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31. Druker BJ, Guilhot F, O'Brien SG, Gathmann I, Kantarjian H, Gattermann N, Deininger MW, Silver RT, Goldman JM, Stone RM, Cervantes F, Hochhaus A, Powell BL, Gabrilove JL, Rousselot P, Reiffers J, Cornelissen JJ, Hughes T, Agis H, Fischer T, Verhoef G, Shepherd J, Saglio G, Gratwohl A, Nielsen JL, Radich JP, Simonsson B, Taylor K, Baccarani M, So C, Letvak L, Larson RA, IRIS Investigators: Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. N Engl J Med; 2006 Dec 7;355(23):2408-17
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  • [Title] Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia.
  • 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.
  • 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).
  • 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]. )
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Benzamides. Cytarabine / administration & dosage. Disease-Free Survival. Female. Follow-Up Studies. Fusion Proteins, bcr-abl / blood. Humans. Imatinib Mesylate. Interferon-alpha / administration & dosage. Kaplan-Meier Estimate. Male. Survival Analysis. Survival Rate. Treatment Outcome


32. Talpaz M, Shah NP, Kantarjian H, Donato N, Nicoll J, Paquette R, Cortes J, O'Brien S, Nicaise C, Bleickardt E, Blackwood-Chirchir MA, Iyer V, Chen TT, Huang F, Decillis AP, Sawyers CL: Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias. N Engl J Med; 2006 Jun 15;354(24):2531-41
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  • [Title] Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias.
  • BACKGROUND: The BCR-ABL tyrosine kinase inhibitor imatinib is effective in Philadelphia chromosome-positive (Ph-positive) leukemias, but relapse occurs, mainly as a result of the outgrowth of leukemic subclones with imatinib-resistant BCR-ABL mutations.
  • We evaluated dasatinib, a BCR-ABL inhibitor that targets most imatinib-resistant BCR-ABL mutations, in patients with chronic myelogenous leukemia (CML) or Ph-positive acute lymphoblastic leukemia (ALL).
  • METHODS: Patients with various phases of CML or with Ph-positive ALL who could not tolerate or were resistant to imatinib were enrolled in a phase 1 dose-escalation study.
  • RESULTS: A complete hematologic response was achieved in 37 of 40 patients with chronic-phase CML, and major hematologic responses were seen in 31 of 44 patients with accelerated-phase CML, CML with blast crisis, or Ph-positive ALL.
  • Responses were maintained in 95 percent of patients with chronic-phase disease and in 82 percent of patients with accelerated-phase disease, with a median follow-up more than 12 months and 5 months, respectively.
  • Nearly all patients with lymphoid blast crisis and Ph-positive ALL had a relapse within six months.
  • Responses occurred among all BCR-ABL genotypes, with the exception of the T315I mutation, which confers resistance to both dasatinib and imatinib in vitro.
  • CONCLUSIONS: Dasatinib induces hematologic and cytogenetic responses in patients with CML or Ph-positive ALL who cannot tolerate or are resistant to imatinib. (ClinicalTrials.gov number, NCT00064233 [ClinicalTrials.gov].).
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Fusion Proteins, bcr-abl / antagonists & inhibitors. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / administration & dosage. Pyrimidines / administration & dosage. Thiazoles / administration & dosage

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  • [Copyright] Copyright 2006 Massachusetts Medical Society.
  • [CommentIn] N Engl J Med. 2006 Sep 7;355(10):1062; author reply 1063-4 [16957155.001]
  • [CommentIn] N Engl J Med. 2006 Jun 15;354(24):2594-6 [16775240.001]
  • [CommentIn] N Engl J Med. 2006 Sep 7;355(10):1062-3; author reply 1063-4 [16960978.001]
  • (PMID = 16775234.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00064233
  • [Grant] United States / NCRR NIH HHS / RR / M01-RR-00865
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
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33. Chen ZC, You Y, Zhu XM, Li QB, Li WM, Zou P: [A clinical study of treating 120 cases of adult chronic myelocytic leukemia with imatinib mesylate]. Zhonghua Nei Ke Za Zhi; 2007 Dec;46(12):1003-6
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  • [Title] [A clinical study of treating 120 cases of adult chronic myelocytic leukemia with imatinib mesylate].
  • OBJECTIVE: To analyze and evaluate the clinical efficacy and safety of imatinib mesylate (IM) as a tyrosine kinase inhibitor on Ph-positive or BCR/ABL positive chronic myelogenous leukemia (CML).
  • METHODS: 120 patients diagnosed as CML with positive Ph chromosome were treated with IM 400 mg/d for CML in chronic phase (CP) (n = 90) or 600 mg/d for CML in accelerated or blastic phase (AP or BP) (n = 30) once daily.
  • Hematological, cytogenetic and molecular effects of IM on the disease process of these patients were evaluated with blood and marrow cells morphology examination, G-band conventional cytogenetics analysis for Ph chromosome and PCR assay for BCR/ABL gene.
  • (1) In CML-CP patients, after a follow-up of 9 ( range 3-42) months, cumulative complete hematological response (CHR), complete cytogenetic response (CCyR) and complete molecular response (CMR) rates were 73.3%, 66.7% and 54.4%, which was not influenced by prior treatment of interferon.
  • CMR was better when time from diagnosis to treatment with IM was < or = 6 months (P < 0.05).
  • It is significant that the time to first CHR and time to first CCyR were related with the time to first CCyR and the time to first negative BCR/ ABL, respectively (both P < 0.05), while there was no relation between the time to first CHR and the time to first negative BCR/ABL (P > 0.05). (2) CHR, CCyR and CMR rates of the patients with progressive course (AP and BP) were 43.3%, 25.9% and 25.0%, respectively.
  • CONCLUSION: IM can lead to considerable hematological, cytogenetic and molecular response rates in CML, especially CML-CP patients, with minor tolerable side effects.
  • [MeSH-major] Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Benzamides. Female. Fusion Proteins, bcr-abl / genetics. Humans. Imatinib Mesylate. Male. Middle Aged. Philadelphia Chromosome. Retrospective Studies. Treatment Outcome

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  • (PMID = 18478917.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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4. Ahmad R, Tripathi AK, Tripathi P, Singh R, Singh S, Singh RK: Oxidative stress and antioxidant status in patients with chronic myeloid leukemia. Indian J Clin Biochem; 2008 Oct;23(4):328-33
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  • [Title] Oxidative stress and antioxidant status in patients with chronic myeloid leukemia.
  • Chronic myeloid leukemia is a myeloproliferative disorder with a unique rearrangement, the Philadelphia chromosome.
  • The aim of this study was to evaluate the role of oxidative stress in pathophysiology of Chronic myeloid leukemia by measuring the circulating plasma lipid peroxide levels in terms of malonyldialdehyde, total lipid hydroperoxide and oxidized proteins as protein carbonyl whereas antioxidant status were estimated in terms of reduced glutathione and total thiol in plasma of Chronic myeloid leukemia patients.
  • The present study included 47 Chronic myeloid leukemia patients and 20 age-and sex-matched healthy subjects.
  • Out of 47 Chronic myeloid leukemia patients, 31 were in chronic phase (CML-CP) and 16 in accelerated phase (CML-AP).
  • The median age of Chronic myeloid leukemia patients was 33 years and that of controls was 32 years.
  • There was a significant increase (p<0.05) in plasma malonyldialdehyde, total lipid hydroperoxide and protein carbonyl levels in Chronic myeloid leukemia patients as compared to healthy subjects.
  • Our results also showed that plasma malonyldialdehyde and protein carbonyl levels were markedly elevated (p<0.05) in both chronic phase (CML-CP) and accelerated phase (CML-AP) as compared to healthy volunteers.
  • Antioxidant status was found to be significantly decreased (p<0.05) in Chronic myeloid leukemia patients and its phases as compared to healthy participants.
  • It could be concluded that oxidative stress may be associated with the pathophysiology of Chronic myeloid leukemia.

