S100A8 and S100A9 in inflammation and cancer.
By C. Gebhardt, J. Nemeth, P. Angel, J. Hess. Biochemical Pharmacology, 2006
703 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/0977c76cae09738db3f24aee0610a981037f6ae1
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
- S. Ostrand-Rosenberg
- P. Sinha
- Larry Norton
- Swarnali Acharyya
- J. Massagué
- Thordur Oskarsson
- D. Gabrilovich
- R. Weinberg
In Molecular Biology
- Larry Norton
- Thordur Oskarsson
- S. Ostrand-Rosenberg
- Venkatraman E. Seshan
- J. Massagué
- P. Sinha
- Eric P. Skaar
- R. Weinberg
In Pulmonary and Respiratory Medicine
Citations in the corpus
- Nutritional immunity beyond iron: a role for manganese and zinc (2009, background): “Calprotectin is a heterodimer of S100A8 and S100A9 that accounts for 40–50% of the protein constituent of the neutrophil cytoplasm [47].”
- A CXCL1 paracrine network links cancer chemoresistance and metastasis (2012, positive): “S100A8/9 are low molecular weight calcium binding proteins that are associated with chronic inflammation and cancer (Gebhardt et al., 2006 À/À bone marrow showed a marked increase in the number of apoptotic cells in the mammary tumors and the lung (Figure 4A).”
- Proinflammatory S100 Proteins Regulate the Accumulation of Myeloid-Derived Suppressor Cells (2008, background): “Up-regulation of S100A8/A9 in various tumors (17), their positive autocrine secretion, and promotion of a feed forward loop involving receptors such as RAGE suggest that these proteins play an important role in inflammation mediated cancer progression.”
- Myeloid-Derived Suppressor Cells: Linking Inflammation and Cancer (2009, background): “They are elevated in patients with a variety of inflammatory diseases (92, 93) where they amplify inflammation by chemoattracting leukocytes that produce additional proinflammatory mediators (94).”