[Expression of human papillomavirus type 16/18 in human cervical carcinomas by the quantum dot fluorescent in-situ hybridization].

OBJECTIVE: To investigate fluorescence in situ hybridization labeled with quantum dots (QDs) for the detection of human papillomavirus 16/18 (HPV16/18) infection in cervical carcinoma patients. METHODS: A total of 80 biopsy samples of squamous carcinoma of cervix were assayed for HPV 16/18 infection by using quantum dot labeled fluorescent in situ hybridization (QD-FISH) and chromogenic in situ hybridization (CISH) techniques, respectively. The results obtained by using two different methods were statistically analyzed. RESULTS: The positive rate for HPV16/18 by QD-FISH was 88.8% (71/80), higher than that (80.0%) by CISH, however, the result was statistically not significant (P=0.127). The positive detection rates for HPV16/18 by using both methods increased coincidentally with raising of the tumor grading stage. CONCLUSION: The sensitivity and specificity of HPV infection detectable by QD-FISH is higher than that by the CISH technique.

[Relationship of MAGE-A1 expression with Ki-67 and tumor-infiltrating lymphocyte response in non-small cell lung carcinoma].

BACKGROUND & OBJECTIVE: Recent studies revealed a possible close association between the expression of some members of tumor-specific antigen MAGE (melanoma antigen) family and actively proliferated infantile cells. But the correlation of MAGE-A1 expression with proliferation of tumor cells and immune response at host local site has not been reported to date. Our study was to investigate the expression of MAGE-A1 in non-small cell lung carcinoma (NSCLC), and its relationship with Ki-67 expression, tumor-infiltrating lymphocyte (TIL) response, histologic grade, and pathological type. METHODS: Thirty NSCLC samples in formalin-fixed, paraffin-embedded sections were examined for MAGE-A1, Ki-67 and TIL response using SP immunohistochemical technique. RESULTS: The positive expression rate of MAGE-A1 was 80.00%(24/30) with high expression rate of 58.33%(14/24) and low expression rate of 41.67%(10/24). The positive expression rate of Ki-67 was 93.33%(28/30) with high expression rate of 57.14%(16/28) and low expression rate of 42.86% (12/28). TIL response was observed in 22 patients. There was a significant relationship between MAGE-A1 positive expression and Ki-67 positive expression (rs=0.578, P< 0.005), as well as between MAGE-A1 positive expression and TIL response (rs=0.505, P< 0.005). However, MAGE-A1 expression was not significantly correlated with histologic grade and pathological type (P >0.05). CONCLUSION: The NSCLC cells with MAGE-A1 positive expression possess high proliferation activity; meanwhile, the up-regulation of MAGE-A1 indicates the increase of antigen in tumor cells and the increase of local TIL response, indicating that MAGE-A1 may have potential to be used as a target for immunotherapy in NSCLC patient.

[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.