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  • [Cites] Clin Chem. 1992 Apr;38(4):594-5 [1568333.001]
  • [Cites] Methods Enzymol. 1990;186:464-78 [1978225.001]
  • [Cites] Free Radic Biol Med. 1990;8(1):15-9 [2157633.001]
  • [Cites] Free Radic Biol Med. 1990;8(6):583-99 [2193855.001]
  • [Cites] Methods Enzymol. 1990;186:421-31 [2233309.001]
  • [Cites] Science. 1985 Jan 25;227(4685):375-81 [2981433.001]
  • [Cites] Mol Cell Biochem. 1988 Dec;84(2):147-53 [3068520.001]
  • [Cites] Lancet. 1983 May 7;1(8332):1010-4 [6133059.001]
  • [Cites] Lancet. 1994 Sep 24;344(8926):862-3 [7916406.001]
  • [Cites] Cancer Chemother Pharmacol. 1994;35(2):132-6 [7987989.001]
  • [Cites] Am J Med. 1994 Sep 26;97(3A):5S-13S; discussion 22S-28S [8085584.001]
  • [Cites] Free Radic Biol Med. 1997;22(1-2):269-85 [8958153.001]
  • [Cites] Free Radic Biol Med. 1999 Feb;26(3-4):410-8 [9895233.001]
  • [Cites] Clin Chem. 1999 Jul;45(7):1084-6 [10388487.001]
  • [Cites] Breast Cancer Res Treat. 2000 Jan;59(2):163-70 [10817351.001]
  • [Cites] Cancer Res. 2001 Jan 15;61(2):778-84 [11212282.001]
  • [Cites] Clin Biochem. 2002 Nov;35(8):621-5 [12498996.001]
  • [Cites] Indian J Exp Biol. 2002 Nov;40(11):1233-9 [13677624.001]
  • [Cites] J Lab Clin Med. 1963 May;61:882-8 [13967893.001]
  • [Cites] Clin Chim Acta. 2003 Dec;338(1-2):143-9 [14637279.001]
  • [Cites] J Biol Chem. 1951 Nov;193(1):265-75 [14907713.001]
  • [Cites] J Nutr. 2004 Mar;134(3):489-92 [14988435.001]
  • [Cites] Contrib Nephrol. 2005;149:240-60 [15876848.001]
  • [Cites] Acta Biochim Pol. 2006;53(1):237-42 [16404476.001]
  • [Cites] Clin Chem. 2006 Apr;52(4):601-23 [16484333.001]
  • [Cites] Blood. 2006 Jul 1;108(1):319-27 [16527898.001]
  • [Cites] Obes Surg. 2007 Oct;17(10):1367-73 [18000722.001]
  • [Cites] Cancer Metastasis Rev. 2006 Dec;25(4):695-705 [17160708.001]
  • [Cites] Cancer Treat Rev. 1997 Jul;23(4):209-40 [9377594.001]
  • [Cites] Wiad Lek. 1998;51 Suppl 4:107-12 [10731952.001]
  • [Cites] J Assoc Physicians India. 1999 Apr;47(4):403-5 [10778525.001]
  • [Cites] J Biol Chem. 2000 Aug 11;275(32):24273-8 [10833515.001]
  • [Cites] Indian J Med Sci. 2000 Feb;54(2):52-4 [11271724.001]
  • [Cites] Indian J Med Sci. 2001 Apr;55(4):215-7 [11665392.001]
  • [Cites] Exp Biol Med (Maywood). 2003 May;228(5):525-8 [12709580.001]
  • [Cites] Ann Intern Med. 2003 May 20;138(10):819-30 [12755554.001]
  • [Cites] Int Urol Nephrol. 2003;35(3):345-50 [15160536.001]
  • [Cites] Mediators Inflamm. 2004 Dec;13(5-6):381-3 [15770058.001]
  • [Cites] Indian J Med Res. 2005 Dec;122(6):529-34 [16518005.001]
  • [Cites] J Cell Mol Med. 2006 Apr-Jun;10(2):389-406 [16796807.001]
  • (PMID = 23105780.001).
  • [ISSN] 0970-1915
  • [Journal-full-title] Indian journal of clinical biochemistry : IJCB
  • [ISO-abbreviation] Indian J Clin Biochem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3453137
  • [Keywords] NOTNLM ; Antioxidants / Chronic myeloid leukemia / Malonyldialdehyde / Oxidative stress / Protein carbonyl / Total lipid hydroperoxide
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35. Jabbour E, Cortés JE, Kantarjian H: Optimizing treatment with Bcr-Abl tyrosine kinase inhibitors in Philadelphia chromosome-positive chronic myeloid leukemia: focus on dosing schedules. Clin Lymphoma Myeloma; 2008 Mar;8 Suppl 3:S75-81
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  • [Title] Optimizing treatment with Bcr-Abl tyrosine kinase inhibitors in Philadelphia chromosome-positive chronic myeloid leukemia: focus on dosing schedules.
  • Chronic myeloid leukemia (CML) is characterized by the presence of the Philadelphia chromosome (Ph), a genetic aberration that codes for bcrabl, which plays a key role in disease pathophysiology.
  • Dose-escalated imatinib (800 mg daily) has shown some limited activity in patients with imatinib-resistant CML, but the development of second-generation tyrosine kinase inhibitors has broadened the treatment options.
  • Dasatinib has demonstrated activity in all phases of CML and Ph+ acute lymphocytic leukemia and is approved for the treatment of adults in this setting.
  • Recent phase III data have demonstrated that, in patients with chronic-phase CML, dasatinib 100 mg once daily is equally effective, with improved tolerability, compared with the previously approved 70-mg twice-daily dose.
  • Nilotinib, which has been recently approved, has increased potency for Brc-Abl compared with imatinib and has demonstrated activity in patients with imatinib-resistant and -intolerant chronic- and accelerated-phase CML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Philadelphia Chromosome. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Clinical Trials as Topic. Dasatinib. Fusion Proteins, bcr-abl. Humans

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  • (PMID = 19254884.001).
  • [ISSN] 1557-9190
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
  • [Number-of-references] 51
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36. Notari M, Neviani P, Santhanam R, Blaser BW, Chang JS, Galietta A, Willis AE, Roy DC, Caligiuri MA, Marcucci G, Perrotti D: A MAPK/HNRPK pathway controls BCR/ABL oncogenic potential by regulating MYC mRNA translation. Blood; 2006 Mar 15;107(6):2507-16
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  • [Title] A MAPK/HNRPK pathway controls BCR/ABL oncogenic potential by regulating MYC mRNA translation.
  • Altered mRNA translation is one of the effects exerted by the BCR/ABL oncoprotein in the blast crisis phase of chronic myelogenous leukemia (CML).
  • Here, we report that in BCR/ABL+ cell lines and in patient-derived CML blast crisis mononuclear and CD34+ cells, p210(BCR/ABL) increases expression and activity of the transcriptional-inducer and translational-regulator heterogeneous nuclear ribonucleoprotein K (hnRNP K or HNRPK) in a dose- and kinase-dependent manner through the activation of the MAPK(ERK1/2) pathway.
  • Furthermore, HNRPK down-regulation and interference with HNRPK translation-but not transcription-regulatory activity impairs cytokine-independent proliferation, clonogenic potential, and in vivo leukemogenic activity of BCR/ABL-expressing myeloid 32Dcl3 and/or primary CD34+ CML-BC patient cells.
  • Mechanistically, we demonstrate that decreased internal ribosome entry site (IRES)-dependent Myc mRNA translation accounts for the phenotypic changes induced by inhibition of the BCR/ABL-ERK-dependent HNRPK translation-regulatory function.
  • Accordingly, MYC protein but not mRNA levels are increased in the CD34+ fraction of patients with CML in accelerated and blastic phase but not in chronic phase CML patients and in the CD34+ fraction of marrow cells from healthy donors.
  • Thus, BCR/ABL-dependent enhancement of HNRPK translation-regulation is important for BCR/ABL leukemogenesis and, perhaps, it might contribute to blast crisis transformation.

