|
BMC Cancer 2012
Increased serum sTRAIL levels were correlated with survival in bevacizumab-treated metastatic colon cancerAbstract: sTRAIL and VEGF levels were measured by ELISA in the sera of 16 bevacizumab-treated metastatic colon cancer patients and 10 presumably healthy age-matched controls. The measurements were taken before and after treatment for comparison purposes.Elevated levels of sTRAIL were found in seven out of 16 patients after bevacizumab treatment. Although these patients had a median survival time of 20.6 months, the remaining bevacizumab-treated patients who did not show an increase in sTRAIL had a median survival time of 9.4 months. As expected, serum VEGF levels were decreased in all patients who received bevacizumab therapy and showed no correlation between serum VEGF levels and patient survival (data not shown).Serum sTRAIL levels might be a useful predictor of prognosis in metastatic colon cancer, in the early evaluation stages following bevacizumab treatment.Colorectal cancer is the third most common cancer and the second leading cause of cancer-related death [1]. Overall, the 5-year survival rate is <10% for stage IV cancer [2]. The cure rate with surgery alone is very low and chemotherapy and radiotherapy are usually needed in patients with untreated metastatic colon cancer. The development of colorectal cancer is characterized by a sequence of events during which normal colonic epithelium gradually transforms to carcinoma tissue, in most cases, via the development of colorectal adenomas [3]. This sequence of events is driven by an accumulation of molecular (epi)genetic alterations causing progressive disorders in cell growth, differentiation and apoptosis [4,5]. Apoptosis, or programmed cell death, plays an important role in the development and maintenance of tissue homeostasis but also represents an effective mechanism by which abnormal cells, such as tumor cells, can be eliminated [6-8]. Abnormalities in apoptotic function or resistance to apoptosis have been identified as important events in the pathogenesis of colorectal cancer and its resistance to chemotherapeut
|