Stromal fibroblasts in cancer initiation and progression
By N. Bhowmick, Eric G. Neilson, H. Moses. Nature, 2004
2,366 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/1c274f7b3a1f80cff94e0e5c2c687fb1e7496525
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Citations in the corpus
- MET signalling: principles and functions in development, organ regeneration and cancer (2010, background): “During tissue repair and cancer invasion, several cytokines that are abundant in the reactive interstitial compartment — for example, interleukin-1 and -6, tumour necrosis factor-α and transforming growth factor-β (TGFβ) — induce transcriptional upregulation of both HGF (in fibroblasts and residen”
- Fibroblast-led collective invasion of carcinoma cells with differing roles for RhoGTPases in leading and following cells (2007, background): “, and the tumour-promoting role of carcinoma-associated fibroblasts is well documente”
- Hallmarks of cancer: interactions with the tumor stroma. (2010, background): “The induction of malignant progression was accompanied by stromal expansion and an increased expression of HGF, leading to augmented signaling by c-Met in epithelial cells.”
- The tumour microenvironment as a target for chemoprevention (2007, background): “This newer version of an old hypothesis now enables us to consider that stromal cells and their associated matrix, as well as cells of the immune system, have important roles in tumour angiogenesis and carcinogenesi”
- Epithelial—mesenchymal and mesenchymal—epithelial transitions in carcinoma progression (2007, background): “Stromal fibroblasts produce ECM proteins and secrete many growth factors and hormones, including HGF, IGF-I, IGF-II, EGF, TGF-a, TGF-b1,-b2, and -b3, FGF-7, -2, and –10, and interleukin-6 (Bhowmick et al., 2004).”
- Targeting the tumour vasculature: insights from physiological angiogenesis (2010, background): “TAFs are increasingly recognized as having an active role in tumorigenesi”
- Keratinocyte-fibroblast interactions in wound healing. (2007, background): “There is strong evidence that these patterns of epithelial–mesenchymal interactions persist in adult life and regulate skin homeostasis, part of the wound-healing response (Martin and Parkhurst, 2004), or become critically involved in tumor cell invasion and tumor progression (Bhowmick et al., 2004;”
- Extracellular matrix: a dynamic niche component during cancer progression (2012, positive): “The main contributors of altered activities of ECM remodeling enzymes and thus abnormal ECM metabolism are stromal cells, including cancer associated fibroblasts (CAFs) and immune cells (Bhowmick et al., 2004; Orimo et al., 2005).”
- Biomechanical remodeling of the microenvironment by stromal Caveolin-1 favors tumor invasion and metastasis (2011, background): “CAFs, the main cell component of the desmoplastic stroma of solid cancers and their metastases (Bhowmick et al., 2004), influence TC growth through paracrine secretion of growth factors and recruit endothelial progenitors to promote angiogenesis (Karnoub et al., 2007; Orimo et al., 2005).”
- Tumor-stroma interactions in pancreatic ductal adenocarcinoma (2007, background): “New evidence indicates that mutations arising in stromal fibroblasts and consequent manifestation of paracrine factors promote growth and proliferation of carcinoma cells (2).”
- Autocrine TGF-β and stromal cell-derived factor-1 (SDF-1) signaling drives the evolution of tumor-promoting mammary stromal myofibroblasts (2010, neutral): “GFP-shRNA 5′-GCAAGCTGACCCTGAAGTTCA-3′ (4) CXCR4-shRNA1 5′-ATGGATTGGTCATCCTGGTCA-3′ (10) CXCR4-shRNA2 5′-ATCCTGGCCTTCATCAGTCTG-3′ (11) SDF-1-shRNA1 5′-TCCTCGTGCTGACCGCGCTCT-3′ SDF-1-shRNA2 5′-AGCTATTCCTACTCTCTCCCC-3′ TβR-II-shRNA1 5′-GAATGACGAGAACATAACACT-3′ (12) TβR-II-shRNA2 5′-GATTCAAGAGTATTCTCACT”
- Mutant p53 in Cancer: New Functions and Therapeutic Opportunities (2014, background): “CAFs, the most abundant cell type in the stroma, secrete cytokines, hormones, and growth factors including hepatocyte growth factor and TGF-b (Bhowmick et al., 2004; Ostman and Augsten, 2009), both of which have been shown to mediate mutant p53-dependent invasion and metastasis (Adorno et al.,…”
- Hallmarks of cancer: the next generation. (2011, positive): “Recruited myofibroblasts and reprogrammed variants of normal tissue-derived fibroblastic cells have been demonstrated to enhance tumor phenotypes, notably cancer cell proliferation, angiogenesis, and invasion and metastasis; their tumorpromoting activities have largely been defined by transplantatio”