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  • [Cites] Exp Hematol. 1993 Oct;21(11):1460-6 [8405226.001]
  • [Cites] Mol Cell Biol. 2002 Apr;22(7):2255-66 [11884611.001]
  • [Cites] Med Oncol Tumor Pharmacother. 1992;9(3):139-47 [1341325.001]
  • [Cites] Nature. 1994 Apr 28;368(6474):867-71 [7512694.001]
  • [Cites] Mol Cell Biol. 1995 Mar;15(3):1324-32 [7862126.001]
  • [Cites] Cancer Res. 1995 Jun 1;55(11):2275-8 [7757976.001]
  • [Cites] Blood. 1995 Sep 15;86(6):2371-8 [7662984.001]
  • [Cites] Mol Cell Biol. 1995 Oct;15(10):5531-41 [7565705.001]
  • [Cites] Mol Cell Biol. 1996 May;16(5):2350-60 [8628302.001]
  • [Cites] J Biol Chem. 1996 Feb 16;271(7):3420-7 [8631943.001]
  • [Cites] Leukemia. 1996 May;10(5):751-6 [8656667.001]
  • [Cites] Leuk Res. 1996 Jan;20(1):85-91 [8632682.001]
  • [Cites] Blood. 1996 Aug 1;88(3):1005-12 [8704208.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):13137-42 [8917557.001]
  • [Cites] EMBO J. 1997 Jun 16;16(12):3587-98 [9218800.001]
  • [Cites] J Exp Med. 2001 Aug 6;194(3):275-84 [11489947.001]
  • [Cites] EMBO J. 2001 Dec 3;20(23):6793-804 [11726515.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):48-58 [11753385.001]
  • [Cites] Oncogene. 2001 Dec 13;20(57):8249-57 [11781839.001]
  • [Cites] Oncogene. 1997 Nov 6;15(19):2333-42 [9393877.001]
  • [Cites] Blood. 1998 Jan 15;91(2):406-18 [9427693.001]
  • [Cites] EMBO J. 1998 Aug 3;17(15):4442-55 [9687511.001]
  • [Cites] Oncogene. 1998 Sep 24;17(12):1597-606 [9794237.001]
  • [Cites] J Biol Chem. 1999 Mar 5;274(10):6553-8 [10037749.001]
  • [Cites] N Engl J Med. 1999 Apr 29;340(17):1330-40 [10219069.001]
  • [Cites] J Biol Chem. 1999 May 21;274(21):15101-9 [10329716.001]
  • [Cites] Proteomics. 2005 Feb;5(3):796-804 [15682461.001]
  • [Cites] Cell Death Differ. 2005 Jun;12(6):534-40 [15846378.001]
  • [Cites] Oncogene. 2005 Sep 22;24(42):6432-40 [16007188.001]
  • [Cites] Cancer Cell. 2005 Nov;8(5):355-68 [16286244.001]
  • [Cites] Ann Hematol. 2000 Aug;79(8):424-31 [10985361.001]
  • [Cites] Nat Cell Biol. 2001 Mar;3(3):325-30 [11231586.001]
  • [Cites] J Biol Chem. 2001 Mar 30;276(13):9699-704 [11121407.001]
  • [Cites] RNA. 2002 Mar;8(3):265-78 [12003487.001]
  • [Cites] Mol Cell Biol. 2002 Jul;22(13):4535-43 [12052863.001]
  • [Cites] Methods. 2002 Feb;26(2):191-8 [12054896.001]
  • [Cites] Oncogene. 2002 Oct 17;21(47):7137-46 [12370803.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):145-60 [12620409.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Aug;37(4):346-58 [12800146.001]
  • [Cites] Oncogene. 2003 Sep 11;22(39):8012-20 [12970749.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5716-22 [14522890.001]
  • [Cites] Curr Top Microbiol Immunol. 2004;279:169-97 [14560958.001]
  • [Cites] Oncogene. 2004 Mar 4;23(9):1693-703 [14647428.001]
  • [Cites] Annu Rev Immunol. 2004;22:247-306 [15032571.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3167-74 [15070699.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4010-22 [14982876.001]
  • [Cites] Cancer Treat Res. 2004;119:239-70 [15164881.001]
  • [Cites] Bioessays. 2004 Jun;26(6):629-38 [15170860.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1314-23 [15142884.001]
  • [Cites] Cancer Genet Cytogenet. 1987 Aug;27(2):349-56 [3474057.001]
  • [Cites] Leuk Res. 1988;12(6):507-16 [3165487.001]
  • [Cites] Cancer. 1988 Sep 15;62(6):1171-8 [3044574.001]
  • [Cites] Cell. 1992 Sep 18;70(6):901-10 [1525828.001]
  • [Cites] Leuk Lymphoma. 1993;11 Suppl 1:45-6 [8251915.001]
  • (PMID = 16293596.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / CA095512; United States / NCI NIH HHS / CA / CA16058
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; 0 / Ribonucleoproteins; 146410-60-8 / HNRNPK protein, human; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1895740
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37. Yin OQ, Gallagher N, Tanaka C, Fisher D, Sethuraman V, Zhou W, Lin TH, Heuman D, Schran H: Effects of hepatic impairment on the pharmacokinetics of nilotinib: an open-label, single-dose, parallel-group study. Clin Ther; 2009;31 Pt 2:2459-69
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  • BACKGROUND: Nilotinib is a second-generation BCR-ABL tyrosine kinase inhibitor approved for the treatment of patients who have imatinib-resistant Philadelphia chromosome-positive chronic myeloid leukemia in the chronic or accelerated phase or who are unable to tolerate imatinib.
  • The mean (SD) t(1/2) was 15.1 (4.97) and 16.0 (9.13) hours in the mild-impairment and control groups, respectively, but was 21.6 (7.77) and 32.4 (10.7) hours in the moderate- and severe-impairment groups, respectively, reflecting the decrease in CL/F and/or increase in Vz/F in the latter 2 groups.
  • [MeSH-minor] Adult. Aged. Area Under Curve. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Male. Middle Aged. Protein-Tyrosine Kinases / antagonists & inhibitors

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  • [Copyright] Copyright 2009 Excerpta Medica Inc. All rights reserved.
  • (PMID = 20110053.001).
  • [ISSN] 1879-114X
  • [Journal-full-title] Clinical therapeutics
  • [ISO-abbreviation] Clin Ther
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00418626
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Pyrimidines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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38. Na IK, Kreuzer KA, Lupberger J, Dörken B, le Coutre P: Quantitative RT-PCR of Wilms tumor gene transcripts (WT1) for the molecular monitoring of patients with accelerated phase bcr/abl + CML. Leuk Res; 2005 Mar;29(3):343-5
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  • [Title] Quantitative RT-PCR of Wilms tumor gene transcripts (WT1) for the molecular monitoring of patients with accelerated phase bcr/abl + CML.
  • The tyrosine kinase inhibitor imatinib inhibits the activity of the bcr/abl fusion protein present in patients with chronic myeloid leukemia.
  • Although in chronic phase patients response to therapy can be monitored by quantitative RT-PCR for bcr/abl mRNA transcripts, in advanced disease (accelerated phase or blast crisis) only few patients respond on a molecular level.
  • We investigated Wilms tumor gene (WT1) and bcr/abl mRNA transcripts in 16 accelerated phase CML patients by quantitative real time PCR.
  • In contrast to the bcr/abl mRNA levels the WT1 mRNA levels were indicative for hematologic relapse (n = 6) versus response (n = 10).
  • [MeSH-major] Biomarkers, Tumor / analysis. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. WT1 Proteins / genetics

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  • (PMID = 15661271.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / WT1 Proteins; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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39. Agis H, Krauth MT, Mosberger I, Müllauer L, Simonitsch-Klupp I, Schwartz LB, Printz D, Böhm A, Fritsch G, Horny HP, Valent P: Enumeration and immunohistochemical characterisation of bone marrow basophils in myeloproliferative disorders using the basophil specific monoclonal antibody 2D7. J Clin Pathol; 2006 Apr;59(4):396-402
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  • In chronic myeloid leukaemia (CML), basophilia is a diagnostic and prognostic determinant.
  • OBJECTIVE: To detect and enumerate basophils in bone marrow sections in patients with CML and other MPD.
  • METHODS: The anti-basophil antibody 2D7 was applied to paraffin embedded bone marrow sections from normal/reactive subjects (n = 31), patients with CML (chronic phase, n = 37; accelerated phase, n = 9), and other MPD (chronic idiopathic myelofibrosis (CIMF), n = 20; polycythaemia vera (PV), n = 20; essential thrombocythaemia (ET), n = 20; indolent systemic mastocytosis (ISM), n = 7).
  • 2D7(+) bone marrow cells were found to increase in CML compared with normal/reactive bone marrow and other MPD (median numbers of 2D7(+) cells/mm(2): CML, 33; normal/reactive bone marrow, 6; CIMF, 10; PV, 6; ET, 5; ISM, 3; p<0.05).
  • The highest basophil counts were recorded in accelerated phase CML (115/mm(2)).
  • This approach should help in the quantification of bone marrow basophils at diagnosis and during anti-leukaemic treatment.

