Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA221790 | ENA |
REPOSITORIES: ENA
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Project description:Identification of genes associated with bone metastatic breast cancer cells
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Project description:Gene expression signatures for breast cancer cells metastatic to bone marrow
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Project description:Bone is the most common metastasis site in patients with breast cancer, and approximately up to 80% of patients with advanced breast cancer (BC) develop bone metastasis (BM), which leads to a worse prognosis with a median survival of 16 months and skeletal-related events (SREs), including severe bone pain, pathological fracture, hypercalcemia and lethal complications. Using quantitative proteomics mass-spectrometry (MS) analysis of the secretome from patient-derived primary BC cells (PBCs) and bone-metastatic BC cells (BMBCs), we identified an unreported breast cancer (BC) cells–secreted microprotein, osteolysin, encoded by tropomyosin 3 pseudogene 9 (TPM3P9) and clinically associated with BC bone-tropism.
2024-07-05 | PXD053732 |
Project description:Identification of genes associated with breast cancer micrometastatic disease in bone marrow disseminated tumor cells (DTCs)
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Project description:Identification of MicroRNAs Inhibiting TGF-beta-Induced IL-11 Production in Bone Metastatic Breast Cancer Cells
2012-11-22 | E-TABM-1220 | biostudies-arrayexpress
Project description:1,322 morphologically unidentified fragmentary bone specimens were analyzed using MALDI-TOF and a subset of 341 bone specimens with LC-MS/MS in order to characterize their proteome for species identification and potential hominin specimens related to the LRJ transitional period derived from the site Ilsenhöhle Ranis, Germany (50°39.7563’N, 11°33.9139’E).
2023-10-20 | PXD043272 | Pride
Project description:Comparing gene-expression profiles between bone-metastatic vs. non bone-metastatic human prostate cancer cells
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Project description:Bone is the primary site of breast cancer metastasis and complications associated with bone metastases can lead to a significantly decreased quality of life in these patients. Thus, it is essential to gain a better understanding of the molecular mechanisms that underlie the emergence and growth of breast cancer skeletal metastases. Methods: To search for novel molecular mediators that influence breast cancer bone metastasis, we generated gene expression profiles from laser capture micro-dissected trephine biopsies of both breast cancer bone metastases and primary breast tumors that metastasized to bone. Bioinformatics analysis identified genes that are differentially expressed in breast cancer bone metastases compared to primary mammary tumors. Results: ABCC5, an ATP-dependent transporter, was found to be overexpressed in breast cancer osseous metastases relative to primary mammary tumors. In addition, ABCC5 was significantly up-regulated in human and mouse breast cancer cell lines with high bone-metastatic potential. Stable knockdown of ABCC5 significant reduced bone metastatic burden and osteolytic bone destruction in mice. The decrease in osteolysis was further associated with diminished osteoclast numbers. Conclusions: Our data, for the first time, suggests that ABCC5 functions as a mediator of breast cancer skeletal metastasis. ABCC5 expression in breast cancer cells is important for the efficient bone resorption mediated by osteoclasts. Hence, ABCC5 may be a potential therapeutic target for breast cancer bone metastasis. primary breast tumors vs. bone trephine biopsies
2012-11-09 | E-GEOD-39494 | biostudies-arrayexpress
Project description:Intratumor mutational heterogeneity has been documented in primary non-small cell lung cancer. Here, we elucidate mechanisms of tumor evolution and heterogeneity in metastatic thoracic tumors (lung adenocarcinoma and thymic carcinoma) using whole-exome and transcriptome sequencing, SNP array for copy number alterations (CNA) and mass spectrometry-based quantitative proteomics of metastases obtained by rapid autopsy. APOBEC-mutagenesis, promoted by increased expression of APOBEC3 region transcripts and associated with a high-risk germline APOBEC3 variant, strongly correlated with mutational tumor heterogeneity. TP53 mutation status was associated with APOBEC hypermutator status. Interferon pathways were enriched in tumors with high APOBEC mutagenesis and IFN- induced expression of APOBEC3B in lung adenocarcinoma cells in culture suggesting a role for the immune microenvironment in the generation of mutational heterogeneity. CNA occurring late in tumor evolution correlated with downstream transcriptomic and proteomic heterogeneity, although global proteomic heterogeneity was significantly greater than transcriptomic and CNA heterogeneity. These results illustrate key mechanisms underlying multi-dimensional heterogeneity in metastatic thoracic tumors.
2019-05-07 | PXD012845 | Pride