Potential mechanisms of disease progression and management of advanced-phase chronic myeloid leukemia

Jabbour, Elias; Hughes, Timothy P.; Cortés, Jorge E.; Kantarjian, Hagop M.; Hochhaus, Andreas

doi:10.3109/10428194.2013.845883

Cited by 38 publications

(29 citation statements)

References 130 publications

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“…The advent of tyrosine kinase inhibitor therapy has tremendously improved the clinical outlook for patients with CML. However, the number of eff ective treatment options is limited in advanced-phase (accelerated phase or blast crisis) CML, and treatment modalities eff ective in chronic-phase CML are not nearly as eff ective in advanced-phase CML (18). Active clinical research of investigational agents and combination regimens is needed to expand treatment options available to patients such as the one presented here.…”

Section: Discussionmentioning

confidence: 99%

“…Available choices for newly diagnosed, tyrosine kinase inhibitor-naïve patients include imatinib, dasatinib, or nilotinib (15)(16)(17). Also, the recent approval of next-generation tyrosine kinase inhibitors like bosutinib and ponatinib provides clinicians multiple treatment options for patients with advanced-phase CML (18). Appropriate patients should be referred early for allogeneic stem cell transplant.…”

Section: Discussionmentioning

confidence: 99%

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Myeloid Sarcoma as the Presenting Symptom of Chronic Myelogenous Leukemia Blast Crisis

Levy

Mardones

Burch

et al. 2014

Baylor University Medical Center Proceedings

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Myeloid Sarcoma as the Presenting Symptom of Chronic Myelogenous Leukemia Blast Crisis

Levy

Mardones

Burch

et al. 2014

Baylor University Medical Center Proceedings

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“…Management of advanced stage chronic myeloid leukemia: All five currently available TKIs are approved in the USA and Europe for treatment of AP CML, and all except nilotinib are also approved for treatment of BC CML [43,63,66,102]. Although TKI therapy is moderately effective in patients with AP/BC CML, the overall effectiveness of TKI therapy in advanced CML is less robust than that observed in early-stage disease.…”

Section: Management Of Chronic Phase Chronic Myeloid Leukemiamentioning

confidence: 99%

Current Management Approaches of Chronic Myeloid Leukemia

Fentie¹,

Woldu²

2017

J Cancer Sci Ther

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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.

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“…В резуль-тате этой транслокации на хромосоме 22 образуется химерный ген BCR-ABL, который кодирует химерный белок с молекулярной массой 210 кДа, имеющий более выраженную тирозинкиназную активность, чем его нормальный прототип р145abl. Активация различных участков химерного гена обусловливает цепь событий, ведущих к повышению клеточной пролиферации [1][2][3].…”

Section: миелоидные новообразованияunclassified

Molecular Genetic Abnormalities in the Pathogenesis of Hematologic Malignancies and Corresponding Changes in Cell Signaling Systems

Тилова¹,

Savinkova²,

Zhidkova³

et al. 2017

Клиническая онкогематология

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Hematological disorders include a wide spectrum of malignancies of hematopoietic and lymphoid tissues. The genetic changes underlying the pathogenesis of the diseases are specific for each disease. High incidence of chromosomal aberrations (deletion, translocation, insertion) is one of the principal characteristics of oncohematological diseases. In addition, mutations in individual genes or blocking of normal regulation of gene functioning in relation to epigenetic events can occur. Progression of oncohematological diseases could be a result of accumulation of different genetic abnormalities. Modern classification of malignancies of hematopoietic and lymphoid tissues is based on the analysis of clinical data, morphological and functional characteristics of tumor cells and identification of specific cytogenetic and molecular-genetic changes. A large number of genetic abnormalities specific for certain types of hematological malignancies has been discovered to date. It allows to optimize the treatment strategy, as well as to design, test and introduce to the clinical practice a number of targeted drugs (inhibitors of chimeric proteins formed as a result of trans-locations and triggering the malignant cell transformation). Drugs based on monoclonal antibodies (Rituximab, Alemtuzumab, etc.) or low molecular weight compounds (Imatinib, Bortezomib, Carfilzomib) form this group of medications. The knowledge about not only specific gene abnormalities but also about the corresponding changes in cell efferent signaling pathways could be of great interest for the development of new targeted molecules or the repurposing of known chemotherapeutic agents. The present review compares genetic aberrations in diseases listed in the 2008 WHO classification (amended in 2016) of hematopoietic and lymphoid tissue malignancies and main changes in cell signaling pathways associated with malignant transformation of hematopoietic cells.

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Potential mechanisms of disease progression and management of advanced-phase chronic myeloid leukemia

Cited by 38 publications

References 130 publications

Myeloid Sarcoma as the Presenting Symptom of Chronic Myelogenous Leukemia Blast Crisis

Myeloid Sarcoma as the Presenting Symptom of Chronic Myelogenous Leukemia Blast Crisis

Current Management Approaches of Chronic Myeloid Leukemia

Molecular Genetic Abnormalities in the Pathogenesis of Hematologic Malignancies and Corresponding Changes in Cell Signaling Systems

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