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  • [Cites] J Allergy Clin Immunol. 2002 Feb;109(2):287-93 [11842299.001]
  • [Cites] Blood. 2001 Dec 15;98(13):3784-92 [11739187.001]
  • [Cites] Scand J Haematol. 1977 Jan;18(1):25-38 [265093.001]
  • [Cites] J Clin Invest. 1980 Feb;65(2):390-9 [6965379.001]
  • [Cites] J Histochem Cytochem. 1981 Apr;29(4):577-80 [6166661.001]
  • [Cites] Cancer. 1981 May 15;47(10):2470-7 [6944141.001]
  • [Cites] Blood. 1982 Jul;60(1):113-20 [6952947.001]
  • [Cites] Fed Proc. 1983 May 15;42(8):2504-9 [6301890.001]
  • [Cites] Blood. 1984 Jul;64(1):78-83 [6234038.001]
  • [Cites] Am J Clin Pathol. 1984 Jul;82(1):1-14 [6588747.001]
  • [Cites] Prog Clin Biol Res. 1984;154:3-17 [6382299.001]
  • [Cites] J Immunol. 1986 May 1;136(9):3447-54 [3007619.001]
  • [Cites] Blood. 1987 Dec;70(6):1872-9 [3118989.001]
  • [Cites] Br J Haematol. 1987 Nov;67(3):281-4 [3479996.001]
  • [Cites] Cancer. 1988 Apr 1;61(7):1441-6 [3162181.001]
  • [Cites] Leukemia. 1988 Mar;2(3):141-3 [3258049.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2288-92 [3258425.001]
  • [Cites] J Med. 1987;18(5-6):293-303 [3505257.001]
  • [Cites] Blood. 1989 Feb 15;73(3):777-81 [2644988.001]
  • [Cites] Blood. 1989 May 15;73(7):1763-9 [2469498.001]
  • [Cites] Int Arch Allergy Appl Immunol. 1990;91(2):198-203 [1971264.001]
  • [Cites] Crit Rev Oncol Hematol. 1990;10(4):327-52 [2278641.001]
  • [Cites] Adv Immunol. 1992;52:333-423 [1332448.001]
  • [Cites] J Pathol. 1993 Oct;171(2):83-98 [7506771.001]
  • [Cites] Allergy. 1994 Dec;49(10):861-5 [7709996.001]
  • [Cites] J Immunol. 1995 Jun 15;154(12):6548-55 [7759888.001]
  • [Cites] Immunology. 1996 Apr;87(4):535-43 [8675206.001]
  • [Cites] Leuk Lymphoma. 1996 Jul;22(3-4):187-204 [8819068.001]
  • [Cites] Sao Paulo Med J. 1996 Jan-Feb;114(1):1083-90 [8984584.001]
  • [Cites] Int Rev Cytol. 1998;180:87-236 [9496635.001]
  • [Cites] J Allergy Clin Immunol. 1998 Mar;101(3):354-62 [9525452.001]
  • [Cites] J Natl Cancer Inst. 1998 Jun 3;90(11):850-8 [9625174.001]
  • [Cites] Am J Surg Pathol. 1998 Sep;22(9):1132-40 [9737247.001]
  • [Cites] Lab Invest. 1999 Jan;79(1):27-38 [9952108.001]
  • [Cites] Prog Histochem Cytochem. 1998;33(3-4):III-IX, 169-320 [10319376.001]
  • [Cites] Blood. 1999 Oct 1;94(7):2343-56 [10498606.001]
  • [Cites] Acta Med Scand. 1963 Aug;174:249-54 [14051143.001]
  • [Cites] Haematologica. 1999 Nov;84(11):978-87 [10553157.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4028-38 [11110670.001]
  • [Cites] Adv Immunol. 2001;77:93-122 [11293121.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3484-90 [11369641.001]
  • [Cites] Hum Pathol. 2001 May;32(5):545-52 [11381374.001]
  • [Cites] J Allergy Clin Immunol. 2001 Aug;108(2):205-11 [11496235.001]
  • [Cites] Clin Exp Allergy. 2001 Nov;31(11):1705-13 [11696046.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2292-302 [12239137.001]
  • (PMID = 16461568.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI020487; United States / NIAID NIH HHS / AI / R21 AI020487; United States / NIAID NIH HHS / AI / R37 AI020487; United States / NIAID NIH HHS / AI / AI20487
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers; 820484N8I3 / Histamine
  • [Other-IDs] NLM/ PMC1860377
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40. Rice L, Popat U: Every case of essential thrombocythemia should be tested for the Philadelphia chromosome. Am J Hematol; 2005 Jan;78(1):71-3
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  • Essential thrombocythemia (ET) and chronic myelogenous leukemia (CML) usually present with distinctive features.
  • By 4 years, both developed leukocytosis, extreme basophilia, and circulating blasts, typical of accelerated CML.
  • We conclude that CML can present in identical fashion as ET.
  • The mandate for routine Philadelphia chromosome testing is magnified by the availability of targeted therapy and its greater efficacy in early stage disease.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Philadelphia Chromosome. Thrombocythemia, Essential / diagnosis. Thrombocythemia, Essential / genetics
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Benzamides. Bone Marrow / pathology. Chronic Disease. Diagnosis, Differential. Female. Humans. Imatinib Mesylate. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 15609281.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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41. Apperley JF, Cortes JE, Kim DW, Roy L, Roboz GJ, Rosti G, Bullorsky EO, Abruzzese E, Hochhaus A, Heim D, de Souza CA, Larson RA, Lipton JH, Khoury HJ, Kim HJ, Sillaber C, Hughes TP, Erben P, Van Tornout J, Stone RM: Dasatinib in the treatment of chronic myeloid leukemia in accelerated phase after imatinib failure: the START a trial. J Clin Oncol; 2009 Jul 20;27(21):3472-9
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  • [Title] Dasatinib in the treatment of chronic myeloid leukemia in accelerated phase after imatinib failure: the START a trial.
  • PURPOSE Patients with chronic myelogenous leukemia in accelerated phase (CML-AP) that is resistant or intolerant to imatinib have limited therapeutic options.
  • Dasatinib, a potent inhibitor of BCR-ABL and SRC-family kinases, has efficacy in patients with CML-AP who have experienced treatment failure with imatinib.
  • We now report follow-up data from the full patient cohort of 174 patients enrolled onto a phase II trial to provide a more complete assessment of the efficacy and safety of dasatinib in this population.
  • PATIENTS AND METHODS Patients with imatinib-resistant (n = 161) or -intolerant (n = 13) CML-AP received dasatinib 70 mg orally twice daily.
  • Responses were achieved irrespective of imatinib status (resistant or intolerant), prior stem-cell transplantation, or the presence of prior BCR-ABL mutation.
  • CONCLUSION Dasatinib is effective in patients with CML-AP after imatinib treatment failure.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / therapeutic use. Thiazoles / therapeutic use. Treatment Failure
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Benzamides. Dasatinib. Disease-Free Survival. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Treatment Outcome. Young Adult


42. Fausel CA: Novel treatment strategies for chronic myeloid leukemia. Am J Health Syst Pharm; 2006 Dec 1;63(23 Suppl 8):S15-20; quiz S21-2
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  • [Title] Novel treatment strategies for chronic myeloid leukemia.
  • PURPOSE: Despite dramatic advances in the treatment of chronic myeloid leukemia (CML), resistance to therapeutic agents has emerged as a significant treatment dilemma.
  • Mutations of the BCR-ABL kinase domain, a common mechanism of resistance to imatinib in CML, are discussed.
  • SUMMARY: Several new targeted kinase inhibitors have reached clinical trials and have proved to be efficacious in halting the oncogenic activity of most BCR-ABL mutants.
  • Dasatinib is 300 times more potent than imatinib at BCR-ABL inhibition, has few side effects, and inhibits the SRC family kinases.
  • Nilotinib inhibits BCR-ABL at 20-50 times more potency than imatinib.
  • Both agents were highly effective in treating chronic phase CML but were less effective at treating accelerated phase CML in early phase clinical trials.
  • CONCLUSION: The new kinase inhibitors, dasatinib and nilotinib, are emerging as plausible therapeutic options for the treatment of imatinib-refractory CML.
  • [MeSH-major] Drug Therapy / methods. Immunotherapy, Active / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy


43. Oki Y, Kantarjian HM, Gharibyan V, Jones D, O'brien S, Verstovsek S, Cortes J, Morris GM, Garcia-Manero G, Issa JP: Phase II study of low-dose decitabine in combination with imatinib mesylate in patients with accelerated or myeloid blastic phase of chronic myelogenous leukemia. Cancer; 2007 Mar 1;109(5):899-906
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  • [Title] Phase II study of low-dose decitabine in combination with imatinib mesylate in patients with accelerated or myeloid blastic phase of chronic myelogenous leukemia.
  • BACKGROUND: Resistance to imatinib is a frequent clinical problem in advanced phase chronic myelogenous leukemia (CML).
  • A Phase II study was performed on low-dose decitabine, a DNA methyltransferase inhibitor, in combination with imatinib in patients with CML in accelerated phase (AP) and myeloid blastic phase (BP).
  • The hematologic response rate was higher in patients without BCR-ABL kinase mutations (10 of 19, 53%) than in those with mutations (1 of 7, 14%).
  • CONCLUSIONS: Combination therapy with decitabine and imatinib is well tolerated and active in advanced phase CML without BCR-ABL kinase mutations.

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  • (PMID = 17236224.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CM / N01-CM-62202; United States / NCI NIH HHS / CA / P50CA100632
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 776B62CQ27 / decitabine; 8A1O1M485B / Imatinib Mesylate; M801H13NRU / Azacitidine
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44. Kumar L: Chronic myelogenous leukaemia (CML): an update. Natl Med J India; 2006 Sep-Oct;19(5):255-63
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  • [Title] Chronic myelogenous leukaemia (CML): an update.
  • The management of chronic myelogenous leukaemia (CML) has undergone a major change over the past 5 years.
  • All newly diagnosed patients of CML are candidates for imatinib mesylate therapy.
  • Almost 95% of patients with early chronic phase CML achieve complete haematological remission (CHR) and nearly 80% achieve complete cytogenetic response (CGR; 0% Philadelphia [Ph] chromosome-positive metaphases).
  • For patients with advanced CML (accelerated phase and blast crisis), achievement of CHR and major (complete and partial) CGR occurs in 25%-37% and 10%-30% of patients, respectively.
  • Most investigators agree that patients who fail to achieve CHR by 12 weeks, have partial cytogenetic response (< 35% Ph-positive metaphases) at 12 months, have CGR by 18 months, who relapse after initial response to imatinib, and those with a high Sokal score or in an advanced phase of CML should be considered for allogeneic stem cell transplantation (SCT).
  • Despite Ph negativity with imatinib treatment, most patients continue to remain BCR-ABL positive on molecular studies, and require treatment indefinitely.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 17203680.001).
  • [ISSN] 0970-258X
  • [Journal-full-title] The National medical journal of India
  • [ISO-abbreviation] Natl Med J India
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; X6Q56QN5QC / Hydroxyurea
  • [Number-of-references] 87
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45. Etienne G, Milpied B, Réa D, Rigal-Huguet F, Tulliez M, Nicolini FE, French Intergroup of CML (Fi-LMC group): [Guidelines for the management of nilotinib (Tasigna)-induced side effects in chronic myelogenous leukemia: recommendations of French Intergroup of CML (Fi-LMC group)]. Bull Cancer; 2010 Aug;97(8):997-1009
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  • [Title] [Guidelines for the management of nilotinib (Tasigna)-induced side effects in chronic myelogenous leukemia: recommendations of French Intergroup of CML (Fi-LMC group)].
  • [Transliterated title] Recommandations du groupe Fi-LMC pour la gestion des effets indésirables du traitement par nilotinib (Tasigna) au cours de la leucémie myéloïde chronique.
  • Nilotinib (Tasigna) is a second-generation BCR-ABL kinase inhibitor, recently introduced and used for the treatment of chronic or accelerated phase CML patients, intolerant or resistant to imatinib.
  • This treatment represents and important step forward for the disease control of such patients but can lead to side effects, sometimes serious, which can limit its optimal use.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / adverse effects. Pyrimidines / adverse effects

