肿瘤血栓临床研究-..(陆舜).pptVIP

* In this hypothesis, it is proposed that heparins may inhibit the adhesion of circulating tumour cells to platelets, leucocytes, and endothelial cells by binding to cell-adhesion molecules such as P-selectin. * * * This was an experimental study comparing the ability of various heparins to interfere with P-selectin-dependent tumour cell interactions. At equivalent concentrations in terms of anti-factor Xa units, nadroparin, but not enoxaparin, significantly inhibited P-selectin-dependent tumour cell interactions. UFH was also effective in this model. * In a mouse experimental model, the nadroparin dose (in anti-Xa units) required to inhibit lung metastases by 50% was five-fold lower than that of enoxaparin. The ability of heparins (UFH, nadroparin and enoxaparin) to inhibit P-selectin-dependent tumour cell interactions in vitro was positively correlated with their ability to inhibit experimental lung metastases in vivo. * * Breast cancer was more frequent in the Fraxiparine? group, whereas colorectal and cervical cancers were seen more often in the placebo group. A small proportion of patients did not have metastatic disease. The types of locally advanced disease in this group included hepatocellular, oesophageal, and pancreatic cancer. * The overall hazard ratio for mortality was 0.75 with a median survival of 8.0 months in the Fraxiparine? group vs. 6.6 months in the placebo group. After adjustment for potential confounders (life expectancy, WHO performance status, concomitant treatment, type and histology of cancer), the beneficial effect of Fraxiparine? on survival remained significant. * In the a priori specified subgroup of patients with a life expectancy of six months or above at enrolment, the hazard ratio for mortality was 0.64, with a median survival of 15.4 and 9.4 months in the Fraxiparine? and placebo groups, respectively. In patients with a shorter life expectancy, the hazard ratio of mortality was 0.88 (95% CI: 0.62 to 1.25). * * Gemcitabine