The effects of surgery, with or without rhGM-CSF, on the angiogenic profile of patients treated for colorectal carcinoma

172: Serum endostatin levels are elevated in colorectal cancer and correlate with invasion and systemic inflammatory markers

“…A similar association has been reported in several human cancers and recently also in gastrointestinal cancers, including CRC, gastric cancer and hepatocellular cancer (Li et al, 2012). It has also been shown that the removal of a primary colorectal tumour leads to a decrease in serum endostatin levels (Wu et al, 2004;Peeters et al, 2005). However, our study suggests that endostatin is unlikely to prove to be a valuable tool in CRC diagnosis or follow-up, because of relatively low AUC (0.618) in discriminating the patients from healthy controls in ROC analysis.…”

Minimally invasive colon resection for malignant colonic conditions is associated with a transient early increase in plasma sVEGFR1 and a decrease in sVEGFR2 levels after surgery

“…The increases noted during the first postoperative month may be a manifestation of wound healing, whereas the later decreases likely reflect the removal of a VEGF-producing cancer [24,25]. Significantly higher VEGF levels have been noted during the first 8 days after resection of a variety of tumors and up to 2 to 4 weeks after minimally invasive colorectal resection (MICR) for colorectal cancer [6,20,21,26,27]. Persistently elevated blood VEGF levels may stimulate the growth of residual tumor cells and tumor microfoci during the first month after surgery.…”

Granulocyte Colony-Stimulating Factor and Granulocyte-Macrophage Colony-Stimulating Factor Promote Malignant Growth of Cells from Head and Neck Squamous Cell Carcinomas In vivo

“…Although originally identified as hematopoietic growth factors (10), both factors are also produced by a variety of nonhematopoietic cells, including fibroblasts, endothelial cells, and keratinocytes (11,12). They induce the proliferation and migration of endothelial cells, thereby contributing to angiogenesis (13,14), and can promote keratinocyte proliferation (5,15,16), resulting in a stimulatory role on wound healing (17)(18)(19). In normal cells (e.g., keratinocytes), the expression of both factors is strictly regulated (20), requiring induction by appropriate stimuli, such as interleukin-1, tumor necrosis factor-a, or lipopolysaccharides (16,21).…”

“…In contrast, the constitutive expression of G-CSF and GM-CSF, frequently together with their respective receptors, is found in numerous solid tumors (3,22), such as skin or head and neck squamous cell carcinoma (HNSCC; refs. 6,8,18,23,24), gliomas (4), and meningiomas (9). G-CSF and GM-CSF contribute to tumor growth and progression by autocrine stimulation of proliferation and migration in skin SCC and gliomas (4)(5)(6) and by enhancing the invasive capacity of human lung cancer cells in vitro (7).…”

“…On the other hand, due to their role as recruitment, proliferation, and maturation factors for granulocytes and macrophages as well as their stimulatory effect on wound healing, G-CSF and GM-CSF are commonly used in cancer therapy to ameliorate mucositis and neutropenia and to accelerate wound healing (18,19,26). In the therapy of HNSCC, oropharyngeal mucositis is a painful, often dose-limiting side effect of radiotherapy and chemotherapy (27).…”