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  • (PMID = 20529767.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Practice Guideline
  • [Publication-country] France
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Recombinant Proteins; 11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
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46. Zhang Y, Jiang Q, Qiu JY, Chen SS, Jiang B, Huang XJ: [The prognostic implications of secondary chromosomal aberrations in Philadelphia chromosome-positive chronic myeloid leukemia patients after imatinib mesylate treatment]. Zhonghua Nei Ke Za Zhi; 2007 Aug;46(8):648-50
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  • [Title] [The prognostic implications of secondary chromosomal aberrations in Philadelphia chromosome-positive chronic myeloid leukemia patients after imatinib mesylate treatment].
  • OBJECTIVE: To investigate the change of Philadelphia chromosome-positive clone with secondary chromosomal aberrations after imatinib mesylate (IM) treatment in patients with chronic myeloid leukemia (CML) and its relation with prognosis.
  • METHODS: 37 cases of CML in accelerated phase and blastic phase were collected and chromosome specimens of bone marrow cells were prepared by with 24-hour culture.
  • The percentage of Philadelphia chromosome-positive clone with secondary chromosomal aberrations showed the following 4 types of change; amplification, no change, decrease and complete remission after treatment with IM.
  • 2 of the 24 cases in CML in accelerated phase gained complete cytogenetic response (CCyR) and 2 of the 13 in blastic phase did so.
  • CONCLUSION: The percentage of Philadelphia chromosome-positive clone with secondary chromosomal aberrations may drop in some CML patients after IM treatment and the patients may gain CCyR with accompanied prolonged survival.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Chronic-Phase / drug therapy. Leukemia, Myeloid, Chronic-Phase / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 17967235.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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47. DeAngelo DJ, Attar EC: Use of dasatinib and nilotinib in imatinib-resistant chronic myeloid leukemia: translating preclinical findings to clinical practice. Leuk Lymphoma; 2010 Mar;51(3):363-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Use of dasatinib and nilotinib in imatinib-resistant chronic myeloid leukemia: translating preclinical findings to clinical practice.
  • The BCR-ABL inhibitor imatinib revolutionized the treatment of chronic myeloid leukemia (CML).
  • The mechanisms underlying resistance are multifactorial and may include mutations in the kinase domain of BCR-ABL, increased production of BCR-ABL, or activation of BCR-ABL-independent pathways.
  • Two second-line BCR-ABL inhibitors are now approved for treatment of patients with resistance or intolerance to imatinib.
  • Dasatinib is a dual BCR-ABL/Src-family kinase (SFK) inhibitor approved for patients with imatinib-resistant and -intolerant CML in any phase and Ph+ ALL.
  • Nilotinib, an analogue of imatinib, is approved for the treatment of imatinib-resistant or -intolerant patients with chronic or accelerated phase CML.
  • Both agents have shown significant clinical activity in patients with imatinib-resistant or -intolerant CML, and their approval represents a major advancement in the treatment options available.
  • The presence of certain disease characteristics (e.g. specific BCR-ABL mutations) or patient comorbidities may facilitate more effective treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Mutation. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use


48. le Coutre P, Ottmann OG, Giles F, Kim DW, Cortes J, Gattermann N, Apperley JF, Larson RA, Abruzzese E, O'Brien SG, Kuliczkowski K, Hochhaus A, Mahon FX, Saglio G, Gobbi M, Kwong YL, Baccarani M, Hughes T, Martinelli G, Radich JP, Zheng M, Shou Y, Kantarjian H: Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is active in patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia. Blood; 2008 Feb 15;111(4):1834-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is active in patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia.
  • Patients with imatinib-resistant or -intolerant accelerated-phase chronic myelogenous leukemia (CML-AP) have very limited therapeutic options.
  • Nilotinib is a highly selective BCR-ABL tyrosine kinase inhibitor.
  • This phase 2 trial was designed to characterize the efficacy and safety of nilotinib (400 mg twice daily) in this patient population with hematologic response (HR) as primary efficacy endpoint.
  • In conclusion, nilotinib is an effective and well-tolerated treatment in imatinib-resistant and -intolerant CML-AP.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Benzamides. Blood Cell Count. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Resistance. Female. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Male. Middle Aged. Mutation. Safety

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  • (PMID = 18048643.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00384228
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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49. Sonmez M, Ovali E, Omay SB: Tumor lysis syndrome during treatment with AMN107 (Nilotinib) in a patient with chronic myelogenous leukemia accelerated phase. J Clin Pharm Ther; 2008 Feb;33(1):91-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor lysis syndrome during treatment with AMN107 (Nilotinib) in a patient with chronic myelogenous leukemia accelerated phase.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Accelerated Phase / drug therapy. Pyrimidines / adverse effects. Tumor Lysis Syndrome / etiology

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  • (PMID = 18211624.001).
  • [ISSN] 1365-2710
  • [Journal-full-title] Journal of clinical pharmacy and therapeutics
  • [ISO-abbreviation] J Clin Pharm Ther
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Pyrimidines
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50. Shah NP: Advanced CML: therapeutic options for patients in accelerated and blast phases. J Natl Compr Canc Netw; 2008 Mar;6 Suppl 2:S31-S36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advanced CML: therapeutic options for patients in accelerated and blast phases.
  • Tyrosine kinase inhibitor (TKI) therapy has impacted the natural course of chronic myelogenous leukemia (CML), because patients diagnosed as having chronic-phase disease can experience long-lasting responses.
  • However, for patients with advanced CML (accelerated and blast phases), the efficacy of all current therapies is reduced.
  • For patients with accelerated-phase CML, imatinib, dasatinib, and nilotinib have been shown to produce meaningful rates of hematologic and cytogenetic response.
  • Imatinib and dasatinib are also approved for blast-phase CML.
  • Moreover, because fewer mechanisms appear to exist for secondary resistance to dasatinib and nilotinib, reducing the potential for disease to escape TKI therapy, these agents may result in improved longer-term outcomes.
  • However, BCR-ABL-independent pathways may also become more important, indicating that other therapeutic targets may also have a future role in managing patients with advanced CML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Protein Kinase Inhibitors / therapeutic use
  • [MeSH-minor] Blast Crisis / pathology. Clinical Trials as Topic. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl / genetics. Humans

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  • (PMID = 18397679.001).
  • [ISSN] 1540-1405
  • [Journal-full-title] Journal of the National Comprehensive Cancer Network : JNCCN
  • [ISO-abbreviation] J Natl Compr Canc Netw
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 33
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51. Guilhot F, Apperley J, Kim DW, Bullorsky EO, Baccarani M, Roboz GJ, Amadori S, de Souza CA, Lipton JH, Hochhaus A, Heim D, Larson RA, Branford S, Muller MC, Agarwal P, Gollerkeri A, Talpaz M: Dasatinib induces significant hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in accelerated phase. Blood; 2007 May 15;109(10):4143-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dasatinib induces significant hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in accelerated phase.
  • Treatment options are limited for patients with imatinib-resistant or -intolerant accelerated phase chronic myeloid leukemia (CML-AP).
  • Dasatinib is a novel, potent, oral, multitargeted kinase inhibitor of BCR-ABL and SRC-family kinases that showed marked efficacy in a phase 1 trial of patients with imatinib-resistant CML.
  • Results are presented for 107 patients with CML-AP with imatinib-resistance or -intolerance from a phase 2, open-label study further evaluating dasatinib efficacy and safety.
  • Response rates for the 60% of patients with baseline BCR-ABL mutations did not differ from the total population.
  • In summary, dasatinib induced significant hematologic and cytogenetic responses in patients with imatinib resistance or intolerance, was well tolerated, and may represent a potent new therapeutic option for CML-AP.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Benzamides. Blood Cell Count. Cytogenetic Analysis. Dasatinib. Disease Progression. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Female. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Male. Middle Aged. Point Mutation. Protein-Tyrosine Kinases / genetics. Treatment Outcome


52. Rosti G, Castagnetti F, Gugliotta G, Palandri F, Martinelli G, Baccarani M: Dasatinib and nilotinib in imatinib-resistant Philadelphia-positive chronic myelogenous leukemia: a 'head-to-head comparison'. Leuk Lymphoma; 2010 Apr;51(4):583-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dasatinib and nilotinib in imatinib-resistant Philadelphia-positive chronic myelogenous leukemia: a 'head-to-head comparison'.
  • Imatinib has revolutionized the treatment of patients with chronic myeloid leukemia (CML).
  • Dasatinib, approved in 2006 for the treatment of patients with CML in all phases who experience imatinib resistance or intolerance, has displayed significant efficacy, with a 2-year follow-up showing durable hematologic and cytogenetic responses, as well as prolonged progression-free and overall survival.
  • Nilotinib was approved in 2007 for the treatment of patients with CML in chronic phase or CML in accelerated phase, resistant or intolerant to prior therapy including imatinib, based on strong efficacy as well as a favorable safety profile.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use

