Project description:HER2 gene amplification and protein overexpression (HER2+) define a clinically challenging subgroup of breast cancer with variable prognosis and response to therapy. Although gene expression profiling has identified an ERBB2 molecular subtype of breast cancer, it is clear that HER2+ tumors reside in all molecular subtypes and represent a genomically and biologically heterogeneous group. Genome-wide DNA copy number profiling, using BAC array comparative genomic hybridization (aCGH) were performed on 200 tumors with mixed clinical characteristics and amplification of HER2. Genomic Identification of Significant Targets in Cancer (GISTIC) was used to identify significant copy number aberrations (CNAs) in HER2+ tumors. This analysis sheds further light on the genomically complex and heterogeneous nature of HER2+ tumors in relation to other subgroups of breast cancer.
Project description:Genomic and expression profiling using 38K BAC array-CGH and Illumina HT-12 beadchips were performed on 97 diploid invasive breast tumors to assess the impact of gene dosage on gene expression patterns and the effect of other mechanisms on transcriptional levels. Patient stratification was performed according to axillary lymph node status (node-negative, pN0; node-positive, pN1) and overall survival (>8-year survivors; breast cancer-specific mortality within 8 years of diagnosis). Array-CGH results was validated by FISH using tumors showing HER2/neu gene amplification and expression profiling was confirmed using qPCR for 16 transcripts.
Project description:An oligo array based high-resolution analysis of copy number alterations in 171 primary breast tumors of relatively small size and low NPI, and 49 breast cancer cell-lines. Objectives of the study were to study the molecular taxonomy and the genomic aberration patterns in a breast cancer cohort representative of breast cancer demographics. Keywords: array comparative genomic hybridisation
Project description:Analysis of genes regulated by RU486 (an progesterone antagonist) in human breast cancer T47D cells and human uterine leiomyoma smooth muscle cells. The hypothesis is that RU486 inhibits tumor growth by inactivating the transcription of multiple genes which trigger critical signaling pathways to induce tumorigenesis in both breast caner and uterine leomyoma. Tissue-specific and common patterns of gene regulation may determine the therapeutic effects of antiprogestins in uterine leiomyoma and breast cancer. Keywords: Expression profiling by array
Project description:Transcriptomic profiling of human breast tumors. Genomic and expression profiling using 38K BAC array-CGH and Illumina HT-12 beadchips were performed on 53 invasive breast tumors to assess the impact of gene dosage on gene expression patterns and the effect of other mechanisms on transcriptional levels. Array-CGH results was validated by FISH using tumors showing 8p11-p12 DNA amplification and expression profiling was confirmed using qPCR for 11 transcripts. Low-level gain, high-level gain/amplification, heterozygous loss and homozygous deletion (henceforth referred to as gain, amplification, loss and deletion) were defined as log2 ratio thresholds set at +0.2, >= +0.5, -0.2 and <=-1.0, respectively.
Project description:MicroRNAs (miRNAs) are small, non-coding, endogenous RNAs involved in many human diseases including breast cancer. miRNA expression profiling of human breast cancers has identified miRNAs related to the clinical diversity of the disease and potentially provides novel diagnostic and prognostic tools for breast cancer therapy. In order to further understand the roles of miRNAs in association with oncogenic drivers and in specifying sub-types of breast cancer, we performed miRNAexpression profiling on mammary tumors from eight well-characterized genetically -engineered Mouse (GEM) models of human breast cancer including MMTV–H-Ras, -Her2/neu, -c-Myc, -PymT, –Wnt1 and C3(1)/SV40 T/t-antigen transgenic mice, BRCA1fl/fl;p53+/-;MMTV-cre and the p53fl/fl ;MMTV-cre transplant model. As supplementary data
Project description:MicroRNAs (miRNAs) are small, non-coding, endogenous RNAs involved in many human diseases including breast cancer. miRNA expression profiling of human breast cancers has identified miRNAs related to the clinical diversity of the disease and potentially provides novel diagnostic and prognostic tools for breast cancer therapy. In order to further understand the roles of miRNAs in association with oncogenic drivers and in specifying sub-types of breast cancer, we performed miRNAexpression profiling on mammary tumors from eight well-characterized genetically -engineered Mouse (GEM) models of human breast cancer including MMTV–H-Ras, -Her2/neu, -c-Myc, -PymT, –Wnt1 and C3(1)/SV40 T/t-antigen transgenic mice, BRCA1fl/fl;p53+/-;MMTV-cre and the p53fl/fl ;MMTV-cre transplant model.
Project description:Genomic and expression profiling using 38K BAC array-CGH and Illumina HT-12 beadchips were performed on 97 diploid invasive breast tumors to assess the impact of gene dosage on gene expression patterns and the effect of other mechanisms on transcriptional levels. Patient stratification was performed according to axillary lymph node status (node-negative, pN0; node-positive, pN1) and overall survival (>8-year survivors; breast cancer-specific mortality within 8 years of diagnosis). Array-CGH results was validated by FISH using tumors showing HER2/neu gene amplification and expression profiling was confirmed using qPCR for 16 transcripts.
Project description:HER2 gene amplification and protein overexpression (HER2+) define a clinically challenging subgroup of breast cancer with variable prognosis and response to therapy. Although gene expression profiling has identified an ERBB2 molecular subtype of breast cancer, it is clear that HER2+ tumors reside in all molecular subtypes and represent a genomically and biologically heterogeneous group. Genome-wide DNA copy number profiling, using BAC array comparative genomic hybridization (aCGH) were performed on 200 tumors with mixed clinical characteristics and amplification of HER2. Genomic Identification of Significant Targets in Cancer (GISTIC) was used to identify significant copy number aberrations (CNAs) in HER2+ tumors. This analysis sheds further light on the genomically complex and heterogeneous nature of HER2+ tumors in relation to other subgroups of breast cancer. Genomic profiling of 200 breast tumors using tiling BAC aCGH (32K, 33K and 38K). A number of cases were hybridized as replicates or dye-swaps.