Badb2f81-2fc7-43fc-924e-9f9eddc9c8e6 - samples
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ABSTRACT:
PROVIDER: EGAD00001010840 | EGA |
REPOSITORIES: EGA
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Project description:This is a multicentre long-term non-interventional study of adult subjects diagnosed with unresectable or metastatic, progressive, well differentiated (G1 and G2), somatostatin receptor positive GEP-NETs who have been prescribed Lutathera in standard clinical practice.
| 2365307 | ecrin-mdr-crc
Project description:Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are rare and heterogeneous tumors presenting a wide spectrum of different clinical and biological characteristics. In these tumors, the histological evaluation is a crucial element of clinical management. Currently, tumor grading, determined by Ki-67 staining and mitotic counts, is the most reliable predictor of prognosis. This scoring method is time-consuming and a high reproducibility cannot be achieved. Novel approaches are needed to support histological evaluation and prognosis. In this study, starting from a microarray analysis, we defined the miRNAs signature for poorly differentiated NETs (G3) compared to well differentiated NETs (G1 and G2) consisting of 56 deregulated miRNAs. Moreover, we identified 8 miRNAs that were expressed in all GEP-NETs grades but at different level. Among these miRNAs, we found miR-96-5p that raised its expression levels from grade 1 to grade 3; inversely, its target FOXO1 was decrease from grade 1 to grade 3. Our results reveal that the miRNAs expression profile of GEP-NET correlates their expression with grading showing a potential advantage of miRNA quantification to aid clinicians in the classification of common GEP-NETs subtypes.
2020-08-04 | GSE135034 | GEO
Project description:Tumors of advanced gastric cancer patients were biopsied and subjected to gene expression profiling using the Affymetrix Human Genome U133 Plus 2.0 Arrays. Patients were then segregated into G1, G2 or G3 groups based on their tumor genomic profiles. Patients in the G1 and G3 cohorts were assigned SOX (oxaliplatin plus S-1) chemotherapy whereas those in the G2 cohort were given SP (cisplatin plus S-1) regimen. This bench-to-bedside effort indicated the feasibility of using molecular profiling to tailor treatment for advanced gastric cancer.
2018-07-31 | GSE100935 | GEO
Project description:The project aimed to determine proteomics changes in Bladder cancer (BCa) tissue from early to more advanced stages of the disease and identify the proteins associated with the progression. The samples used in this study were fresh frozen BCa tissues from patients collected immediately after surgery, with histopathologicaly confirmed disease. Samples were grouped according to the histopathological report in 3 groups: 1) Group 1 (pTa, G1), 2) Group 2 (T1, G2-G3) and 3) Group 3 (pT2-T3, G3). Patients were aged 28–82 years with no significant differences among groups regarding age: Median age (Group 1 (pTa, G1)) =62; Median age (Group 2 (T1, G2-G3)) =58 and Median age (Group 3 (pT2-T3, G3)) =73.5. Each group had 6 samples or 18 samples in total were used for the comparative proteomics analysis by label-free data-independent LC-MS/MS.
2023-10-22 | PXD044432 | Pride
Project description:Interventions: This is a three-arm, single-blind, randomized controlled clinical trial. Patients (n = 36) will be randomly distributed into three blocks (G1,G2,G3). Patients will be randomly assigned to three blocks (G1,G2,G3) in a 1:1 ratio to receive probiotics (G1 group) with formulation: Lactobacillus acidophilus NCFM, Lactobacillus paracasei Lpc-37 TM, Bifidobacterium lactis Bi-04TM, Bifidobacterium lactis Bi-07TM, Bifidobacterium bifidum Bb-02TM), associated with a standard nutritional guidance protocol. In the G2 (control) group, conventional treatment will be performed with a standard nutritional guidance protocol, without the use of probiotics. The intervention product (probiotic capsules) will be distributed and packaged according to the days of the research and inpatient ward, which will not be disclosed during the entire period of the research, the tests will be carried out on alternate days as detailed in the recruitment, in order not to cross-referencing of information between previously blinded participants. In the case of the G3 group, they will receive the probiotic capsules at the same time as the G1 group. Both groups that will use probiotic capsules should continue using them for 7 days, without any break in follow-up. The groups will be monitored twice a day in person or by telephone, in order to avoid loss of capsule intake.;G07.203.300.456.500
