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Analysis of the response to PD1 therapy in B16R2L mouse melanoma tumors knockdown for Mdk.

ABSTRACT: Analysis of the response to PD1 therapy in B16R2L mouse melanoma tumors knockdown for Mdk.

PROVIDER: PRJNA631978 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11778100.fastq.gz	Fastqsanger.gz
	SRR11778101.fastq.gz	Fastqsanger.gz
	SRR11778102.fastq.gz	Fastqsanger.gz
	SRR11778103.fastq.gz	Fastqsanger.gz
	SRR11778104.fastq.gz	Fastqsanger.gz

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Analysis of the response to PD1 therapy in B16R2L mouse melanoma tumors knockdown for Mdk.

Project description:Gene expression analysis in tumors generated by B16R2L cells injected in C57BL/6J mice and treated with anti-PD1 (clone RMP1-14, 10 gr/Kg) or the corresponding IgG2a control.

2020-10-18 | GSE150401 | GEO

Proteomic profiling to predict therapeutic response to anti-PD1 therapy in advanced melanoma – Orbitrap Elite dataset depleted serum

Project description:MS-based proteomics based on data-dependent acquisition / shotgun MS was used to study the response of melanoma patients to anti-PD1 therapy. Human serum samples were collected from patients at the start of their therapy and later categorized into responders and non-responders based on clinical outcome. Samples were subjected to immunodepletion and proteins were identified by bottom-up proteomics.

2023-08-18 | PXD027849 | Pride

Proteomic profiling to predict therapeutic response to anti-PD1 therapy in advanced melanoma – SWATH MS dataset - glycopeptides

Project description:MS-based proteomics based on data-independent acquisition / SWATH MS was used to study the response of melanoma patients to anti-PD1 therapy. Human serum samples were collected from patients at the start of their therapy and later categorized into responders and non-responders based on clinical outcome. Samples were subjected to glycocapture and glycopeptides were quantified by SWATH MS followed by analysis using mapDIA to protein levels.

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Effect of MDK expressing Melanoma cells conditioned media in Human LEC

Project description:Gene expression analysis in hLECs treated with gain of function or loss of function of MDK in human melanoma cells.

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Supplementation with α-ketoglutarate improved the efficacy of anti-PD1 melanoma treatment through epigenetic modulation of PD-L1

Project description:Patients with advanced melanoma have shown an improved outlook after receiving anti-PD1 therapy, but the low response rate restricts clinical benefit; therefore, enhancing anti-PD1 therapy efficacy remains a major challenge. Here, our findings show significantly higher abundance of α-KG in healthy controls, anti-PD1-sensitive melanoma-bearing mice, and anti-PD1-sensitive melanoma patients; moreover, supplementation with α-KG enhanced the efficacy of anti-PD1 immunotherapy and increased PD-L1 expression in melanomas via STAT1/3. We also found that supplementation with α-KG significantly increased methylcytosine dioxygenase TET2/3, which led to an increased 5-hydroxymethylcytosine (5-hmC) level in the PD-L1 promoter. As a consequence, STAT1/3 had been recognized and stabilized in PD-L1 promoter to upregulate PD-L1 expression. Importantly, single-cell sequencing of preclinical samples and analysis of clinical data revealed that the TET2/3-STAT1/3-CD274 signaling was associated with sensitivity to anti-PD1 treatment in melanoma. Taken together, we provide a novel insight into α-KG's function in melanoma anti-PD1 treatment and supplement of α-KG is a novel promising strategy to improve the efficacy of anti-PD1 therapy.

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Proteomic profiling to predict therapeutic response to anti-PD1 therapy in advanced melanoma

Project description:Purpose Antibody-blockade of PD-1 shows durable responses, but so far, few biomarkers accurately predict if patients with metastatic melanoma will respond. Experimental design We analyzed baseline serum samples (n=56) and tumor cell cultures (n=8), from melanoma patients treated with anti-PD1 therapy. Two approaches concentrating low abundant proteins in serum and two different mass spectrometry (MS) methods were applied: depletion of high abundant proteins with shotgun-MS, and N-glycosite enrichment combined with SWATH-MS. Tumor cell cultures were processed as whole cell lysates with subsequent shotgun-MS. Results Focusing on the non-responder proteome, we identified pathways such as inflammatory processes, cell adhesion and migration, scavenger receptor activity, RAGE receptor binding, platelet aggregation, neutrophil degranulation and integrin signaling to be upregulated. Analyzing the tumor cell proteome revealed a distinctive immunophenotype with CD antigens highly overexpressed in non-responders. Validation of a subset of these markers, performed by immunofluorescence staining of a tissue microarray, revealed a higher mean of positive cells in the tumor microenvironment of non-responders. Validation of serum proteome markers on a second baseline cohort by using a timsTOF for ion mobility MS, revealed significant differences between responder and non-responder for the proteins ORM2, SERPINA1, EFEMP1, and VASN. TCGA survival analysis demonstrated prognostic significance for multiple proteins of our signature correlating with lower overall survival in melanoma patients. Based on this study, we suggest a protein-panel for responsiveness to PD-1 blockade consisting of 14 serum and 33 tumor cell markers that will be the basis for further research.

