A new study examined outcomes in infants with acute lymphoblastic leukemia treated with a lymphoid course of therapy vs a myeloid course.
This study identified risk factors for TH-ED in a large cohort of patients with APL, which enriched clinical information on identifying patients at high risk of TH-ED.
Publication date: Available online 1 August 2019Source: Stem Cell ReportsAuthor(s): Juan Bautista Menendez-Gonzalez, Milica Vukovic, Ali Abdelfattah, Lubaid Saleh, Alhomidi Almotiri, Leigh-anne Thomas, Aloña Agirre-Lizaso, Aleksandra Azevedo, Ana Catarina Menezes, Giusy Tornillo, Sarah Edkins, Kay Kong, Peter Giles, Fernando Anjos-Afonso, Alex Tonks, Ashleigh S. Boyd, Kamil R. Kranc, Neil P. RodriguesSummarySubversion of transcription factor (TF) activity in hematopoietic stem/progenitor cells (HSPCs) leads to the development of therapy-resistant leukemic stem cells (LSCs) that drive fulminant acute myeloid leukemia…
ConclusionThe use of a pediatric-inspired protocol for high-risk AYA ALL patients was effective and well tolerated with improvement in OS and DFS compared with historical data using adult protocols in such populations.
Publication date: Available online 1 August 2019Source: Clinical Lymphoma Myeloma and LeukemiaAuthor(s): Evandro D. Bezerra, Megan Othus, Carole Shawn, Mary-Elizabeth Percival, Kelda Gardner, Roland B. Walter, Pamela S. Becker, Paul C. Hendrie, Elihu H. Estey
Growing evidence has demonstrated that epigenetic dysregulation is a common pathological feature in human cancer cells. Global alterations in the epigenetic landscape are prevalent in malignant cells across different solid tumours including, prostate cancer, non-small-cell lung cancer, renal cell carcinoma, and in haemopoietic malignancy. In particular, DNA hypomethylation and histone hypoacetylation have been observed in acute myeloid leukaemia (AML) patient blasts, with histone methylation being an emerging area of study.
Histone 3 lysine 9 trimethylation (H3K9me3) is a post-translational modification known to be invol…
T(4;11) MLL-AF4 acute lymphoblastic leukemia is an aggressive subtype of infant and pediatric leukemia that originates in utero, with monozygotic twin studies having shown a 100% penetrance . We are starting to gain more insights into how the disease develops through the use of pre-leukemia and leukemia mouse models [2-8]. Using a pre-leukemia mouse model, in which expression of Mll-AF4 initiates in all definitive hematopoietic cells formed during embryonic development (Mll-AF4 invertor mouse crossed with VEC-Cre), we have previously identified the fetal liver as the starting point of MLL-AF4-driven leukemogenesis [4,7].
In conclusion, NF-κB-94 ins/del ATTG and CARD8 (rs2043211) genotypes might serve as novel biomarkers and potential targets for ALL.
The Notch receptor is a key mediator of developmental programs and cell-fate decisions. Imbalanced Notch signaling leads to developmental disorders and cancer. To fully characterize the Notch signaling pathway and exploit it in novel therapeutic interventions, a comprehensive view on the regulation and requirements of Notch signaling is needed. Notch is regulated at different levels, ranging from ligand binding, stability to endocytosis. Using an array of different techniques, including reporter gene assays, immunocytochemistry, and ChIP-qPCR we show here, to the best of our knowledge for the first time, regulation of Notc…