We are analyzing https://link.springer.com/article/10.1007/s10142-024-01524-7.

Title:
Pan-cancer secreted proteome and skeletal muscle regulation: insight from a proteogenomic data-driven knowledge base | Functional & Integrative Genomics
Description:
Large-scale, pan-cancer analysis is enabled by data driven knowledge bases that link tumor molecular profiles with phenotypes. A debilitating cancer-related phenotype is skeletal muscle loss, or cachexia, which occurs partly from tumor products secreted into circulation. Using the LinkedOmicsKB knowledge base assembled from the Clinical Proteomics Tumor Analysis Consortium proteogenomic analysis, along with catalogs of human secretome proteins, ligand-receptor pairs and molecular signatures, we sought to identify candidate pan-cancer proteins secreted to blood that could regulate skeletal muscle phenotypes in multiple solid cancers. Tumor proteins having significant pan-cancer associations with muscle were referenced against secretome proteins secreted to blood from the Human Protein Atlas, then verified as increased in paired tumor vs. normal tissues in pan-cancer manner. This workflow revealed seven secreted proteins from cancers afflicting kidneys, head and neck, lungs and pancreas that classified as protein-binding activity modulator, extracellular matrix protein or intercellular signaling molecule. Concordance of these biomarkers with validated molecular signatures of cachexia and senescence supported relevance to muscle and cachexia disease biology, and high tumor expression of the biomarker set associated with lower overall survival. In this article, we discuss avenues by which skeletal muscle and cachexia may be regulated by these candidate pan-cancer proteins secreted to blood, and conceptualize a strategy that considers them collectively as a biomarker signature with potential for refinement by data analytics and radiogenomics for predictive testing of future risk in a non-invasive, blood-based panel amenable to broad uptake and early management.
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Keywords {🔍}

pubmed, article, google, scholar, cas, cancer, central, cell, muscle, cachexia, wang, zhang, protein, chen, skeletal, nat, tumor, kim, analysis, human, liu, growth, sci, yang, secreted, mice, lee, pancancer, res, med, tgfbeta, factor, secretome, signaling, expression, rev, cells, clinical, biol, mol, biomarkers, inhibitor, patients, proteins, physiol, role, promotes, data, clin, sparc,

Topics {✒️}

c-src-akt-lkb1-ampkalpha pathway nfkappab-bmp signaling cross-talk tumor cell-derived tgf-beta nitric-oxide synthase-dependent mechanism interferon-gamma-producing tumor cells month download article/chapter tgf-beta signalling-related markers blood-based multi-cancer detection high-fat-fed c57bl/6 mice stetler-stevenson wg transforming growth factor-beta1 amp-activated protein kinase function-related proteome profiling single-cell antigen-specific landscape tumor lipid-mobilizing factor multi-cancer early detection plasma cell-free dna nanotechnology-based multidimensional harvesting pan-cancer secreted proteome immunomodulatory tgf-beta signaling liquid biopsy-based biomarkers igf1-akt/pkb pathway wnt/beta-catenin signaling induce pro-fibrotic activation liquid-biopsy proteomics combined myc/mtor-driven model specific multi-cancer detection cell-free dna approaches fstl-1-mediated glucose uptake degraded ffpe-rna samples regulate tgfbeta-induced expression aptamer-based discovery platform tgf-beta signal augmentation significant pan-cancer associations multicancer detection tests g1 cell-cycle control fak/akt signaling pathway c26 tumour-bearing mice protein-binding activity modulator senescence atlas reveals pai-1-regulated mir-21 defines debilitating cancer-related phenotype mediating igf-independent effects multicentre case-control study blood-based panel amenable human protein atlas tumor-supportive immune microenvironment protein tumour markers tumor suppressor skeletal muscle atrophy

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      description:Large-scale, pan-cancer analysis is enabled by data driven knowledge bases that link tumor molecular profiles with phenotypes. A debilitating cancer-related phenotype is skeletal muscle loss, or cachexia, which occurs partly from tumor products secreted into circulation. Using the LinkedOmicsKB knowledge base assembled from the Clinical Proteomics Tumor Analysis Consortium proteogenomic analysis, along with catalogs of human secretome proteins, ligand-receptor pairs and molecular signatures, we sought to identify candidate pan-cancer proteins secreted to blood that could regulate skeletal muscle phenotypes in multiple solid cancers. Tumor proteins having significant pan-cancer associations with muscle were referenced against secretome proteins secreted to blood from the Human Protein Atlas, then verified as increased in paired tumor vs. normal tissues in pan-cancer manner. This workflow revealed seven secreted proteins from cancers afflicting kidneys, head and neck, lungs and pancreas that classified as protein-binding activity modulator, extracellular matrix protein or intercellular signaling molecule. Concordance of these biomarkers with validated molecular signatures of cachexia and senescence supported relevance to muscle and cachexia disease biology, and high tumor expression of the biomarker set associated with lower overall survival. In this article, we discuss avenues by which skeletal muscle and cachexia may be regulated by these candidate pan-cancer proteins secreted to blood, and conceptualize a strategy that considers them collectively as a biomarker signature with potential for refinement by data analytics and radiogenomics for predictive testing of future risk in a non-invasive, blood-based panel amenable to broad uptake and early management.
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         Secretome
         Human protein atlas
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         Plant Genetics and Genomics
         Microbial Genetics and Genomics
         Biochemistry
         general
         Bioinformatics
         Animal Genetics and Genomics
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            address:
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            address:
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