[Relationship between hMSH2 and FHIT gene expression in non-small cell lung cancer].

BACKGROUND & OBJECTIVE: Abnormality of FHIT gene has been proved to be frequent in certain malignant tumors closely related to environmental oncogenic factors, such as lung cancer. Foreign scholars have begun to explore the relationship between FHIT gene and other tumor suppressor genes, which are implicated in the pathogenesis of lung cancer. This study was designed to investigate the relationship between hMSH(2) and FHIT protein expression and to explore the correlation of hMSH(2) and FHIT protein expression with clinicopathologic features of lung cancer. METHODS: Immunohistochemical analysis of hMSH(2) and FHIT protein expression in 40 lung cancer cases and 15 adjacent non-cancer lung tissues was performed; the positive rates of FHIT and hMSH(2) proteins were measured by image analysis system. RESULTS: (1)The positive rates of FHIT and hMSH(2) proteins were 58.2% and 45.8% respectively in lung cancer tissues compared with 89.1% and 65.3% in non-cancer lung tissues. The expression levels of FHIT and hMSH(2) proteins were significantly lower in lung cancer tissues than that in non-cancer lung tissues (P< 0.01). (2)Reduced expression levels of both proteins were significantly related to tumor histology. The positive rate of the FHIT protein was 52.2% in squamous cell carcinoma compared with 63.4% in adenocarcinomas(P< 0.01), whereas the positive rate of the hMSH(2) protein was 35.6% in adenocarcinomas compared with 53.2% in squamous cell carcinoma(P< 0.01). (3)A correlation between FHIT reduced expression and lymph node metastasis was observed(P< 0.01). The positive rate of the FHIT protein was 54.1% in lung cancer tissues with metastasis compared with 60.5% in lung cancer tissues without metastasis. No association was found between hMSH(2) reduced expression and nodal metastasis(P >0.05). (4)Loss of FHIT protein correlated significantly with lasting and heavy smoking(P< 0.01). The positive rate of the FHIT protein was 53.1% in smoking group compared with 66.1% in non-smoking group. The reduction of hMSH(2) expression was not associated with smoking(P >0.05). (5)An inverse correlation was found between hMSH(2) reduced expression and FHIT protein loss (P< 0.01, RR=-0.54). CONCLUSION: FHIT gene may be a negative regulatory gene of hMSH(2) gene, and play an important role in the inactivation mechanism of hMSH(2) gene.

[Helical dual-phase CT scan in evaluating blood supply of primary heptocellular carcinoma after transcatheter hepatic artery chemoembolization with lipiodol].

OBJECTIVE: To evaluate the blood supply of low density viable area of primary heptocellular carcinoma after transcatheter hepatic artery chemoembolization using lipiodol (LP-TACE), by helical dual-phase CT scanning and three dimensional CT (3DCT). METHODS: Thirty-four patients with primary heptocellular carcinoma after LP-TACE were examined by hepatic helical dual-phase CT. 3DCT model of the maximum intensity projection (MIP), surface shaded display (SSD) reconstruction of the hepatic artery and portal vein were simultaneously done in 5 cases. RESULTS: Viable tumor areas of 34 cases of primary heptocellular carcinoma after LP-TACE were divided into four types: peripheral, lateral, central and diffused types. Enhanced tumor vessel or tissue in viable tumor area was found during hepatic dual-phase in 17 cases, during hepatic artery-phase only in 8 and hepatic portal vein-phase only in 3. The viable tumor areas were found to have blood supply from the hepatic vein in 2 cases. The viable tumor area unenhanced during hepatic dual-phase was found in 6 cases. In 5 cases, the relation between the viable tumor area and branches of hepatic artery and portal vein was showed by MIP and SSD of hepatic artery and portal vein. CONCLUSION: Hepatic helical dual-phase CT scan with 3DCT is effective in evaluating the blood supply of viable tumor areas and the therapeutic effect of primary heptocellular carcinoma after LP-TACE.

[Expression of HIF-1 alpha and its relationship to apoptosis and proliferation in lung cancer].

BACKGROUND & OBJECTIVES: Hipoxia-inducible factor-1 is a transcriptive factor that regulates genes involved in metabolism, angiogenesis, proliferation, and apoptosis. This study was designed to investigate the expression of hypoxia inducible facter-1 alpha(HIF-1 alpha) and its relationship to bcl-2, Bax, PCNA in lung cancer. METHOD: Immunohistochemical streptavidin/peroxidase(SP) was used to examine the expression of HIF-1a, bcl-2, Bax, and PCNA in 60 cases of lung cancer. RESULTS: In 60 cases of lung cancer, positive rate for HIF-1a was 28.3% (17/60), specially the positive rate of small cell lung cancer(66.7%) was significantly higher than non-small cell lung cancer (21.6%). HIF-1a expression increased as clinical stage and metastasis increased(P < 0.01). The positive rate of bcl-2, Bax, and PCNA were 31.7% (19/60), 40.0% (24/60), 76.7% (46/60), respectively. Inverse relationship was found between the expression of HIF-1 alpha and bcl-2; while the correlation of HIF-1 alpha and Bax was positive(P < 0.01). The relationship between HIF-1 alpha and Bax was positive(P < 0.01). The relationship between HIF-1 alpha and PCNA was not observed(P > 0.05). CONCLUSION: HIF-1 alpha is correlated with apopotosis, but has no relationship with proliferation.