Galectin-3 is reported to be overexpressed in a variety of neoplastic cells and is suggested to be involved in tumour metastasis by, e.g. enhancing adhesion between tumour cells and extracellular matrix, promoting embolization. However, no generalized conclusion on the role of Gal-3 in cancer has yet been established. The lectin is not only produced and secreted into the plasma by tumour tissues, but also by peritumoural inflammatory cells and stromal cells.
Elevated Gal-3 levels in the serum/plasma have been reported in some cancers, e.g., metastatic breast and gastrointestinal cancer. However, decreased levels of this lectin have been observed in metastatic breast, endometrial and ovary carcinomas, while the levels in Non-Hodgkin's lymphoma and melanoma  have not been observed to change. Elevated levels of circulating Gal-3 have not only been observed in cancers, but also in chronic inflammations, e.g. inflammatory bowel disease , obesity, type 2 diabetes , and heart failure [7, 8]. The present studies showed that a higher circulating Gal-3 concentration was observed in liver cancer (NS) and echinococcosis patients than in the healthy control group. The results concerning the cancerous patients, even if not significant, seem to be consistent with the results mentioned above  as well as with those reported by Matsuda et al. , who observed a higher level of the circulating lectin in liver cancer than in the control group and subjects with chronic liver disease. However, the present report would seem to be the first to compare the levels of Gal-3 in the plasma of cancer patients, echinoccosis patients and healthy volunteers. The highest level observed in echinococcosis could be the result of inflammation related to parasite invasion. Nevertheless, liver cancer is also associated with inflammation and exhibited similar CRP levels to, and higher leukocyte levels than, echinococcosis. Factors other than the inflammation that occurs in echinococcosis might therefore influence the Gal-3 level in the plasma.
sE-cadherin is a form, cleaved from E-cadherin by proteases such as MMP-3, MMP-7 , plasmin , ADAM10 , ADAM15 , whereas sN-CAD is cleaved by ADAM10 , MT1-MMP , MT5-MMP , MMP-9, MMP-12 , and Presenilin 1 . The induction/upregulation of various MMPs (e.g. MMP-2, MMP-3, MMP-7 and/or MMP-9) has been detected in tumourous liver tissues obtained from, e.g. hepatocellular carcinoma (HCC) patients, whereas the expression of plasminogen activators appears to be largely confined to stromal and inflammatory cells. Inflammation also enhances the expression of MMPs, e.g. in endothelial cells, lymphocytes and macrophages. Furthermore, the expression of certain MMPs and plasminogen activators is also increased in liver cells during liver regeneration [19, 20].
Elevated sE-Cad was observed in the serum or plasma of patients with gastric carcinoma , bladder cancer , non-small cell lung cancer , melanoma , late-stage colorectal carcinoma , and hepatocellular carcinoma . However, higher levels of that cadherin have also been found in gastroesophageal reflux disease , multiorgan dysfunction , endometriosis , familial adenomatous polyposis , and acute pancreatitis . Higher amounts of the serum sN-CAD have been described in a group of cancerous patients suffering from prostate carcinoma, breast cancer, ovarian cancer, and gastrointestinal carcinoma, and have been mentioned as being present in diabetes and liver cirrhosis (data not shown) as well . The present study exhibited a higher plasma concentration of sE-CAD in the liver cancer group than the healthy group. This is consistent with the results reported by Sayoma et al. .
Moreover, the level of the marker was observed to be lower in the echinococcosis group than the healthy control group. This suggests that sE-cadherin would be a valuable marker of HCC not only because of its association with early recurrence and extrahepatic metastasis , but also owing to its ability to distinguish between liver cancer and echinococcosis. In the present study, the plasma sN-CAD concentration in liver cancer was also observed to be lower than that in the healthy group. These results are difficult to explain and require further analysis. Moreover, they seem to be inconsistent with the results reported by Derycke et al. . However, there is no information about the presence of liver carcinoma in the cancerous group examined by them.
The lower levels of the plasmas sN-CAD and sE-CAD in echinococossis patients than in healthy subjects could be explained by the ability of Echinococcus granulosus to evade certain defence mechanisms by such means as modulating the host's immune system and resisting the host's proteolytic enzymes by dealing efficiently with, e.g. MMP-9 [19, 30]. Discriminant analysis revealed that the association of two or more markers significantly increased their efficiency. These results seem to encourage other scientists to combine two or more markers, which are not effective enough when used separately.