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Preclinical Evaluation of Carfilzomib for Infant KMT2A-Rearranged Acute Lymphoblastic Leukemia

Infants with KMT2A-rearranged B-cell precursor acute lymphoblastic leukemia (ALL) have poor outcomes. There is an urgent need to identify novel agents to improve survival. Proteasome inhibition has emerged as a promising therapeutic strategy for several hematological malignancies. The aim of this study was to determine the preclinical efficacy of the selective proteasome inhibitor carfilzomib, for infants with KMT2A-rearranged ALL.

DYRK1A regulates B cell acute lymphoblastic leukemia through phosphorylation of FOXO1 and STAT3

DYRK1A is a serine/threonine kinase encoded on human chromosome 21 (HSA21) that has been implicated in several pathologies of Down syndrome (DS), including cognitive deficits and Alzheimer's disease. Although children with DS are predisposed to developing leukemia, especially B cell acute lymphoblastic leukemia (B-ALL), the HSA21 genes that contribute to malignancies remain largely undefined. Here, we report that DYRK1A is overexpressed and required for B-ALL. Genetic and pharmacologic inhibition of DYRK1A decreased leukemic cell expansion and suppressed B-ALL development in vitro and in vivo.

Flt3L-mediated tumor cDC1 expansion enhances immunotherapy by priming stem-like CD8+ T cells in lymph nodes

Immune checkpoint blockade (ICB) evokes antitumor immunity through the reinvigoration of T cell responses. T cell differentiation status controls response, with less differentiated cells having an enhanced capacity to proliferate after ICB. Given that conventional type 1 dendritic cells (cDC1) maintain precursor exhausted T cells (TPEX), we hypothesized that expansion of cDC1s with Flt3L could enhance responses to ICB. 

Tumor site-directed A1R expression enhances CAR T cell function and improves efficacy against solid tumors

Citation: Sek K, Chen AXY, Cole T, Armitage JD, Tong J, ……… Waithman J, Parish IA, et al. Tumor site-directed A1R expression enhances CAR T cell

Rewiring endogenous genes in CAR T cells for tumour-restricted payload delivery

The efficacy of chimeric antigen receptor (CAR) T cell therapy in solid tumours is limited by immunosuppression and antigen heterogeneity. To overcome these barriers, 'armoured' CAR T cells, which secrete proinflammatory cytokines, have been developed. However, their clinical application has been limited because of toxicity related to peripheral expression of the armouring transgene. 

Human erythroleukemia genetics and transcriptomes identify master transcription factors as functional disease drivers

Acute erythroleukemia (AEL or acute myeloid leukemia [AML]-M6) is a rare but aggressive hematologic malignancy. Previous studies showed that AEL leukemic cells often carry complex karyotypes and mutations in known AML-associated oncogenes.

SNAIL trail in myeloid malignancies

Transcription factors known to induce the epithelial-to-mesenchymal transition (EMT) (such as ZEB1/2 [zinc finger E-box binding homeobox 1/2], SNAI1/2/3, and TWIST1/2) have been undoubtedly implicated in tumorigenesis, cancer progression, metastasis, and chemoresistance in solid tumors; however, their role in normal and malignant hematopoiesis has been underappreciated for many years.

A CHAF1B-Dependent Molecular Switch in Hematopoiesis and Leukemia Pathogenesis

Here we report that CHAF1B is required for normal hematopoiesis while its overexpression promotes leukemia

Efficacy of DYRK1A inhibitors in novel models of Down syndrome acute lymphoblastic leukemia

Despite significant advances, outcomes for children with Down syndrome (DS, trisomy 21) who develop acute lymphoblastic leukemia remain poor. Reports of large DS-ALL cohorts have shown that children with DS have inferior event-free survival and overall survival compared to children without DS.

Transcriptional rewiring in CD8+ T cells: implications for CAR-T cell therapy against solid tumours

T cells engineered to express chimeric-antigen receptors (CAR-T cells) can effectively control relapsed and refractory haematological malignancies in the clinic. However, the successes of CAR-T cell therapy have not been recapitulated in solid tumours due to a range of barriers such as immunosuppression, poor infiltration, and tumour heterogeneity.