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Loss of TGF-β signaling in mice leads to promoted hypertrophic conversion of articular chondrocytes, which process is suggested to be linked to progression of osteoarthritis (OA).
While Gaucher patients are frequently reported to demonstrate alterations in cytokine/chemokine production that could be linked to progression of multiple myeloma, there is no consistent pattern that implicates the involvement of one or more specific mediators.
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Declining levels of endothelial progenitor cells within systemic circulation have likewise been linked to progression of cardiovascular diseases.
The CD44v6 adhesion molecule has been linked to progression of various carcinomas, but its role in relation to oral-cancer development is not clear.
Angiogenesis and disruption of liver vascular architecture have been linked to progression to cirrhosis and liver cancer (HCC) in chronic liver diseases, which contributes both to increased hepatic vascular resistance and portal hypertension and to decreased hepatocyte perfusion.
Furthermore, prior studies in humans found lower levels of magnesium (thus, higher serum calcium/magnesium ratio) lead to inflammation and insulin resistance which have been linked to progression of prostate cancer.
Overexpression of these proteins has been linked to progression and metastasis of breast cancer.
TGF-β accumulation in valves has been linked to progression of valve fibrosis and subsequent calcification (3).
Human SPINT2 (HAI-2) is a physiological inhibitor of matrix cleaving proteases and decreased expression of SPINT2 has been linked to progression of several cancers [ 107- 109].
Nuclear localisation has been linked to progression of colorectal carcinogenesis when a certain threshold tumour size is exceeded (Brabletz et al, 2000).
GTPases from the Rho family have been linked to progression of human cancer, and the Rho/ROCK pathway is considered to be involved in tumor progression by regulating the actin cytoskeleton [ 15- 17].
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