Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA316575 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression profiling of early stage cervical cancer tumours with and without lymph node metastasis, in order to predict lymph node metastasis before treatment. Subsequently, comparing gene expression profiles between healthy cervical tissue and early stage cervical cancer tissue. Experiment Overall Design: All patients had clinical FIGO stage IB-IIA cervical cancer, the low-risk group (N) included 19 patients without unfavourable prognostic factors (positive lymph nodes, parametrial invasion, positive margins or a combination of unfavourable prognostic factors); the high risk group (P) consisted of 16 patients with lymph node metastasis, who were treated with adjuvant radiation therapy with or without chemotherapy. Healthy cervical tissue biopsies (H) were collected from 5 non-cervical carcinoma patients who underwent hysterectomy for benign reasons. RNA pooled from all tumour tissue samples was used as reference sample. Log-ratios of five technical replicates were used for normalization.
2008-04-05 | E-GEOD-7410 | biostudies-arrayexpress
Project description:Background: Cervical lymph node metastasis is a potent prognostic factor in oral squamous cell carcinoma (OSCC). However, lymph nodes resected by sentinel node biopsy or neck dissection are usually diagnosed by examining only one or two sections of the maximal cut surface. Accurate diagnosis of the metastasis in lymph nodes is important but depends on a heavy workload of the pathologist. In this study, we have attempted to identify novel molecular markers to find the harboring cancer cells in the lymph node and establish rapid detection method. Methods: We determined the gene expression profiles of 7 metastatic lymph nodes from patients with OSCC and 1 normal lymph node and 5 salivary glands from non-cancerous patients by microarray analysis. We found the overexpression genes in all metastatic lymph nodes. Subsequently, we examined the expression of these genes in newly 23 metastatic lymph nodes and 9 normal lymph nodes by real-time quantitative RT-PCR (qRT-PCR) assay. Moreover, the rapid detection of lymph node metastasis by these genes was examined using the reverse transcription loop-mediated isothermal amplification (RT-LAMP) method. Result: Among the 4 genes identified by microarray analysis, annexin A8 (ANXA8) and desmoglein 3 (DSG3) were detected in all metastatic lymph nodes at a much higher level but not in normal lymph nodes at all by qRT-PCR. Furthermore, RT-LAMP method targeting ANXA8 rapidly detected almost lymph nodes with metastasis. Conclusions: ANXA8 could be a useful marker for detecting lymph node metastasis in OSCC. Using AB1700 system, we determined the gene expression profiles of lymph nodes with metastasis of OSCC. Normal lymph node and salivary gland tissues were used as control samples.
2015-12-21 | E-GEOD-70604 | biostudies-arrayexpress
Project description:Secreted extracellular vesicles are known to influence the tumor microenvironment and promote metastasis. In this work, we have analyzed the involvement of extracellular vesicles in the establishment of lymph node pre-metastatic niches by melanoma cells. We found that small extracellular vesicles (sEVs) derived from highly metastatic melanoma cell lines spread broadly through the lymphatic system and were taken up by lymphatic endothelial cells, reinforcing lymph node metastasis. Melanoma-derived sEVs induce lymphangiogenesis, a hallmark of pre-metastatic niche formation, in vitro and in lymphoreporter mice in vivo. We found that neural growth factor receptor (NGFR) is secreted in melanoma-derived small extracellular vesicles and shuttled to lymphatic endothelial cells, inducing lymphangiogenesis and tumor cell adhesion through the activation of ERK and NF-B pathways and ICAM1 expression. Importantly, ablation or inhibition of NGFR in sEVs reversed the lymphangiogenic phenotype, decreased melanoma lymph node metastasis and extended the survival. Importantly, analysis of NGFR expression in lymph node metastases and matched primary tumors shows that levels of MITF+NGFR+ lymph node metastatic cells are correlated with disease outcome. Our data support the idea that NGFR secreted in sEVs favors lymph node pre-metastatic niche formation and lymph node metastasis in melanoma
2021-08-05 | PXD024852 | Pride
Project description:Secreted extracellular vesicles are known to influence the tumor microenvironment and promote metastasis. In this work, we have analyzed the involvement of extracellular vesicles in establishing the lymph node pre-metastatic niche by melanoma cells. We found that small extracellular vesicles (sEVs) derived from highly metastatic melanoma cell lines spread broadly through the lymphatic system and are taken up by lymphatic endothelial cells reinforcing lymph node metastasis. Melanoma-derived sEVs induce lymphangiogenesis, a hallmark of pre-metastatic niche formation, in vitro and in lymphoreporter mice in vivo. Analysis of involved factors demonstrated that the neural growth factor receptor (NGFR) is secreted in melanoma-derived small extracellular vesicles and shuttled to lymphatic endothelial cells inducing lymphangiogenesis and tumor cell adhesion through the activation of ERK and NF-B pathways and ICAM1 expression. Importantly, ablation or inhibition of NGFR in sEVs reversed the lymphangiogenic phenotype, decreased melanoma lymph node metastasis and extended mice survival. Importantly, analysis of NGFR expression in lymph node metastases and matched primary tumors shows that levels of MITF+NGFR+ lymph node metastatic cells are correlated with disease outcome. Our data support that NGFR is secreted in sEVs favoring lymph node pre-metastatic niche formation and lymph node metastasis in melanoma.
