Affymetrix SNP6.0 array data for isogenic melanoma cell lines
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE96708 | GEO | 2020/03/16
REPOSITORIES: GEO
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Project description:Here we report on a bulk culture termed MCM1, which was derived from a 61 year old male diagnosed with a nodular melanoma stage T2a, N0. At passage three of culturing, DNA was isolated and Affymetrix SNP6.0 array hybridizations were performed. Cultured MCM1 cells revealed overall identical copy number gains and losses as compared with the primary patient-derived lesion and were therefore used in this study.
2012-06-18 | GSE35991 | GEO
Project description:Here we report on a bulk culture termed MCM1, which was derived from a 61 year old male diagnosed with a nodular melanoma stage T2a, N0. At passage three of culturing, DNA was isolated and Affymetrix SNP6.0 array hybridizations were performed. Cultured MCM1 cells revealed overall identical copy number gains and losses as compared with the primary patient-derived lesion and were therefore used in this study. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA, which was extracted from a patient derived melanoma sample and from a cellline generated from the same melanoma sample at passage three.
2012-06-17 | E-GEOD-35991 | biostudies-arrayexpress
Project description:We aimed at identifying lymphangiogenic subpopulations by comparative analysis of single cell clones derived from a melanoma of a single patient. Selected clones were grafted into SCID mice, where they induced lymphangiogenesis and metastasized into sentinel nodes, whereas non-lymphangiogenic clones from the same patient did not metastasize. RNA isolated from primary SCID mouse tumors were used for transcriptome analysis. A total of 16 Samples were analysed, 4 per group. Parental pool MCM1(C), nonlymphangiogenic MCM1G(G), lymphangiogenic MCM1D(D1), lymphangiogenic and very metastatic MCM1DLN(D2).
2012-06-17 | E-GEOD-36035 | biostudies-arrayexpress
Project description:Cutaneous melanoma first metastasizes into sentinel lymph nodes that control the lymphatic drain from the area of the primary tumor. This observation is used clinically for melanoma patients with primary melanomas thicker than 1mm (tumor stage ≥T2a), for these patients sentinel lymph node biopsy has become an important and routinely performed diagnostic procedure. The importance of sentinel node analysis is reflected by a significant better prognosis of melanoma patients with tumor free sentinel nodes compared to patients with metastatic sentinel nodes. Although intensively studied, not much is known about mechanisms responsible for the development of melanoma metastasis.To analyze gene expression in mouse SLNs of M24met tumor bearing animals as compared to tumor free control animals, SLNs were taken at different time points and analyzed for the presence of human M24met to classify SLNs into control, negative, macro metastatic SLN. After categorized SLNs were subjected to microarray analysis.
2011-07-15 | GSE30688 | GEO
Project description:To determine differential expression of miRNA in classical Hodgkin lymphoma diseased nodes compared to non-malignant lymph nodes, we used agilent microarray release 16 and quantile normalisation using Genespring GX software to quantify and compare miRNA expression.. Total RNA was extracted from 8 non-malignant lymph node and 14 classical Hodgkin lymphoma diseased node (6 mixed cellularity and 8 nodular sclerosing) formalin-fixed paraffin-embedded tissue samples
2013-03-19 | E-GEOD-45264 | biostudies-arrayexpress
Project description:Cutaneous melanoma first metastasizes into sentinel lymph nodes that control the lymphatic drain from the area of the primary tumor. This observation is used clinically for melanoma patients with primary melanomas thicker than 1mm (tumor stage ≥T2a), for these patients sentinel lymph node biopsy has become an important and routinely performed diagnostic procedure. The importance of sentinel node analysis is reflected by a significant better prognosis of melanoma patients with tumor free sentinel nodes compared to patients with metastatic sentinel nodes. Although intensively studied, not much is known about mechanisms responsible for the development of melanoma metastasis.To analyze gene expression in mouse SLNs of M24met tumor bearing animals as compared to tumor free control animals, SLNs were taken at different time points and analyzed for the presence of human M24met to classify SLNs into control, negative, macro metastatic SLN. After categorized SLNs were subjected to microarray analysis. To analyze gene expression in mouse SLNs of human M24met tumor bearing animals as compared to tumor free control animals, SLNs were taken at different time points and analyzed for the presence of human M24met to classify