RESUMEN
We examined gastric outlet obstruction (GOO) patients who received two weeks of strengthening pre-operative enteral nutrition therapy (pre-EN) through a nasal-jejenal feeding tube placed under a gastroscope to evaluate the feasibility and potential benefit of pre-EN compared to parenteral nutrition (PN). In this study, 68 patients confirmed to have GOO with upper-gastrointestinal contrast and who accepted the operation were randomized into an EN group and a PN group. The differences in nutritional status, immune function, post-operative complications, weight of patients, first bowel sound and first flatus time, pull tube time, length of hospital stay (LOH), and cost of hospitalization between pre-operation and post-operation were all recorded. Statistical analyses were performed using the chi square test and t-test; statistical significance was defined as p < 0.05. The success rate of the placement was 91.18% (three out of 31 cases). After pre-EN, the levels of weight, albumin (ALB), prealbumin (PA), and transferrin (TNF) in the EN group were significantly increased by pre-operation day compared to admission day, but were not significantly increased in the PN group; the weights in the EN group were significantly increased compared to the PN group by pre-operation day and day of discharge; total protein (TP), ALB, PA, and TNF of the EN group were significantly increased compared to the PN group on pre-operation and post-operative days one and three. The levels of CD3+, CD4+/CD8+, IgA, and IgM in the EN group were higher than those of the PN group at pre-operation and post-operation; the EN group had a significantly lower incidence of poor wound healing, peritoneal cavity infection, pneumonia, and a shorter first bowel sound time, first flatus time, and post-operation hospital stay than the PN group. Pre-EN through a nasal-jejunum feeding tube and placed under a gastroscope in GOO patients was safe, feasible, and beneficial to the nutrition status, immune function, and gastrointestinal function, and sped up recovery, while not increasing the cost of hospitalization.
Asunto(s)
Cicatriz/cirugía , Nutrición Enteral , Obstrucción de la Salida Gástrica/cirugía , Intubación Gastrointestinal , Complicaciones Posoperatorias/prevención & control , Cuidados Preoperatorios , Neoplasias Gástricas/cirugía , Adulto , China/epidemiología , Cicatriz/diagnóstico , Cicatriz/economía , Costos y Análisis de Costo , Nutrición Enteral/efectos adversos , Nutrición Enteral/economía , Estudios de Factibilidad , Femenino , Obstrucción de la Salida Gástrica/diagnóstico , Obstrucción de la Salida Gástrica/economía , Costos de Hospital , Humanos , Incidencia , Intubación Gastrointestinal/efectos adversos , Intubación Gastrointestinal/economía , Yeyuno , Tiempo de Internación , Masculino , Persona de Mediana Edad , Estado Nutricional , Nutrición Parenteral/efectos adversos , Nutrición Parenteral/economía , Complicaciones Posoperatorias/economía , Complicaciones Posoperatorias/epidemiología , Complicaciones Posoperatorias/terapia , Cuidados Preoperatorios/economía , Pronóstico , Neoplasias Gástricas/diagnóstico , Neoplasias Gástricas/economía , Cicatrización de HeridasRESUMEN
AIM: To examine the effect of aberrant methylation of the KISS1 promoter on the development of colorectal cancer (CRC) and to investigate reversing aberrant methylation of the KISS1 promoter as a potential therapeutic target. METHODS: KISS1 promoter methylation, mRNA expression and protein expression were detected by methylation-specific polymerase chain reaction (PCR), real-time quantitative PCR and Western blotting, respectively, in 126 CRC tissues and 142 normal colorectal tissues. Human CRC cells with KISS1 promoter hypermethylation and poor KISS1 expression were treated in vitro with 5-aza-2'-deoxycytidine (5-Aza-CdR). After treatment, KISS1 promoter methylation, KISS1 mRNA and protein expression and cell migration and invasion were evaluated. RESULTS: Hypermethylation of KISS1 occurred frequently in CRC samples (83.1%, 105/126), but was infrequent in normal colorectal tissues (6.34%, 9/142). Moreover, KISS1 methylation was associated with tumor differentiation, the depth of invasion, lymph node metastasis and distant metastasis (P < 0.001). KISS1 methylation was also associated with low KISS1 expression (P < 0.001). Furthermore, we observed re-expression of the KISS1 gene and decreased cell migration after 5-Aza-CdR treatment in a CRC cell line. CONCLUSION: These data suggest that KISS1 is down-regulated in cancer tissues via promoter hypermethylation and therefore may represent a candidate target for treating metastatic CRC.
