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Links from GEO DataSets

Items: 6

1.

Expression data from chronic lymphocytic leukemia (CLL) tumors in two time points

(Submitter supplied) As part of a large genetic evolution study we also acquired 3'UTR expression arrays at two time points for the same 18 patients with CLL. We have analysed the data to evaluate whether genetic evolution (somatic mutations and Somatic copy number alterations) also manifested at the transcriptome level, either globally, or at the level of pre-defined curated geneset that correspond to specfic evolving genetic lesions.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
40 Samples
Download data: CEL
Series
Accession:
GSE37168
ID:
200037168
2.

Clonal evolution, genomic drivers, and effects of therapy in chronic lymphocytic leukemia

(Submitter supplied) The identification of gene mutation and structural genomic aberrations that are critically involved in CLL pathogenesis is still evolving. One may postulate that genomic driver lesions with effects on CLL proliferation, apoptosis thresholds, or chemotherapy resistance should increase in frequency over time when measured sequentially in a large CLL cohort. We sequentially sampled a large, well-characterized CLL cohort at a mean of 4 years between samplings. more...
Organism:
Homo sapiens
Type:
Genome variation profiling by SNP array
Platform:
GPL6801
496 Samples
Download data: CEL
Series
Accession:
GSE45565
ID:
200045565
3.

Longitudinal Genome Wide Analysis of Chronic Lymphocytic Leukemia Reveals Complex Evolution of Clonal Architecture at Disease Progression and at the Time of Relapse

(Submitter supplied) Little is known about the extent of intraclonal heterogeneity of CLL tumor cells. We performed longitudinal whole genome analysis in 22 CLL cases with evidence of clinical progression and/or clinical relapse post therapy. We demonstrate the striking and unanticipated presence of genetic clonal heterogeneity, with at least 27% of patients exhibiting clonal evolution and 18% showing evidence of multiple subclones. more...
Organism:
Homo sapiens
Type:
Genome variation profiling by genome tiling array
Platform:
GPL8736
54 Samples
Download data: TXT
Series
Accession:
GSE30217
ID:
200030217
4.

Affymetrix SNP array data for Chronic Lymphocytic Leukemia_diagnostic sample_patient samples

(Submitter supplied) High-resolution genomic microarrays provides simultaneous detection of copy-number aberrations such as the known recurrent aberrations in Chronic Lymphocytic Leukemia_diagnostic sample_patient (del(11q), del(13q), del(17p) and trisomy 12), and copy-number neutral loss of heterozygosity. We screened 369 newly diagnosed Chronic Lymphocytic Leukemia_diagnostic sample_patient patient samples from a population-based cohort using 250K single nucleotide polymorphism-arrays.
Organism:
Homo sapiens
Type:
Genome variation profiling by SNP array; SNP genotyping by SNP array
Platform:
GPL3718
369 Samples
Download data: CEL, CNCHP
Series
Accession:
GSE28030
ID:
200028030
5.

Affymetrix CytoScan HD array data for del(17p) Chronic Lymphocytic Leukemia samples

(Submitter supplied) We performed whole genome profiling in order to determine the landscape of genetic alterations assoicated with a subset of CLL that is characterized by deletions in 17p The number of copy number alterations predicted shorter time to treatment among patients untreated at sampling. Chromosome 3p, 4p, and 9p were frequently deleted in del(17p) CLL and strongly associated with shorter OS. We conclude that del(17p) has a unique genomic profile characterized typically by TP53 mutation with novel CNAs and novel drivers, with increasing genomic complexity of any type associated with worse overall survival.
Organism:
Homo sapiens
Type:
Genome variation profiling by genome tiling array; Genome variation profiling by SNP array
Platform:
GPL16131
86 Samples
Download data: CEL
Series
Accession:
GSE74239
ID:
200074239
6.

Affymetrix SNP array data for chronic lymphocytic leukemia samples

(Submitter supplied) Although in 80% of CLL cases that require therapy is possible to achieve a complete remission using a combination of fludarabine, anti-CD20 in conjunction with cyclophosphamide and/or mitoxantrone, 20% of patients do not achieve disease control with this conventional approach. The main reason of complete remission failure is chemorefractoriness to fludarabine that occurs in up to 10% of patients requiring treatment. more...
Organism:
Homo sapiens
Type:
Genome variation profiling by SNP array; SNP genotyping by SNP array
Platform:
GPL6801
52 Samples
Download data: CEL, CHP, TXT
Series
Accession:
GSE51711
ID:
200051711
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