Wei Y.Y.,Shanghai University |
Wei Y.Y.,Shanghai JiaoTong University |
Zhang T.H.,Shanghai JiaoTong University |
Chow A.,Changi General Hospital |
And 13 more authors.
BMC Psychiatry | Year: 2016
Background: The reported rates of personality disorder (PD) in subjects with schizophrenia (SZ) are quite varied across different countries, and less is known about the heterogeneity of PD among subjects with SZ. We examined the co-morbidity of PD among patients who are in the stable phase of SZ. Method: 850 subjects were randomly sampled from patients diagnosed with SZ in psychiatric and psycho-counseling clinics at Shanghai Mental Health Center. Co-morbidity of PDs was assessed through preliminary screening and patients were administered several modules of the SCID-II. Evidence of heterogeneity was evaluated by comparing patients diagnosed with SZ with those who presented with either affective disorder or neurosis (ADN). Results: 204 outpatients (24.0 %) in the stable phase of SZ met criteria for at least one type of DSM-IV PD. There was a higher prevalence of Cluster-A (odd and eccentric PD) and C (anxious and panic PD) PDs in SZ (around 12.0 %). The most prevalent PD was the paranoid subtype (7.65 %). Subjects with SZ were significantly more likely to have schizotypal PD (4.4 % vs. 2.1 %, p = 0.003) and paranoid PD (7.6 % vs. 5.4 %, p = 0.034), but much less likely to have borderline, obsessive-compulsive, depressive, narcissistic and histrionic PD. Conclusions: These findings suggest that DSM-IV PD is common in patients with SZ than in the general population. Patterns of co-morbidity with PDs in SZ are different from ADN. © 2016 The Author(s).
Yuan W.,Bio X Institutes |
Zhang Z.,Shanghai JiaoTong University |
Liu J.,Zhengzhou Translational Medicine Research CenterZhengzhou Sixth Peoples HospitalZhengzhou |
Liu Y.,Institute of Biomedical SciencesFudan UniversityShanghai China |
And 2 more authors.
Cancer | Year: 2016
BACKGROUND: Genomic alterations of small bowel cancers remain poorly understood due to the rarity of these diseases. In the current study, the authors report the identification of somatic mutations from patients with duodenal adenocarcinoma by whole-exome sequencing. METHODS: Whole-exome sequencing and follow-up analysis were conducted in 12 matched tumor-normal tissue duodenal adenocarcinoma tissue pairs to examine the genetic characteristics of this disease. Somatic mutations (single-nucleotide variants and short insertion/deletions) were obtained and filtered and then searched for recurrently mutated genes and pathways. RESULTS: An excess of C-to-T transitions at the CpG dinucleotide was observed in the substitution of bases. The authors identified recurrent mutations in tumor protein p53 (TP53), KRAS, catenin (cadherin-associated protein) β-1 (CTNNB1), AT-rich interactive domain 2 (ARID2), adenomatous polyposis coli (APC), erb-b2 receptor tyrosine kinase 2 (ERBB2), ARID1A, cadherin-related family member 1 (CDHR1), NRAS, Bcl-2-related ovarian killer (BOK), radial spoke head 14 homolog (chlamydomonas) (RTDR1), cell division cycle 27 (CDC27), catalytic subunit of phosphoinositide-3-kinase (PIK3CA), and SMAD family member 4 (SMAD4). Pathway scan indicated that the Wnt signaling pathway, regulation of the actin cytoskeleton pathway, ErbB signaling pathway, and the pathway of focal adhesion were the most extensively affected pathways. CONCLUSIONS: This genomic characterization of duodenal adenocarcinoma provides researchers with insight into its somatic landscape and highlights the vital role of the Wnt/β-catenin signaling pathway. The study data also indicate that duodenal adenocarcinomas have a genetic resemblance to gastric and colorectal cancers. These discoveries may benefit the future development of molecular diagnosis and personalized therapies. © 2016 American Cancer Society.
Ruan X.,Bio X Institutes |
Zuo Q.,Shanghai University |
Jia H.,Bio X Institutes |
Chau J.,Institute of Molecular and Cell Biology |
And 7 more authors.
Journal of Molecular Cell Biology | Year: 2015
The DNA damage response helps to maintain genome integrity, suppress tumorigenesis, and mediate the effects of radiotherapy and chemotherapy. Our previous studies have shown that Smad1 is upregulated and activated by Atm in DNA damage response, which can further bind to p53 and promote p53 stabilization. Herewe report another aspect of the interplay between p53 and Smad1. Comparison of rectal tumor against paired paraneoplastic specimens and analysis of >500 colorectal tumors revealed that Smad1 was upregulated in tumor samples, which was attributable to p53 defects. Using MEFs as a model, we found that knockdown of the elevated Smad1 in p53-/- MEFs promoted cell proliferation, E1A/Ras-induced cell transformation, and tumorigenesis. Mechanistic studies suggest that elevated Smad1 and momentary activation inhibit cell proliferation by upregulating p57Kip2 and enhancing Atm-Chk2 activation. Surprisingly, elevated Smad1 appears to have a negative effect on chemotherapy, as colorectal tumors, primary cancer cells, and cell lines with Smad1 knockdown all showed an increase in chemosensitivity, which could be attributable to elevated p57Kip2. These findings underscore the significance of Smad1-p53 interaction in tumor suppression and reveal an unexpected role for Smad1 in chemoresistance of colorectal cancers. © The Author (2015).
Lin X.-B.,Shanghai University |
Hu G.-H.,Shanghai University |
Fu H.-L.,Bio X Institutes |
Jin W.-L.,Bio X Institutes
Nano Biomedicine and Engineering | Year: 2014
The most common types of primary brain tumors in adults are gliomas. Glioblastoma multiforme (GBM) is the most highly aggressive type of glioma. GBM contains various numbers of cells with characteristics of activated or dysmorphic macrophages/microglia. Among them, some cell types provide significant support for tumor growth, while others are able to inhibit tumor progression. These cells are generally considered part of the tumor stroma and are often described as TAMs (tumourassociated macrophages). The presence of TAMs has been linked to increased tumor grade and poor clinical outcome in GBM, suggesting that depletion or inhibition of these cells may suppress tumor growth. A better understanding of tumor microenvironment in the brain would therefore be expected to contribute to the development of improved therapies for brain tumors that are urgently required due to a poor availability of treatments for these malignancies. This review summarizes some of the known interactions between brain tumors and different stromal cells, and also discusses potential therapeutic approaches within this context. © 2014 Xian-Bin Lin, Guo-Han Hu, Hua-Lin Fu and Wei-Lin Jin.