Publications by authors named "B J Eisfelder"
Article Synopsis
- Myeloid neoplasms, which are linked to clonal hematopoiesis (CH), may also play a role in acute lymphoblastic leukemia (ALL), with 18% of adult ALL cases having TP53 mutations and 16% carrying myeloid CH-related mutations.
- ALL associated with these myeloid mutations displays unique genetic traits and poorer survival outcomes, suggesting it is a high-risk disease.
- Research indicates that myeloid mutations can develop years before an ALL diagnosis, with certain clones becoming dominant, while B-ALL cases respond better to immunotherapy due to alterations in cell survival genes.
Article Synopsis
- Relapsed T-acute lymphoblastic leukemia (T-ALL) has limited treatment options and this study explores resistance mechanisms to BH3 mimetics and the effectiveness of a new drug, NWP-0476, both alone and in combination.
- The research used BH3 profiling and phosphokinase arrays to reveal that T-ALL cells rely on different proteins (BCL-xL and BCL-2) for survival, leading to the discovery of enhanced LCK and ACK1 activity in resistant cells as potential resistance factors.
- The study concluded that targeting the LCK and ACK1 signaling pathways, along with combining BH3 mimetics and tyrosine kinase inhibitors, could offer a promising treatment strategy for relapsed T-
Article Synopsis
- T-cell acute lymphoblastic leukemia (T-ALL) is a serious blood cancer that shows varying drug responses, with about 44% of children and 17% of adults responding well to the drug dasatinib.
- Research found that the activation of a specific signaling pathway (preTCR-LCK) is key to why some T-ALL cases are sensitive to dasatinib, while other cases are resistant to a different drug called venetoclax.
- The study highlights that the developmental stage of T-cells in leukemia influences which signaling pathways are active, suggesting potential for developing targeted therapies based on a patient's specific leukemia characteristics.
Internal tandem duplication (-ITD) mutations of Fms-like tyrosine kinase 3 (FLT3) provide growth and pro-survival signals in the context of established driver mutations in FLT3 mutant acute myeloid leukemia (AML). Maternal embryonic leucine zipper kinase (MELK) is an aberrantly expressed gene identified as a target in AML. The MELK inhibitor OTS167 induces cell death in AML including cells with FLT3 mutations, yet the role of MELK and mechanisms of OTS167 function are not understood.
View Article and Find Full Text PDFAlthough trauma in pregnancy is rare, it is one of the most common causes of morbidity and mortality to pregnant women and fetus. Pathophysiology of trauma is generally time sensitive, and this is still true in pregnant patients, with the additional challenge of rare presentation and balancing the management of two patients concurrently. Successful resuscitation requires understanding the physiologic changes to the woman throughout the course of pregnancy.
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