NPM1 mutation is one of the most common recurrent genetic lesions in AML, and is relatively specific for AML; it occurs in 2―8 % of childhood cases and 27―35 % of adult cases overall, as well as in 45―64 % of adult cases with...
Briefly, ScRNA-seq is a powerful tool for development and optimization of CAR T-cell therapy. Researchers can improve the design of CAR constructs to make T cells more persistent, more effective at killing cancer cells, and better at secreting cytokines by looking at the transcriptional profiles ...
The p53 tumor suppressor gene is mutated in over half of human solid cancers. However, in hematological malignancies the frequency of p53 mutation is relatively low, and the majority of tumors express a wild-type, transcriptionally competent protein. Nevertheless, leukemia cells have abnormalities in...
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and HLA-DR. The hypothesis was that AML blasts inducing HGF expression might be a mechanism for resistance to anti-HGF therapy. Researchers performed unsupervised gene module analysis to identify additional biomarkers of resistance to anti-HGF therapy, and discovered 20 groups of co-regulated genes ...
[72]. Patients were enrolled in two cohorts, both with R/R AML regardless ofFLT3mutation status as follows: patients aged ≥ 60 years with R/R disease within 1 year after first-line therapy (cohort 1; n = 157), and patients aged ≥ 18 years with R/R disease after ...
In addition, CyTOF (single-cell mass cytometry) analysis could be used to select patients with the best response based on pre- and on-therapy apoptotic and signaling pathway profiles [57]. Targeting TP53 mutation The TP53 gene, located on chromosome 17p13.1, is commonly mutated in tumors ...
and balanced abnormalities and excluded cases of therapy related AML and AML with recurrent genetic abnormalities, such as t(8;21), inv(3), and t(6;9), the latter two of which may have multilineage dysplasia [4]. Whether the presence of dysplastic morphologic features alone warrants classi ...
In addition, myelomonocytic leukemia, upregulation of BCL2A1 and CLEC7A, as well as mutations of PTPN11 and KRAS, confer resistance to VEN-based therapy [27]. More recently, Dohner et al. have reported that TP53, FLT3-ITD, NRAS, and KRAS mutation status are associated with three different ...
“Despite the poor outcomes in this setting, several novel immune and cellular therapy approaches, including those with potentially p53-agnostic mechanisms of action, could hold promise,” said Abhishek Maiti, MD, during an interview with Targeted Therapies in Oncology™. Maiti is an assistant prof...