The pattern of genomic instability during bladder cancer progression (part 1)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE50666 | GEO | 2014/07/01
SECONDARY ACCESSION(S): PRJNA218315
REPOSITORIES: GEO
Similar Datasets
Project description:The Illumina SNP bead arrays were done for two metachronous tumors and the blood from a given patient. It was used to define copy number abnormalities in order to support subclonal population analysis in this patient. Three samples were analysed concerning two metachronous tumor samples and a blood sample from the same patient.
2014-07-01 | E-GEOD-50666 | biostudies-arrayexpress
Project description:The Affymetrix SNP6.0 arrays were done for two metachronous tumors and the blood from three patients. It was used to define copy number abnormalities in order to support subclonal population analysis in this patient. Nine samples were analysed concerning two metachronous tumor samples and a blood sample from the three different patients.
2014-07-01 | E-GEOD-50667 | biostudies-arrayexpress
Project description:The Affymetrix SNP6.0 arrays were done for two metachronous tumors and the blood from three patients. It was used to define copy number abnormalities in order to support subclonal population analysis in this patient.
2014-07-01 | GSE50667 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2014-07-01 | E-GEOD-50668 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2014-07-01 | GSE50668 | GEO
Project description:Colorectal cancer (CRC) patients suffer from the second highest mortality among all cancer entities. In half of all CRC patients, colorectal cancer liver metastases (CRLM) can be observed. Metastatic colorectal cancer is associated with poor overall survival and limited treatment options. Even after successful surgical resection of the primary tumor, metachronous liver metastases occur in one out of eight cases. The only available curative intended treatment is hepatic resection, but metachronous CRLM frequently recur after approximately one year. In this study, we performed a proteome analysis of three recurrent liver metastases of a single CRC patient by mass spectrometry. Despite surgical resection of the primary CRC and adjuvant chemotherapy plus cetuximab treatment, the patient developed three metachronous CRLM which occurred consecutively after 9, 21 and 31 months. We identified a set of 1,132 proteins expressed in the three metachronous CRLM, of which 481 were differentially regulated, including 81 proteins that were associated with the extracellular matrix (ECM). 56 ECM associated proteins were identified as upregulated in the third metastasis, 26 (46%) of which were previously described as negative prognostic markers in CRC, including tenascin C, nidogen 1, fibulin1 and vinculin. These data may reflect an ascending trend of malignancy from the first to the third metachronous colorectal cancer liver metastasis. Additionally, the results indicate different ECM phenotypes for recurrent metachronous metastasis, associated with different grades of malignancy and highlights the importance of individual analysis of molecular features in different, consecutive metastatic events in a single patient.
2021-09-09 | PXD020109 | Pride
Project description:We present the first computational approach to reconstruct the sequence of copy number alterations driving carcinogenesis from the analysis of several tumor samples of a same patient. Applied to BAC array-CGH and SNP array data from bladder and breast cancers, this method proved highly valuable to establish the clonal relationships between primary tumors and recurrences and to identify the chromosome aberrations at the initiation of tumorigenesis. An algorithm was developed to reconstruct tumors lineage and the sequence of copy number alterations along tumorigenesis from the analysis of several samples from a same patient. The data here consist in Illumina SNP data from 20 bladder tumors. 15 of these tumors (REF1 to REF15) come from independent samples and were used to compute the frequencies of breakpoints at each location. The 5 other samples (S4_A, S4_B, S5_A, S5_B, and S5_C) are multiple tumors from 2 patients. They were used to reconstruct the sequence of chromosome aberrations along cancer development in these 2 patients.
2010-06-25 | E-GEOD-19189 | biostudies-arrayexpress
Project description:During pancreatic cancer progression, heterogeneous subclonal populations evolve in the primary tumor that possess differing capacities to metastasize and cause patient death. However, the genetics of metastasis reflects that of the primary tumor, and PDAC driver mutations arise early. This raises the possibility than an epigenetic process could be operative late. Using an exceptional resource of paired patient samples, we found that different metastatic subclones from the same patient possessed remarkably divergent malignant properties and global epigenetic programs. Global reprogramming was targeted to thousands of large chromatin domains across the genome that collectively specified malignant divergence. This was maintained by a metabolic shift within the pentose phosphate pathway, independent of KRAS driver mutations. Analysis of paired primary and metastatic tumors from multiple patients uncovered substantial epigenetic heterogeneity in primary tumors, which resolved into a terminally reprogrammed state in metastatic lesions. This supports a model whereby driver mutations accumulate early to initiate pancreatic tumorigenesis, followed by a period of subclonal evolution that generates sufficient intra-tumor heterogeneity for selection of epigenetic programs that may increase fitness during malignant progression and metastatic spread. To map the epigenomic landscape of pancreatic cancer progression as it evolves within patients. BS-Seq of 4 patients (A13, A38, A124 and A125). Patient A38 included local peritoneal metastasis and 2 distant metastsis (liver and lung mets). Patient A13 included 2 primary tumors and 1 distant lung metastasis. Each sample has been done with replicates. Patient A124 included 2 primary tumors and 1 normal pancreas.
2016-10-24 | E-GEOD-63123 | biostudies-arrayexpress
Project description:During pancreatic cancer progression, heterogeneous subclonal populations evolve in the primary tumor that possess differing capacities to metastasize and cause patient death. However, the genetics of metastasis reflects that of the primary tumor, and PDAC driver mutations arise early. This raises the possibility than an epigenetic process could be operative late. Using an exceptional resource of paired patient samples, we found that different metastatic subclones from the same patient possessed remarkably divergent malignant properties and global epigenetic programs. Global reprogramming was targeted to thousands of large chromatin domains across the genome that collectively specified malignant divergence. This was maintained by a metabolic shift within the pentose phosphate pathway, independent of KRAS driver mutations. Analysis of paired primary and metastatic tumors from multiple patients uncovered substantial epigenetic heterogeneity in primary tumors, which resolved into a terminally reprogrammed state in metastatic lesions. This supports a model whereby driver mutations accumulate early to initiate pancreatic tumorigenesis, followed by a period of subclonal evolution that generates sufficient intra-tumor heterogeneity for selection of epigenetic programs that may increase fitness during malignant progression and metastatic spread. To map the epigenomic landscape of pancreatic cancer progression as it evolves within patients. RNA-Seq of 2 patients (A13 and A38). Patient A38 included local peritoneal metastasis and 2 distant metastsis (liver and lung mets), and 6AN treated and DMSO control samples. Patient A13 included 2 primary tumors and 1 distant lung metastasis. Each sample has been done with replicates.
2016-10-24 | E-GEOD-63124 | biostudies-arrayexpress
Project description:The present study was carried out on a proband affected by Partial Androgen Insensitivity Syndrome (PAIS) and his family. The patient developed the primary RSC at 27 years. Three years after primary surgery, the patient developed a second primary (metachronous) rectal cancer relapsed one year later. The PAIS was also diagnosed in his cousin. Both cousins were found positive for the same missense androgen receptor (AR) gene mutation that was inherited from their asymptomatic mothers. The aim of this study was to identify constitutional genetic events that could have played a role in early onset of RSC in the proband. SNP-array analyses were carried out to investigate Copy Number Variations and Uniparental Disomy events as possible genetic causes linked to Colorectal Cancer pathogenesis.
2016-06-05 | GSE69613 | GEO