Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA136693 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: Presence of pelvic lymph node metastases is the main prognostic factor in early stage cervical cancer patients, primarily treated with surgery. Aim of this study was to identify cellular tumor pathways associated with pelvic lymph node metastasis in early stage cervical cancer. Experimental Design: Gene expression profiles (Affymetrix U133 plus 2.0) of 20 patients with negative (N0) and 19 with positive lymph nodes (N+), were compared with gene sets that represent all 285 presently available pathway signatures. Validation immunostaining of tumors of 274 consecutive early stage cervical cancer patients was performed for representatives of the identified pathways. Results: Analysis of 285 pathways resulted in identification of five pathways (TGF-β, NFAT, ALK, BAD, and PAR1) that were dysregulated in the N0, and two pathways (β-catenin and Glycosphingolipid Biosynthesis Neo Lactoseries) in the N+ group. Class comparison analysis revealed that five of 149 genes that were most significantly differentially expressed between N0 and N+ tumors (P<0.001) were involved in β-catenin signaling (TCF4, CTNNAL1, CTNND1/p120, DKK3 and WNT5a). Immunohistochemical validation of two well-known cellular tumor pathways (TGF-β and β-catenin) confirmed that the TGF-β pathway (positivity of Smad4) was related to N0 (OR:0.20, 95%CI:0.06-0.66) and the β-catenin pathway (p120 positivity) to N+ (OR:1.79, 95%CI:1.05-3.05). Conclusions: Our study provides new, validated insights in the molecular mechanism of lymph node metastasis in cervical cancer. Pathway analysis of the microarray expression profile suggested that the TGF-β and p120-associated non-canonical β-catenin pathways are important in pelvic lymph node metastasis in early stage cervical cancer. For the microarray experiment, we selected fresh frozen primary cervical cancer tissue, containing at least 80% tumor cells, of patients with histologically confirmed N0 (n=20) and of patients with N+ (n=19). The N0 and N+ groups were matched for age, FIGO stage and histology (all squamous cell carcinoma).
2011-02-15 | E-GEOD-26511 | biostudies-arrayexpress
Project description:Purpose: Presence of pelvic lymph node metastases is the main prognostic factor in early stage cervical cancer patients, primarily treated with surgery. Aim of this study was to identify cellular tumor pathways associated with pelvic lymph node metastasis in early stage cervical cancer. Experimental Design: Gene expression profiles (Affymetrix U133 plus 2.0) of 20 patients with negative (N0) and 19 with positive lymph nodes (N+), were compared with gene sets that represent all 285 presently available pathway signatures. Validation immunostaining of tumors of 274 consecutive early stage cervical cancer patients was performed for representatives of the identified pathways. Results: Analysis of 285 pathways resulted in identification of five pathways (TGF-β, NFAT, ALK, BAD, and PAR1) that were dysregulated in the N0, and two pathways (β-catenin and Glycosphingolipid Biosynthesis Neo Lactoseries) in the N+ group. Class comparison analysis revealed that five of 149 genes that were most significantly differentially expressed between N0 and N+ tumors (P<0.001) were involved in β-catenin signaling (TCF4, CTNNAL1, CTNND1/p120, DKK3 and WNT5a). Immunohistochemical validation of two well-known cellular tumor pathways (TGF-β and β-catenin) confirmed that the TGF-β pathway (positivity of Smad4) was related to N0 (OR:0.20, 95%CI:0.06-0.66) and the β-catenin pathway (p120 positivity) to N+ (OR:1.79, 95%CI:1.05-3.05). Conclusions: Our study provides new, validated insights in the molecular mechanism of lymph node metastasis in cervical cancer. Pathway analysis of the microarray expression profile suggested that the TGF-β and p120-associated non-canonical β-catenin pathways are important in pelvic lymph node metastasis in early stage cervical cancer.