SLNs into control, negative, macro metastatic SLN. Briefly, explanted SLNs were stored in RNA later (Ambion, Austin, TX) and DNA as well as RNA was extracted using AllPrep DNA/RNA Mini Kit and RNeasy Micro Kit (Qiagen, Valencia, CA) according to manufacturer’s instructions. To detect human cells in mouse SLNs we used a polymerase chain reaction method for the detection of a human-specific 850-bp fragment of the alpha-satellite DNA on human chromosome 17. For analysis of gene expression RNA from control SLN from tumor free animals (control), RNA from tumor negative SLN (negative), and RNA from macro metastatic SLN (positive) from tumor bearing animals was used to analyze gene expression on Mouse Genome 430A 2.0 Arrays (Affymetrix, Santa Clara, CA)
2011-07-14 | E-GEOD-30688 | biostudies-arrayexpress
Project description:Using gene expression microarrays, we tested whether lung SCCs that have metastasised to loco-regional lymph nodes (N1/2m) are different to those that directly invade and involve local nodes (N1d). Using 22,323 element microarrays, a non-parametric test identified 126 genes/transcripts that discriminated between N0 (n=35) and N1/2m (n=16) tumours (Wilcoxon-Mann-Whitney U test, P<0.01). Hiearchical clustering of all 59 tumours (including 8 N1d tumours) demonstrated the N1d tumours clustered with the N0 tumours rather than the N1/2m tumours. Next, we built class prediction models from the 35 N0 tumours and 16 N1/2m tumours to predict the class of N1d tumours. All models consistently classified N1d tumours as similar to N0 tumours. This could explain some of the variable response of some N1 tumours to adjuvant chemotherapy, and suggest refinement of the TNM "N" stage nomenclature to adjust for this biological observation to ensure appropriate patients benefit from treatment. Keywords: non-small cell lung carcinoma, squamous cell, nodal metastasis, TNM staging, expression profiling
2007-05-01 | GSE5828 | GEO
Project description:Evolution of melanoma from a primary tumor to widespread metastasis is crucially dependent on lymphatic spread. The mechanisms regulating the initial step in metastatic dissemination via regional lymph nodes remain largely unknown. We have previously described a dysfunctional immune profile that precedes evidence of metastasis in the first node draining from the primary tumor, the sentinel lymph node (SLN). Herein, we explore the role of melanoma-derived extracellular vesicles (EVs) as mediators of this pre-metastatic niche through cargo-specific polarization of dendritic cells (DCs). Utilizing mass cytometry, pre-metastatic SLNs demonstrate compromised co-stimulatory CD80 expression compared to healthy lymph nodes. Similarly, DCs matured in vitro in the presence of melanoma EVs showed impaired co-stimulation and polarization towards a chronic inflammatory cytokine milieu. Profiling of melanoma EV cargo identified shared proteomic and RNA signatures including the signaling axis S100A8, S100A9 and cognate receptor TLR4. Mechanistically, S100A8 and S100A9 compromised DC maturation, a phenotype which was partially recovered following TLR4 blockade. Early evidence demonstrates similar EVs can be isolated from human afferent lymphatic fluid ex vivo. Taken together, we propose synergistic interactions among melanoma EV cargo are responsible for suppressing DC maturation, potentially explaining the survival of malignant melanocytes metastasizing into seemingly “normal” regional lymph nodes.
2018-10-26 | PXD005539 | Pride
Project description:Using gene expression microarrays, we tested whether lung SCCs that have metastasised to loco-regional lymph nodes (N1/2m) are different to those that directly invade and involve local nodes (N1d). Using 22,323 element microarrays, a non-parametric test identified 126 genes/transcripts that discriminated between N0 (n=35) and N1/2m (n=16) tumours (Wilcoxon-Mann-Whitney U test, P<0.01). Hiearchical clustering of all 59 tumours (including 8 N1d tumours) demonstrated the N1d tumours clustered with the N0 tumours rather than the N1/2m tumours. Next, we built class prediction models from the 35 N0 tumours and 16 N1/2m tumours to predict the class of N1d tumours. All models consistently classified N1d tumours as similar to N0 tumours. This could explain some of the variable response of some N1 tumours to adjuvant chemotherapy, and suggest refinement of the TNM "N" stage nomenclature to adjust for this biological observation to ensure appropriate patients benefit from treatment. Keywords: non-small cell lung carcinoma, squamous cell, nodal metastasis, TNM staging, expression profiling Expression profiling using 22K element microarrays of 59 primary lung squamous cell carcinomas.
2007-05-01 | E-GEOD-5828 | 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. 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