A selection of Blod research on September 24, 2020.

Adding repamycin to GVHD prevention programmes can significantly improve HLA antigen misalluaring HCT patient prognostic https://doi.org/10.1182/blood.202000533 8 (Xinhua) -- Researchers recently evaluated the efficacy of adding reparamycin to postoperative anti-host disease (GVHD) of hematopoietic cell transplantation (HCT) mismatched with repamycin in the treatment of cyclosporine and McCorphenolates.
to recruit patients with hematological malignant diseases that can be treated with the allogeneic HCT.
conditioning options include fluorodarabin (90 mg/m2) and 2-3 Gy full body radiotherapy.
GVHD prevention is cyclosporine and McCorphenolates and repamycin.
assessment was whether the cumulative occurrence of type II-IV acute GVHD could be reduced to less than 70% in HCT patients with type I or type II HLA misaltags.
as of December 12, 2018, 77 subjects had been recruited, 76 of whom had completed the study intervention.
follow-up for 47 months.
100 days, the cumulative rate of ii-IV acute GVHD was 36%, reaching the main endpoint.
, the cumulative rates of non-recurrence deaths and relapses/progress were 18 per cent and 30 per cent, respectively, and the overall survival rate was 62 per cent.
. Quantitative proteomics reveals the unique metabolic characteristics of AML stem cells https://doi.org/10.1182/blood.2019003654 Acute myeloid leukemia (AML) is characterized by the accumulation of cloned myelocell cell cells that cannot differentiate into mature white blood cells.
can relieve most patients, but the recurrence rate is high and leads to poor clinical prognostication.
this is mainly caused by chemotherapy-resistant leukemia stem cells (LSCs), LSC must be eradicated to improve patient survival.
to study LSC mainly at the transcription level, so there is a lack of information about post-transcription regulatory genes and related networks.
Raffel et al. extended past reports on LSC proteomics to healthy age-matching hematopoietic stem cells and ancestral cells (HSPC) and associated proteomics with corresponding transcription groups.
By comparing LSC with leukemia mother cells and healthy HSPC, Raffel et al. validated the candidate markers for LSC and highlighted new, potentially targetable proteins that are not present or rarely expressed in HSPC.
, the data provide strong evidence that LSC has unique energy metabolism, adhesive molecular composition, and RNA processing properties.
association of proteomics and transcription data from samples of the same individual also highlights the importance of proteomic analysis, which is particularly effective in detecting changes in metabolic pathlines.
IKAROS and CK2 regulate high-risk B-ALL BCL-XL expression and chemotherapy sensitivity https://doi.org/10.1182/blood.2019002655 High-risk type B cell acute lymphoblastic leukemia (B-ALL) is an invasive disease characterized by chemotherapy resistance.
common feature of high-risk type B-ALL is the loss of function of tumor suppressor IKAROS (encoded by the IKZF1 gene).
researchers recently found that IKAROS regulates the expression of the BCL2L1 gene (encoded bcl-xl protein) in human B-ALL.
of functional accessibility and loss of function showed that IKAROS combined with the BCL2L1 promoter, recruited histone deacetylase HDAC1, and inhibited the expression of BCL2L1 through chromatin remodeling.
in leukemia, cancer-causing casein kinase II (CK2) is highly expressed in B-ALL, impairing IKAROS function.
CK2 phosphate reduced the combination of IKAROS on the BCL2L1 launcher and the HDAC1 collected.
this leads to the loss of ICL2L1 expression inhibition and an increase in BCL-XL expression mediated by IKAROS.
increased expression of BCL-XL and/or CK2, as well as decreased expression of IKAROS, were associated with drug resistance in dolbi-star therapy.
inhibition of CK2 with the specific inhibitor CX-4945 can increase the binding of IKAROS with BCL2L1 promoters and enhance the inhibition of IKAROS-mediated BCL2L1 in B-ALL.
CX-4945 therapy enhances B-ALL's sensitivity to doody stars and reverses B-ALL's resistance to dosoded stars.
in-body and preclinical models of high-risk B-ALL in combination with CX-4945 and dorous star therapy.
. In adults, the liver-based hormone iron-iron-tuning (HAMP) regulates the overall iron levels of the whole body by blocking iron-output protein-to-iron protein (FPN), iron absorption and re-absorption points in the late stages of pregnancy.
damage to HAMP expression or abnormal FPN reaction to HAMP can lead to iron overload.
HAMP is also expressed in the fetal liver, but its role in regulating fetal iron storage is unclear.
In order to address the role of HAMP in regulating fetal iron storage without being affected by a mix of maternal iron stabilization factors, the researchers established fetal mice that carried the parent-inherited HAMP resistance fpnC326Y gene.
addition, to avoid any confuse of changes in the iron state of the placenta, the researchers created mice with fpnC326Y liver specific knock-in or hamp gene knock-out.
results showed that these fetuses had reduced liver iron reserves and hemoglobin, and a significant increase in FPN in the liver, but normal in the placenta.
, the researchers speculated that HAMP in the mouse liver could operate autonomously in cells to increase iron storage in the fetal liver.
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