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Transcriptome Analysis of Tumor Associated High Endothelial Venules in Breast Cancer

ABSTRACT: Transcriptome Analysis of Tumor Associated High Endothelial Venules in Breast Cancer

PROVIDER: PRJNA806936 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18016623.fastq.gz	Fastqsanger.gz
	SRR18016624.fastq.gz	Fastqsanger.gz
	SRR18016625.fastq.gz	Fastqsanger.gz
	SRR18016626.fastq.gz	Fastqsanger.gz
	SRR18016627.fastq.gz	Fastqsanger.gz

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Transcriptome Analysis of Tumor Associated High Endothelial Venules in Breast Cancer

Project description:High endothelial venules (HEVs) are specialized post-capillary venules that recruit naïve lymphocytes to the lymph nodes and are essential for the development of adaptive immunity. HEVs can also develop in tumors. These specialized tumor vessels are thought to be important for recruiting naïve T cells and B cells into tumors and locally enhancing anti-tumor immunity by supporting the formation of tertiary lymphoid structures. By a comparative transcriptome analysis in human breast cancer, we investigated differentially expressed genes between tumor-associated HEVs and the rest of the tumor vasculature. Tumor vessels highly expressing HEV-upregulated genes, such as the homeobox gene MEOX2 and the tetraspanin gene TSPAN7, were associated with extensive infiltration of T and B lymphocytes and the occurrence of tertiary lymphoid structures, which is known to predict therapeutic responses to immune checkpoint inhibitors. Moreover, high transcript counts of these genes in clinical tumor specimens were associated with a significant survival benefit in advanced breast cancer. The molecular signature of HEVs identified here may be useful for guiding immunotherapies and provide a new direction for investigating tumor-associated HEVs and their clinical significance.

2022-03-31 | GSE196703 | GEO

Effect of recombinant IGLL5 treatment on gene expressing of high endothelial venules

Project description:High endothelial venules (HEVs) are key component in the formation of tertiary lymphatic structure. Our previous studies have shown that IGLL5+B cells adhere to and inhibit the functional phenotype of HEVs. In addition, we found that IGLL5 binds to the LTβR receptor on the membrane of HEVs.

2025-08-01 | GSE272276 | GEO

Lymphoma-induced regression of high endothelial venules impairs homeostatic lymphocyte trafficking

Project description:Lymphoma-induced regression of high endothelial venules impairs homeostatic lymphocyte trafficking

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Molecular Signature of Tumor-Associated High Endothelial Venules That Can Predict Breast Cancer Survival.

Project description:High endothelial venules (HEV) are specialized post-capillary venules that recruit naïve lymphocytes to lymph nodes. HEVs are essential for the development of adaptive immunity. HEVs can also develop in tumors where they are thought to be important for recruiting naïve T cells and B cells into the tumors and locally enhancing antitumor immunity by supporting the formation of tertiary lymphoid structures. Herein, we used comparative transcriptome analysis of human breast cancer to investigate genes differentially expressed between tumor-associated HEVs and the rest of the tumor vasculature. Tumor vessels highly expressing HEV-upregulated genes, such as the homeobox gene MEOX2 and the tetraspanin gene TSPAN7, were associated with extensive infiltration of T and B cells and the occurrence of tertiary lymphoid structures, which is known to predict therapeutic responses to immune-checkpoint inhibitors. Moreover, high transcript counts of these genes in clinical tumor specimens were associated with a significant survival benefit in advanced breast cancer. The molecular signature of HEVs identified herein may be useful for guiding immunotherapies and provides a new direction for investigating tumor-associated HEVs and their clinical significance. See related Spotlight by Gallimore, p. 371.

| S-EPMC8976767 | biostudies-literature

Interferon responsive high endothelial venules drive tumor tertiary lymphoid structure formation and predict response to anti-PD-1 immunotherapy in nasopharyngeal carcinoma

Project description:The outcome of immune checkpoint blockade (ICB) therapy largely hinges on the antitumor immune response of tertiary lymphoid structures (TLSs), but the driver factors behind tumor TLS formation remain poorly understood. Through integrated analysis of spatial and pan-cancer single-cell transcriptomics, we reveal the characteristics of TLSs in nasopharyngeal carcinoma (NPC) and identify a subset of interferon responsive high endothelial venules (IFN-HEVs) that is responsible for the emergence of tumor-specific chemokines, especially CXCL9. Functionally, IFN-HEVs facilitate the recruitment of CD4+ T cells into TLSs via the CXCL9-CXCR3 axis. IFN-HEV-related phenotypes are strongly correlated with positive prognostic outcomes and better responses to ICB therapy. Leveraging these phenotypes, we develop a pretreatment CXCL9-TLS Response-predictive scoring system (CTRscore) to forecast the efficacy of ICB therapy and validate its predictive efficiency in three independent NPC cohorts. Our study provides biological and functional insights into the IFN-HEVs in tumor TLSs, highlighting their potential role in the development of biomarkers and predictors for the success of ICB therapy.

