Rat model of breast cancer to dissect mechanisms of immune escape and immunotherapy sensitivity
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA702999 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13745000_1.fastq.gz | Fastqsanger.gz | |||
| SRR13745000_2.fastq.gz | Fastqsanger.gz | |||
| SRR13745001.fastq.gz | Fastqsanger.gz | |||
| SRR13745002.fastq.gz | Fastqsanger.gz | |||
| SRR13745003.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 155 |
Similar Datasets
Project description:NMU-induced sprague dawley rat model of breast cancer treated with immunotherapy to prevent tumor progression
2022-04-10 | GSE167102 | GEO
Project description:Immunotherapy has revolutionized the management of numerous cancers; however, a substantial proportion that initially respond subsequently acquire means of immune escape and relapse. Analysis of recent clinical trials permits us to preliminarily understand how immunotherapies exert evolutionary pressures: selecting cancer subclones deficient in antigenicity and/or immunogenicity, thereby facilitating immune escape.
| S-EPMC6249768 | biostudies-literature
Project description:Background and aimUrothelial bladder cancer (UBC) is a common malignant tumor of the urogenital system with a high rate of recurrence. Due to the sophisticated and largely unexplored mechanisms of tumorigenesis of UBC, the classical therapeutic approaches including transurethral resection and radical cystectomy combined with chemotherapy have remained unchanged for decades. However, with increasingly in-depth understanding of the microenvironment and the composition of tumor-infiltrating lymphocytes of UBC, novel immunotherapeutic strategies have been developed. Bacillus Calmette-Guerin (BCG) therapy, immune checkpoint blockades, adoptive T cell immunotherapy, dendritic cell (DC) vaccines, etc., have all been intensively investigated as immunotherapies for UBC. This review will discuss the recent progress in immune escape mechanisms and immunotherapy of UBC.MethodsBased on a comprehensive search of the PubMed and ClinicalTrials.gov database, this review included the literature reporting the immune escape mechanisms of UBC and clinical trials assessing the effect of immunotherapeutic strategies on tumor or immune cells in UBC patients published in English between 1999 and 2020.ResultsImmune surveillance, immune balance, and immune escape are the three major processes that occur during UBC tumorigenesis. First, the role of immunosuppressive cells, immunosuppressive molecules, immunosuppressive signaling molecules, and DCs in tumor microenvironment is introduced elaborately in the immune escape mechanisms of UBC section. In addition, recent progress of immunotherapies including BCG, checkpoint inhibitors, cytokines, adoptive T cell immunotherapy, DCs, and macrophages on UBC patients are summarized in detail. Finally, the need to explore the mechanisms, molecular characteristics and immune landscape during UBC tumorigenesis and development of novel and robust immunotherapies for UBC are also proposed and discussed.ConclusionAt present, BCG and immune checkpoint blockades have been approved by the US Food and Drug Administration for the treatment of UBC patients and have achieved encouraging therapeutic results, expanding the traditional chemotherapy and surgery-based treatment for UBC.Relevance for patientsImmunotherapy has achieved desirable results in the treatment of UBC, which not only improve the overall survival but also reduce the recurrence rate and the occurrence of treatment-related adverse events of UBC patients. In addition, the indicators to predict the effectiveness and novel therapy strategies, such as combination regimen of checkpoint inhibitor with checkpoint inhibitor or chemotherapy, should be further studied.
| S-EPMC8445627 | biostudies-literature
Project description:Multiple myeloma (MM) is a neoplasia of bone marrow (BM) plasma cells that remains largely incurable with current treatment. Advancing therapeutic discoveries has been hampered by the lack of genetically heterogeneous models of MM. To circumvent this limitation, we engineered fifteen mouse models carrying combinations of eight MM genetic drivers, which fulfilled the pathogenesis of human disease including progression from premalignant states under immune surveillance. Integrative analyses of ⁓500 mice and ⁓1,000 patients revealed a MAPK-MYC genetic pathway that regulates time to progression and immune escape mechanisms across genetically heterogeneous tumors. During progression, MYC-dependent and independent remodeling of the BM microenvironment divided MM into immune categories with predominance of selected T-cell subpopulations, which dictated immunotherapy responses. Experimental targeting of the cytotoxic or immunosuppressive T-cell states observed in refractory MM patients enhanced immunotherapy effectiveness. Our resource enabled characterization of MM cell-intrinsic and immunological traits at unprecedented levels, which will accelerate the translation of personalized immunotherapy.