Primary outcome(s): To evaluate the use of perioperative probiotics to improve the nutritional and immunological clinical status of patients undergoing gastrectomy for gastric cancer
| 2756417 | ecrin-mdr-crc
Project description:Neuroblastoma (NB) is an aggressive tumor that affects both infants and children. The disease outcome is greatly influenced by age of patient, stage, chromosome copy number aberrations (CNAs) and gene expression abnormalities. We analyzed, by microarray technology, genome and transcriptome of 3 groups of tumors of patients with metastatic disease: G1, stage 4S and MYCN single copy; G2, stage 4 younger than 18 months of age, MYCN single copy with no disease progression and G3, stage 4, older than 19 months, with unfavorable outcome. We found an accumulation of structural copy number aberrations (CNAs) in G3 whereas G1 tumors had mostly numerical (N) CNAs and G2 showed an intermediate behavior. Pair wise comparisons demonstrated that the average of N CNAs significantly decreased from G1 to G2 to G3 (9.6 G1 < 7.2 G2 < 3.6 G3); in contrast S CNAs significantly increased in G3 (0.7 G1 < 3.7 G2 < 7.0 G3). Interestingly, we observed several intra-chromosomal rearrangements in G3 tumors on chromosomes not usually involved in NB. Excluding MYCN amplified tumors by G3 we found a high frequency of S CNAs in this group. Gene expression analysis showed a deregulation of downstream genes of Ras and Rho signaling pathway among the 3 groups. It has been also observed a progressive switch off of development and adhesion genes and a switch on of cell cycle genes from G1 to G2 to G3. Moreover, the telemorase genes were significantly expressed in G3 with respect to remaining groups. Present data show an accumulation of S CNAs from stage 4S to 4. The deregulation of genes Rho/Ras pathway may explain the increase of tumor aggressiveness from G1 to G2 to G3. The increase of cell cycle and telomerase genes expression associated with G3 would provide unlimited replicative potential for these tumors and may be responsible for accumulation of S CNAs. Finally, we can argue that accumulation of structural aberrations and gene deregulation is age-dependent and it is associated with a more aggressive tumor phenotype.
2012-01-01 | GSE25771 | GEO
Project description:Neuroblastoma (NB) is an aggressive tumor that affects both infants and children. The disease outcome is greatly influenced by age of patient, stage, chromosome copy number aberrations (CNAs) and gene expression abnormalities. We analyzed, by microarray technology, genome and transcriptome of 3 groups of tumors of patients with metastatic disease: G1, stage 4S and MYCN single copy; G2, stage 4 younger than 18 months of age, MYCN single copy with no disease progression and G3, stage 4, older than 19 months, with unfavorable outcome. We found an accumulation of structural copy number aberrations (CNAs) in G3 whereas G1 tumors had mostly numerical (N) CNAs and G2 showed an intermediate behavior. Pair wise comparisons demonstrated that the average of N CNAs significantly decreased from G1 to G2 to G3 (9.6 G1 < 7.2 G2 < 3.6 G3); in contrast S CNAs significantly increased in G3 (0.7 G1 < 3.7 G2 < 7.0 G3). Interestingly, we observed several intra-chromosomal rearrangements in G3 tumors on chromosomes not usually involved in NB. Excluding MYCN amplified tumors by G3 we found a high frequency of S CNAs in this group. Gene expression analysis showed a deregulation of downstream genes of Ras and Rho signaling pathway among the 3 groups. It has been also observed a progressive switch off of development and adhesion genes and a switch on of cell cycle genes from G1 to G2 to G3. Moreover, the telemorase genes were significantly expressed in G3 with respect to remaining groups. Present data show an accumulation of S CNAs from stage 4S to 4. The deregulation of genes Rho/Ras pathway may explain the increase of tumor aggressiveness from G1 to G2 to G3. The increase of cell cycle and telomerase genes expression associated with G3 would provide unlimited replicative potential for these tumors and may be responsible for accumulation of S CNAs. Finally, we can argue that accumulation of structural aberrations and gene deregulation is age-dependent and it is associated with a more aggressive tumor phenotype. We analyzed 133 samples of metastatic neuroblastoma from patients divided into three groups: G1 49 patients stage 4S and MYCN single copy; G2 37 patients stage 4 younger than 18 months of age at diagnosis, MYCN single copy with no disease progression; G3 47 patients stage 4 older than 19 months of age at diagnosis, with unfavorable outcome.