2025-05-02 | GSE289272 | GEO

Effect of recombinant IGLL5 treatment on gene expressing of high endothelial venules

Project description:Effect of recombinant IGLL5 treatment on gene expressing of high endothelial venules

| PRJNA1136005 | ENA

Human Breast Tumor-associated Endothelial Cells Favor Interactions with Nanomedicines

Project description:Human Breast Tumor-associated Endothelial Cells Favor Interactions with Nanomedicines

| PRJNA1066841 | ENA

Lymphoma-induced regression of high endothelial venules impairs homeostatic lymphocyte trafficking

Project description:Lymphoma growth is facilitated by the well-balanced infrastructure of the microenvironment in lymph nodes (LN). LNs undergo rapid expansion during lymphoma progression, often accompanied by excessive blood vessel growth. Here we report that aggressive lymphoma cause severe high endothelial venule (HEV) regression which impairs lymphocyte recirculation. In this study, we used transferred (i.v.) Eµ-Myc tumor cells as a mouse model of aggressive lymphoma. Blood endothelial cells from tumor bearing and control LNs were isolated by FACS and processed for single-cell RNA sequencing. The results revealed a detrimental mechanisms causing HEV-dedifferentiation during lymphoma growth with potential implications on tumor-targeting immune surveillance and strategies of immune therapy in LNs

2021-10-14 | E-MTAB-10389 | biostudies-arrayexpress

Human Breast Tumor-associated Endothelial Cells Favor Interactions with Nanomedicines

Project description:Nanomedicines, designed to improve the effectiveness of cancer treatment, have not met anticipated outcomes owing to suboptimal delivery efficiency to tumors. While the enhanced permeability and retention (EPR) effect has been explored, recent research challenges the predominant passive accumulation theory. This study explores the mechanisms governing nanoparticle entry into tumors by comparing human breast tumor-associated endothelial cells (HBTECs) and healthy human mammary macrovascular endothelial cells (HMMECs). Our results demonstrate that HBTECs exhibit higher nanoparticle uptake, involving three major endocytic pathways. Gene expression analysis reveals the upregulation of transport-related genes, especially motor protein genes, in tumor-associated endothelial cells. These insights highlight the need for comprehensive investigations into nanoparticle transport mechanisms and associated factors within the tumor microenvironment, essential for advancing drug delivery and therapeutic outcomes.

2024-09-01 | GSE253737 | GEO

Single cell RNA-sequencing of Tumor-Associated High Endothelial Cells (TA-HECs) and comparison to their counterparts in homeostatic and inflamed mouse lymph nodes

Project description:High endothelial venules (HEVs) are specialized postcapillary venules that mediate lymphocyte trafficking from the blood into lymph nodes. HEV-like blood vessels are found in solid tumors in association with CD8+ T cell infiltration.This study uses single cell RNA-sequencing using the Fluidigm C1 system as a method to evaluate the transcriptome in lymph node and tumor-associated HEV endothelial cells (LN-HECs and TA-HECs). We isolated MECA-79+ TA-HECs and CD31+MECA-79- tumor-associated endothelial cells (TA-ECs) by cell sorting and we compared their transcriptome to those of their counterparts in homeostatic (LN-HECs and LN-ECs) or inflamed (iLN-HECs) lymph nodes. TA-HECs express high levels of endothelial cell markers Cdh5 and Pecam1 (CD31), post-capillary venule marker Ackr1 (DARC) and venous transcription factor Nr2f2, indicating that they correspond to post-capillary venule endothelium, like their lymph node counterparts. The genes encoding HEV sialomucins decorated by the sulfated MECA-79 epitope (CD34 and Emcn, endomucin) and the core 1 branching enzyme B3gnt3 that is essential for its biosynthesis, are equally expressed in all HEC populations, whereas sulfotransferases Chst2 and Chst4 are expressed at lower levels in TA-HECs. Although TA-HECs are molecularly distinct from lymph node HECs, they share several important characteristics with iLN-HECs, including the upregulation of endothelial selectins (Selp, Sele) and inflammatory chemokines CXCL9 and CXCL10, the ligands for chemokine receptor CXCR3 on effector T cells. Finally, endothelial cell adhesion molecules ICAM1, ICAM2 and VCAM1 that are important for lymphocyte sticking to HEVs, are expressed at similar levels in all HECs. Together, these findings indicated that MECA-79+ TA-HECs, similar to HECs in immune-stimulated lymph nodes, exhibit an inflamed phenotype characterized by co-expression of MECA-79+ antigens with endothelial selectins and inflammatory chemokines.

2021-12-14 | GSE154898 | GEO

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