Bladder cancer is characterized by high incidence and high recurrence; however, the mechanism of pathogenesis, especially of recurrence is still unclear. This paper reviews the molecular characteristics of bladder cancer, urothelial somatic mutation, driver genes and mutation characteristics, and prospects the future research directions.

Objective:To overview the systematic reviews/meta analysis of the treatment of external therapy of TCM for gastroesophageal reflux disease (GERD).Methods:Systematic reviews/meta analysis of the treatment of external therapy of TCM for GERD were retrieved from CNKI, Wanfang Data, VIP, CBM, PubMed, Embase and Cochrane Library databases from the establishment of the databases to 31st, December 2022. The AMSTAR 2 tool, PRISMA 2020 reporting specifications, and GRADE guidelines were used to evaluate the methodological quality, reporting quality, and evidence quality of the included literature. A multiple evaluation was performed in six dimensions: year of publication, type of study design, methodological quality score, reporting quality score, degree of homogeneity, and risk of publication bias evaluation.Results:A total of 9 systematic reviews/meta analysis were included, of which 1 was of low quality methodological quality and 8 was of very low quality. GRADE guidelines evidence quality grading results showed 33 outcome indicators, 9 of which were with moderate evidence, 21 of which were with low evidence, and 3 of which were with very low evidence. 9 articles had reporting quality scores ranging from 16 to 24, of which 1 report was relatively complete and 8 had some deficiencies. The rank mean scores of multiple evaluations indicated that 2 articles were of high quality and 1 article was of poor quality.Conclusions:The quality of evidence for the treatment of external therapy of TCM for GERD is intermediate in terms of improving the cure rate and reducing adverse effects, and is recommended for clinical use. However, the methodological quality and reporting quality of the current systematic reviews/meta analysis of the treatment of external therapy of TCM for GERD need to be improved, and users of the evidence ought to use the above evidence with caution for decision making.

Objective To investigate the effect of GTPase activating protein Git2 on metastasis in breast cancer. Methods Git2 gene over?expression was induced by Git2 cDNA, and Git2 gene knockdown was induced by Git2 ShRNA lentivirus in four breast cancer cell lines. Six?week old wide type female mice were also used in this study. The cells were tagged with luciferase and injected into wide type female mice by tail vein or 4th mammary fat pad, respectively, to establish a cancer metastasis model. In vivo real time imaging system and immunohistochemical staining were used to detect the cancer metastasis. Results The relative mRNA expression level of Git2 ( normalized by GAPDH) in the 4T1,4TO7,168FARN and 67NR cells were 0.91 ± 0. 03, 0. 125 ± 0. 06, 0. 131 ± 0. 04 and 0. 92 ± 0. 04, respectively. The expression of EMT marker E?cadherin was inhibited and N?cadherin and vimentin were enhanced when Git2 was over?expressed in 168FARN cells and 4TO7 cells expressing low level of Git2, whereas the expression of E?cadherin was increased and N?cadherin and vimentin were decreased when Git2 was knocked down in 67NR cells and 4T1 cells expressing high level of Git2. Furthermore, over?expression of Git2 promoted 4TO7 cells to progress from micro?metastasis to macro?metastasis. The down?regulation of Git2 pushed 67NR cells to intravasate into blood circulation and suppressed the metastatic ability of 4T1 cells. The number of bioluminescence photos of lung metastatic 4T1?Luc?KD cells was (0.4±0.05) ×106, compared with (3.0±0.04) ×106 in the control 4T1?Luc cells, showing a significant difference (P<0.05). Conclusion Our results indicate that Git2 is involved in breast cancer initiation and metastatic colonization.

Objective To investigate the effect of GTPase activating protein Git2 on metastasis in breast cancer. Methods Git2 gene over?expression was induced by Git2 cDNA, and Git2 gene knockdown was induced by Git2 ShRNA lentivirus in four breast cancer cell lines. Six?week old wide type female mice were also used in this study. The cells were tagged with luciferase and injected into wide type female mice by tail vein or 4th mammary fat pad, respectively, to establish a cancer metastasis model. In vivo real time imaging system and immunohistochemical staining were used to detect the cancer metastasis. Results The relative mRNA expression level of Git2 ( normalized by GAPDH) in the 4T1,4TO7,168FARN and 67NR cells were 0.91 ± 0. 03, 0. 125 ± 0. 06, 0. 131 ± 0. 04 and 0. 92 ± 0. 04, respectively. The expression of EMT marker E?cadherin was inhibited and N?cadherin and vimentin were enhanced when Git2 was over?expressed in 168FARN cells and 4TO7 cells expressing low level of Git2, whereas the expression of E?cadherin was increased and N?cadherin and vimentin were decreased when Git2 was knocked down in 67NR cells and 4T1 cells expressing high level of Git2. Furthermore, over?expression of Git2 promoted 4TO7 cells to progress from micro?metastasis to macro?metastasis. The down?regulation of Git2 pushed 67NR cells to intravasate into blood circulation and suppressed the metastatic ability of 4T1 cells. The number of bioluminescence photos of lung metastatic 4T1?Luc?KD cells was (0.4±0.05) ×106, compared with (3.0±0.04) ×106 in the control 4T1?Luc cells, showing a significant difference (P<0.05). Conclusion Our results indicate that Git2 is involved in breast cancer initiation and metastatic colonization.