4.5, and undetectable transcripts (UND), i.e., BCR-ABL/ABL of ≤0.1, ≤0.01, ≤0.0032%, and undetectable transcripts, respectively. Four hundred eighty-three patients received imatinib 400 mg/day (IM400, 71, July 2000 to April 2001), imatinib 800 mg/day (IM800, 204, June 2001 to July 2005), nilotinib (106, July 2005 to date), or dasatinib (102, November 2005 to date). UND rates at 36 months were 18.1, 30.6, 29.2, and 28.6%, respectively. Patients achieving UND have superior transformation-free survival (TFS) and overall survival (OS) versus those obtaining ≤MMR, but not other MR levels. At the 18- and 24-month landmark analysis, patients achieving UND have no advantage in TFS and OS compared to those achieving a lesser degree of MR. Among patients achieving MR4.5, those who maintain it for ≥2 years (susMR4·5) have no additional benefit in TFS or OS. Most patients with early CP CML receiving TKI achieve MMR. BCR-ABL transcripts become undetectable in a significant fraction of them. Deeper MR at 18 or 24 months are not associated with a benefit in TFS or OS. Furthermore, achieving susMR4·5 does not appear to further reduce the risk of transformation or death. Most patients with chronic myeloid leukemia (CML) in chronic phase (CP) treated with tyrosine kinase inhibitors (TKI) achieve complete cytogenetic response (CCyR). An increasing number of patients also achieve deep molecular responses (MR). We determined the frequency and significance of deep MR after TKI therapy for CML in CP. MR included: major molecular response (MMR), MR4, MR4.5, and undetectable transcripts (UND), i.e., BCR‐ABL/ABL of ≤0.1, ≤0.01, ≤0.0032%, and undetectable transcripts, respectively. Four hundred eighty‐three patients received imatinib 400 mg/day (IM400, 71, July 2000 to April 2001), imatinib 800 mg/day (IM800, 204, June 2001 to July 2005), nilotinib (106, July 2005 to date), or dasatinib (102, November 2005 to date). UND rates at 36 months were 18.1, 30.6, 29.2, and 28.6%, respectively. Patients achieving UND have superior transformation‐free survival (TFS) and overall survival (OS) versus those obtaining ≤MMR, but not other MR levels. At the 18‐ and 24‐month landmark analysis, patients achieving UND have no advantage in TFS and OS compared to those achieving a lesser degree of MR. Among patients achieving MR4.5, those who maintain it for ≥2 years (susMR4·5) have no additional benefit in TFS or OS. Most patients with early CP CML receiving TKI achieve MMR. BCR‐ABL transcripts become undetectable in a significant fraction of them. Deeper MR at 18 or 24 months are not associated with a benefit in TFS or OS. Furthermore, achieving susMR4·5 does not appear to further reduce the risk of transformation or death. Am. J. Hematol. 88:1024–1029, 2013. © 2013 Wiley Periodicals, Inc. Most patients with chronic myeloid leukemia (CML) in chronic phase (CP) treated with tyrosine kinase inhibitors (TKI) achieve complete cytogenetic response (CCyR). An increasing number of patients also achieve deep molecular responses (MR). We determined the frequency and significance of deep MR after TKI therapy for CML in CP. MR included: major molecular response (MMR), MR4, MR4.5, and undetectable transcripts (UND), i.e., BCR‐ABL/ABL of ≤0.1, ≤0.01, ≤0.0032%, and undetectable transcripts, respectively. Four hundred eighty‐three patients received imatinib 400 mg/day (IM400, 71, July 2000 to April 2001), imatinib 800 mg/day (IM800, 204, June 2001 to July 2005), nilotinib (106, July 2005 to date), or dasatinib (102, November 2005 to date). UND rates at 36 months were 18.1, 30.6, 29.2, and 28.6%, respectively. Patients achieving UND have superior transformation‐free survival (TFS) and overall survival (OS) versus those obtaining ≤MMR, but not other MR levels. At the 18‐ and 24‐month landmark analysis, patients achieving UND have no advantage in TFS and OS compared to those achieving a lesser degree of MR. Among patients achieving MR4.5, those who maintain it for ≥2 years ( sus MR4·5) have no additional benefit in TFS or OS. Most patients with early CP CML receiving TKI achieve MMR. BCR‐ABL transcripts become undetectable in a significant fraction of them. Deeper MR at 18 or 24 months are not associated with a benefit in TFS or OS. Furthermore, achieving sus MR4·5 does not appear to further reduce the risk of transformation or death. Am. J. Hematol. 88:1024–1029, 2013. © 2013 Wiley Periodicals, Inc. Most patients with chronic myeloid leukemia (CML) in chronic phase (CP) treated with tyrosine kinase inhibitors (TKI) achieve complete cytogenetic response (CCyR). An increasing number of patients also achieve deep molecular responses (MR). We determined the frequency and significance of deep MR after TKI therapy for CML in CP. MR included: major molecular response (MMR), MR4, MR4.5, and undetectable transcripts (UND), ie BCR-ABL/ABL of ≤0.1%, ≤0.01%, ≤0.0032%, and undetectable transcripts, respectively. 483 patients received imatinib 400mg/day (IM400, 71, July 2000-April 2001), imatinib 800mg/day (IM800, 204, June 2001-July 2005), nilotinib (NILO, 106, July 2005 to date), or dasatinib (DASA, 102, November 2005 to date). UND rates at 36 months were 18.1%, 30.6%, 29.2%, and 28.6%, respectively. Patients achieving UND have superior transformation-free survival (TFS) and overall survival (OS) versus those obtaining ≤MMR, but not other MR levels. At the 18- and 24-month landmark analysis patients achieving UND have no advantage in TFS and OS compared to those achieving a lesser degree of MR. Among patients achieving MR4.5, those who maintain it for ≥2 years ( sus MR4·5) have no additional benefit in TFS or OS. Most patients with early CP CML receiving TKI achieve MMR. BCR-ABL transcripts become undetectable in a significant fraction of them. Deeper MR at 18 or 24 months are not associated with a benefit in TFS or OS. Furthermore, achieving sus MR4·5 does not appear to further reduce the risk of transformation or death. |
