GuLan chun, Fujun,2023.11.17

Description

OEP004747

meiyao he, ,2023.11.16

Description

OEP004742

Cheng Cheng, Shanghai Jiaotong University School of Medicine affiliated Xinhua Hospital,2023.11.07

Description

Proteomic and phospho-proteomic raw data of Wilms' tumor tissue and normal adjacent kidney tissue from Wilms tumor patients. mRNA expression data of Wilm's tumor cell line after knockdown of EHMT2.

OEP004700

Yijun Shen, Fudan University Shanghai Cancer Center,2023.11.13

Description

OEP004732

Xiaoyuan Feng, ,2023.11.13

Description

Four novel Yoonia strains from brackish lake Zhangnai on the Tibetan Plateau.

OEP004731

Tan Xiaoli, Shanghai Jiao Tong University,2023.07.11

Description

resequencing

OEP004233

Yakai Fu, Renji Hospital, Shanghai Jiaotong University School of Medicine,2023.11.05

Description

Objective: Gastrointestinal (GI) involvements were scarcely reported in adult anti-NXP2 dermatomyositis (NXP2+DM). In this study, we investigated the clinical, pathological, and molecular features as well as treatment options of this rare yet life-threatening disease. Patients and Methods: We retrospectively collected the data of the cohort of NXP2+ DM from 2012 to 2022 in our hospital. RNAseq was performed in intestinal samples of perforated patients compared to healthy controls dataset. Results: A total of 56 adult NXP2+DM patients were collected including 10 cases with GI involvements. Abdominal pain and melena were the initial manifestations for GI involvements with a median 10-month time lag after the diagnosis of NXP2+DM when myositis largely subsided. Within weeks, GI perforation occurred in eight of ten patients, while five patients underwent eight surgical interventions subsequently. The short-term mortality was observed in four patients. NXP2+DM with GI involvements presented with more extramuscular systemic manifestations such as interstitial lung disease and subcutaneous calcinosis. The GI pathological features encompassed vasculitis/vasculopathy with high MxA expression, intestinal smooth muscle necrosis, and serosal calcinosis. Gene expression profile validated the type-I interferon activation and revealed that epithelial mesenchymal transition and focal adhesion pathway may also contribute. Finally, Vedolizumab, an anti-α4β7‑integrin monoclonal antibody, exhibited promising therapeutic signals which should be further investigated. Conclusions: GI involvement is an unique complication in adult NXP2+ DM patients. Timely recognition and targeted therapy may turn out to be lifesaving.

OEP004694

Lei Zhang, Shandong University,2023.11.02

Description

There is, in fact, increasing evidence suggesting that bacterial dysbiosis may have a significant impact on the pathogenesis of IgAV . However, the specific mechanisms by which the gut microbiota affects IgAV development and progression are still obscure.Here, we investigate the gut microbiome of 127 IgAV child-mother pairs and 62 matched healthy child-mother pairs to investigate the taxonomic and functional shifts of the gut microbiome and its correlation between mother and child.

OEP004691

Yongxin Lv, Shanghai Jiaotong UNI,2020.05.22

Description

OEP000957

Yuexiang Wang, Shanghai Institute of Nutrition and Health,2023.01.11

Description

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy and bears dismal prognosis due to the lack of effective treatments. While immunotherapy has made great strides in other cancers, the outcomes of immune checkpoint inhibitors (ICIs) treatment in PDAC are disheartening. Here we demonstrate that tumor cell-intrinsic Setd2-knockout sensitizes PDAC tumors to ICIs immunotherapy in syngeneic murine models. Mechanistically, via an integrated multiomics analysis using ATAC-seq, ChIP-seq and RNA-seq, we reveal that SETD2 inactivation reduces NR2F1 transcription by impairing H3K36me3 deposition and chromatin accessibility. As a repressive transcription factor to STAT1, down-regulated NR2F1 activates IFNγ-STAT1 pathway to promote chemokine production, PD-L1 expression and enhance MHC-I antigen presentation. Upregulated chemokines reprogram intratumoral immune cells and inflame the tumor microenvironment with high-infiltrated T cells through bulk and single-cell RNA-seq analysis. Enhanced MHC-I antigen presentation profoundly promotes the cytotoxity of CD8+ T cells. With a blockade to the highly expressed PD-L1, the inflamed intratumoral immune cells significantly inhibits the tumor growth in PDAC. The SETD2-NR2F1-STAT1 regulatory axis is conserved in human and murine PDAC, suggesting a sign of clinical benefit for patients harboring SETD2 deficiency. Together, our findings provide novel insights into the regulation of tumor cell-intrinsic SETD2 inactivation to immune microenvironment, and reveal a potential biomarker for ICIs treatment in refractory PDAC.

OEP003840