Asunto(s)
Biomarcadores de Tumor/genética , Neoplasias Colorrectales/genética , Metilación de ADN , Kisspeptinas/genética , Anciano , Biomarcadores de Tumor/metabolismo , Estudios de Casos y Controles , Movimiento Celular , Neoplasias Colorrectales/metabolismo , Neoplasias Colorrectales/patología , Metilación de ADN/efectos de los fármacos , Metilasas de Modificación del ADN/antagonistas & inhibidores , Metilasas de Modificación del ADN/metabolismo , Progresión de la Enfermedad , Regulación hacia Abajo , Inhibidores Enzimáticos/farmacología , Femenino , Regulación Neoplásica de la Expresión Génica , Células HCT116 , Humanos , Kisspeptinas/metabolismo , Masculino , Persona de Mediana Edad , Invasividad Neoplásica , Regiones Promotoras Genéticas , ARN Mensajero/metabolismoRESUMEN
OBJECTIVE: To investigate the change of expression level of metastasis suppressor gene Kiss-1 in the colorectal cancer cell line SW480 after radiation, and to determine its association with the proliferation and apoptosis of SW480 cells. METHODS: SW480 cells were divided into control group (0 Gy) and study groups (2, 4, 6, 8 Gy). Cells in the study groups were irradiated by 6-MV X-ray radiation for 48 hours. Immunohistochemistry and real-time PCR methods were used to investigate the influence of radiation on Kiss-1 gene expression of SW480. Colony formation assay was used to detect the proliferation of SW480. Flow cytometry-Annexin- V/PI assay was used to observe the change of the apoptosis rate. RESULTS: Compared with the control group, Kiss-1 protein expression increased after radiation of 6, 8 Gy (P<0.05), but no significant changes were observed after radiation of 2, 4 Gy(P>0.05). Kiss-1 gene mRNA level increased after radiation of 2, 4, 6 Gy, while no obvious change was observed for 8 Gy radiation. The apoptosis rates increased for 4, 6, 8 Gy radiation(P<0.05), however, there was no significant difference for 2 Gy radiation (P<0.05). CONCLUSION: Radiation may increase Kiss-1 gene expression in SW480 cells, which results in decreases proliferation and increases apoptosis in residual surviving cells.
Asunto(s)
Apoptosis , Proliferación Celular , Neoplasias Colorrectales/metabolismo , Kisspeptinas/metabolismo , Línea Celular Tumoral , Neoplasias Colorrectales/patología , Humanos , Kisspeptinas/genética , Kisspeptinas/efectos de la radiación , ARN Mensajero/genética , Rayos XRESUMEN
BACKGROUND: Solid-pseudopapillary tumor of the pancreas (SPTP) is an uncommon and enigmatic pancreatic neoplasm that occurs mainly in young women. Although more and more cases have been reported in recent years, misdiagnosis and incorrect treatment still frequently take place. This study was designed to stimulate consideration of this tumor. METHODS: We retrospectively reviewed the experience of diagnosis and treatment of 15 patients with SPTP and compared them with 516 patients with pancreatic cancer from January 1997 to March 2007. RESULTS: Most of the SPTP cases were asymptomatic except for one palpable mass. Almost all SPTPs demonstrated a solid structure with hypo- or iso-attenuation, cystic structure with hypo-attenuation on pre-contrast CT scan, and enhancement of solid portions on post-contrast CT scan. By contrast, most cases of pancreatic carcinoma had multiple symptoms and abnormal blood results. The tumors showed hypo-attenuation on both pre-contrast and post-contrast CT scan, and only a few showed iso-attenuation on post-contrast CT scan. All cases of SPTP in our group were cured by surgical resection, while only 16.86% of patients with pancreatic carcinoma could undergo a radical resection. CONCLUSIONS: Clinical features and CT scans were helpful to differentiate SPTP from pancreatic carcinoma. Radical surgical resection was the most effective and safe method for the treatment of SPTP.