| Author | Verma, Dushyant O'Brien, Susan Garcia‐Manero, Guillermo Borthakur, Gautam Verstovsek, Srdan Wang, Xuemei Quintás‐Cardama, Alfonso Falchi, Lorenzo Kantarjian, Hagop M. Jabbour, Elias J. Cortes, Jorge E. Burger, Jan A. Ravandi‐Kashani, Farhad Luthra, Raja |
| AuthorAffiliation | 2 Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX 3 Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX 1 Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX |
| AuthorAffiliation_xml | – name: 1 Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX – name: 2 Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX – name: 3 Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX |
| Author_xml | – sequence: 1 givenname: Lorenzo surname: Falchi fullname: Falchi, Lorenzo organization: The University of Texas MD Anderson Cancer Center – sequence: 2 givenname: Hagop M. surname: Kantarjian fullname: Kantarjian, Hagop M. organization: The University of Texas MD Anderson Cancer Center – sequence: 3 givenname: Xuemei surname: Wang fullname: Wang, Xuemei organization: The University of Texas MD Anderson Cancer Center – sequence: 4 givenname: Dushyant surname: Verma fullname: Verma, Dushyant organization: The University of Texas MD Anderson Cancer Center – sequence: 5 givenname: Alfonso surname: Quintás‐Cardama fullname: Quintás‐Cardama, Alfonso organization: The University of Texas MD Anderson Cancer Center – sequence: 6 givenname: Susan surname: O'Brien fullname: O'Brien, Susan organization: The University of Texas MD Anderson Cancer Center – sequence: 7 givenname: Elias J. surname: Jabbour fullname: Jabbour, Elias J. organization: The University of Texas MD Anderson Cancer Center – sequence: 8 givenname: Farhad surname: Ravandi‐Kashani fullname: Ravandi‐Kashani, Farhad organization: The University of Texas MD Anderson Cancer Center – sequence: 9 givenname: Gautam surname: Borthakur fullname: Borthakur, Gautam organization: The University of Texas MD Anderson Cancer Center – sequence: 10 givenname: Guillermo surname: Garcia‐Manero fullname: Garcia‐Manero, Guillermo organization: The University of Texas MD Anderson Cancer Center – sequence: 11 givenname: Srdan surname: Verstovsek fullname: Verstovsek, Srdan organization: The University of Texas MD Anderson Cancer Center – sequence: 12 givenname: Jan A. surname: Burger fullname: Burger, Jan A. organization: The University of Texas MD Anderson Cancer Center – sequence: 13 givenname: Raja surname: Luthra fullname: Luthra, Raja organization: The University of Texas MD Anderson Cancer Center – sequence: 14 givenname: Jorge E. surname: Cortes fullname: Cortes, Jorge E. organization: The University of Texas MD Anderson Cancer Center |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23913852$$D View this record in MEDLINE/PubMed |
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| Notes | This research has been supported in part by MD Anderson Cancer Center Support (Grant CA016672) and the National Institute of Health (Grant P01 CA049639). Conflict of interest: H.K.M. has received research funding from Bristol‐Myers Squibb, Ariad, Pfizer, and Novartis. E.J.J. has received honoraria from Pfizer, Novartis, and Bristol‐Myers Squibb. F.R. has received research funding from Bristol‐Myers‐Squibb and has received honoraria from Bristol‐Myers Squibb, Novartis, and Pfizer. J.E.C.: is consultant for Ariad, Pfizer, and Teva and has received research funding from Ariad, Bristol‐Myers Squibb, Novartis, Chemgenex, and Pfizer. L.F., X.W., D.V., S.O., G.B., A.Q., G.G., S.V., and J.A.B. declare no conflicts of interest. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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| SubjectTerms | Adolescent Adult Aged Aged, 80 and over Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Benzamides - pharmacology Benzamides - therapeutic use Biomarkers, Tumor Dasatinib Disease-Free Survival Female Fusion Proteins, bcr-abl - antagonists & inhibitors Fusion Proteins, bcr-abl - blood Fusion Proteins, bcr-abl - genetics Hematology Humans Imatinib Mesylate Leukemia Leukemia, Myeloid, Chronic-Phase - blood Leukemia, Myeloid, Chronic-Phase - drug therapy Leukemia, Myeloid, Chronic-Phase - genetics Male Medical research Middle Aged Neoplasm Proteins - antagonists & inhibitors Neoplasm Proteins - blood Neoplasm Proteins - genetics Piperazines - pharmacology Piperazines - therapeutic use Protein Kinase Inhibitors - pharmacology Protein Kinase Inhibitors - therapeutic use Pyrimidines - pharmacology Pyrimidines - therapeutic use Real-Time Polymerase Chain Reaction RNA, Messenger - blood RNA, Neoplasm - blood Survival Analysis Thiazoles - pharmacology Thiazoles - therapeutic use Treatment Outcome Young Adult |
| Title | Significance of deeper molecular responses in patients with chronic myeloid leukemia in early chronic phase treated with tyrosine kinase inhibitors |
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