ABSTRACT
BackgroundThe meibomian gland carcinoma is an eyelid malignant tumor with a domestic incidence after basal cell carcinoma.Meibomian gland carcinoma is not sensitive to radiation therapy and chemotherapy,and the related factors with its recurrence and metastasis are rarely reported.ObjectiveThis study was to investigate the clinical and pathologic features of meibomian gland carcinoma with multiple operations and the effectiveness of histologically controlled excision.MethodsThe clinical data and the histopathologic sections of 34 cases of the meibomian gland carcinoma diagnosed by pathology were retrospectively analyzed at Zhongshan Ophthalmic Center in September 2003 to April 2011,and the treating effectiveness of histologically controlled excision was evaluated. ResultsIn this group of cases,the appearing rate of the meibomian gland carcinoma was resemble in both lateral eyes.A higher morbidity was on the upper eyelid (26/34,76.5％) and then the lower eyelids (5/34,14.7％ ) and both (3/34,8.8％).The average ages of these cases were 57.5 years old.Sixteen of 21 misdiagnosed cases were identified as chalazion at the first visit,and no histopathological examination was performed in 11 cases after initial operation.Twenty-six cases(76.5％ )were identified as meibomian gland carcinoma in initial histopathologic diagnosis.Two cases had histologically controlled excision and 16 cases had simple excision while 16 cases had chalazion enucleation in the first operation.All the patients had histologically controlled excision in Zhongshan Ophthalmic Center with 58.8％ of the patients having pagetoid invasion.Sixteen cases were followed up for 5 months to 8 years after histologically controlled excision,in which none died of recurrence and metastasis of meibomian gland carcinoma.No significant differences were found in the pathological feature between 16 lost patients and 18 followed-up patients(P ＞ 0.05 ).Conclusions Misdiagnosis of meibomian gland as chalazion is a main cause of repeat operations of meibomian gland carcinoma.Histologically controlled excision is a feasible therapy for the recurrence and metastasis of meibomian gland carcinoma.
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Objective: To explore the therapeutic efficacy of transduction of p53 gene with Tie2-mediated gene delivery system in the treatment of lung cancer and provide experimental basis for future clinical application. Methods: GA3, a small peptide against Tie 2, was conjugated with PEI by bifunctional crosslinking agent SMCC to construct Tie2-targeted gene vector. Then pCMV-luciferase cDNA was combined with GA3-PEI to form an electrostatic complex. GA3-PEI/luciferase cDNA complex was transduced into Tie2-positive SPC-A1 lung cancer cells and Tie2-negative SMMC7721 hepatic cancer cells in vitro. The activity of luciferase was measured 24 h later. The GA3-PEI/β-gal complex was injected into peri-tumorous tissues of the transplanted SPC-A1 tumors in nude mice in vivo. Meanwhile, PEI/β-gal gene was injected as control. The nude mice were decapitated 24 h later. The heart, liver, spleen, lung, kidney and tumor tissues were excised and stained with X-gal. Human lung cancer SPC-A1 cells were inoculated subcutaneously into the 4-week-old female athymic mice (BALB/c). The mice were randomly divided into 5 groups (NS, GA3, p53, PEI/p53, and GA3-PEI/p53) with 6 mice in each group. GA3-PEI/ p53 1 μg was subcutaneously injected into peri-tumorous tissues once every two days. The tumor volume was calculated according to formula (V = πab2/6). The tumor-inhibiting ratio was calculated regarding NS group as control. Results: The activity of luciferase of GA3-PEI/luciferase was significantly higher in SPC-A1 cells than that in SMMC7721 cells (P<0.05). A lot of blue-stained cells were observed in transplanted tumor tissues but not in heart, liver, spleen, and kidney tissues except lung bronchial mucosa. Compared with NS group, GA3-PEI/p53 significantly inhibited the growth of tumor by 61.29%. Conclusion: Transfer of p.53 gene by GA3 gene delivery system remarkably inhibits tumor growth.
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HCAP1 is a novel hepatic cancer related gene located on human chromosome 17p13.3. The loss of heterozygosity occurred at 17p13.3 in various human cancers. In order to investigate the effects of exogenous HCAP1 gene products on cell proliferation of T lymphoma Jurkat cell line, HCAP1 gene! was transfected into Jurkat cells mediated by liposome, and the cells stably expressing exogenous HCAP1 were screened with G418. The effects of HCAP1 products on cell proliferation were assessed by viable cell count, cell growth curve and colony formation assay in soft agar. The results showed that the HCAP1 transgenic Jurkat cells displayed slow growth rate, extended doubling time and reduced colony formation capability, as compared with the cells transfected with pBK/CMV empty vector (P < 0.01). It is concluded that exogenous HCAP1 gene products could inhibit the proliferation of Jurkat cells.
Subject(s)
Humans , Carcinoma, Hepatocellular , Genetics , Cell Division , Jurkat Cells , Liver Neoplasms , Genetics , Neoplasm Proteins , Genetics , Peptides , TransfectionABSTRACT
Aim To investigate the possible mechanism of human promyelocytic leukemia cells differentiation and apoptosis induced by all trans_retinoic acid (ATRA) and Ara_c. Methods The effects of ATRA and Ara_c on the tolomerase activity of HL_60 cells were detected by PCR_ELISA. Results The tolomerase activity of HL_60 cells declined during the course of differentiation and apoptosis induced by ATRA and Ara_c. Conclusion These findings suggest that ATRA and Ara_c can inhibit tolomerase activity of HL_60 cells. It may be one of the important mechanisms of human promyelocytic leukemia cells differentiation and apoptosis induced by ATRA and Ara_c.