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  • (PMID = 20302388.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
  • [Number-of-references] 30
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53. Nakazato T, Suzuki K, Mihara A, Sanada Y, Kakimoto T: [Successful induction of complete cytogenetic response with low-dose imatinib mesylate in an accelerated phase chronic myelogenous leukemia patient who developed severe bone marrow aplasia following standard-dose imatinib mesylate therapy]. Gan To Kagaku Ryoho; 2010 Mar;37(3):539-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Successful induction of complete cytogenetic response with low-dose imatinib mesylate in an accelerated phase chronic myelogenous leukemia patient who developed severe bone marrow aplasia following standard-dose imatinib mesylate therapy].
  • Bone marrow appearance was consistent with CML-AP, and t (9;22) (q34;q11) was detected on karyotyping.
  • Bone marrow biopsy showed severe bone marrow aplasia with no morphological evidence of disease progression.
  • This case also suggests that low-dose imatinib would be tolerable and effective for some CML patients who are intolerant of a standard dose of imatinib.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Bone Marrow / drug effects. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / administration & dosage. Piperazines / adverse effects. Pyrimidines / administration & dosage. Pyrimidines / adverse effects

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  • (PMID = 20332700.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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54. Kantarjian H, Talpaz M, O'Brien S, Giles F, Faderl S, Verstovsek S, Garcia-Manero G, Shan J, Rios MB, Champlin R, de Lima M, Cortes J: Survival benefit with imatinib mesylate therapy in patients with accelerated-phase chronic myelogenous leukemia--comparison with historic experience. Cancer; 2005 May 15;103(10):2099-108
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survival benefit with imatinib mesylate therapy in patients with accelerated-phase chronic myelogenous leukemia--comparison with historic experience.
  • BACKGROUND: The effect of imatinib mesylate on survival in the accelerated phase of chronic myelogenous leukemia (CML) is unknown.
  • The objectives of this study were to update the long-term experience with imatinib in patients who had accelerated-phase CML and to compare outcomes with historic experience.
  • METHODS: The outcomes of 176 patients who received treatment with imatinib were reviewed and compared with the outcomes of 213 historic control patients with accelerated-phase CML who received treatment with interferon-alpha or with other modalities.
  • This may have implications in relation to subsequent therapy, because, according to the outcomes of patients who underwent allogeneic transplantation in accelerated phase at the authors' institution and from literature reports, the estimates of 5-year survival were 25-30%.
  • CONCLUSIONS: The current results suggest that imatinib improved survival compared with other therapies in patients with accelerated-phase CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Anemia / chemically induced. Benzamides. Bone Marrow Transplantation. Cohort Studies. Cytogenetic Analysis. Female. Follow-Up Studies. Fusion Proteins, bcr-abl / analysis. Hemoglobins / analysis. Humans. Imatinib Mesylate. Interferon-alpha / therapeutic use. Longitudinal Studies. Male. Middle Aged. Remission Induction. Survival Rate. Treatment Outcome

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  • (PMID = 15830345.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Hemoglobins; 0 / Interferon-alpha; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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55. Kantarjian H, le Coutre P, Cortes J, Pinilla-Ibarz J, Nagler A, Hochhaus A, Kimura S, Ottmann O: Phase 1 study of INNO-406, a dual Abl/Lyn kinase inhibitor, in Philadelphia chromosome-positive leukemias after imatinib resistance or intolerance. Cancer; 2010 Jun 1;116(11):2665-72
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  • [Title] Phase 1 study of INNO-406, a dual Abl/Lyn kinase inhibitor, in Philadelphia chromosome-positive leukemias after imatinib resistance or intolerance.
  • BACKGROUND: : INNO-406, a dual v-abl Abelson murine leukemia viral oncogene homolog (Abl)/v-yes-1 Yamaguchi sarcoma viral-related oncogene homolog (Lyn) tyrosine kinase inhibitor (TKI), has demonstrated specific Lyn kinase inhibitory activity with no or limited activity against other sarcoma (Src) family member kinases.
  • Several breakpoint cluster region (Bcr)-Abl kinase domain mutations are sensitive to INNO-406 in vitro, including mutations that involve a phenylalanine-to-leucine or phenylalanine-to-valine substitution at codon 317 (F317L and F317V, respectively).
  • In the current study, the authors evaluated the use of INNO-406 in patients with Philadelphia (Ph) chromosome-positive chronic myelogenous leukemia (CML) or acute lymphocytic leukemia (ALL) after imatinib resistance or intolerance.
  • Of 31 patients with CML in chronic phase who received INNO-406, the major cytogenetic response rate was 19%.
  • No responses were observed in patients who had CML in accelerated phase, CML in blastic phase, or Ph-positive ALL.
  • CONCLUSIONS: : INNO-406 had anti-CML efficacy in a heavily pretreated study population.
  • On the basis of the classic determinations of both DLT and MTD, the recommended phase 2 dose of oral INNO-406 was 240 mg twice daily.

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  • [Copyright] (c) 2010 American Cancer Society.
  • [Cites] N Engl J Med. 1999 Jul 15;341(3):164-72 [10403855.001]
  • [Cites] Haematologica. 2008 Sep;93(9):1389-93 [18603549.001]
  • [Cites] Science. 2001 Aug 3;293(5531):876-80 [11423618.001]
  • [Cites] N Engl J Med. 2003 Oct 9;349(15):1451-64 [14534339.001]
  • [Cites] Oncologist. 2004;9(3):259-70 [15169981.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1321-31 [15215876.001]
  • [Cites] Cancer Chemother Rep. 1966 May;50(4):219-44 [4957125.001]
  • [Cites] J Natl Compr Canc Netw. 2005 Nov;3(6):757-68 [16316612.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1061-6 [16642048.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2531-41 [16775234.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2542-51 [16775235.001]
  • [Cites] N Engl J Med. 2006 Dec 7;355(23):2408-17 [17151364.001]
  • [Cites] Ann Intern Med. 2006 Dec 19;145(12):913-23 [17179059.001]
  • [Cites] Blood. 2007 Jan 1;109(1):306-14 [16954504.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2303-9 [17138817.001]
  • [Cites] Cancer. 2007 Jun 1;109(11):2171-81 [17431887.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3540-6 [17715389.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2007;:371-5 [18024653.001]
  • [Cites] Haematologica. 2008 Feb;93(2):186-92 [18223278.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Leuk Res. 2008 Jun;32(6):980-3 [18191450.001]
  • [Cites] Expert Rev Anticancer Ther. 2008 Sep;8(9):1387-98 [18759691.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3948-54 [16105974.001]
  • (PMID = 20310049.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA100632-070007; United States / NCI NIH HHS / CA / CA100632-070007; United States / NCI NIH HHS / CA / P01CA049639; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / P01 CA049639
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 859212-16-1 / bafetinib; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ NIHMS189694; NLM/ PMC2876208
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56. Brave M, Goodman V, Kaminskas E, Farrell A, Timmer W, Pope S, Harapanhalli R, Saber H, Morse D, Bullock J, Men A, Noory C, Ramchandani R, Kenna L, Booth B, Gobburu J, Jiang X, Sridhara R, Justice R, Pazdur R: Sprycel for chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia resistant to or intolerant of imatinib mesylate. Clin Cancer Res; 2008 Jan 15;14(2):352-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sprycel for chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia resistant to or intolerant of imatinib mesylate.
  • Food and Drug Administration approved dasatinib (Sprycel; Bristol-Myers Squibb), a new small-molecule inhibitor of multiple tyrosine kinases, for the treatment of adults with chronic phase, accelerated phase, or myeloid or lymphoid blast phase chronic myeloid leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph(+) ALL) with resistance or intolerance to prior therapy including imatinib.
  • The primary efficacy end point in chronic phase CML was major cytogenetic response.
  • The primary end point in accelerated phase, myeloid phase, and lymphoid blast phase CML, and Ph(+) ALL was major hematologic response.
  • In patients with chronic phase CML, the major cytogenetic response rate was 45% with a complete cytogenetic response rate of 33%.
  • Major hematologic response rates in patients with accelerated phase CML, myeloid CML, lymphoid blast CML, and Ph(+) ALL were 59%, 32%, 31%, and 42%, respectively.
  • Median response durations in chronic phase, accelerated phase, and myeloid phase CML had not been reached.
  • The median durations of major hematologic response were 3.7 months in lymphoid blast CML and 4.8 months in Ph(+) ALL.
  • CONCLUSIONS: This report describes the Food and Drug Administration review supporting the approval of dasatinib for CML and Ph(+) ALL based on the rates and durability of cytogenetic and hematologic responses.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Chronic-Phase / drug therapy. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Benzamides. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Dasatinib. Drug Approval. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Multicenter Studies as Topic. Protein Kinase Inhibitors / adverse effects. Protein Kinase Inhibitors / chemistry. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. United States. United States Food and Drug Administration


