Project description:This study is a repository for all RNAseq data obtained from High Throuput Seqeuncing of Patient Derived Xenograft models of Breast Cancer studied at the Baylor College of Medicine Breast Center.
Project description:Goal: To define the digital transcriptome of three breast cancer subtypes (TNBC, Non-TNBC, and HER2-positive) using RNA-sequencing technology. To elucidate differentially expressed known and novel transcripts, alternatively spliced genes and differential isoforms and lastly expressed variants in our dataset. Method: Dr. Suzanne Fuqua (Baylor College of Medicine) provided the human breast cancer tissue RNA samples. All of the human samples were used in accordance with the IRB procedures of Baylor College of Medicine. The breast tumour types, TNBC, Non-TNBC and HER2-positive, were classified on the basis of immunohistochemical and RT-qPCR classification. Results: Comparative transcriptomic analyses elucidated differentially expressed transcripts between the three breast cancer groups, identifying several new modulators of breast cancer. We discovered subtype specific differentially spliced genes and splice isoforms not previously recognized in human transcriptome. Further, we showed that exon skip and intron retention are predominant splice events in breast cancer. In addition, we found that differential expression of primary transcripts and promoter switching are significantly deregulated in breast cancer compared to normal breast. We also report novel expressed variants, allelic prevalence and abundance, and coexpression with other variation, and splicing signatures. Additionally we describe novel SNPs and INDELs in cancer relevant genes with no prior reported association of point mutations with cancer
Project description:Whole striatum were dissected from wild-type, as well as in mice where Dnmt3a or MeCP2 was conditional deleted in inhibitory neurons. Inhibitory neuronal nuclei were also conditionally tagged with GFP in all mice. Tissues were snap-frozen in liquid nitrogen until further analysis. Inhibitory neurons were sorted from whole striatum using anti-GFP-488 and anti-NeuN-647 signals and snap frozen until further analysis. Total nuclear RNA was purified from each sample using the Single Cell RNA Purification Kit from Norgen Biotek according to manufactures instructions and stored at -80C until library preparation at the Genomic and RNA Profiling Core at Baylor College of Medicine. NuGEN Ovation RNA-Seq v2 & Rubicon ThruPlex DNA-Seq kits were utilized for library preparation. A paired-end 100 cycle run was used to sequence the flowcell on a HiSeq 2500 Sequencing System.
Project description:The purpose of this study was to search for microgravity-sensitive genes, specifically for apoptotic genes influenced by the microgravity environment and other genes related to immune response. Experiment Overall Design: Two-group design with paired samples, i.e., one 1G and one MMG culture came from the same donor. Therefore, 6 samples came from 3 different donors. Experiment Overall Design: Donor 1 :GSM96146,GSM96147 Experiment Overall Design: Donor 2: GSM96148, GSM96149 Experiment Overall Design: Donor 3: GSM96150,GSM96151 Experiment Overall Design: Total RNA was submitted to, and then labeled, hybridized and data generated by the Baylor College Medicine Microarray Core Facility (333E One Baylor Plaza, Houston, TX 77030).
Project description:Goal: To define the digital transcriptome of three breast cancer subtypes (TNBC, Non-TNBC, and HER2-positive) using RNA-sequencing technology. To elucidate differentially expressed known and novel transcripts, alternatively spliced genes and differential isoforms and lastly expressed variants in our dataset. Method: Dr. Suzanne Fuqua (Baylor College of Medicine) provided the human breast cancer tissue RNA samples. All of the human samples were used in accordance with the IRB procedures of Baylor College of Medicine. The breast tumour types, TNBC, Non-TNBC and HER2-positive, were classified on the basis of immunohistochemical and RT-qPCR classification. Results: Comparative transcriptomic analyses elucidated differentially expressed transcripts between the three breast cancer groups, identifying several new modulators of breast cancer. We discovered subtype specific differentially spliced genes and splice isoforms not previously recognized in human transcriptome. Further, we showed that exon skip and intron retention are predominant splice events in breast cancer. In addition, we found that differential expression of primary transcripts and promoter switching are significantly deregulated in breast cancer compared to normal breast. We also report novel expressed variants, allelic prevalence and abundance, and coexpression with other variation, and splicing signatures. Additionally we describe novel SNPs and INDELs in cancer relevant genes with no prior reported association of point mutations with cancer mRNA profiles of 17 breast tumor samples of three different subtypes (TNBC, non-TNBC and HER2-positive) and normal human breast organoids (epithelium) samples (NBS) were sequenced using Illumina HiSeq.
Project description:The below table includes a smaller list of data that was analyzed by dChip and filtered by pvalue such that a file with about 4600 genes was obtained, which allowed for ease of use from 40,000 genes. Experiment Overall Design: The total RNA was extracted from 2T3 pre-osteoblast cells exposed to static or simulated microgravity (Rotating Wall Vessel) conditions. The RNA was then sent to Affymetrix microarray core facility at Baylor College of Medicine (Houston, TX) for microarray analysis.
Project description:We applied DNA content flow cytometry to ten patient derived triple negative breast cancer (TNBC) xenografts (PDXs) from the Baylor College of Medicine (BCM). We interrogated purified sorted tumor fractions from each sample with whole genome copy number variant (CNV) analyses. These identified a variety of somatic genomic lesions that are common in TNBC including three cases with 9p24.1 amplification targeting PD-L1-PDL2 and JAK2 (PDJ amplicon) and recurring focal amplicons of oncogenic drivers found commonly in the TNBC PDXs including MYC and EGFR. In addition, homozygous deletions of known tumor suppressor genes including PTEN, CDKN2A, RB1, and BRCA2, and unique targets such as CUX1 and FYN were identified. Of the three PDJ-positive amplified PDXs, 2/3 two had focal MYC amplifications and 1/3 had a RB1 homozygous deletion.