2012-01-01 | E-GEOD-25771 | biostudies-arrayexpress
Project description:Histological grading of breast cancer defines morphological subtypes informative of metastatic potential, although not without considerable inter-observer disagreement and clinical heterogeneity particularly among the moderately differentiated grade II (G2) tumors. We posited that a gene expression signature capable of discerning tumors of grade I (G1) and grade III (G3) histology might provide a more objective measure of grade with prognostic benefit for patients with moderately differentiated disease. To this end, we studied the expression profiles of 347 primary invasive breast tumors analyzed on Affymetrix microarrays. Using class prediction algorithms, we identified 264 robust grade-associated markers, six of which could accurately classify G1 and G3 tumors, and separate G2 tumors into two highly discriminant classes (termed G2a and G2b genetic grades) with patient survival outcomes highly similar to those with G1 and G3 histology, respectively. Statistical analysis of conventional clinical variables further distinguished G2a and G2b subtypes from each other, but also from histologic G1 and G3 tumors. In multivariate analyses, genetic grade was consistently found to be an independent prognostic indicator of disease recurrence comparable to that of lymph node status and tumor size. When incorporated into the Nottingham Prognostic Index, genetic grade enhanced detection of patients with less harmful tumors, likely to benefit little from adjuvant therapy. Our findings show that a genetic grade signature can improve prognosis and therapeutic planning for breast cancer patients, and support the view that low and high grade disease, as defined genetically, reflect independent pathobiological entities rather than a continuum of cancer progression. Three separate breast cancer cohorts were analyzed: 1) Uppsala (n=249), 2) Stockholm (n=58), 3) Singapore (n=40). The Uppsala and Singapore data can be accessed here. The Stockholm cohort data can be accessed at GEO Series GSE1456. Experiment Overall Design: All tumor specimens were assessed on U133 A and B arrays.
2008-06-15 | E-GEOD-4922 | biostudies-arrayexpress
Project description:Histological grading of breast cancer defines morphological subtypes informative of metastatic potential, although not without considerable inter-observer disagreement and clinical heterogeneity particularly among the moderately differentiated grade II (G2) tumors. We posited that a gene expression signature capable of discerning tumors of grade I (G1) and grade III (G3) histology might provide a more objective measure of grade with prognostic benefit for patients with moderately differentiated disease. To this end, we studied the expression profiles of 347 primary invasive breast tumors analyzed on Affymetrix microarrays. Using class prediction algorithms, we identified 264 robust grade-associated markers, six of which could accurately classify G1 and G3 tumors, and separate G2 tumors into two highly discriminant classes (termed G2a and G2b genetic grades) with patient survival outcomes highly similar to those with G1 and G3 histology, respectively. Statistical analysis of conventional clinical variables further distinguished G2a and G2b subtypes from each other, but also from histologic G1 and G3 tumors. In multivariate analyses, genetic grade was consistently found to be an independent prognostic indicator of disease recurrence comparable to that of lymph node status and tumor size. When incorporated into the Nottingham Prognostic Index, genetic grade enhanced detection of patients with less harmful tumors, likely to benefit little from adjuvant therapy. Our findings show that a genetic grade signature can improve prognosis and therapeutic planning for breast cancer patients, and support the view that low and high grade disease, as defined genetically, reflect independent pathobiological entities rather than a continuum of cancer progression. Three separate breast cancer cohorts were analyzed: 1) Uppsala (n=249), 2) Stockholm (n=58), 3) Singapore (n=40). The Uppsala and Singapore data can be accessed here. The Stockholm cohort data can be accessed at GEO Series GSE1456. Keywords: Tumor sample comparisons
2006-05-31 | GSE4922 | GEO
Project description:Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are rare and highly heterogeneous neoplasms whose incidence has
markedly increased over the last decades. A grading system based on the tumor cells' proliferation index predicts high-risk for G3
NETs. However, low-to-intermediate grade (G1/G2) NETs have an unpredictable clinical course that varies from indolent to highly
malignant. Cultures of human cancer cells enable to perform functional perturbation analyses that are instrumental to enhance our
understanding of cancer biology. To date, no tractable and reliable long-term culture of G1/G2 NET has been reported to permit
disease modeling and pharmacological screens. Here, we report of the first long-term culture of a G2 metastatic small intestinal
NET that preserves the main genetic drivers of the tumor and retains expression patterns of the endocrine cell lineage.
Replicating the tissue, this long-term culture showed a low proliferation index, and yet it could be propagated continuously
without dramatic changes in the karyotype. The model was readily available for pharmacological screens using targeted agents
and as expected, showed low tumorigenic capacity in vivo. Overall, this is the first long-term culture of NETs to faithfully
recapitulate many aspects of the original neuroendocrine tumor.
| EGAS00001007108 | EGA