Project description:Proliferative breast lesions, such as simple ductal hyperplasia (SH) and atypical ductal hyperplasia (ADH), are candidate precursors to ductal carcinoma in situ (DCIS) and invasive cancer. To better understand their relationship to more advanced disease, we used microdissection and DNA microarrays to profile the gene expression of patient-matched histologically normal (HN), ADH, and DCIS from 12 patients with ER+ sporadic breast cancer. SH were profiled from a subset of cases. We found 837 differentially expressed genes between DCIS-HN and 447 between ADH-HN, with >90% of the ADH-HN genes also present among the DCIS-HN genes. Only 61 genes were identified between ADH-DCIS. Expression differences were reproduced in an independent cohort of patient-matched lesions by qRT-PCR. Many breast cancer-related genes and pathways were dysregulated in ADH and maintained in DCIS. Particularly, cell adhesion and extracellular matrix (ECM) interactions were overrepresented. Focal adhesion was the top pathway in each gene set. We conclude that ADH and DCIS share highly similar gene expression and are distinct from HN. In contrast, SH appear more similar to HN. These data provide genetic evidence that ADH (but not SH) are often precursors to cancer and suggest cancer-related genetic changes, particularly adhesion and ECM pathways, are dysregulated prior to invasion and even before malignancy is apparent. These findings could lead to novel risk stratification, prevention, and treatment approaches. Patient-matched (HN, SH, ADH, DCIS) samples were isolated from within patients with ER+ sporadic breast cancers via laser capture microdissection. Use of patient-matched samples decreases between patient variations.
Project description:This single cell RNA-seq experiment was performed to quantify DLL3 expression in tumor cells in small cell lung cancer patients.Tumors were rapidly dissociated after the surgical procedure using the Miltenyi Biotec Human Tumor Dissociation kit (cat# 130-095-929). Libraries were constructed using the VDJ NextGEM v1.1 10x Genomics Chromium kit according to the manufacturer's instructions. Samples were sequenced on a NextSeq 550 sequencer (Illumina). Corresponding EGA study number: EGAS50000001400, EGA dataset number: EGAD50000002034.
Project description:Here, we investigated tumor tissue from 26 patients affected by AT/RT to identify signatures of recurrences in comparison to matched primary tumor samples.
Project description:Prostate adenocarcinoma and matched adjacent normal samples were profiled by deep transcriptional sequencing to analyze transcription-induced chimeras and gene fusions. Reference samples from the MAQC and brain and universal reference libraries were also sequenced.
Project description:Here, we investigated tumor tissue from 26 patients affected by AT/RT to identify signatures of recurrences in comparison to matched primary tumor samples. Therefore, we performed histological analysis and DNA methylation and gene expression profiling.
Project description:CTCF ChIP-seq of 39 primary samples derived from human acute leukemias, namely AML, T-ALL and mixed myeloid/lymphoid leukemias with CpG Island Methylator Phenotype (CIMP). Due to patient confidentiality considerations, the raw data files for this dataset have been deposited to the EGA controlled-access archive under the accession numbers EGAS00001007094 (study); EGAD00001011059 (dataset).
Project description:Proliferative breast lesions, such as simple ductal hyperplasia (SH) and atypical ductal hyperplasia (ADH), are candidate precursors to ductal carcinoma in situ (DCIS) and invasive cancer. To better understand their relationship to more advanced disease, we used microdissection and DNA microarrays to profile the gene expression of patient-matched histologically normal (HN), ADH, and DCIS from 12 patients with ER+ sporadic breast cancer. SH were profiled from a subset of cases. We found 837 differentially expressed genes between DCIS-HN and 447 between ADH-HN, with >90% of the ADH-HN genes also present among the DCIS-HN genes. Only 61 genes were identified between ADH-DCIS. Expression differences were reproduced in an independent cohort of patient-matched lesions by qRT-PCR. Many breast cancer-related genes and pathways were dysregulated in ADH and maintained in DCIS. Particularly, cell adhesion and extracellular matrix (ECM) interactions were overrepresented. Focal adhesion was the top pathway in each gene set. We conclude that ADH and DCIS share highly similar gene expression and are distinct from HN. In contrast, SH appear more similar to HN. These data provide genetic evidence that ADH (but not SH) are often precursors to cancer and suggest cancer-related genetic changes, particularly adhesion and ECM pathways, are dysregulated prior to invasion and even before malignancy is apparent. These findings could lead to novel risk stratification, prevention, and treatment approaches. Patient-matched (HN, SH, ADH, DCIS) samples were isolated from within patients with ER+ sporadic breast cancers via laser capture microdissection. Use of patient-matched samples decreases between patient variations. Forty total samples were analyzed via Affymetrix U133A. Patient age ranged from 48-92. Case numbers correspond to individual patients. Each sample is identified by case number, histologic lesion and corresponding microarray ID.
Project description:H3K27ac ChIP-seq of 79 primary samples derived from human acute leukemias, namely AML, T-ALL and mixed myeloid/lymphoid leukemias with CpG Island Methylator Phenotype (CIMP). In addition, 4 samples derived from CD34+ cord blood cells of healthy donors were included. Due to patient confidentiality considerations, the raw data files for this dataset have been deposited to the EGA controlled-access archive under the accession numbers EGAS00001007094 (study); EGAD00001011060 (dataset).