Current Management Approaches of Chronic Myeloid Leukemia

Abstract

Chronic myeloid leukemia is a slowly progressive and clonal myeloproliferative disorder characterized by the presence of Philadelphia chromosome. Even if the global incidence is unknown, CML accounts for 15% to 20% cases of adult leukemia's in USA and is predominantly the disease of adults. It has three phases reflecting the grade of malignancy; chronic phase, accelerated phase and blast crisis phase. Initial diagnosis and monitoring of treatment response is based on hematologic, cytogenetic and molecular assessments that need to be regularly checked. The treatment in each phase had undergone a profound progress over a relatively short period of time, starting with arsenic therapy, radiotherapy, allogeneic hematopoietic stem cell transplantation, recombinant interferon-alfa, busulfan, and hydroxyurea, and more recently with the tyrosine kinase inhibitors. Among tyrosine kinase inhibitors national comprehensive cancer network puts imatinib, dastinib and nilotinib as category 1 recommendation for initial treatment of chronic phase chronic myeloid leukemia. Second generation tyrosine kinase inhibitors; nilotinib, dasatinib, bosutinib and ponatinib had shown inducing higher rates of early optimal responses, although their impact on long-term overall survival remains to be determined. There are also drugs for the treatment of chronic myeloid leukemia such as histone deacetylase inhibitors, proteasome inhibitors and farnesyl transferase inhibitors which are under investigation. In addition to these vaccines are under investigation as a part of treatment for chronic myeloid leukemia which still needs further research.

Inorganic Nanoparticles as Drug Delivery Systems and Their Potential Role in the Treatment of Chronic Myelogenous Leukaemia

“…Unfortunately, the prognosis of CML is worse in both the accelerated phase and the blast phase of the disease with fewer successful pharmaceutical treatments and transplants. 27,28 As previously stated, Imatinib (on account of its superior anti-leukemic effects) is currently mainstay therapy used in CML treatment. 29 However, Imatinib resistance has been described and has been associated with BCR/ABL mutations in most cases.…”

“…Unfortunately, the prognosis of CML is worse in both the accelerated phase and the blast phase of the disease with fewer successful pharmaceutical treatments and transplants. 27,28…”

“…Finally, stem cell transplantation is especially helpful for patients who have been successful in finding a suitable donor and remains the only treatment to cure CML. 27,28 Within 1 year of chronic-phase CML treatment with imatinib, up to 70% of patients showed complete cytogenetic response (CCyR) and even higher response rate with the newer TKIs. Moreover, complete molecular response (CMR) was observed after a year in many patients.…”

A short review about chronic myeloid leukemia

“…A slow-progressing and clonal myeloproliferative disorder, chronic myeloid leukemia (CML) is the result of neoplastic transformation of the primitive hematopoietic stem cell (HSC), which is monoclonal in heritage and affects myeloid, erythroid, monocytic, megakaryocytic, B-cell, and sometimes T-cell lineages (Fentie et al, 2017). Philadelphia chromosome (also known as Ph1 chromosome) (Fig.…”

“…Oxidative DNA damage is caused by an increase in the number of DNA point mutations and double strand breaks, which, in turn, leads to abnormal chromosomal changes as a result of dishonest and incompetent DNA repair processes (Gunnarsson, 2017), in another words, an unstable genome might lead to a rise in medication resistance and cancerous growth (Dolinska, 2019). There is no actual explanation for this chromosomal translocation, but it is believed to be the result of many chromosomal breaks and repairs happening at the same time during mitosis, which is made easier by the near area of chromosomes 9 and 22 in the interphase nucleus (Fentie et al, 2017). Most patients with CML have the Ph1 chromosome, which is found in myeloid and erythroid precursor cells as well as megakaryocytes.…”