Inflammation and EMT: an alliance towards organ fibrosis and cancer progression

By J. López-Novoa, M. Nieto. EMBO Molecular Medicine, 2009

654 citations recorded by the source corpus.

Recent advances in our understanding of the molecular pathways that govern the association of inflammation with organ fibrosis and cancer point to the epithelial to mesenchymal transition (EMT) as the common link in the progression of these devastating diseases. The EMT is a crucial process in the development of different tissues in the embryo and its reactivation in the adult may be regarded as a physiological attempt to control inflammatory responses and to ‘heal’ damaged tissue. However, in pathological contexts such as in tumours or during the development of organ fibrosis, this healing response adopts a sinister nature, steering these diseases towards metastasis and organ failure. Importantly, the chronic inflammatory microenvironment common to fibrotic and cancer cells emerges as a decisive factor in the induction of the pathological EMT.

Subfields: Genetics, Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/c987d18b5d07c4ae76778bb6fca8b58799716e8a

How researchers see this paper

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

In Genetics

1. J. P. Thiery
2. M. Nieto
3. Valerie M. Weaver
4. Arul M. Chinnaiyan
5. F. Greten
6. M. Egeblad
7. H. Acloque
8. R. Weinberg

In Oncology

1. M. Nieto
2. J. P. Thiery
3. R. Huang
4. Valerie M. Weaver
5. H. Acloque
6. F. Greten
7. Morten G. Rasch
8. M. Egeblad

In Pulmonary and Respiratory Medicine

1. J. P. Thiery
2. M. Nieto
3. R. Huang
4. Arul M. Chinnaiyan
5. R. Weinberg
6. Jormay Lim

Citations in the corpus

• Epithelial-Mesenchymal Transition in Cancer: Parallels Between Normal Development and Tumor Progression (2010, background): “While EMT is a critical normal process during development and wound healing, recently properties of EMT have been implicated in human pathology, including fibrosis and cancer metastasis [12].”
• IL-6R/STAT3/miR-34a feedback loop promotes EMT-mediated colorectal cancer invasion and metastasis. (2014, background): “Growing evidence suggests that inflammation promotes EMT (5).”
• Epithelial-mesenchymal transitions in development and disease. (2009, background): “Interestingly, recent studies point to the inflammation-induced EMT as critical to this connection (López-Novoa and Nieto, 2009).”
• Dynamic interplay between the collagen scaffold and tumor evolution (2010, background): “Fibrosis is an accumulation of ECM proteins, including type I collagen [8].”
• The ins and outs of the epithelial to mesenchymal transition in health and disease. (2011, background): “MET: mesenchymal to epithelial transition the stroma in breast tumors (Ramón y Cajal 1890; see also López-Novoa & Nieto 2009).”
• Integrative Clinical Genomics of Metastatic Cancer (2017, positive): “Metastatic tumors fall into two main subtypes: an EMT-like subtype associated with inflammation signatures 29 , and a proliferative subtype associated with increased metabolism and systemic stress.”