Angiogenesis plays a crucial role in multiple myeloma and its prognosis, with the success of antiangiogenic therapies being limited. Exosomes mediate cell-to-cell cross talk during the progression of cancer by transporting their molecular cargo, which include long non-coding RNAs (lncRNAs); their role in multiple myeloma was investigated.
The development of resistance and relapse during the blast phase of chronic myeloid leukemia poses a challenge in the management of this pathology, with half of the cases accounting for FLT3 pathway activation that, in turn, contributes to tyrosine kinase inhibitor resistance.
B-cell lymphoma 6 (BCL6) is up-regulated in several B-cell malignancies where it acts as a transcription factor activity mediator to induce and maintain lymphomagenesis.
Researchers from Lund University presented data from a study that aimed to identify novel targets for immunotherapy in acute myeloid leukemia (AML). To identify differentially expressed cell surface proteins in the primitive CD34+CD38- cell populations, an arrayed antibody screen was performed on primary bone marrow samples from patients with AML as well as healthy donors.
The first oral session in the acute myeloid leukemia (AML) translational research track of June 15, was given by Eliza Yankova, from the University of Cambridge, who presented collaborative studies done together with Storm Therapeutics Ltd. outlining pharmacological inhibition of METTL1 as a therapeutic strategy in AML treatment.
The c-MYB oncogene plays an important role in hematopoietic cell differentiation and proliferation. Dysregulation of MYB downstream effector signaling is thought to be behind these abnormalities by modulation of genes such as BCL2, MYC or FLT3, and as such an attractive therapeutic target for acute myeloid leukemia (AML).
Myeloproliferative neoplasms (MPNs) can only be cured, to date, using allogeneic stem cell transplantation which, in turn, only works for up to 20% of patients. As calreticulin (CALR) frameshift mutations are the second most common cause of MPNs, targeting this endoplasmic reticulum resident protein is one of the strategies emerging at the forefront of hematological malignancies research.