An increasing number of molecular markers are being identified that correlate with cancer metastasis or a poor prognosis. Typically these markers were examined based on the potential for a biologic activity that would act to enhance cancer cell growth and metastasis. There are also reports of various cytokine or growth factor receptors that are constitutively activated via autocrine or paracrine loops thus supporting cancer cell growth. While granulocyte colony-stimulating factor (G-CSF) expression has been shown for a wide variety of cancer cell types, an increasing number of reports are being published regarding the aberrant expression of the G-CSF receptor (G-CSFR) by various non-hematopoietic human cancers and cancer cell lines.
Our aim i s to clearly demonstrate that G-CSF expression coupled with aberrant G-CSFR expression by transitional cell carcinoma (TCC) can be used as a predictor of more aggressive behavior. We will demonstrate the biological impact of G-CSF/G-CSFR expression in in vitro and also in vivo by using a murine TCC model. Thus the aberrant G-CSFR expression that is being demonstrated by an expanding variety of solid tumors may serve as both a marker of specific tumor cell capabilities impacting clinical outcome and as a mechanism for many of these tumor-enhancing functions.
| Chakraborty, Arup; Guha, Sushovan (2007) Granulocyte colony-stimulating factor/granulocyte colony-stimulating factor receptor biological axis promotes survival and growth of bladder cancer cells. Urology 69:1210-5 |
| Chakraborty, Arup; White, Scott M; Guha, Sushovan (2006) Granulocyte colony-stimulating receptor promotes beta1-integrin-mediated adhesion and invasion of bladder cancer cells. Urology 68:208-13 |