2021-07-16 | PXD024108 | Pride
Project description:N4-acetylcytidine (ac4C) is a posttransciptional RNA modification regulating in various important bioprocess. However, the role in human cancer, especially lymph node metastasis, remains largely unknown. Here, we showed NAT10, as the only “writer” of ac4C mRNA modification, was highly expressed in HNSCC patients with lymph node metastasis. High NAT10 levels in lymph node of HNSCC patients predicted poor overall survival. Moreover, we found the high expression of NAT10 was positively upregulated by NRF1 transcription factor. Gain and loss-of-function displayed that NAT10 promoted cell metastasis in mice. Mechanistically, NAT10 induced ac4C modification of GLMP and stabilized its mRNA, which triggered the activation of MAPK/ERK signaling pathway. Lastly, the NAT10’s specific inhibitor Remodelin could inhibit HNSCC tumorigenesis via 4-NQO-induced murine tumor model and remodel the tumor microenvironment, including angiogenesis, CD8+ T cell and Treg recruitment. These results demonstrated that NAT10 promoted lymph node metastasis of HNSCC via ac4C-dependent stabilization of GLMP transcript, providing a potential epitranscriptomic-targeted therapeutic strategy for HNSCC.
2023-08-08 | GSE239900 | GEO
Project description:Background: Cervical lymph node metastasis is a potent prognostic factor in oral squamous cell carcinoma (OSCC). However, lymph nodes resected by sentinel node biopsy or neck dissection are usually diagnosed by examining only one or two sections of the maximal cut surface. Accurate diagnosis of the metastasis in lymph nodes is important but depends on a heavy workload of the pathologist. In this study, we have attempted to identify novel molecular markers to find the harboring cancer cells in the lymph node and establish rapid detection method. Methods: We determined the gene expression profiles of 7 metastatic lymph nodes from patients with OSCC and 1 normal lymph node and 5 salivary glands from non-cancerous patients by microarray analysis. We found the overexpression genes in all metastatic lymph nodes. Subsequently, we examined the expression of these genes in newly 23 metastatic lymph nodes and 9 normal lymph nodes by real-time quantitative RT-PCR (qRT-PCR) assay. Moreover, the rapid detection of lymph node metastasis by these genes was examined using the reverse transcription loop-mediated isothermal amplification (RT-LAMP) method. Result: Among the 4 genes identified by microarray analysis, annexin A8 (ANXA8) and desmoglein 3 (DSG3) were detected in all metastatic lymph nodes at a much higher level but not in normal lymph nodes at all by qRT-PCR. Furthermore, RT-LAMP method targeting ANXA8 rapidly detected almost lymph nodes with metastasis. Conclusions: ANXA8 could be a useful marker for detecting lymph node metastasis in OSCC.
2015-12-21 | GSE70604 | GEO
Project description:Purpose: Lymph node invasion is a hallmark of breast cancer disease progression, but current treatment strategies lack guidance from lymph node biomarkers. We investigated JAGGED1 (JAG1) as a promoter of lymph node metastasis and a prognostic biomarker in metastatic lymph node specimens. Experimental Design: We used mouse models to assess the role of JAG1 expression in human and mouse breast cancer cells on lymphovascular invasion, lymph node metastatic potential, transcriptional profiles, and tumor interactions with lymphatic endothelium. We examined breast and lymph node samples from 284 breast cancer patients to determine the correlative and prognostic value of tumoral JAG1 expression in the lymph node. Results: In matched human breast tumor and lymph node samples, tumor cells that invaded lymph nodes showed higher JAG1 expression than their associated primary tumors (P value < 0.0001). In multiple models, breast cancer cells with high JAG1 expression showed increased lymphovascular invasion, lymph node metastasis, lymph node metastatic outgrowth, and migration through lymphatic endothelium. Transcriptomic analysis indicated that tumoral JAG1 regulates both juxtacrine and paracrine signaling pathways that induce inflammatory and pro-metastatic genes in lymphatic endothelium. When examining patients with identical surgical treatments, patients with lymph node JAG1 H-scorelow showed increased 5-year recurrence free survival rates than patients with lymph node JAG1 H-scorehi (87% vs 70%, P=0.016). Conclusions: JAG1 expression promotes lymphovascular invasion and lymph node metastasis in murine models. In patients, high expression of JAG1 in tumor cells in lymph node metastases predicts reduced recurrence free survival.
