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Xiong-Zhi Wu

Publications and source records attributed to Xiong-Zhi Wu.

9 recordsLinked to original sources
PubMed2007

Bone marrow-derived cells: roles in solid tumor. Minireview.

The role of cancer stem cells has been demonstrated for some cancers. Recently, research indicated that solid tumors may originate from bone marrow stem cells. Bone marrow-derived cells have recently been shown to contribute to stromal formation, especially angiogenesis and lymphvasculogenesis. Moreover, the interaction and the cell fusion between cancer cells and bone mesenchymal stem cells could enhance the aggregative ability of cancer cells. Bone marrow derived cells home to tumor-specific pre-metastatic sites to provide a permissive niche for incoming tumor cells. Since bone marrow-derived cells play an important role in carcinogenesis, angiogenesis and metastasis, bone marrow-derived cells are not only the tool for cancer therapy, but also the targets for cancer therapy.

Bone Marrow Cells↗
PubMed2006

A new classification system of anticancer drugs - based on cell biological mechanisms.

The arrival of a great number of new anticancer agents has made it necessary to reclassify all of them. We established a new classification system based on cell biological mechanisms. Anticancer drugs were grouped as cytotoxic drug and modifier, which could regulate the interaction of tumor, host and drugs. The modifiers were subdivided into three groups: cell biological modifier which reverses the abnormal biological behaviour of tumor cells, biological response modifier which regulates the host response of tumor and biochemical modulator which affects the host's metabolic pathway of cytotoxic drug to enhance the chemosensitivity or reduce the adverse reaction. Combination with cell biological modifiers and cytotoxic drugs play a double role of killer and rectifier for tumor cells, whereas biological response modifiers and cytotoxic drugs are combined to regulate the tumor-host interaction. Biochemical modulators and cytotoxic drugs are combined to enhance the chemosensitivity or improve the dose of cytotoxic drugs.

Animals↗
PubMed2006

Helicobacter pylori and hepatocellular carcinoma: correlated or uncorrelated?

Helicobacter pylori can be detected in liver tissue resected from patients with hepatocellular carcinoma. Conflicting reports regarding the relationship between H. pylori and hepatocellular carcinoma mean it is uncertain whether H. pylori acts as a troublemaker, co-risk factor or innocent bystander to the development of hepatocellular carcinoma. Clinical studies in patients without known causes of hepatocellular carcinoma are important to discover whether H. pylori is involved in the carcinogenesis of hepatocellular carcinoma. High quality prospective studies in patients with hepatocellular carcinoma, hepatitis C virus infection and no cirrhosis are needed to determine whether H. pylori is a co-risk factor for hepatocellular carcinoma.

Carcinoma, Hepatocellular↗
PubMed2006

Origin of hepatocellular carcinoma: role of stem cells.

The question of whether hepatocellular carcinoma (HCC) arises from the differentiation block of stem cells or dedifferentiation of mature cells remains controversial. Recently, researchers suggested that HCC may originate from the transdifferentiation of bone marrow cells. Interestingly, there are four levels of cells in the hepatic stem cell lineage: bone marrow cells, hepato-pancreas stem cells, oval cells and hepatocytes. Hematopoietic stem cells and the liver are known to have a close relationship in early development. Bone marrow stem cells could differentiate into oval cells, which could differentiate into hepatocytes and duct cells. The development of pancreatic and liver buds in embryogenesis suggests the existence of a common progenitor cell to both the pancreas and liver. Cellular events during hepatocarcinogenesis illustrate that HCC may arise from cells at various stages of differentiation in the hepatic stem cell lineage.

Animals↗
PubMed2004

Early diagnosis of bacterial and fungal infection in chronic cholestatic hepatitis B.

AIM: To investigate the early diagnostic methods of bacterial and fungal infection in patients with chronic cholestatic hepatitis B. METHODS: One hundred and one adult in-patients with chronic hepatitis B were studied and divided into 3 groups: direct bilirubin (DBil)/total bilirubin (TBil) > or = 0.5, without bacterial and fungal infection (group A, n=38); DBil/TBil <0.5, without bacterial and fungal infection (group B, n=23); DBil/TBil> or = 0.5, with bacterial or fungal infection (group C, n=40). The serum biochemical index and pulse rate were analyzed. RESULTS: Level of TBil, DBil, alkaline phosphatase (ALP) and DBil/ALP in group A increased compared with that in group B. The level of ALP in group C decreased compared with that in group A, whereas the level of TBil, DBil and DBil/ALP increased (ALP: 156+/-43, 199+/-68, respectively, P<0.05; TBil: 370+/-227, 220+/-206, respectively, P<0.01; DBil: 214+/-143, 146+/-136, respectively, P<0.01; DBil/ALP: 1.65+/-1.05, 0.78+/-0.70, respectively, P<0.001). The level of DBil and infection affected DBil/ALP. Independent of the effect of DBil, infection caused DBil/ALP to rise (P<0.05). The pulse rate in group A decreased compared with that in group B (63.7+/-6.4, 77.7+/-11.4, respectively, P<0.001), and the pulse rate in group C increased compared with that in group A (81.2+/-12.2, 63.7+/-6.4, respectively, P<0.001). The equation (infection=0.218 pusle rate +1.064 DBil/ALP -16.361), with total accuracy of 85.5%, was obtained from stepwise logistic regression. Pulse rate (> or =80/min) and DBil/ALP (> or =1.0) were used to screen infection. The sensitivity was 62.5% and 64.7% respectively, and the specificity was 100% and 82.8% respectively. CONCLUSION: Bacterial and fungal infection deteriorate jaundice and increase pulse rate, decrease serum ALP and increase DBil/ALP. Pulse rate, DBil/ALP and the equation (infection=0.218 pusle rate+1.064 DBil/ALP-16.361) are helpful to early diagnosis of bacterial and fungal infection in patients with chronic cholestatic hepatitis B.

Bacterial Infections↗