Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA277850 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We analysed a cohort of pure DCIS cases treated only with wide local excision for genome-wide copy number and loss of heterozygosity using Affymetrix OncoScan® MIP arrays. Cases included those without recurrence within 6 years (n=25) and with recurrence between 1-5 years after diagnosis (n=15). Additional cases were excluded for low grade (n=6) or non-clonal recurrence (n=2). Recurrence tumour was available for 8 cases. Pure DCIS were broadly similar in copy number changes compared to invasive breast cancer, with the consistent exception of a greater frequency of ERBB2 amplification in DCIS. There were no significant differences in age or ER status between the cases with a recurrence versus those without. Overall, the DCIS cases with recurrence had more copy number events than the DCIS without recurrence. The increased copy number appeared non-random with several genomic regions showing an increase in frequency in recurrent cases including 20q gain, ERBB2 amplification and 15q loss. Copy number changes may provide prognostic information for DCIS recurrence but validation in additional cohorts is required.
2015-12-01 | GSE66746 | GEO
Project description:Overexpression of NUCKS1 in colorectal cancer correlates with recurrence after curative surgery (copy number analysis)
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Project description:Colorectal adenomas are common precancerous lesions with the potential for malignant transformation to colorectal adenocarcinoma. Endoscopic polypectomy provides an opportunity for cancer prevention, however, recurrence rates are high. We collected formalin-fixed paraffin-embedded tissue of fourteen primary adenomas with recurrence, fourteen primary adenomas without recurrence, and fourteen matched pair samples (primary adenoma and the corresponding recurrent adenoma). These samples were analysed by array-based comparative genomic hybridisation (aCGH) to understand the dynamics of copy number alterations (CNAs) and to identify molecular markers to predict recurrence. ACGH analysis confirmed the genetic landscape specific for colorectal tumorigenesis, i.e., CNAs of chromosomes 7 (13.7%), 13q (13.7%), 18 (5.8%) and 20q (13.7%). CNAs were detected in 41/51 (80.4%) of colorectal adenomas (2N). Focal aberrations (≤10 Mbp) were mapped to chromosome bands 6p22.1-p21.33 (33.3%), 7q22.1 (31.4%) and 16q21 (29.4%). Gains of CDX2 were exclusively seen in adenomas with recurrence compared to adenomas without recurrence. However, the average number of copy alterations failed to discriminate primary adenomas with recurrence from primary adenomas without recurrence.
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