2011-02-15 | GSE26511 | GEO
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. Keywords: Disease stage analysis
2008-03-01 | GSE7410 | GEO
Project description:We report that NEK2 protein level is overexpressed and correlated with the tumor stage and lymph node metastasis in cervical cancer. Furthermore, we provided evidence that NEK2-depleted cervical cancer cells exhibit impaired oncogenesis and enhanced radiosensitivity. Using RNA sequencing, we identify Wnt1 as a key downstream effector of NEK2. Knockdown of NEK2 downregulates the mRNA and protein levels of Wnt1, thereby inhibiting the activation of the Wnt/β-catenin signaling pathway. More importantly, the observed consequences induced by NEK2 depletion in cervical cancer cells can be partially rescued by Wnt1 overexpression. Taken together, these results demonstrate that NEK2 activates the Wnt/β-catenin signaling pathway via Wnt1 to drive oncogenesis and radioresistance in cervical cancer, indicating that NEK2 may be a promising target for the radiosensitization of cervical cancer.
2021-04-30 | GSE148531 | GEO
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:To investigate the differences in miRNA profiles specially related to lymph node metastasis in cervical cancer, six primary cervical cancer tissues derived from stage І-ІІ patients with (n=3) or without (n=3) lymph node metastasis were collected. The differential expression of seven representative miRNAs (top seven miRNAs included: miR-135-5p, miR-221-3p, miR-25-3p, miR-96-5p, miR-182-5p, miR-183-5p, and miR-144-3p) was verified using qRT-PCR in the same tissues used for microarray analysis.
2017-08-24 | GSE102969 | GEO
Project description:Lymph node status is a crucial predictor for the overall survival of invasive breast cancer. However, lymph node involvement is only detected in about half of HER2 positive patients. Currently, there are no biomarkers available for distinguishing small size HER2-positive breast cancers with different lymph node statuses. Thus, in the present study, we applied label-free quantitative proteomic strategy to construct plasma proteomic profiles of ten patients with small size HER2-positive breast cancers (5 patients with lymph node metastasis versus 5 patients with lymph node metastasis).
2018-02-08 | PXD007217 | Pride
Project description:Malignant melanoma is characterized by frequent metastasis, however specific changes that regulate this process have not been clearly delineated. Although it is well known that Wnt signaling is frequently dysregulated in melanoma, the functional implications of this observation are unclear. By modulating beta-catenin levels in a mouse model of melanoma that is based on melanocyte-specific Pten loss and BrafV600E mutation, we demonstrate that beta-catenin is a central mediator of melanoma metastasis to lymph node and lung. In addition to altering metastasis, beta-catenin levels control tumor differentiation and regulate both MAPK/Erk and PI3K/Akt signaling. Highly metastatic tumors with beta-catenin stabilization are very similar to a subset of human melanomas; together these findings establish Wnt signaling as a metastasis regulator in melanoma.
2011-10-13 | GSE32907 | GEO
Project description:Malignant melanoma is characterized by frequent metastasis, however specific changes that regulate this process have not been clearly delineated. Although it is well known that Wnt signaling is frequently dysregulated in melanoma, the functional implications of this observation are unclear. By modulating beta-catenin levels in a mouse model of melanoma that is based on melanocyte-specific Pten loss and BrafV600E mutation, we demonstrate that beta-catenin is a central mediator of melanoma metastasis to lymph node and lung. In addition to altering metastasis, beta-catenin levels control tumor differentiation and regulate both MAPK/Erk and PI3K/Akt signaling. Highly metastatic tumors with beta-catenin stabilization are very similar to a subset of human melanomas; together these findings establish Wnt signaling as a metastasis regulator in melanoma. MoGene-1_0-st-v1: Four samples total. Two biological replicates of uncultured Pten/Braf murine melanomas and two biological replicates of uncultured Pten/Braf/Bcat-STA murine melanomas. MoEx-1_0-st-v1: Two samples total. Dissociated tumor and FACS-enriched Pten/Braf and Pten/Braf/Bcat-STA murine melanoma.
2011-10-12 | E-GEOD-32907 | biostudies-arrayexpress
Project description:Microarray was used to find out the differentially expressed in tumor sites of early-stage oral squamous cell carcinoma compared with Normal parts. Furthermore, we compared cases of early-stage oral squamous cell carcinoma with lymph node metastasis with cases without lymph node metastasis. The miRNAs obtained may not only serve as predictive biomarkers for lymph node metastasis, but may also be used further to understand disease.
2023-08-22 | GSE241289 | GEO