Subscribe to RSS

DOI: 10.1055/s-0039-1698546
Success and Challenges in the Management of Chronic Myeloid Leukemia
Publication History
Publication Date:
11 October 2019 (online)

Abstract
Chronic myeloid leukemia (CML) is one of the most common myeloproliferative neoplasms characterized by the presence of Philadelphia chromosome, that is, t(9:22), a reciprocal translocation between long arms of chromosomes 9 and 22. In its natural course CML has three phases, that is, chronic phase, accelerated phase, and blast crises phase. Peripheral blood shows marked leukocytosis and left shift. Diagnosis is confirmed by demonstration of specific molecular abnormality by polymerase chain reaction (PCR), fluorescence in situ hybridization (FISH) method or cytogenetics. The drug of choice is tyrosine kinase inhibitor (TKI); imatinib. Other TKIs are dasatinib and nilotinib. Most patients respond and have almost normal life span. However, challenges remain. At present the drug is prescribed for lifelong. Recent studies have shown that the drug may be stopped in certain groups of which around 50% remain in long term remission (operational cure). However, around 20% did not respond and showed resistance. Research is in progress to find out the mechanism of resistance and newer therapeutic modalities or agents.
-
References
- 1 Singhal MK, Sengar M, Nair R. Summary of the published Indian data on chronic myeloid leukemia. South Asian J. Cancer 2016; 5 (03) 162-165
- 2 Bansal S, Prabhash K, Parikh P. Chronic myeloid leukemia data from India. Indian J Med Paediatr Oncol 2013; 34 (03) 154-158
- 3 Savage DG, Antman KH. Imatinib mesylate–a new oral targeted therapy. N Engl J Med 2002; 346 (09) 683-693
- 4 Tripathi AK, Verma SP, Kumar N. Mutation analysis in chronic myeloid leukemia patient in chronic phase on Imatinib having delayed achievement of milestones or loss of response. Indian J Hematol Blood Transfus 2017; 33 (03) 316-320
- 5 Bajpai P, Tripathi AK, Agrawal D. Genetic polymorphism of CYP3A5 in Indian chronic myeloid leukemia patients. Mol Cell Biochem 2010; 336 (1,2) 49-54
- 6 Agarwal D, Tripathi AK, Bajpai P. Association between GSTM1, GSTT1, and GSTP1 genetic polymorphism and risk to chronic myeloid leukemia. Hematologica 2007; 92: 197
- 7 Bajpai P, Tripathi AK, Agrawal D. Increased frequencies of glutathione-S-transferase (GSTM1 and GSTT1) null genotypes in Indian patients with chronic myeloid leukemia. Leuk Res 2007; 31 (10) 1359-1363
- 8 Bajpai P, Agarwal D, Tripathi AK. Genetic polymorphism of glutathione S-transferase M1 and T1 and risk to chronic myeloid leukemia. 97th Annual Meeting of American Society of Cancer Research. Washington DC: April 1–5, 2006 (Abstract 4588)
- 9 Tripathi AK, Tripathi P, Ahmad R, Chaudhary PD, Verma SK. S-phase fraction as response marker in patients with chronic myeloid leukemia. Leuk Lymphoma 2009; 50 (07) 1223-1225
- 10 Ahmad R, Tripathi AK, Tripathi P, Singh R, Singh S, Singh RK. Studies on lipid peroxidation and non-enzymatic antioxidant status as indices of oxidative stress in patients with chronic myeloid leukaemia. Singapore Med J 2010; 51 (02) 110-115
- 11 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; 23 (04) 328-333
- 12 Ahmad R, Tripathi AK, Tripathi P, Singh S, Singh R, Singh RK. Malondialdehyde and protein carbonyl as biomarkers for oxidative stress and disease progression in patients with chronic myeloid leukemia. In Vivo 2008; 22 (04) 525-528
- 13 Tripathi AK, Jain M, Singh AK. et al. Alterations in the circulating nitrite levels and expression of NOS isoforms in the neutrophils of AML patients. Blood (ASH Annual Meeting Abstracts) 2012; 120: 4325
- 14 Jyoti A, Singh A, Kesari R. et al. Nitric oxide synthtase-Nitric oxide involvement in the human neutrophil free radical generation: Role of iNOS and Rac 2 interaction. Blood (ASH abstract) 2012; 120: 1036