Delving into the Latest Updates on 商丘肿瘤防治研究所 with Synapse

概览

疾病领域	数量

肿瘤	1

排名前五的药物类型	数量

重组多肽	1

排名前五的靶点	数量

TNFRSF21(肿瘤坏死因子受体超家族成员21)	1

关联

1

项与商丘肿瘤防治研究所相关的药物

CN114478693

专利挖掘

靶点

TNFRSF21

作用机制-

在研机构

商丘肿瘤防治研究所

原研机构

商丘肿瘤防治研究所

在研适应症

肿瘤

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期-

100 项与商丘肿瘤防治研究所相关的临床结果

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0 项与商丘肿瘤防治研究所相关的专利（医药）

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1,231

项与商丘肿瘤防治研究所相关的文献（医药）

2025-06-02·Journal of Cell Biology

ZBTB17/MIZ1 promotes peroxisome biogenesis by transcriptional regulation of PEX13

Article

作者: Zhuang, Guanglei ; Zhu, Zheng-Jiang ; Liu, Hongqin ; Wang, Hanlin ; Chen, Xi ; Zhuang, Min

Peroxisomes are integral metabolic organelles involved in both catabolic and anabolic processes in humans, with defects linked to diseases. The functions of peroxisomes are regulated at transcriptional, translational, and posttranslational levels. In this study, we employed the CRISPR/Cas9-based screening of a ubiquitin ligase library to identify regulators of human peroxisomes. We discovered that ZBTB17 (MIZ1) plays a role in regulating the import of proteins into peroxisomes. Independent of its ubiquitin ligase activity, ZBTB17/MIZ1 operates as a transcription factor to modulate the expression of key importer PEX13, influencing the localization of peroxisomal enzymes. Furthermore, metabolomic profiling reveals that knockdown of ZBTB17 or PEX13 results in similar metabolic alterations, with downregulated purine synthesis. Collectively, we identify ZBTB17 as a key regulator of peroxisomal protein import, thereby affecting peroxisomal function and nucleotide metabolism. Our findings provide insights into the multifaceted regulation of peroxisomes in complex human cells and shed light on the molecular mechanisms underlying ZBTB17’s role as a transcriptional regulator.

2025-06-01·Journal of Controlled Release

Quercetin liposomes conjugated with hyaluronidase: An efficient drug delivery system to block pancreatic cancer

Article

作者: Wu, Ying ; Shao, Rong ; Xu, Hang ; Li, Jiekai ; Liu, Yingbin ; Sun, Ge ; Li, Yiping ; Tong, Peilin ; Yang, Mingjie ; Kong, Xianming

Pancreatic cancer characterized with intense hydraulic tissue in tumor extracellular matrix (ECM) resists most of chemotherapeutic drugs. Increased levels of hyaluronic acid (HA) represent the primary component of the hydraulic tissue, rendering tumors protective from drug targeting. Quercetin (Que), a natural flavonoid, has the ability to inhibit tumor cell growth in a number of cancers; however, its poor water solubility and low bioavailability largely limit its application in cancer therapy. Hence, we developed an efficient drug delivery system by encapsulation of Que. into liposomes and conjugation with hyaluronidase (HAase) at liposome surface, termed as HQL. In the presence of HAase, HQL were predominantly accumulated at tumor with enhanced permeability and retention effect. Treatment of xenografted tumor mice with HQL gave rise to suppressed tumor growth, while no toxic effects were observed in mice. HQL demonstrated the strong ability to inhibit cell proliferation, promote cell apoptosis, and induce arrest at G2/M cell cycle in pancreatic cancer lines, three-dimensional cultured cell spheroids and pancreatic ductal adenocarcinoma (PDAC)-derived organoids. Mechanistically, HQL downregulated expression of cell cycle-associated protein (CCNB1, CDK1 and PLK1) and cell apoptosis-associated factors PI3K/AKT and Bcl-2. In summary, HQL degraded HA in the tumor microenvironment to enhance nano-particle penetration and inhibited tumor cell growth, eliciting efficacy of anti-tumor therapy. Thereof, HQL may provide a novel efficient drug delivery approach for the adjuvant treatment of pancreatic cancer.

2025-05-01·Gut

Mutational signatures define immune and Wnt-associated subtypes of ampullary carcinoma

Article

作者: Gao, Yu-Tang ; Andersen, Jesper B ; Oliveira, Rui Caetano ; Pea, Antonio ; Taranta, Andrzej ; O'Rourke, Colm J ; Rashid, Asif ; Chang, David ; Zhuravleva, Ekaterina ; Koshiol, Jill ; Hsing, Ann W ; Lewinska, Monika

Background and objectiveAmpullary carcinoma (AMPAC) taxonomy is based on morphology and immunohistochemistry. This classification lacks prognostic reliability and unique genetic associations. We applied an approach of integrative genomics characterising patients with AMPAC exploring molecular subtypes that may guide personalised treatments.DesignWe analysed the mutational landscapes of 170 patients with AMPAC. The discovery included 110 tumour/normal pairs and the validation comprised 60 patients. In a tumour subset, we interrogated the transcriptomes and DNA methylomes. Patients were stratified based on mutational signatures and associated with molecular and clinical features. To evaluate tumour and immune cellularity, 22 tumours were independently assessed histomorphologically and by digital pathology.ResultsWe defined three patient clusters by mutational signatures independent of histomorphology. Cluster 1 (C1) was defined by spontaneous deamination of DNA 5-methylcytosine and defective mismatch repair. C2 and C3 were related to the activity of transcription-coupled nucleotide excision repair but C3 was further defined by the polymerase eta mutational process. C1–2 showed enrichment of Wnt pathway alterations, aberrant DNA methylation profiles, immune cell exclusion and patients with poor prognosis. These features were associated with a hypermutator phenotype caused by C>T alterations at CpGs. C3 patients with improved overall survival were associated with activation of immune-related pathways, immune infiltration and elevated expression of immunoinhibitory checkpoint genes.ConclusionImmunogenicity and Wnt pathway associations, emphasised by the mutational signatures, defined patients with prospective sensitivity to either immunotherapy or Wnt pathway inhibitors. This emphasises a novel mutational signature-based AMPAC classification with prognostic potential, suggesting prospective implications for subgroup-specific management of patients with AMPAC.

100 项与商丘肿瘤防治研究所相关的药物交易

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100 项与商丘肿瘤防治研究所相关的转化医学

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