2023-01-31 | GSE220997 | GEO
Project description:Tumor immune escape has emerged as the most significant barrier to cancer therapy. A thorough understanding of tumor immune escape therapy mechanisms is critical for further improving clinical treatment strategies. Currently, research indicates that combining several immunotherapies can boost antitumor efficacy and encourage T cells to play a more active part in the immune assault. To generate a more substantial therapeutic impact, it can establish an ideal tumor microenvironment (TME), encourage T cells to play a role, prevent T cell immune function reversal, and minimize tumor immune tolerance. In this review, we will examine the mechanisms of tumor immune escape and the limits of tumor immune escape therapy, focusing on the current development of immunotherapy based on tumor immune escape mechanisms. Individualized tumor treatment is becoming increasingly apparent as future treatment strategies. In addition, we forecast the future research direction of cancer and the clinical approach for cancer immunotherapy. It will serve as a better reference for researchers working in cancer therapy research.
| S-EPMC8989557 | biostudies-literature
Project description:X chromosome inactivation (XCI) silences most genes on one X chromosome in female mammals, but some genes escape XCI. To identify escape gene in vivo and to explore molecular mechanisms that regulate this process we analyzed the allele-specific expression and chromatin structure of X-linked genes in mouse tissues and cells with skewed XCI and distinguishable alleles based on single nucleotide polymorphisms. Using a new method to estimate allelic expression, we demonstrate a continuum between complete silencing and significant expression from the inactive X (Xi). Few genes (2-3%) escape XCI to a significant level and only a minority differs between mouse tissues, suggesting stringent silencing and escape controls. Allelic profiles of DNase I hypersensitivity and RNA polymerase II occupancy of genes on the Xi correlate with escape from XCI. Allelic binding profiles of the DNA binding protein CCCTC-binding factor (CTCF) in different cell types indicate that CTCF binding at the promoter correlates with escape. Importantly, CTCF binding at the boundary between escape and silenced domains may prevent the spreading of active escape chromatin into silenced domains. Examination of allelic expression in mouse hybrid tissues.
2015-02-20 | E-GEOD-59777 | biostudies-arrayexpress
Project description:X chromosome inactivation (XCI) silences most genes on one X chromosome in female mammals, but some genes escape XCI. To identify escape gene in vivo and to explore molecular mechanisms that regulate this process we analyzed the allele-specific expression and chromatin structure of X-linked genes in mouse tissues and cells with skewed XCI and distinguishable alleles based on single nucleotide polymorphisms. Using a new method to estimate allelic expression, we demonstrate a continuum between complete silencing and significant expression from the inactive X (Xi). Few genes (2-3%) escape XCI to a significant level and only a minority differs between mouse tissues, suggesting stringent silencing and escape controls. Allelic profiles of DNase I hypersensitivity and RNA polymerase II occupancy of genes on the Xi correlate with escape from XCI. Allelic binding profiles of the DNA binding protein CCCTC-binding factor (CTCF) in different cell types indicate that CTCF binding at the promoter correlates with escape. Importantly, CTCF binding at the boundary between escape and silenced domains may prevent the spreading of active escape chromatin into silenced domains. Examination of CTCF and RNA PolIIS5p occupancy in mouse hybrid cells and adult tissues.
2015-02-20 | E-GEOD-59778 | biostudies-arrayexpress
Project description:Tumor-associated neutrophils attenuate the immuno-sensitivity of hepatocellular carcinoma and curtail immunotherapy response
| PRJNA1005345 | ENA
Project description:Lung cancer is the most common malignant tumor of lung and bronchus, with the highest mortality rate, and its immunotherapy is easy to cause drug resistance. In order to understand the molecular mechanism of immune escape in patients and develop prediction and therapeutic targets, this study carried out analytical experiments by single-cell sequencing.
2024-05-17 | GSE267108 | GEO