57. Altintas A, Cil T, Kilinc I, Kaplan MA, Ayyildiz O: Central nervous system blastic crisis in chronic myeloid leukemia on imatinib mesylate therapy: a case report. J Neurooncol; 2007 Aug;84(1):103-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Central nervous system blastic crisis in chronic myeloid leukemia on imatinib mesylate therapy: a case report.
  • Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by a reciprocal translocation between chromosomes 9 and 22.
  • Imatinib mesylate is a potent and selective inhibitory of the BCR/ABL tyrosine kinase.
  • Imatinib is a first choice of treatment of chronic phase CML.
  • It has also shown activity in patients with CML in accelerated or blastic phases.
  • Herein, we report a patient with CML in accelerated phase that developed central nervous system disease while on imatinib mesylate therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blast Crisis / drug therapy. Central Nervous System Neoplasms / secondary. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Sarcoma, Myeloid / drug therapy


58. Cohen MH, Johnson JR, Pazdur R: U.S. Food and Drug Administration Drug Approval Summary: conversion of imatinib mesylate (STI571; Gleevec) tablets from accelerated approval to full approval. Clin Cancer Res; 2005 Jan 1;11(1):12-9
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  • [Title] U.S. Food and Drug Administration Drug Approval Summary: conversion of imatinib mesylate (STI571; Gleevec) tablets from accelerated approval to full approval.
  • Imatinib mesylate (Gleevec, Novartis Pharmaceuticals East Manruer, NJ) received accelerated approval on May 10, 2001 for the treatment of patients with chronic myeloid leukemia (CML) in (a) chronic phase after failure of IFN-alpha therapy, (b) accelerated phase, and (c) blast crisis.
  • The accelerated approval was accompanied by a postmarketing commitment by Novartis Pharmaceuticals to continue patient follow-up to determine duration of treatment response and survival.
  • The present review, based on a safety and efficacy report submitted on December 20, 2002, summarizes data applicable to the conversion of these three CML indications to full approval status.
  • RESULTS: Chronic phase CML: Five hundred thirty-two chronic phase CML patients who had not benefited from prior IFN therapy were treated at a starting imatinib mesylate dose of 400 mg p.o. qd; dose escalation to 800 mg p.o. qd was allowed.
  • Patients had received a median of 14 months of IFN therapy at doses > or =25 million IU/wk and were all in late chronic phase, with a median time from diagnosis of 32 months.
  • After 2 years of treatment, an estimated 85.4% of patients were free of progression to accelerated phase or blast crisis, and the estimated overall survival was 90.8% (95% confidence interval, 88.3-93.2).
  • Accelerated phase CML: Patients enrolled totaled 293: 235 with CML accelerated phase, 48 with relapsed/refractory acute lymphocytic leukemia, 2 with relapsed/refractory acute myelocytic leukemia, and 8 with relapsed/refractory CML in lymphoid blast crisis.
  • The median survival in the advanced leukemia population (acute lymphocytic leukemia, acute myelocytic leukemia, and lymphoid blast crisis) was only 5 months, and only two patients are still on treatment.
  • Blast crisis CML: A total of 260 patients were recruited.
  • CONCLUSIONS: The results confirm those of the interim analysis and suggest that imatinib mesylate represents an effective therapeutic agent for the treatment of patients with CML in chronic phase after failure of IFN-alpha therapy, in blast crisis, and in accelerated phase.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / pharmacology. Pyrimidines / pharmacology

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  • (PMID = 15671523.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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59. Li X, Yang J, Chen X, Liu J, Li H, Zheng J, He Y, Chen Z, Huang S: A report of early cytogenetic response to imatinib in two patients with chronic myeloid leukemia at accelerated phase and carrying the e19a2 BCR-ABL transcript. Cancer Genet Cytogenet; 2007 Jul 15;176(2):166-8
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  • [Title] A report of early cytogenetic response to imatinib in two patients with chronic myeloid leukemia at accelerated phase and carrying the e19a2 BCR-ABL transcript.
  • The development of imatinib is a milestone in the treatment of chronic myeloid leukemia (CML), and its therapeutic effect has been extensively investigated in CML patients carrying M-bcr and m-bcr BCR/ABL fusion transcripts.
  • However, our knowledge about its therapeutic effect on CML patients with rare BCR/ABL fusion transcripts e19a2(u-bcr) remains sparse.
  • Here, we report on two CML patients with e19a2 transcripts who rapidly progressed into the accelerated phase, further confirming the possibility that 19a2 might be associated with an unfavorable prognosis in CML.
  • [MeSH-major] Gene Expression Regulation, Leukemic / drug effects. Genes, abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Benzamides. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Cytogenetic Analysis. Disease Progression. Exons. Female. Humans. Imatinib Mesylate. Male. Middle Aged. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Time Factors. Translocation, Genetic. Treatment Outcome

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  • (PMID = 17656262.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate
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60. Yu HH, Lu MY, Lin DT, Lin KH, Tang JL, Jou ST: Pathological fracture as a manifestation of extramedullary blastic crisis in chronic myelogenous leukemia: report of one case. Acta Paediatr Taiwan; 2006 May-Jun;47(3):150-4
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  • [Title] Pathological fracture as a manifestation of extramedullary blastic crisis in chronic myelogenous leukemia: report of one case.
  • A three-year-old girl with chronic myelogenous leukemia (CML) experienced a pathological fracture of her femur after a demonstrated osteolytic bone lesion.
  • Extramedullary disease (EMD) was diagnosed following the histologic findings of a biopsy of the osteolytic lesion.
  • This was the youngest patient to have been reported in English literature of Philadelphia chromosome positive (Ph+) CML with isolated bony EMD and pathological fracture.
  • Treatment with a tyrosine kinase inhibitor, imatinib mesylate (Gleevec), in bone marrow accelerated phase of CML was failed to reverse the progression of blastic transformation, neither in the extramedullary bone lesion nor in the bone marrow.
  • [MeSH-major] Blast Crisis / complications. Femoral Fractures / etiology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology

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  • (PMID = 17078470.001).
  • [ISSN] 1608-8115
  • [Journal-full-title] Acta paediatrica Taiwanica = Taiwan er ke yi xue hui za zhi
  • [ISO-abbreviation] Acta Paediatr Taiwan
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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61. Kantarjian H, Cortes J, Kim DW, Dorlhiac-Llacer P, Pasquini R, DiPersio J, Müller MC, Radich JP, Khoury HJ, Khoroshko N, Bradley-Garelik MB, Zhu C, Tallman MS: Phase 3 study of dasatinib 140 mg once daily versus 70 mg twice daily in patients with chronic myeloid leukemia in accelerated phase resistant or intolerant to imatinib: 15-month median follow-up. Blood; 2009 Jun 18;113(25):6322-9
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  • [Title] Phase 3 study of dasatinib 140 mg once daily versus 70 mg twice daily in patients with chronic myeloid leukemia in accelerated phase resistant or intolerant to imatinib: 15-month median follow-up.
  • Dasatinib is the most potent BCR-ABL inhibitor, with 325-fold higher potency than imatinib against unmutated BCR-ABL in vitro.
  • Studies have demonstrated the benefits of dasatinib 70 mg twice daily in patients with accelerated-phase chronic myeloid leukemia intolerant or resistant to imatinib.
  • A phase 3 study compared the efficacy and safety of dasatinib 140 mg once daily with the current twice-daily regimen.
  • Here, results from the subgroup with accelerated-phase chronic myeloid leukemia (n = 317) with a median follow-up of 15 months (treatment duration, 0.03-31.15 months) are reported.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Accelerated Phase / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Benzamides. Dasatinib. Drug Resistance, Neoplasm. Female. Follow-Up Studies. Fusion Proteins, bcr-abl / analysis. Fusion Proteins, bcr-abl / genetics. Gastrointestinal Diseases / chemically induced. Genes, abl. Heart Diseases / chemically induced. Hematologic Diseases / chemically induced. Humans. Imatinib Mesylate. Kaplan-Meier Estimate. Male. Middle Aged. Mutation. Piperazines / adverse effects. Piperazines / pharmacology. Young Adult


62. Bryant BJ, Alperin JB, Elghetany MT: Paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed chronic myelogenous leukemia. Am J Hematol; 2007 Feb;82(2):150-4
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  • [Title] Paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed chronic myelogenous leukemia.
  • Extramedullary tumors, also known as granulocytic sarcomas (GS), occur most frequently in acute myelogenous leukemia (AML).
  • They may signal the onset of the accelerated phase of chronic myelogenous leukemia (CML) or the blastic transformation of a myeloproliferative disorder.
  • Occasionally, a GS may be the presenting sign of undiagnosed AML, and rarely the presenting sign of undiagnosed CML or aleukemic leukemia.
  • Paraplegia due to a spinal cord GS is an extremely rare presentation of undiagnosed leukemia.
  • This is the first case report of paraplegia as the presenting manifestation of extramedullary megakaryoblastic transformation of previously undiagnosed CML.
  • The CBC revealed a leukocyte count of 238,300/microl and a differential consistent with CML.
  • Further immunohistochemical studies of the tumor were consistent with extramedullary acute megakaryoblastic blast transformation of CML.
  • Although extramedullary blast crises herald the accelerated phases in approximately 10% of CML cases, megakaryoblastic blast transformation of CML accounts for less than 3% of these cases.
  • The combination of acute paraplegia and megakaryoblastic transformation in a previously undiagnosed patient with CML is extremely rare and may pose a diagnostic dilemma.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Lymphocyte Activation. Paraplegia / pathology. Spinal Cord Compression / pathology. Spinal Cord Neoplasms / pathology
  • [MeSH-minor] Combined Modality Therapy. Female. Humans. Middle Aged. Splenic Neoplasms / diagnosis. Splenic Neoplasms / pathology. Splenic Neoplasms / secondary. Splenic Neoplasms / therapy

