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Copy number analysis by low coverage whole genome sequencing using ultra low-input DNA from formalin-fixed paraffin embedded tumour tissue

ABSTRACT: We analysed a cohort of Lifepool IDC cases treated only with wide local excision for genome-wide copy number and loss of heterozygosity using Affymetrix OncoScan® MIP arrays. Cases included IDC (n=4).Benign cases were available for 2 cases. We have analysed copy number calling from the same samples using low-coverage whole genome sequencing in order to investigate the concordance between the two techniques.

ORGANISM(S): Homo sapiens

PROVIDER: GSE85035 | GEO | 2016/08/02

SECONDARY ACCESSION(S): PRJNA336004

REPOSITORIES: GEO

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Copy number analysis by low coverage whole genome sequencing using ultra low-input DNA from formalin-fixed paraffin embedded tumour tissue

Project description:We analysed a cohort of Lifepool IDC cases treated only with wide local excision for genome-wide copy number and loss of heterozygosity using Affymetrix OncoScanÂ® MIP arrays. Cases included IDC (n=4).Benign cases were available for 2 cases. We have analysed copy number calling from the same samples using low-coverage whole genome sequencing in order to investigate the concordance between the two techniques. 4 cases of lifepool invasive ductal carcinoma (IDC) and 2 benign cases were microdissected from FFPE tissue and analysed by molecular inversion probe (MIP) copy number arrays. The data in this submission are CN values for the ~300,000 probes common to two batches performed.

2016-08-02 | E-GEOD-85035 | biostudies-arrayexpress

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Identification of copy number alterations associated with the progression of DCIS to Invasive Ductal Carcinoma

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2012-09-04 | E-GEOD-31892 | biostudies-arrayexpress

Integrated Copy Number Analysis of Epstein Barr Virus (EBV)-Positive Diffuse Large B-Cell Lymphoma (DLBCL)

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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.

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Project description:Invasive lobular carcinoma (ILC) is a histological subtype of breast cancer with distinct molecular and clinical features from the more common subtype invasive ductal carcinoma (IDC). ILC cells exhibit anchorage-independent growth in ultra-low attachment (ULA) suspension cultures, which is largely attributed to the loss of E-cadherin. In addition to anoikis resistance, herein we show that human ILC cell lines exhibit enhanced cell proliferation in ULA cultures as compared to IDC cells. Proteomic comparison of ILC and IDC cell lines identified induction of PI3K/Akt and p90-RSK pathways specifically in ULA culture in ILC cells. Further transcriptional profiling uncovered unique upregulation of the inhibitors of differentiation family transcription factors ID1 and ID3 in ILC ULA culture, the knockdown of which diminished the anchorage-independent growth of ILC cell lines through cell cycle arrest. We find that ID1 and ID3 expression is higher in human ILC tumors as compared to IDC, correlated with worse prognosis uniquely in patients with ILC and associated with upregulation of angiogenesis and matrisome-related genes. Altogether, our comprehensive study of anchorage independence in human ILC cell lines provides mechanistic insights and clinical implications for metastatic dissemination of ILC and implicates ID1 and ID3 as novel drivers and therapeutic targets for lobular breast cancer.

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