Collection: Blood Research Selected on June 25, 2020

1The primary cell-like chronic myeloid leukemia model based on genetic heterogeneityBCR-ABL1 kinase targeted therapy revolutionized the treatment of chronic stage (CP) chronic myeloid leukemia (CML)In contrast, themanagementof the primary cell vision (BC) CML remains challengingTo better understand BC, the researchers conducted a comprehensive multi-group analysis of 74 CP and BC samples through genome-wide and exome sequencing, transcription and methylation spectra, chromatinimmunoprecipitation and high-throughput sequencingIt was found by path-enrichment analysis that in the BC genome, the mutations that affect the components of the initiation complex (PRC) signaling pathway were significantly enrichedHowever, transcriptomic analysis showed that in BC progenitor cells, PRC1-related genes were enriched, while PRC2-related gene sets were missingBy integrating the database, the researchers identified the development of BC progenitor cells through EPIGENETIC reprogramming driven by PRC to a convergent transcription stateSpecifically, PRC2 mediates high methylation of BC cell DNA, which in turn silences key genes involved in myelin differentiation and tumor suppression gene function through so-called "epigenetic transformation", while PRC1 inhibits an overlapping set of different genes, including the new BC tumor suppressor genethe prognosis for the treatment of hodgkinlymphomasynosy lymphoma (NLPHL) is a rare heliosphor mutation, and the best treatment for I-II NLPHL is uncertain researchers conducted a multi-center editing study that included patients with I-II NLPHL diagnosed between 1995 and 2018 who were diagnosed with a variety of treatments, including radiotherapy (RT), combined modal therapy (CMT-RT-chemotherapy), chemotherapy (CT), post-excision observation, ritusoxiaandasandand and RT, and litoxie monotherapy (R) The evaluation indicators are Progressless Survival (PFS), Pre-Transplant Time, and Overall Survival Rate (OS) 559 patients were included in the study, with the median age of 39, 72.3% male and 54.9% in stage I Median follow-up 5.5 years (range: 3.1-10.1) The five-year PFS and OS of the entire queue were 87.1% and 98.3%, respectively Initial treatment with RT, CMT, CT, observation, rituximab, RT or rituximab monotherapy patients had 257 cases (46.0%), 184 cases (32.9%), 47 cases (8.4%), 37 cases (6.6%), 19 (3.4%) and 15 (2.7%) THE FIVE-YEAR PFS AFTER RT, CMT, CT, OBSERVATION, RITUXIXAINE PLUS RT OR RITUXICYT MONOTHERAPY WAS 91.1%, 90.5%, 77.8%, 73.5%, 80.8% AND 38.5%, RESPECTIVELY the prognosis of abnormal hematopoietic function in patients with new myeloma the risk of myeloma hyperplasia syndrome (MDS) in patients with multiple myeloma (MM) and MGUS patients increased significantly, but the incidence and sequelae of hematopoietic dysfunction at diagnosis were not clear researchers screened 285 MM patients using multidimensional flow cytomeomenos (MFC) to analyze the presence of MDS-related phenotype changes (MDS-PA) in the bone marrow diagnosed, 33 (11.6%) patients had MDS-PA Bulk and single-cell targeted sequencing of recurrent mutations of MDS gene in 67 patients with CD34-progenitor cells (and stunted spectrum) showed that 13/26 (50%) MDS-PA patients had cloned hematopoietic blood, 9/41 (22%) non-MDS-PA patients had cloned blood, and TET2 and NRAS were the most common mutant genes An assessment of MDS-PA dynamics at the time of diagnosis and post-autologous transplantation in 86/285 patients found that in most cases (69/86, 80%), the presence or failure of MDS-PA remained constant for a long time It is important to note that MDS-related mutations are rarely seen after high-dose treatment Based on MFC analysis, the researchers also found changes in the hematopoietic and Treg distribution seconditiony and Treg in tumor microenvironments in patients with MDS-PA Importantly, the presence of mononucleosis MDS-PA at the time of diagnosis indicates a higher risk of hematotoxicity and is independently associated with poor progression-free survival and total survival a new model for the study of susceptibility to Tissue Damage by T-cell
researchers recently designed an in vitro platform using mechanical observation in preclinical animal models to reconstruct genetic susceptibility to T-cell-mediated damage intestinal transplantantite serorhaging host disease (GVHD) is a life-threatening complication of allo-HCT The researchers found that in mice with atg16L1 (a polymorphic autophagy gene) defect, intraintestinal GVHD was reversed by inhibiting necrosis In addition, the researchers found that allogeneic T cells co-cultured small intestine organs from the atg16L1 mutation that could kill mice, which were associated with abnormal signaling of epithelial interferon Using this information, the researchers demonstrated that transduction from drug-suppressing necrosis or interferon signals protects organs of the same gene T-cell from people carrying common ATG16L1 variants Source: MedSci Original