RESUMO
BACKGROUND/AIM: The authors aimed to determine the clinical value of colonoscopy by evaluating the frequency of colorectal neoplasm (CRN) detection in patients with early gastric cancer (EGC) as compared with healthy controls and analysed the risk factors of advanced CRN in patients with EGC. METHODS: The medical records of 201 patients diagnosed as EGC and age- and gender-matched healthy controls were retrospectively reviewed. Frequencies and clinical features of colorectal polyps of patients and controls were compared. Risk factors of advanced CRN in patients with EGC were also analysed. RESULTS: Frequencies of CRN in patients and controls were 49.8 and 49.3% respectively (P = 0.90). They were more common in the right colon in patients (P < 0.05). Advanced CRN were found in 10.3% of patients and in 3% of controls (P < 0.05). Multivariate analysis revealed that old age and smoking history were risk factors of an advanced CRN in patients with EGC. CONCLUSION: The prevalence of a coexisting advanced CRN was higher in EGC patients. The study shows colonoscopy plays an important role with respect to the detection of synchronous advanced CRN in patients with EGC.
Assuntos
Neoplasias Colorretais/diagnóstico , Neoplasias Colorretais/epidemiologia , Detecção Precoce de Câncer/métodos , Neoplasias Gástricas/diagnóstico , Neoplasias Gástricas/epidemiologia , Adenoma/diagnóstico , Adenoma/epidemiologia , Adulto , Fatores Etários , Idoso , Idoso de 80 Anos ou mais , Colonoscopia/métodos , Neoplasias Colorretais/cirurgia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Fatores de Risco , Fumar/efeitos adversos , Fumar/epidemiologia , Neoplasias Gástricas/cirurgiaRESUMO
Syntenin, a tandem PDZ domain containing scaffold protein, functions as a positive regulator of cancer cell progression in several human cancers. We report here that syntenin positively regulates transforming growth factor (TGF)-ß1-mediated Smad activation and the epithelial-to-mesenchymal transition (EMT) by preventing caveolin-1-mediated internalization of TGF-ß type I receptor (TßRI). Knockdown of syntenin suppressed TGF-ß1-mediated cell migration, transcriptional responses and Smad2/3 activation in various types of cells; however, overexpression of syntenin facilitated TGF-ß1-mediated responses. In particular, syntenin knockdown abolished both the basal and TGF-ß1-mediated repression of E-cadherin expression, as well as induction of vimentin expression along with Snail and Slug upregulation; thus, blocking the TGF-ß1-induced EMT in A549 cells. In contrast, overexpression of syntenin exhibited the opposite effect. Knockdown of syntenin-induced ubiquitination and degradation of TßRI, but not TGF-ß type II receptor, leading to decreased TßRI expression at the plasma membrane. Syntenin associated with TßRI at its C-terminal domain and a syntenin mutant lacking C-terminal domain failed to increase TGF-ß1-induced responses. Biochemical analyzes revealed that syntenin inhibited the interaction between caveolin-1 and TßRI and knockdown of syntenin induced a massive internalization of TßRI and caveolin-1 from lipid rafts, indicating that syntenin may increase TGF-ß signaling by inhibiting caveolin-1-dependent internalization of TßRI. Moreover, a positive correlation between syntenin expression and phospho-Smad2 levels is observed in human lung tumors. Taken together, these findings demonstrate that syntenin may act as an important positive regulator of TGF-ß signaling by regulating caveolin-1-mediated internalization of TßRI; thus, providing a novel function for syntenin that is linked to cancer progression.
Assuntos
Caveolina 1/genética , Neoplasias Pulmonares/genética , Proteínas Serina-Treonina Quinases/genética , Receptores de Fatores de Crescimento Transformadores beta/genética , Sinteninas/genética , Fator de Crescimento Transformador beta1/genética , Caveolina 1/metabolismo , Linhagem Celular Tumoral , Movimento Celular/genética , Transição Epitelial-Mesenquimal/genética , Regulação Neoplásica da Expressão Gênica , Técnicas de Silenciamento de Genes , Humanos , Neoplasias Pulmonares/patologia , Fosforilação , Proteínas Serina-Treonina Quinases/biossíntese , Receptor do Fator de Crescimento Transformador beta Tipo I , Receptor do Fator de Crescimento Transformador beta Tipo II , Receptores de Fatores de Crescimento Transformadores beta/biossíntese , Transdução de Sinais , Proteína Smad2/genética , Sinteninas/metabolismo , Fator de Crescimento Transformador beta1/metabolismo , UbiquitinaçãoRESUMO
Vibrio cholerae O139 first appeared in India and Bangladesh in 1992. Surveillance for O139 was started at three hospitals in Thailand in 1993. By 1994 all three hospitals surveyed in Thailand had experienced an increase in Vibrio cholerae O139 infections.