Blastic phase of chronic myelogenous leukemia

  title={Blastic phase of chronic myelogenous leukemia},
  author={Merat Karbasian Esfahani and Evelyn L Morris and Janice P. Dutcher and Peter H Wiernik},
  journal={Current Treatment Options in Oncology},
Opinion statementChronic myelogenous leukemia (CML), also known as chronic myelocytic or chronic myeloid leukemia, is a clonal disorder of hematopoiesis that arises in a hematopoietic stem cell or early progenitor cell. This is characterized by the dysregulated production of mature non-lymphoid cells with normal differentiation. Eventually, in spite of the term chronic, there is progression to acute leukemia, usually of the myeloid variety, which is highly resistant to current therapies… 
Chronic myelogenous leukemia in the age of imatinib: assessing response, acceleration, and blast phase
Problems facing the diagnostic pathologist in this “Age of Imatinib” include accurate diagnosis and determination of CML disease phase prior to therapy, evaluating response to Therapy, and assessing for disease progression on therapy.
Unrelated Allogeneic Stem Cell Transplantation in a Patient with Chronic Myeloid Leukemia in Blast Crisis
The following article presents the case of a 49-year-old patient diagnosed with Philadelphia-negative CML in blastic transformation, where after multiple conventional acute leukemia induction chemotherapy regimens an unrelated allogeneic hematopoietic stem cell transplant was performed.
Monocytic crisis of chronic myeloid leukemia in the era of tyrosine kinase inhibitor.
A 47-year-old man with Philadelphia chromosome-positive chronic myeloid leukemia (CML) died of pneumonia in March 2012 after being treated with low-dose nilotinib following cytoreduction with MEC (mitoxantrone, etoposide, and cytarabine) chemotherapy.
Case Study Monocytic Crisis of Chronic Myeloid Leukemia in the Era of Tyrosine Kinase Inhibitor
A 47-year-old man was diagnosed with Philadelphia chromosome-positive chronic myeloid leukemia (CML) in October 2005. He could not receive treatment with imatinib mesylate due to his economic
Chronic Myeloid Leukemia with Extramedullary Blast Crisis: Two Unusual Sites with Review of Literature
A case of CML who suffered from two discrete episodes of EBC at atypical locations (scalp and paravertebral) within an interval duration of nine months is presented.
Understanding and Monitoring Chronic Myeloid Leukemia Blast Crisis: How to Better Manage Patients
Overall, selecting optimal treatment endpoints to predict survival and successful TFR improves the quality of life of patients, and identifying risk factors and developing risk-adapted therapeutic options may contribute to a better outcome for advanced-phase patients.
The data show that the rational drug combination of TKI and Ruxolitinib may enhance the eradication of primary human Ph+ cells homed in BM stroma niche, and it is proved that JAK inhibitor Ruxolaninib, that inhibits STAT3 phosphorylation (a marker of JAK activity), synergizes with TKIs in the induction of apoptosis in CML primary cells.
Overcoming resistance in chronic myelogenous leukemia
This review describes agents which overcome the T315I mutation, as well as native BCR-ABL, via several mechanisms, including increased degradation of BCR, ABL, optimization of direct inhibition of the BCR -ABL kinase, and inhibition of B CR-ABl-mediated cell growth via interruption of the T 315I-mediated transcription, protein synthesis or post-translational modification.


Accelerated and blastic phase of chronic myeloid leukemia
Patients whose accelerated phase reverts to chronic phase after treatment may become candidates for bone marrow transplantation, and nontransplant regimens for accelerated phase that produce long-term benefit are urgently needed.
Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study.
It is demonstrated that imatinib has substantial activity and a favorable safety profile when used as a single agent in patients with CML in blast crisis and additional clinical studies are warranted to explore the efficacy and feasibility of imatinIB used in combination with other antileukemic drugs.
Chronic Myelogenous Leukemia: Biology and Therapy
This review updates the clinically relevant biology and treatment advances in chronic myelogenous leukemia and emphasizes the need to continue investigating better strategies for patients who may not benefit as much as younger patients from recent treatment discoveries.
Pathobiology of lymphoid and myeloid blast crisis and management issues.
  • R. Ilaria
  • Biology, Medicine
    Hematology. American Society of Hematology. Education Program
  • 2005
The effect of imatinib on primitive CML progenitors and how this might influence the pathophysiology of blast crisis are examined and a rational framework for deciding how best to integrate stem cell transplantation, traditional chemotherapy,Imatinib, and other BCR-ABL kinase inhibitors in the care ofblast crisis patients are discussed.
Blastic phase of chronic myelogenous leukemia.
This work reviews the molecular biology and evolution of treatment of the blastic phase of CML, the molecular changes during its evolution to blastics phase, and the potential for therapeutic interventions.
The biology of CML blast crisis.
Validation of the critical role of certain secondary changes (ie, loss of p53 or C/EBPalpha function) in murine models of CML blast crisis and in in vitro assays of BCR/ABL transformation of human hematopoietic progenitors might lead to the development of novel therapies based on targeting BCR /ABL and inhibiting or restoring the gene activity gained or lost during disease progression.
Molecular pathogenesis of chronic myeloid leukemia: implications for new therapeutic strategies
This review focuses on the current understanding of Bcr-Abl-induced signal transduction and outlines its importance for the biological effects of B CRM, the so-called Philadelphia chromosome resulting in the bcr-abl fusion gene.
A phase 2 study of imatinib in patients with relapsed or refractory Philadelphia chromosome-positive acute lymphoid leukemias.
Imatinib therapy resulted in a clinically relevant hematologic response rate in relapsed or refractory Ph(+) acute lymphoid leukemia patients, but development of resistance and subsequent disease progression were rapid.
The CNS is a sanctuary for leukemic cells in mice receiving imatinib mesylate for Bcr/Abl-induced leukemia.
In the mouse, the limited ability of imatinib mesylate to cross the blood-brain barrier allowed the CNS to become a sanctuary for Bcr/Abl-induced leukemia, and this model will be a useful tool for the future study of novel anti-CML drugs and in better defining the mechanisms for limitedImatinib Mesylate penetration into the CNS.