RESEARCH REPORT Dave Levitan An international group of experts say that the costs of cancer medications, and those used to treat chronic myeloid leukemia (CML) in particular, have skyrocketed to levels that make treating patients extremely difficult. The group published a perspective piece in the journal Blood online ahead of print on April 25.
A majority of patients on imatinib for treatment of GIST or CML had low or absent levels of osteocalcin, a bone marker secreted by osteoblasts, and about 50% of patients had a decrease in bone mineral density, signaling that long-term treatment may affect bone health in these patients.
CML patients treated with nilotinib had fewer treatment-emergent BCR-ABL mutations than those treated with imatinib, and among patients who did have a mutation, those treated with nilotinib had reduced rates of progression to accelerated phase and blast phase of the disease.
Contrary to previous laboratory findings, a new study has shown for the first time the effect of stem cell burden on treatment outcome, discovering that tyrosine kinase inhibitors, including imatinib and dasatinib, can rapidly eradicate most chronic myeloid leukemia stem cells.
The European Medicines Agency adopted a “positive opinion” earlier this year regarding conditional marketing approval for bosutinib for the treatment of Philadelphia chromosome-positive chronic myeloid leukemia.
As patients and physicians gain experience with a second generation of relatively effective therapies for chronic myeloid leukemia, there is increasing need to quickly understand who will fare best with these drugs.
New research suggests that a novel, investigative drug could help alleviate some of the resistance to tyrosine kinase inhibitor treatment seen in chronic myeloid leukemia (CML). The drug, a pan-BCL2 inhibitor called sabutoclax, could sensitize malignant leukemic stem cells in the bone marrow niche to TKI treatment.
Researchers have identified an enzyme that plays an important role in the reprogramming of malignant progenitor cells in chronic myeloid leukemia. The enzyme, ADAR1, could represent a target for selecting and eradicating leukemia stem cells.
Chromosomal abnormalities, like deletions, amplifications, inversions or translocations, are recurrent features in haematological malignancies. However, the precise molecular breakpoints are frequently not determined. Here we describe a rapid analysis of genetic imbalances combining fine tiling comparative genomic hybridization (FT-CGH) and ligation-mediated PCR (LM-PCR). We clarified an inv(14)(q11q32) in a case of T cell acute lymphoblastic leukaemia with a breakpoint in the TRA/D in 68% of cells
Precursor mRNA splicing is catalyzed by the spliceosome, a macromolecule composed of small nuclear RNAs associated with proteins. The SF3B1 gene encodes subunit 1 of the splicing factor 3b, which is important for anchoring the spliceosome to precursor mRNA. In 2011, whole-exome sequencing studies showed recurrent somatic mutations of SF3B1 and other genes of the RNA splicing machinery in patients with myelodysplastic syndrome or myelodysplastic/myeloproliferative neoplasm. SF3B1 m
Background: Trough imatinib plasma concentration, intracellular drug levels and expression of drug transporters can be indicative of clinical responses in chronic myelocytic leukemia (CML) patients receiving imatinib. We aimed to determine plasma imatinib concentration, intracellular imatinib concentration, human organic cation transporter 1 (hOCT1) and adenosine triphosphate-binding cassette subfamily B member 1 (ABCB1) mRNA expression in bone marrow cells of CML patients in order to evaluate the
The Epstein-Barr virus (EBV) is a member of the herpes family of viruses and is very common in humans. EBV is most often associated with infectious mononucleosis. However, it is estimated that 1% of tumors including lymphoproliferative, epithelial and mesenchymal are linked to EBV infection. EBV has a tropism for certain epithelial cells, lymphocytes and myocytes. Like other herpesviruses, EBV has both lytic and latent phases of infection. In the latent form, EBV-encoded genes ensure the survival of the v
Chronicmyeloidleukemia (CML) is a stem cell disease in which BCR/ABL plays an important role as an oncoprotein and a molecular and immunogenic target. Despite the success of targeted therapy using tyrosine kinase inhibitors (TKIs), CML remains largely incurable, most likely due to the treatment resistance of leukemic stem cells. Several immunotherapies have been developed for CML in different stages and relapse after allogeneic stem cell transplantation. In the this review, several specific immunotherap
Full Text View. Irinotecan and Cytarabine in Treating Patients With Refractory or Recurrent Acute MyeloidLeukemia or Chronic Myelogenous Leukemia. ... Leukemia, Myeloid, Acute. Leukemia, Myeloid. Leukemia, Myelogenous, Chronic, BCR-ABL Positive.
Full Text View. Expanded Access Program of AMN107 in Imatinib-resistant or Intolerant Adult Patients With ChronicMyeloidLeukemia. ... nilotinib. enact. Additional relevant MeSH terms:. Leukemia. Leukemia, Myeloid. Leukemia, Myelogenous, Chronic,
A hematologically stable CML patient developed a solitary, exquisitely painful ulceration, 7 cm × 5 cm, located on the mid-medial foreleg. There was never any evidence of venous insufficiency. The patient denied the possibility of a spider bite. What is the likely cause of this lesion?