Can we use GP73 as a biomarker for the detection of hepatocellular carcinoma?

Hepatocellular carcinoma [HCC] is one of the top five leading causes of death in Egypt and its prevalence is increasing in the next 10-20 years. We aimed to detect the serum Golgi protein 73 [GP73] in patients with cirrhosis and with HCC, and to determine its sensitivity and specificity as a screening tool for the detection of HCC in this study. Serum GP73 was estimated in 93 participants [patients with HCC, patients with cirrhosis, and healthy controls]. GP73 was elevated in patients with HCC and liver cirrhosis; serum level was very high in HCC patients [P<0.01] when compared with the other studied groups. GP73 had sensitivity of 76%, specificity of 75%, at a cut-off value of 16.2 ng/ml with area under the receiver operator characteristic of 0.825 when compared with alpha-fetoprotein that showed a sensitivity of 63%, specificity of 43% at a cut-off value of 16.5 ng/ml and area under the receiver operator characteristic of 0.611. By combining alpha-fetoprotein and GP73 for the diagnosis of HCC, sensitivity and specificity were [93 and 25%], respectively. There is a significant positive correlation between diameter of the focal lesion and GP73 [P=0.01 and r=0.071]. Nonsignificant positive correlation was detected as regards serum GP73 and the number of HCC. GP73 can be used as a screening tool for the detection of HCC. Moreover, it shows a higher serum level with larger lesions

cDNA Microarray Analysis of Differential Gene Expression in Gastric Cancer Cells Sensitive and Resistant to 5-Fluorouracil and Cisplatin / Journal of the Korean Cancer Association, 대한암학회지

PURPOSE: Gastric cancer is one of the most prevalent cancers worldwide. 5-fluorouracil (5-FU) and cisplatin are the most commonly used drugs for the treatment of gastric cancer. However, a significant number of tumors often fail to respond to chemotherapy. MATERIALS AND METHODS: To better understand the molecular mechanisms underlying drug resistance in gastric cancer the gene expression in gastric cancer cells, which were either sensitive or resistant to 5-FU and cisplatin, were examined using cDNA microarray analysis. To confirm the differential gene expression, as determined using the microarray, semiquantitative RT-PCR was performed on a subset of differentially expressed cDNAs. RESULTS: 69 and 45 genes, which were either up-regulated (9 and 22 genes) or down-regulated (60 and 25 genes), were identified in 5-FU- and cisplatin-resistant cells, respectively. Several genes, such as adaptor-related protein complex 1 and baculoviral IAP repeat-containing 3, were up-regulated in both drug-resistant cell types. Several genes, such as the ras homolog gene family, tropomyosin, tumor rejection antigen, protein disulfide isomerase-related protein, melanocortin 1 receptor, defensin, cyclophilin B, dual specificity phosphatase 8 and hepatocyte nuclear factor 3, were down-regulated in both drug-resistant cell types. CONCLUSION: These findings show that cDNA microarray analysis can be used to obtain gene expression profiles that reflect the effect of anticancer drugs on gastric cancer cells. Such data may lead to the assigning of signature expression profiles of drug-resistant tumors, which may help predict responses to drugs and assist in the design of tailored therapeutic regimens to overcome drug resistance.