objective　To study the expression of CD44v3 and CD44v6 and its relationship with lymph node metastasis in non small cell lung cancer (NSCLC). Methods　Specimens (lung tissues) from 52 c ases of NSCLS and 12 normal lung tissue were used to detect the expression of CD 44v3 and CD44v6 by immunohistochemical method (SP method) and flow cytometry, co rrelation was analysed between the expression of CD44v3 or CD44v6 a nd lymph node metastasis of the lung cancer. Results　CD44v3 and CD44v6 were not, or weakly expressed in all normal lung tissues from 12 cases. In contrast, the expression levels of CD44v3 and CD44v6 were obviously higher in lung cancer than that in normal tissue(P<0.05). The expression of CD44v 3 and CD44v6 were much higher in patients with lymph node metastasis than those without lymph node metastasis(P<0.05). Conclusion　① CD44v3 and CD44v6 are expressed with different degree in NSCLC. ②There is a close rel ationship between high expression of CD44v6 and lymph node metastasis, and CD44v 6 may be a co-marker for predicting the potentiality of lymph node metastasis i n lung cancer.

Objective To investigate the immunoregulatory ability of human lung-derived mesenchymal stem cells (MSCs) on T cells. Methods MSCs were isolated and cultured from human fetal lung. The immune phenotype was tested by flow cytometry and T lymphocyte proliferation assessed by thymidine incorporation. Results HLA-DR, CD86, and CD80 were not expressed in human lung-derived mesenchymal stem cells. The proliferation of peripherial blood-derived T cells was suppressed and this suppression seemed dependent on the concentration of MSCs. Conclusion Human lung-derived MSCs have been proved to possess immunomodulatory ability.

BACKGROUNDLung cancer cells can upregulate the expression of Fas ligand (FasL) and counterattack tumor-infiltration lymphocyte (TIL) expressing Fas via the FasL/Fas pathway, therefore escape from immunosurveillance and impair local anti-tumor immune capacity. The aim of this study is to investigate the effects of reducing FasL expression on T cell apoptosis in lung cancer cell line H460 via small interfering RNA (siRNA) technology.

METHODSIn vitro chemically synthesized siRNA targeting FasL as well as constructed plasmid vector were transfected into H460 cells, wherein the interfering effect and alterations in T cell apoptosis were observed.

RESULTSSequence-specific interfering effect was detected at RNA and protein levels by RT-PCR and Western blot in the H460 si group, and the reduction of FasL expression was capable of rescuing T cell apoptosis induced by lung cancer cells.

CONCLUSIONSFasL can be utilized as a new target in gene therapy of lung cancer.

BACKGROUNDOverexpression of CD44v6 is associated with occurrence, development and metastasis of a variety of human malignant tumors. The aim of this study is to determine the expression of CD44v6 and its prognostic significance in non-small cell lung cancer (NSCLC).

METHODSCD44v6 expression was detected in 52 NSCLC tissues and 12 normal pulmonary tissues by reverse transcription polyme-(rase) chain reaction (RT-PCR) and immunohistochemistry (SP method).

RESULTSThe positive expression rate of CD44v6 was 69.2% (SP method) and 75.0% (RT-PCR method) in NSCLC, respectively. Significantly higher expression of CD44v6 was demonstrated in poorly differentiated tumors than that in moderately/well differentiated tumors (P < 0.05). The expression of CD44v6 was remarkably higher in patients with lymphatic metastasis than that in those without lymphatic metastasis (P < 0.01). CD44v6 expression in stage III NSCLC was remarkably higher than that in stage I and II NSCLC (P < 0.05). Survival rate of patients with negative CD44v6 expression was significantly higher than that of those with positive CD44v6 expression (P=(0.0115)). Multi-variate logistic analysis showed the expression of CD44v6 (P=0.048) and pTNM stage (P=0.035) were significantly prognostic factors.

CONCLUSIONSOverexpression of CD44v6 is very common in lung cancer tissues. Detection of CD44v6 expression may be helpful to predict the prognosis of NSCLC patients.

Objective To investigate the variations of mtDNA from high and low metastatic mouse hepatocarcinoma cell sublines Hca-F and Hca-P, and the relationship between mutations of mtDNA and carcinogenesis. Methods The variations of D-loop, ND3 and tRNA Met+Glu+Ile gene fragments of mtDNA from Hca-F and Hca-P cells were analyzed by PCR-RFLP and sequencing techniques. Results No amplification fragment length polymorphism and restriction fragment length polymorphism were observed in tRNA Met+Glu+Ile , ND3 and D-loop of mtDNA from the 2 cell sublines. Sequence difference between these 2 cell sublines were found in mtDNA D-loop region by sequencing. Conclusions Genetic alteration of mtDNA non-coding region in tumors, which may reflect the environmental and genetic influences operative during tumor progression, can be linked to their tumorigenic phenotype.

Objective To study the 4 977 bp deletion of mitochondrial DNA in lung cancer, paraneoplastic tissue and normal lung tissue from non-lung cancer subjects and its significance in the development of cancer. Methods Lung cancer tissues and paraneoplastic tissues from 37 non-small lung cancer patients, and normal lung tissues from 20 patients without lung cancer were analyzed by long PCR technique. Results Mitochondrial DNA 4 977 bp deletion was detected in 54.1%(20/37) of lung cancer tissues, 59.5%(22/37) of paraneoplastic tissues and 30.0%(6/30) of normal lung tissues. The correlation between 4 977 bp deletion and age, smoking was present in our data. Conclusion Mitochondrial DNA 4 977 bp deletion, which may reflect the environmental and genetic influences during tumor progression, is not specific to lung cancer and unlikely to play an important role in carcinogenesis.