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Objective To investigate the association between clinicopathological characteristics and familial history of malignant neoplasms (MN-FH) in patients with colorectal cancer. Methods The clinical data of 652 cancer patients in Zhengzhou University Affiliated Cancer Hospital from December 2014 to December 2015 were analyzed retrospectively. Patients were grouped based on with or without MN-FH. The clinical and pathological features of the patients were analyzed by χ 2test. Results One hundred and thirty cases (19.9 %) of colorectal cancer had MN-FH. Compared with NO MN-FH group, MN-FH group had the features of low differentiation degree, late clinical stage, deep infiltration, and also prone to lymph node metastasis and distant metastasis, associated with cancer nodules, vascular thrombosis, nerve invasion, multiple primary tumor, MSI-H (χ 2values were 30.825, 12.270, 12.122, 8.502, 53.969, 4.502, 12.861, 11.680, 6.272, 17.460, all P < 0.05). Conclusions Colorectal cancer patients with MN-FH has high malignant degree,the early diagnosis and treatment are the key to survival of patients with MN-FH.
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Screening has been proven to be effective for the control of colorectal cancer (CRC).The target of CRC screening is shifting from CRC to colorectal neoplasia (CN),the precursors of CRC.Based on the the latest national guideline,the Consensus of Screening for CRC and CN,and the recent research of precursors both at home and abroad.This paper summarizes the progress in the research of risk factors,risk prediction model,screening strategy optimization,colonoscopy quality control,sessile serrated adenoma identification and follow up as well as the recognition of precursors.
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Screening has been proven to be effective for the control of colorectal cancer (CRC).The target of CRC screening is shifting from CRC to colorectal neoplasia (CN),the precursors of CRC.Based on the the latest national guideline,the Consensus of Screening for CRC and CN,and the recent research of precursors both at home and abroad.This paper summarizes the progress in the research of risk factors,risk prediction model,screening strategy optimization,colonoscopy quality control,sessile serrated adenoma identification and follow up as well as the recognition of precursors.
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Objective To detect the expression levels of metallothionein1 H(MT1 H)in children and adoles-cents osteosarcoma serums,and to analyze its relationship with clinicopathological features,and to explore the effect of MT1 H on cell proliferation of osteosarcoma cells and its mechanism.Methods Enzyme -linked immuno sorbent assay (ELISA)was performed to detect the expression of MT1 H in children and adolescents osteosarcoma serums and non-neoplastic disease serums.MT1 H vector was transfected into the osteosarcoma U2OS cells.Reverse transcription -poly-merase chain reaction(RT -PCR)and Western blot were used to detect the expression of the mRNA and protein of MT1 H,respectively.Methylthiazolyldiphenyl -tetrazolium bromide(MTT)was used to detect the cell growth.Western blot was performed to detect the expression of nuclear factor(NF)-κB,and inhibitor of κB (IκB)-αprotein. Results The expressions of MT1 H in osteosarcoma serums and nonneoplastic disease serums was (0.51 ± 0.52)μg/L and (2.17 ±0.78)μg/L,respectively,with a significant difference between the 2 groups(t =-8.966, P <0.05).The expression of MT1 H in stage Ⅰ -ⅡA andⅡB -Ⅲ was (1 .98 ±0.69)μg/L and (2.45 ±0.82)μg/L,respectively,showing a gradual increase depending on clinical staging(t =-2.343,P <0.05).The expressions of MT1 H mRNA and protein were elevated in osteosarcoma U2OS cells after MT1 H vector transfection(all P <0.05). MTT assay showed that,the A value in blank control group,blank vector group,MT1 H vector group were 0.38 ±0.03, 0.36 ±0.03,0.42 ±0.03,respectively,the cell proliferation in the MT1 H vector group was significantly promoted when compared with these in the blank vector group and blank control group(F =4.213,P <0.05)from the third day.West-ern blot showed that,the relative expression of NF -κB in blank control group,blank vector group,MT1 H vector group were 0.56 ±0.05,0.53 ±0.05,0.92 ±0.07,respectively,the relative expression of IκB -αprotein were 0.64 ± 0.06,0.62 ±0.09,0.34 ±0.08,respectively,the expression of NF -κB protein was up -regulated and the expression of IκB -αprotein was down -regulated in the MT1 H vector group when compared with those in the blank vector group and blank control group(F =44.581 ,14.927,all P <0.05).Conclusions The expression of MT1 H is increased in children and adolescents osteosarcoma serums compared with that in nonneoplastic disease serums.The clinical stage is later,the expression of MT1 H is higher.MT1 H promotes cell proliferation through regulating the NF -κB pathway.
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Objective To establish the effect of curcumin on PTX-resistant esophageal cancer cell line EC9706/PTX and to investigate the mechanism of curcumin on the epithelial stromalization (EMT) of EC9706/PTX cells.Methods EC9706/PTX cells were established by medium concentration intermittent method.The drug resistance index and cross resistance were measured by MTT assay.The inhibitory effects of different concentrations of curcumin on EC9706/PTX cell proliferation were detected.The effects of curcumin on the morphological changes,migration and invasion of EC9706/PTX cells were examined by cytostatic staining,scratching and transwell invasion assay.The effects of curcumin on the expression of E-cadherin,N-cadherin,vimentin and fibronectin in EC9706/PTX cells at mRNA and protein levels were detected by fluorescence quantitative PCR and Western blot.The effect of curcumin on the expressions of NF-κB p65 and Snail in EC9706/PTX cells were detected by Western blot.Results The drug resistance index of EC9706/PTX was 28.4,which was cross-resistant to cisplatin and doxorubicin.Curcumin could inhibit the proliferation of EC9706/PTX cells.The migration and invasion of EC9706/PTX cells were significantly decreased under the action of curcumin at 20 μmol/L concentration.Fluorescence quantitative PCR and Western blot analysis showed that the expression of Ecadherin was down-regulated and the expression of N-cadherin was up-regulated,and curcumin reversed this phenomenon.Western blot analysis showed that the expression of NF-κB p65 and Snail protein was enhanced after PTX-resistant generated in EC cell,but curcumin reversed this phenomenon.Conclusion Curcumin can inhibit the proliferation,migration and invasion of EC9706/PTX cells.The mechanism maybe that curcumin inhibits the NF-κB-Snail pathway.