Stromal myofibroblasts are drivers of invasive cancer growth

By O. De Wever, Pieter Demetter, M. Mareel, M. Bracke. International Journal of Cancer, 2008

742 citations recorded by the source corpus.

Subfields: Oncology, Pulmonary and Respiratory Medicine, Surgery

View Paper: https://www.semanticscholar.org/paper/f24701ad3d609dbc9216925496c829256093f38c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Oncology

1. B. Hinz
2. M. Mareel
3. O. De Wever
4. Valerie M. Weaver
5. Peter C. Searson
6. Denis Wirtz
7. K. Konstantopoulos

In Pulmonary and Respiratory Medicine

1. B. Hinz
2. V. Thannickal
3. Nikolaos G. Frangogiannis
4. TA Wynn

In Surgery

1. B. Hinz
2. Nikolaos G. Frangogiannis

Citations in the corpus

• Recent developments in myofibroblast biology: paradigms for connective tissue remodeling. (2012, background): “CAFs are thought to arise from several mobilized cell types, such as tissue-resident MSCs or fibroblasts, as well as recruited bone marrow– derived MSCs and fibrocytes.(122) Alternatively, or in addition, CAFs may originate from multiple resident precursors, such as endothelial cells, myoepithelial ”
• The extracellular matrix at a glance (2010, background): “Tissue inflammation potentiates stromal fibroblast activation and induces their trans - differentiation into myofibroblasts, thus exacerbating and promoting tissue desmoplasia (De Wever et al., 2008; Desmouliere et al., 2004).”
• 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”
• The myofibroblast: paradigm for a mechanically active cell. (2010, background): “Myofibroblasts further contribute to the evolution of atheromatous plaque after blood vessel injury (Bochaton-Piallat and Gabbiani, 2006) and play a crucial role in the stroma reaction to epithelial tumors (De Wever et al., 2008; Desmouliere et al., 2004).”
• The physics of cancer: the role of physical interactions and mechanical forces in metastasis (2011, positive): “and lysyl-oxidase-mediated crosslinking of the collagen fibres by tumour-associated fibroblast”
• The myofibroblast matrix: implications for tissue repair and fibrosis (2013, neutral): “A number of recent reviews have considered the nature of myofibroblastprogenitors in different organs [21], including resident fibroblasts [3,19,22-25], fibrocytes[26-28],smooth muscle cells [29], pericytes[30-33], epithelial and endothelial cells undergoing endothelial (EndoMT) or epithelial-to-mes”
• Cancer-Associated Fibroblasts: Their Characteristics and Their Roles in Tumor Growth (2015, background): “Fibroblasts in cancer tissues are similar in morphology to myofibroblasts, which are large spindle-shaped cells that are activated during the wound healing process [3].”
• Fibroblasts and myofibroblasts in wound healing (2014, positive): “5–7 The role of myofibroblasts in driving fibrotic diseases, and the recent finding that cancer-associated myofibroblasts likely influence tumor growth and correlate with poor clinical prognosis, has increased our interest in their cellular origins, their regulation, and their role in repair and…”