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Breast metastatic tumors in lung can be substituted by lung-derived tumorsBreast metastatic tumors in lung can be substituted by lung-derived tumors

ABSTRACT: Breast metastatic tumors in lung can be substituted by lung-derived tumorsBreast metastatic tumors in lung can be substituted by lung-derived tumors

PROVIDER: PRJNA922464 | ENA |

REPOSITORIES: ENA

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Breast metastatic tumors in lung can be substituted by lung-derived tumorsBreast metastatic tumors in lung can be substituted by lung-derived tumors

Project description:Metastasis accounts for most cancer-associated deaths; yet, this complex process remains poorly understood, particularly the relationship between distant metastasis and primary site-derived cells. Here, we modified the classical MMTV-PyMT breast carcinoma model to trace the fate of mammary-derived carcinoma cells. We show that within the lung, when the metastatic breast carcinoma cells are conditionally depleted, transformed lung epithelial cells generate new metastases. Metastatic breast carcinoma cells transmit H19 long non-coding (lnc) RNA to lung epithelial cells through exosomes. SF3B1 bearing mutations at arginine-625 alternatively splices H19 lncRNA in lung epithelial cells, which selectively acts like a molecular sponge to sequester let-7a and induces Myc up-regulation. Under the conditional elimination of primary site-derived breast carcinoma cells, lung malignant cells expressing the mutated SF3B1 splice variant dominate the newly created tumors. Our study suggests that these new carcinoma cells originating from within the colonized organ can replace the primary site-derived malignant cells whenever their expansion is abrogated using an inducible diphtheria toxin receptor in our designed system. These findings should call for a better understanding of metastatic tumors with the specific origin during cancer metastasis.

2023-04-11 | GSE222524 | GEO

Array comparative genomic hybridization analysis of metastatic lung tumors

Project description:Array comparative genomic hybridization analysis of metastatic lung tumors

| PRJNA661554 | ENA

Proteomics profiling in primary tumors of metastatic and non-metastatic breast cancers

Project description:Analysis of different proteomics profile in primary tumors of metastatic and non-metastatic breast cancers.

2023-03-09 | PXD037288 | Pride

Lung tumors

Project description:Lung tumors

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Gene expression profiling of HNSCC cells derived from primary and matched metastatic tumors

Project description:To look at genes/pathways differentially expressed in metastatic and primary tumor cells we performed global gene expression profiling of the 3 sets of HNSCC lines derived from primary tumors and matched metastatic sites. Illumina HT-12 v4 BeadChip arrays were used. The data suggest that HNSCC lines derived from metastatic sites exhibit phenotypes distinct from those found in cells derived from the corresponding primary tumors. Metastatic cell lines upregulated several pathways involved in stem cell self-renewal, invasion and migration, which are well known characteristics of metastatic progression. We conclude that the cell lines derived from primary patient tumors and matched metastatic sites represent a reliable model to study HNSCC metastasis.

2018-07-27 | GSE117753 | GEO

Detecting metastatic tumors after γ-irradiation using longitudinal molecular imaging and gene expression profiling of metastatic tumor nodules

Project description:Microarray analysis in the mouse metastatic tumor after ɣ-irradiation(ɣ-IR): non-irradiated primary tumor vs. radiated primary tumor vs. metastatic tumor after ɣ-irradiation Metastatic tumors in C6-L (rat glioma cells ) xenografted mice were studied after local treatment with fractionated γ-IR. To accurately detect the metastatic nodules after γ-IR, we observed the effect of γ-IR on distant metastatic tumor growth. Metastatic nodules after γ-IR indicated extensive colonization of C6-L cells in the lungs within 6 weeks after γ-IR. Identified and described the molecular events occurring after γ-IR through gene expression profiling to elucidate genetic changes (differentially expressed genes between the γ-IR primary tumors vs. non-γ-IR primary tumors and metastatic lung nodules vs. γ-IR primary tumors). We investigated the change of gene expression profile in the γ-IR primary tumors vs. non-γ-IR primary tumors and metastatic lung nodules vs. γ-IR primary tumors in rat glioma (C6-L cell) xenograft model.

2015-09-18 | E-GEOD-73116 | biostudies-arrayexpress

Expression data from lung adenocarcinoma mouse tumors

Project description:To identify altered signal transduction pathways involved in the progression and metastases of Lkb1 deficient lung tumors, we have performed an unbiased microarray analysis of primary and metastatic mouse lung tumors We used microarrays to detail the global programme of gene expression underlying metastatic progression

2010-06-18 | GSE21581 | GEO

Expression data from lung adenocarcinoma mouse tumors

2010-07-08 | E-GEOD-21581 | biostudies-arrayexpress

RNA-seq of prostate cancer Patient‐Derived Xenografts derived from primary and metastatic tumors at different stages of progression

Project description:Patient-Derived Xenografts from primary (PNPCa) and metastatic (LuCaP series) prostate tumors have been implanted in immunocompromised mice and then subjected to PolyA+ RNA-sequencing.

2020-12-10 | E-MTAB-9656 | biostudies-arrayexpress

APOBEC mutagenesis and copy number alterations are drivers of proteogenomic tumor evolution and heterogeneity in metastatic thoracic tumors

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

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