State Key Laboratory for Oncogenes and Related Genes

Shanghai, China

State Key Laboratory for Oncogenes and Related Genes

Shanghai, China

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Li Y.-T.,Shanghai JiaoTong University | Li Y.-T.,Key Laboratory of Gastroenterology and Hepatology | Li Y.-T.,State Key Laboratory for Oncogenes and Related Genes | Cai H.-F.,Shanghai JiaoTong University | And 11 more authors.
Alimentary Pharmacology and Therapeutics | Year: 2016

Background Clostridium difficile infection is a major cause of nosocomial diarrhoea. Aim To evaluate long-term (≥90 days) efficacy and safety of faecal microbiota transplantation for C. difficile infection and explore the factors affecting the faecal microbiota transplantation outcomes. Methods MEDLINE, the Cochrane Library and EMBASE were searched and only observational studies that utilised faecal microbiota transplantation for C. difficile infection with long-term follow-up duration (≥90 days) were included. Primary cure rate, overall recurrence rate and early (<90 days) and late (≥90 days) recurrence rate were calculated. Results Eighteen observational studies with 611 patients were included. The primary cure rate was 91.2% (95% confidence interval, CI 86.7-94.8%). The overall recurrence rate was 5.5% (95% CI 2.2-10.3%). The early recurrence rate and late recurrence rate were 2.7% (95% CI 0.7-6.0%) and 1.7% (95% CI 0.4-4.2%) respectively. Most adverse events were expected, short-lived, self-limited and manageable. The association between faecal microbiota transplantation therapy and adverse events such as inflammatory bowel disease flare, infectious disease and autoimmune disease was a concern but remained insignificant. Old age (≥65 years) was identified as a risk factor for after faecal microbiota transplantation therapy. Upper gastrointestinal administration also results in less frequent primary cure. Conclusions Faecal microbiota transplantation seems to be a highly effective and robust therapy for recurrent C. difficile infection. However, more quality studies, such as randomised controlled trials and cohort studies with control groups, are needed to confirm its long-term efficacy and safety. © 2015 John Wiley & Sons Ltd.


Wang H.,State Key Laboratory for Oncogenes and Related Genes | Liang L.,State Key Laboratory for Oncogenes and Related Genes | Fang J.-Y.,State Key Laboratory for Oncogenes and Related Genes | Xu J.,State Key Laboratory for Oncogenes and Related Genes
Oncogene | Year: 2015

Colorectal cancer (CRC) results from the accumulation of genetic alterations, and somatic copy number alterations (CNAs) are crucial for the development of CRC. Genome-wide survey of CNAs provides opportunities for identifying cancer driver genes in an unbiased manner. The detection of aberrant CNAs may provide novel markers for the early diagnosis and personalized treatment of CRC. A major challenge in array-based profiling of CNAs is to distinguish the alterations that play causative roles from the random alterations that accumulate during colorectal carcinogenesis. In this view, we systematically discuss the frequent CNAs in CRC, focusing on functional genes that have potential diagnostic, prognostic and therapeutic significance.Oncogene advance online publication, 10 August 2015; doi:10.1038/onc.2015.304. © 2015 Macmillan Publishers Limited


Liang L.,State Key Laboratory for Oncogenes and Related Genes | Fang J.-Y.,State Key Laboratory for Oncogenes and Related Genes | Xu J.,State Key Laboratory for Oncogenes and Related Genes
Oncogene | Year: 2015

Gastric cancer (GC) is among the most common malignancy in the world with poor prognosis and limited treatment options. It has been established that gastric carcinogenesis is caused by a complex interaction between host and environmental factors. Copy number variation (CNV) refers to a form of genomic structural variation that results in abnormal gene copy numbers, including gene amplification, gain, loss and deletion. DNA CNV is an important influential factor for the expression of both protein-coding and non-coding genes, affecting the activity of various signaling pathways. CNV arises as a result of preferential selection that favors cancer development, and thus, targeting the amplified 'driver genes' in GC may provide novel opportunities for personalized therapy. The detection of CNVs in chromosomal or mitochondrial DNA from tissue or blood samples may assist the diagnosis, prognosis and targeted therapy of GC. In this review, we discuss the recent CNV discoveries that shed light on the molecular pathogenesis of GC, with a specific emphasis on CNVs that display diagnostic, prognostic or therapeutic significances in GC.Oncogene advance online publication, 15 June 2015; doi:10.1038/onc.2015.209. © 2015 Macmillan Publishers Limited

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