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.
Arsenic Trioxide (ATO) has shown remarkable efficacy for the treatment of multiple myeloma (MM). However, the mechanism by which ATO exerts its inhibitory effect on the proliferation of myeloma cells remains to be clarified. We study the inhibitory effect of ATO at various concentrations on the proliferation of the myeloma cell line RPMI 8226 and discussed the molecular mechanism of ATO on myeloma cell line. Our results proved that ATO had a significant dose-dependent and time-dependent inhibitory effect
Malignant mesothelioma is an asbestos-related fatal disease with no effective cure. We studied whether a green tea polyphenol, epigallocathechin-3-gallate (EGCG), could induce cell death in five human mesothelioma cell lines. We found that EGCG induced apoptosis in all five mesothelioma cell lines in a dose-dependent manner. We further clarified the cell killing mechanism. EGCG induced reactive oxygen species (ROS), and impaired the mitochondrial membrane potential. As treatment with ROS scavengers, catal
PURPOSE: Phase II trial to study the effectiveness of STI571 in treating patients who have chronicmyeloidleukemia that has not responded to interferon alfa. ... PrimaryPurpose: Treatment. Official Title:. A Study to Determine the Safety and
Full Text View. 17-N-Allylamino-17-Demethoxygeldanamycin and Cytarabine in Treating Patients With Relapsed or Refractory Acute MyeloidLeukemia, Acute Lymphoblastic Leukemia, Chronic Myelogenous Leukemia, Chronic Myelomonocytic Leukemia, or
Hematologic malignancy, including any of the following:. Acute myeloidleukemia ( AML) not curable with chemotherapy and meeting any of the following criteria:. ... Myelofibrosis. Polycythemia vera. Essential thrombocythemia. Chronicmyeloidleukemia (
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?