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Pathway Signatures Derived from On-treatment Tumor Specimens Predict Response to Anti-PD1 Blockade in Metastatic Melanoma

Project description:Both genomic and transcriptomic signatures have been developed to predict responses of metastatic melanoma to immune checkpoint blockade (ICB) therapies; however, most of these signatures were derived from pre-treatment biopsy samples. Here, we developed pathway-based signatures that predict response of metastatic melanoma to anti-PD1-based therapies in four independent datasets with RNAseq and clinical response data available for both pre- and on-treatment metastatic melanomas. We first identified pathway signatures that were significantly enriched in tumor specimens from anti-PD1 responders (R) compared to non-responders (NR) at pre-treatment and on-treatment time points, respectively. We also identified pathway signatures that were differentially expressed in pre-treatment versus on-treatment samples derived from R. Finally, we interrogated the capacity of the two types of signatures in predicting response of metastatic melanoma to anti-PD1 therapies in comparison with existing gene expression signatures. And we also investigated the effect of biopsy sites at the same biopsy time point on predictive performance of response to anti-PD1 therapy. Overall, we demonstrate that pathway-based signatures derived from on-treatment tumor specimens are highly predictive of response to anti-PD1 blockade therapies in patients with metastatic melanoma.

2021-08-15 | GSE168204 | GEO

miRNA expression between CD4+PD1+ and CD4+PD1- T cells

Project description:Recent success in cancer immunotherapy has come from the blockade of inhibitory receptors on T cells, such as programmed cell death-1, which can induce a state of T cell exhaustion upon constant antigen stimulation. Understanding miRNA regulation of PD1 can be useful to discover miRNAs for use in therapy or as prognostic markers in various diseases including cancer, autoimmunity and transplantation. We used microarrays to discover global miRNA expression changes upon PD1 upregulation and identified miRNAs that are both up- and down-regulated. B16F10 cells were injected subcutaneously into C57BL/6 mice and 16 days later CD4+PD1+ and CD4+PD1- were sorted from the lymph nodes and spleen for RNA extraction and hybridization on Affymetrix miRNA array.

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Eubacterium rectale improves the efficacy of anti-PD1 immunotherapy in melanoma via L-serine-mediated NK-cell activation

Project description:NK cells, as a type of key immune cell, play essential roles in tumor cell immune escape and immunotherapy. Accumulating evidence has demonstrated that the gut microbiota community affects the efficacy of anti-PD1 immunotherapy and that remodeling the gut microbiota structure is a promising strategy to enhance anti-PD1 immunotherapy responsiveness in advanced melanoma patients; however, the details of the mechanism remain elusive. In this study, we found that Eubacterium rectale (E. rectale) was significantly enriched in melanoma patients who responded to anti-PD1 immunotherapy and a high E. rectale abundance was related to longer survival in melanoma patients. Furthermore, administration of E. rectale remarkably improved the efficacy of anti-PD1 therapy and benefited the overall survival of tumor-bearing mice; moreover, application of E. rectale significantly recruited NK cells into the tumor microenvironment. Interestingly, conditioned medium isolated from an E. rectale culture system dramatically enhanced NK-cell function. Through GC-MS/ UHPLC-MS/MS-based metabolomic analysis, L-serine production was found to be significantly decreased in the E. rectale group; moreover, administration of an L-serine synthesis inhibitor dramatically increased NK-cell activation, which led to enhanced anti-PD1 immunotherapy effects. Mechanistically, supplementation with L-serine or application of the L-serine synthesis inhibitor affected NK-cell activation through Fos/Fosl. In summary, our findings reveal the role of bacteria-modulated serine metabolic signaling in NK-cell activation and provide a novel therapeutic strategy to improve the efficacy of anti-PD1 immunotherapy in melanoma.

2023-04-14 | GSE225920 | GEO

Single-cell characterization of anti-LAG3+anti-PD1 treatment in melanoma patients

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