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17019692.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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63. Dutcher JP, Lee S, Gallagher RE, Makary AZ, Hines JD, Londer H, Farnen JP, Bennett JM, Paietta E, Rowe JM, Goloubeva O, Wiernik PH, Eastern Cooperative Oncology Group: Phase II study of all-trans retinoic acid in the accelerated phase or early blastic phase of chronic myeloid leukemia: a study of the Eastern Cooperative Oncology Group (E1993). Leuk Lymphoma; 2005 Mar;46(3):377-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of all-trans retinoic acid in the accelerated phase or early blastic phase of chronic myeloid leukemia: a study of the Eastern Cooperative Oncology Group (E1993).
  • The aims of this study were to evaluate the safety and efficacy of all-trans retinoic acid (ATRA) in the treatment of the accelerated and blastic phase of chronic myeloid leukemia (CML) and to evaluate in vitro correlates of biological activity.
  • ATRA was administered in an intermittent schedule to patients with CML in the accelerated or blastic phases for a 6 week induction period, which was continued if there was evidence of clinical response or stable disease.
  • Laboratory correlative studies were performed prior to treatment and at intervals during treatment to evaluate effects on maturation and differentiation, and on CML progenitor cell growth by assessment of colony-forming cells (CFC).
  • ATRA demonstrated clinical and hematological activity in 5 of 18 patients with the accelerated phase of CML, and there was evidence of a biological effect in laboratory studies of 3 of the 5 patients' progenitor cells.
  • Combination therapy with other differentiating agents may be useful in this disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Tretinoin / administration & dosage
  • [MeSH-minor] Adult. Aged. Blast Crisis. Combined Modality Therapy. Cytogenetic Analysis. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Interferon-alpha / administration & dosage. Interferon-alpha / adverse effects. Male. Middle Aged. Recombinant Proteins. Survival Analysis. Time Factors

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  • (PMID = 15621827.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 11083; United States / NCI NIH HHS / CA / CA 14548; United States / NCI NIH HHS / CA / CA 14958; United States / NCI NIH HHS / CA / CA 23318; United States / NCI NIH HHS / CA / CA 66636; United States / NCI NIH HHS / CA / CA21115
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Recombinant Proteins; 5688UTC01R / Tretinoin; 76543-88-9 / interferon alfa-2a
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64. Sessions J: Chronic myeloid leukemia in 2007. Am J Health Syst Pharm; 2007 Dec 15;64(24 Suppl 15):S4-9
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  • [Title] Chronic myeloid leukemia in 2007.
  • PURPOSE: Chronic myeloid leukemia (CML), a hematopoietic stem cell cancer representing 15-20% of adult leukemias, is discussed.
  • SUMMARY: CML is a myeloproliferative disorder that affects all lineages of hematopoiesis.
  • Final confirmation of CML comes with detection of the Philadelphia Chromosome (Ph) or BCR-ABL transcripts.
  • The disease presents in one of three phases: chronic phase, accelerated phase, or blast crisis.
  • Progression from chronic phase to accelerated phase usually involves the accumulation of additional cytogenetic aberrations and the arising of resistance to therapy.
  • Although at one point mortality associated with CML was high, new kinase inhibitor therapies have markedly extended the life-span of these patients.
  • These inhibitors were derived through the initial observation of the association of the Ph with CML and the eventual identification of the BCR-ABL oncogene which arises from this translocation.
  • Analysis of the mechanism by which BCR-ABL transforms cells identified this protein as a tyrosine kinase and led to the targeting of this activity.
  • The majority of patients present in chronic phase, which is where these kinase inhibitors have their greatest efficacy.
  • Monitoring of disease progression is of critical importance as the prognosis drops significantly for patients with advanced disease.
  • Blood counts, cytogenetics, and polymerase chain reaction (PCR) are currently used to assess disease.
  • CONCLUSION: Our understanding of BCR-ABL has allowed the development of therapies, which may keep patients with CML in chronic phase indefinitely.
  • This has created a situation in which patient monitoring is essential for detecting changes in the status of CML.
  • The tests described here provide a comprehensive assessment of disease status allowing for effective patient management.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis
  • [MeSH-minor] Clinical Trials as Topic. Drug Resistance, Neoplasm. Humans. Leukemia, Myeloid, Chronic-Phase / diagnosis. Leukemia, Myeloid, Chronic-Phase / genetics. Leukemia, Myeloid, Chronic-Phase / therapy. Neoplasm Staging


65. Breccia M, Muscaritoli M, Cannella L, Stefanizzi C, Frustaci A, Alimena G: Fasting glucose improvement under dasatinib treatment in an accelerated phase chronic myeloid leukemia patient unresponsive to imatinib and nilotinib. Leuk Res; 2008 Oct;32(10):1626-8
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  • [Title] Fasting glucose improvement under dasatinib treatment in an accelerated phase chronic myeloid leukemia patient unresponsive to imatinib and nilotinib.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Blood Glucose / analysis. Diabetes Complications / drug therapy. Leukemia, Myeloid, Accelerated Phase / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use

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  • (PMID = 18321570.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Blood Glucose; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; RBZ1571X5H / Dasatinib
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66. Plosker GL, Robinson DM: Nilotinib. Drugs; 2008;68(4):449-59; discussion 460-1
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  • Nilotinib is an orally administered BCR-ABL tyrosine kinase inhibitor that has shown good clinical efficacy in imatinib-resistant or -intolerant, Philadelphia chromosome-positive, chronic myeloid leukaemia (CML) in a phase I/II trial.
  • The phase I component of the trial established the dosage regimen used in the phase II part of the trial, which included several arms.
  • Three of these arms, or phase II trials, evaluated nilotinib in each of the three phases of CML (chronic, accelerated or blast crisis).I n the phase II trial in patients with chronic-phase CML, major cytogenetic response (primary endpoint) was achieved in 48% of the 280 patients who received nilotinib and had a follow-up period of > or = 6 months.
  • Major cytogenetic response rates did not differ between imatinib-resistant and -intolerant patients, and nilotinib was effective in patients with BCR-ABL mutations (except T315I).
  • Haematologic response rate (primary endpoint) was 47% in the phase II trial with nilotinib in patients with accelerated-phase CML (n = 119).
  • Complete haematologic response was achieved in 26% of patients and 21% had no evidence of leukaemia or returned to chronic-phase CML.
  • Data from the phase II trial in patients with CML in blast crisis (n = 135) also showed promising results, with 39% of patients achieving haematologic response with nilotinib.
  • [MeSH-minor] Animals. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

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  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2531-41 [16775234.001]
  • [Cites] Br J Cancer. 2006 Jun 19;94(12):1765-9 [16721371.001]
  • [Cites] Pharmacol Rev. 2003 Sep;55(3):401-23 [12869662.001]
  • [Cites] Drugs. 2007;67(2):299-320 [17284091.001]
  • [Cites] Cancer Cell. 2005 Feb;7(2):129-41 [15710326.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4500-5 [15930265.001]
  • [Cites] Leukemia. 2002 Nov;16(11):2190-6 [12399961.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2311-5 [17611564.001]
  • [Cites] Blood. 2002 May 15;99(10):3547-53 [11986206.001]
  • [Cites] N Engl J Med. 1999 Apr 29;340(17):1330-40 [10219069.001]
  • [Cites] CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30 [16514137.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1758-66 [10688835.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3207-13 [17185463.001]
  • [Cites] Crit Rev Oncol Hematol. 2006 Feb;57(2):145-64 [16213151.001]
  • [Cites] Blood. 2008 Feb 15;111(4):1834-9 [18048643.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2594-6 [16775240.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2303-9 [17138817.001]
  • [Cites] Expert Opin Investig Drugs. 2007 May;16(5):679-87 [17461740.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3540-6 [17715389.001]
  • [Cites] Blood. 2007 May 15;109(10):4143-50 [17264298.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2542-51 [16775235.001]
  • [Cites] N Engl J Med. 2006 Dec 7;355(23):2408-17 [17151364.001]
  • [Cites] N Engl J Med. 2002 Feb 28;346(9):645-52 [11870241.001]
  • [Cites] Cancer. 2005 Sep 15;104(6):1230-6 [16078266.001]
  • [Cites] Clin Cancer Res. 2005 Jul 1;11(13):4941-7 [16000593.001]
  • (PMID = 18318563.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Pyrimidines
  • [Number-of-references] 36
  •  go-up   go-down






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