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).
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:Patient samples were recruited from a series of female patients with metastatic primary breast cancer (PBC) and biopsy-confirmed breast cancer lung or pleural metastasis (BCLPM) at the Department of Thoracic Surgery, Thoraxklinik, Univ. of Heidelberg, Germany. All patients were included who had received lung or pleural metastasis biopsies from 2003 to 2014 and had a prior history of PBC at the Department of Gynaecology and Obstetrics, Univ. Hospital. Formalin-fixed and paraffin-embedded tissue samples were provided by the Tissue Bank at the National Center for Tumor Diseases (NCT, Heidelberg, Germany) in accordance with the regulations of the Tissue Bank and approval of the Ethics Committee at the Medical Faculty of the Univ. of Heidelberg, approval no. S-716/2018.
Project description:We developed MHC1-TIP: an optimized mild acid elution-based immunopeptidomics workflow that leverages data independent acquisition and the Astral mass analyzer to enable scalable, single-tube and cost-effective MHC-I ligandome profiling. This dataset includes immunopeptidomics and proteomics data from the A375 melanoma cell line, colorectal cancer patient-derived organoids, and renal cell carcinoma tumour fragments. We show the effects of TGF-beta treatment on the proteome and immunopeptidome of A375 cells and interferon-gamma treatment on patient-derived organoids. We also explore immunopeptidome and proteome heterogeneity in patient-derived tumour fragments. MB_30: A375 immunopeptidomes in DDA (wildtype and B2M knockout); MB_38: Proteomes with and without mild acid treatment with A375 cells; MB_39: Proteomes and immunopeptidomes from TGFb treated A375 cells; MB_41: MHC1-TIP and MHC-I immunoprecipitation data from different A375 cell input numbers; MB_43: immunopeptidomes of A375 cells treated with different doses of interferon-gamma; MB_45: immunopeptidomes of A375 cells with MHC1-TIP and immunoprecipitation after mild acid elution to identify intracellular peptides; MB_46: Proteomics and immunopeptidomics data from 15 ex-vivo cultured patient-derived tumour fragments; MB_49: Proteomics and immunopeptidomics data from 3 patient-derived organoid lines.
Project description:We searched for putative phenotypic and genotypic differences between primary lesions and melanoma metastasis. Therefore we investigated melanoma cells derived either from the primary tumor or from lymph node metastasis of the same individual patient. In vitro studies revealed high migratory and anchorage independent growth of metastasis-derived cells. Unexpectedly, whole genome DNA analysis displayed a total of 10 homozygous losses in the primum-derived cell line, whereas the metastasis–derived cell line only shared 5 of those losses. We further tested these cells in a mouse model for intradermal melanoma growth and detected fast growth of the metastasis-derived cell line and no growth of primum-derived cells. Therefore we suggest that tumor cell progression at the metastatic niche can occur parallel and independently from the primary tumor. Additionally we screened melanoma samples isolated from patients and could identify one case were the primum harboured deletions not present in the metastatic lesion. We propose that for mutation-targeted therapy genotyping should be performed not only from primary, but foremost from metastatic melanoma cells.
Project description:Accumulating evidence indicates that patient- derived organoids (PDOs) can predict drug responses in the clinic. Metastasis is the main cause of death in colorectal cancer patients, and the treatment of patients with liver metastasis remains poor. Tumor heterogeneity is the cause of treatment failure. In this study, we aim the investigate the consistency of drug sensitivity for the matched primary and metastatic tumor in patients with liver metastasis.