2026-07-27 | GSE252950 | GEO
Project description:Purpose: Lymph node invasion is a hallmark of breast cancer disease progression, but current treatment strategies lack guidance from lymph node biomarkers. We investigated JAGGED1 (JAG1) as a promoter of lymph node metastasis and a prognostic biomarker in metastatic lymph node specimens. Experimental Design: We used mouse models to assess the role of JAG1 expression in human and mouse breast cancer cells on lymphovascular invasion, lymph node metastatic potential, transcriptional profiles, and tumor interactions with lymphatic endothelium. We examined breast and lymph node samples from 284 breast cancer patients to determine the correlative and prognostic value of tumoral JAG1 expression in the lymph node. Results: In matched human breast tumor and lymph node samples, tumor cells that invaded lymph nodes showed higher JAG1 expression than their associated primary tumors (P value < 0.0001). In multiple models, breast cancer cells with high JAG1 expression showed increased lymphovascular invasion, lymph node metastasis, lymph node metastatic outgrowth, and migration through lymphatic endothelium. Transcriptomic analysis indicated that tumoral JAG1 regulates both juxtacrine and paracrine signaling pathways that induce inflammatory and pro-metastatic genes in lymphatic endothelium. When examining patients with identical surgical treatments, patients with lymph node JAG1 H-scorelow showed increased 5-year recurrence free survival rates than patients with lymph node JAG1 H-scorehi (87% vs 70%, P=0.016). Conclusions: JAG1 expression promotes lymphovascular invasion and lymph node metastasis in murine models. In patients, high expression of JAG1 in tumor cells in lymph node metastases predicts reduced recurrence free survival.
2026-07-27 | GSE253035 | GEO
Project description:Purpose: Lymph node invasion is a hallmark of breast cancer disease progression, but current treatment strategies lack guidance from lymph node biomarkers. We investigated JAGGED1 (JAG1) as a promoter of lymph node metastasis and a prognostic biomarker in metastatic lymph node specimens. Experimental Design: We used mouse models to assess the role of JAG1 expression in human and mouse breast cancer cells on lymphovascular invasion, lymph node metastatic potential, transcriptional profiles, and tumor interactions with lymphatic endothelium. We examined breast and lymph node samples from 284 breast cancer patients to determine the correlative and prognostic value of tumoral JAG1 expression in the lymph node. Results: In matched human breast tumor and lymph node samples, tumor cells that invaded lymph nodes showed higher JAG1 expression than their associated primary tumors (P value < 0.0001). In multiple models, breast cancer cells with high JAG1 expression showed increased lymphovascular invasion, lymph node metastasis, lymph node metastatic outgrowth, and migration through lymphatic endothelium. Transcriptomic analysis indicated that tumoral JAG1 regulates both juxtacrine and paracrine signaling pathways that induce inflammatory and pro-metastatic genes in lymphatic endothelium. When examining patients with identical surgical treatments, patients with lymph node JAG1 H-scorelow showed increased 5-year recurrence free survival rates than patients with lymph node JAG1 H-scorehi (87% vs 70%, P=0.016). Conclusions: JAG1 expression promotes lymphovascular invasion and lymph node metastasis in murine models. In patients, high expression of JAG1 in tumor cells in lymph node metastases predicts reduced recurrence free survival.
2026-07-27 | GSE252953 | GEO
Project description:Purpose: Lymph node invasion is a hallmark of breast cancer disease progression, but current treatment strategies lack guidance from lymph node biomarkers. We investigated JAGGED1 (JAG1) as a promoter of lymph node metastasis and a prognostic biomarker in metastatic lymph node specimens. Experimental Design: We used mouse models to assess the role of JAG1 expression in human and mouse breast cancer cells on lymphovascular invasion, lymph node metastatic potential, transcriptional profiles, and tumor interactions with lymphatic endothelium. We examined breast and lymph node samples from 284 breast cancer patients to determine the correlative and prognostic value of tumoral JAG1 expression in the lymph node. Results: In matched human breast tumor and lymph node samples, tumor cells that invaded lymph nodes showed higher JAG1 expression than their associated primary tumors (P value < 0.0001). In multiple models, breast cancer cells with high JAG1 expression showed increased lymphovascular invasion, lymph node metastasis, lymph node metastatic outgrowth, and migration through lymphatic endothelium. Transcriptomic analysis indicated that tumoral JAG1 regulates both juxtacrine and paracrine signaling pathways that induce inflammatory and pro-metastatic genes in lymphatic endothelium. When examining patients with identical surgical treatments, patients with lymph node JAG1 H-scorelow showed increased 5-year recurrence free survival rates than patients with lymph node JAG1 H-scorehi (87% vs 70%, P=0.016). Conclusions: JAG1 expression promotes lymphovascular invasion and lymph node metastasis in murine models. In patients, high expression of JAG1 in tumor cells in lymph node metastases predicts reduced recurrence free survival.
2026-07-27 | GSE252952 | GEO