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Lian-Hai Zhang

Publications and source records attributed to Lian-Hai Zhang.

5 recordsLinked to original sources
PubMed2005

Dominant expression of 85-kDa form of cortactin in colorectal cancer.

PURPOSE: Cortactin is commonly expressed in several human cancers, which may alter their invasive or metastatic properties. Eighty five kilodalton form (p85) and 80-kDa form (p80) of cortactin are two separate bands in SDS-PAGE representing different conformational states. The objective of this study was to investigate cortactin expression in colorectal cancer (CRC). EXPERIMENTAL DESIGN: Cortactin expression was studied in an eight paired laser capture microdissection (LCM) CRC tissues and matched non-cancerous epithelia by immunoblotting. The expression in 58 CRC and two cell lines, HCT8 and HCT116, was studied respectively by immunohistochemistry and confocal laser scanning immunofluorescence. RESULTS: Dominant expression of p85 was identified in LCM-procured CRC tissues compared with equal intensity of p85 and p80 forms in non-cancerous tissues, while the amount of total cortactin was approximate. Immunohistochemistry analysis demonstrated that cortactin located in the cytoplasm of tumor cells and adjacent non-cancerous cells, and its expression was negatively correlated with TNM staging and lymphatic invasion status. However, the invasion fronts in 3 of 58 primary tumors and 28 of 39 available lymph node metastases were intensively stained. Further, immunofluorescence analysis showed that cortactin was distributed in cytoplasm and enriched in the front of the extending lamellipodia at adhering side of cultured cancer cells. CONCLUSIONS: Our results demonstrated the dominant expression of p85 form of cortactin in CRC for the first time. The enrichment of cortactin in the invasion front of some tumor cells and in the extending lamellipodia of cultured cancer cells suggests that cortactin may help cancer cell movement.

Biomarkers, Tumor↗
PubMed2005

Molecular profiling of hepatocellular carcinomas by cDNA microarray.

Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. Conventional diagnosis and treatment of this malignancy have been dismal and should be complemented by novel tools. The development and progress of HCC are believed to be caused by the accumulation of genetic changes resulting in altered expression of thousands of cancer-related genes, which can be measured by globe genetic analysis. Gene expression profiling of HCC has been employed to elucidate hepatocarcinogenesis and disclose molecular mechanisms underlying complex clinical features. Identifying phenotype-associated genes/profiles has impacts on current diagnosis and management strategy of HCC. In spite of some pitfalls of this technology and challenges in improving the research process, scrutinous validation of profiling data of HCC combined with other approaches will eventually benefit the patients.

Carcinoma, Hepatocellular↗
PubMed2003

Allelic imbalance regions on chromosomes 8p, 17p and 19p related to metastasis of hepatocellular carcinoma: comparison between matched primary and metastatic lesions in 22 patients by genome-wide microsatellite analysis.

To understand the molecular mechanisms of metastasis in hepatocellular carcinoma (HCC), it is necessary to identify the accumulating genetic alterations during its progression as well as those responsible for the acquisition of metastatic potential in cancer cells. In our previous study, using comparative genomic hybridization (CGH), we found that loss on chromosome 8p is more frequent in metastatic lesions than in matched primary tumors of HCC. Thus, 8p deletion might contribute to HCC metastasis. To narrow the location of metastasis-related alteration regions, we analyzed 22 primary and matched metastatic lesions of HCC by genome-wide microsatellite analysis. Common regions with high levels of allelic imbalance (AI) were identified on 17p, 8p11-cen, 8p21-23, 4q32-qter, 4q13-23, 16q, and 1p33. Regions with increased AI in metastatic lesions were 8p23.3, 8p11.2, 17p11.2-13.3, 4q21-22, 4q32-qter, 8q24.1, 9p11, 9q31, 11q23.1, 13q14.1-31, 13q32-qter, 16p13.3, 16q13, 16q22, and 19p13.1, and these were considered to be related to the metastasis phenotype. Among them, loss on 8p was again proved to be related to progression and metastasis of HCC, and 8p23.3 and 8p11.2 were two likely regions harboring metastasis-related genes. It was also shown for the first time in HCC that AI of 19p13.1 might also be related to metastatic potential. These results provide some candidate regions for further study to identify putative genes suppressing metastasis of HCC.

Adult↗
PubMedDate not supplied

Loss of heterozygosity at D14S62 and D14S51 detected by a simple and non-radioactive method in plasma DNA is a potential marker of metastasis and recurrence after curative hepatic resection in hepatocellular carcinoma.

BACKGROUND/AIMS: Recurrence and metastasis in hepatocellular carcinoma remains a major challenge to further improve survival. High frequency of loss of heterozygosity at D14S62 and D14S51 in tumor tissue has been shown to be closely related to metastasis and recurrence in breast cancer. But, loss of heterozygosity on 14q in plasma and tumor tissue DNA of hepatocellular carcinoma patients has not been investigated. To establish a way to predict metastasis and recurrence after curative hepatic resection, we analyzed loss of heterozygosity on 14 q in plasma and tumor tissue DNA of hepatocellular carcinoma patients with curative resection. METHODOLOGY: We used a simple, rapid and non-radioactive method to analyze loss of heterozygosity at D14S62 and D14S51 in paired plasma, lymphocyte and tumor tissue DNA of 85 hepatocellular carcinoma patients with curative resection. RESULTS: From 79 cases informative for D14S62 and 78 cases informative for D14S51 of 85 hepatocellular carcinoma tissue DNA, loss of heterozygosity at D14S62 and D14S51 was present in 45 (57.0%) and 41 (52.6%) cases respectively. And in 96.0% of the tissues which showed loss of heterozygosity we were able to detect loss of heterozygosity in their matched plasma. In matched 85 cases of hepatocellular carcinoma plasma DNA, we detected loss of heterozygosity at D14S62 in 55.7% and at D14S51 in 50.0% of the respective informative DNA samples. The loss of heterozygosity patterns of plasma DNA were almost identical to their corresponding tumor tissues. A comparison of these genetic changes with clinicopathological data of these checked hepatocellular carcinoma patients showed that loss of heterozygosity at D14S62 and D14S51 was adversely correlated significantly with the presence of tumor size, with 35.4% at both the D14S62 and D14S51 locus in the HTMR (high-tendency to metastasis and recurrence) group compared with 72.9% and 59.4% in the LTMR (low-tendency to metastasis and recurrence) group at D14S62 and D14S51, respectively (P = 0.001 and P = 0.027, respectively). CONCLUSION: Our results suggest that loss of heterozygosity at D14S62 and D14S51 plays an important role in the metastasis and recurrence of hepatocellular carcinoma patients following curative resection. Loss of heterozygosity at D14S62 and D14S51 in the plasma DNA of hepatocellular carcinoma patients detected by a simple and non-radioactive method has great potentials to be clinically used to predicate metastasis and recurrence after curative hepatic resection.

Biomarkers, Tumor↗