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Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Lung Cancer is the property of Chinese Journal of Lung Cancer and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Cancer can exhibit different forms depending on the site of origin, cell types, the different forms of genetic mutations which also affect cancer therapeutic effect. Although many genes have been demonstrated to change a direct result of the change in phenotype, however, many cancers lineage complex molecular mechanisms are still not fully elucidated. Therefore, The Cancer Genome Atlas (TCGA) Research Network analyzed a large human tumors, in order to find the molecular changes in DNA, RNA, protein and epigenetic level, The results contain a wealth of data provides us with an opportunity for common, personality and new ideas throughout the cancer lineages form a whole description. Pan-cancer genome program first compares the 12 kinds of cancer types. Analysis of different tumor molecular changes and their functions, will tell us how effective treatment method is applied to a similar phenotype of the tumor. [ABSTRACT FROM AUTHOR]

Long non-coding RNA (lncRNA), once regarded as "noise" in genomic transcription process, were ignored by the scientific community. However, more attentions are paid to lncRNA nowadays because recent studies have shown that they are not "junk" but functional RNAs. Although researches regarding to lncRNA are less because they are just "rising stars" in comparison to short non-coding RNA, these literatures have shown that lncRNA play important roles in the regulation of gene expression and provide immeasurable scientific value for future diagnosis and treatment of clinical disease especially for cancer. In this review, we summarized researches in the current status of the functions, mechanisms of lncRNA and their roles in the development of gynecological tumors. [ABSTRACT FROM AUTHOR]

Background and objective It has been shown that carbonic anhydrase IX (CAIX) was closely related to tumor hypoxia. Proliferating cell nuclear antigen (Ki67) is considered to be an objective indicator which could reliable and comprehensive response to cell population proliferation; vascular endothelial growth factor (VEGF) was positively correlated with tumor angiogenesis. The aim of this study is to investigate the significance of the expression of CAIX in non-small cell lung cancer (NSCLC) tissues by analyzing the correlation between CAIX and clinical characteristics of patients with lung cancer and VEGF, Ki67 expressions. Methods CAIX, VEGF and Ki67 protein were detected in 76 cases of NSCLC and 10 cases of lung inflammatory pseudotumor by immunohistochemistry. Results CAIX was expressed in 45 of 64 cases of NSCLC and not expressed in benign lesion pulmonary tissues. VEGF was expressed in 55 of 76 cases and Ki67 was expressed in 30 of 76 cases. The expression of CAIX in squamous cell carcinoma (SC) was higher than that in adenocarcinoma (AC)(69.7% vs 27.9%, P=0.001). In 34 cases who received radiotherapy, the objective response rates of CAIX positive and negative groups were 27.8% and 62.5% respectively; the expression of CAIX was positively correlated with VEGF (r=0.231, P=0.043) and was not correlated with Ki67 (r=0.064, P=0.583). Conclusion Compared with benign lesion pulmonary tissue, the expression of CAIX in NSCLC tissues is significantly increased and is positively correlated with VEGF. The expression of CAIX was also correlated with the objective response rate of radiotherapy, which provided new evidence about that hypoxia can increase NSCLC radiotherapy resistance. [ABSTRACT FROM AUTHOR]

Background and objective It has been proved that protein phosphorylation and dephosphorylation were important mechanisms in lung cancer development, and tobacco smoking is an important risk factor of lung cancer. The aim of this study is to investigate the expression and clinical significance of protein tyrosine phosphatase SHP2 in non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC); the relationship between tobacco smoking and the expression of SHP2 is also studied. Methods Immunohistochemistry (Invision) and fluorescence in situ hybridization (FISH) were used to detect the expression of SHP2 and the augment of SHP2 mRNA in the 53 lung cancer specimens. Results The weak positive rate of SHP2 was 80% (which was also the total positive rate) in normal bronchial epithelium. The weak, moderate and strong positive rates were 35.4%, 43.8% and 6.2% (total positive rate was 85.4%) in 48 NSCLC patients, 0%, 80% and 20% (total positve rate was 100%) in 5 SCLC patients, 40.7%, 37.4% and 3.7% (total positive rate was 81.5%) in the tumor tissues of 27 NSCLC patients who didn't smoke and 23.8%, 71.4% and 4.7% (total positive rate was 100%) in the tumor tissues of 21 NSCLC patients whose smoking indexes were ⩾400. Significant differences of SHP2 expression were observed between tumor tissues and normal bronchial epithelium, NSCLC and SCLC, and between different smoking indexes (P<0.05). Conclusion The enhancement of SHP2 expression in the tumor tissues of NSCLC patients who smoke may be correlated with tobacco smoking; SHP2 may play certain role in the development of lung cancer; SHP2 prospectively provides new ideas for the drug research and development of lung cancer treatment. [ABSTRACT FROM AUTHOR]

Background and objective The excision repair cross-complementing gene 1 (ERCC1), which is important in the repair of cisplatin-DNA adducts, was reported to be related to cisplatin resistance in tumor cells. The aim of this study is to investigate the changes of cisplatin sensitivity by silencing ERCC1 gene in lung cancer cell. Methods The small interfering RNA (siRNA) targeting ERCC1 gene was designed and synthesized, and transfected to lung cancer cell A549/DDP. The mRNA and protein expression levels of ERCC1 were evaluated by RT-PCR and Western blot. The changes of cisplatin sensitivity after RNA interference were examined by methyl thiazolyl assay. Results In A549/DDP cell, the mRNA and protein levels of ERCC1 were decreased and the sensitivity to cisplatin was increased from 12.49 μg/mL to 9.27 μg/mL after transfection. Conclusion The sensitivity to cisplatin of lung cancer cell A549/DDP could be enhanced by RNA interfering ERCC1 gene targeted code 346. [ABSTRACT FROM AUTHOR]

Background and objective Bufalin, a component of the Chinese medicine chan'su, induces apoptosis in various human tumor cell lines. The aim of this study is to investigate the mechanism of anti-proliferation and the induction of apoptosis of Bufalin on non-small cell lung cancer cell. Methods The effect of Bufalin on A549 cell proliferation was measured using MTT assay; the morphological change was observed with Wright-Giemsa stain; cell cycle phase distribution and hypodiploid DNA were determined by flow cytometry with PI; expressions of Livin, Caspase-3 were detected by Western blot. Results MTT assay showed that Bufalin inhibited A549 cell proliferation in time and dose-dependent manner. The inhibition concentration of 50% cell growth (IC50) at 48 h, 72 h and 96 h were (56.14±6.72) nmol/L, (15.57±4.28) nmol/L and (7.39±4.16) nmol/L, respectively; apoptosis of A549 cells could be effectively induced by Bufalin; apoptotic bodies and sub-G1 peak (representing apoptosis) emerged when cells were treated with different concentrations, compared with the untreated control group (P<0.01). The expression of Livin protein was downregulated (P<0.01) and Caspase-3 protein was activated during Bufalin-induced apoptosis in A549 cells. Conclusion Bufalin suppresses the growth of A549 cells and induces apoptosis; inhibition of Livin and activation of Caspase-3 may be involved in its mechanism. [ABSTRACT FROM AUTHOR]