Asunto(s)
Carcinoma Papilar/diagnóstico , Neoplasias Pancreáticas/diagnóstico , Adolescente , Adulto , Carcinoma Papilar/cirugía , Diagnóstico Diferencial , Femenino , Estudios de Seguimiento , Humanos , Masculino , Persona de Mediana Edad , Pancreatectomía/métodos , Neoplasias Pancreáticas/cirugía , Pronóstico , Estudios Retrospectivos , Tomografía Computarizada por Rayos XRESUMEN
OBJECTIVE: To investigate the clinical characteristics,diagnosis and treatment of hepatoid adenocarcinoma of the stomach. METHODS: Clinical data of 13 hepatoid adenocarcinomas of the stomach, collected from 201 cases of gastric cancer, were analyzed retrospectively. RESULTS: Of the 201 gastric carcinomas, there were 13 AFP-producing adenocarcinomas of the stomach, the positive rate was 6.5%. Morphologically, the tumor cells formed glandular, medullary and linear structures. Of the 13 hepatoid adenocarcinomas of the stomach, 10 cases were in gastric antrum and 10 cases were poorly differentiated. The metastasis rates of liver and lymph node in hepatoid adenocarcinoma of stomach were higher than those in non-hepatoid adenocarcinoma of stomach. The treatment of hepatoid adenocarcinoma of stomach depended mainly on radical resection, and adjuvant chemotherapy was needed.The prognosis of hepatoid adenocarcinoma of stomach was poor. CONCLUSION: Hepatoid adenocarcinoma of the stomach has its own special tumor biological behavior and poor prognosis. Special attention should be paid to this disease.
Asunto(s)
Adenocarcinoma/diagnóstico , Adenocarcinoma/terapia , Neoplasias Gástricas/diagnóstico , Neoplasias Gástricas/terapia , Adenocarcinoma/patología , Adulto , Anciano , Anciano de 80 o más Años , Quimioterapia Adyuvante , Femenino , Gastrectomía , Humanos , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Neoplasias Gástricas/patología , alfa-Fetoproteínas/metabolismoRESUMEN
OBJECTIVE: To observe the effect of inhibition of serine/threonine kinase15 (STK15) gene expression on apoptosis induction in gastric cancer cell line-MKN45 and discuss the role of STK15 in viability of gastric cancer cells. METHODS: The STK15 expression was inhibited by chemically synthesized siRNA. The STK15 mRNA and protein level were respectively measured by real-time quantitative PCR and western blotting,the change of cell cycle distribution and apoptosis rate were detected by flow-cytometry, cell morphological change was observed by Hoechst staining,and pro-caspase 3 level was also detected by western blot. RESULTS: After treatment by siRNA targeting STK15 after 48 h, STK15 mRNA and protein level decreased obviously. More MKN45 cells accumulated at G(2)/M phase (P< 0.05). The apoptosis rate of STK15 siRNA treated MKN45 cells was higher than that of control cells(P< 0.05) with the pro-caspase 3 level decreased. CONCLUSIONS: Inhibition of STK15 gene expression may induce apoptosis in MKN45 cells through the pathway of caspase3. STK15 gene play a key role in proliferation and viability of MKN45 cells.
Asunto(s)
Apoptosis , Silenciador del Gen , Proteínas Serina-Treonina Quinasas/genética , Aurora Quinasa A , Aurora Quinasas , Línea Celular Tumoral , Regulación Neoplásica de la Expresión Génica , Humanos , ARN Interferente Pequeño , Neoplasias GástricasRESUMEN
OBJECTIVE: To observe the effect of polo-like kinase 1 (PLK1) gene depletion on mitosis phenotype and elucidate its vital role in gastric cancer cell line (MKN45) mitosis. METHODS: The PLK1 expression in MKN45 cells was blocked by RNA interference (RNAi), the expression level of PLK1 mRNA and protein were measured by real-time quantitative PCR and Western blot, respectively. The morphological change of microtubules and mitosis phenotype in MKN45 cells were observed by immunofluorescence staining and laser confocal microscopy, the morphological changes of cells were observed by reverse microscopy, the variation of cell cycle distribution was detected by flow-cytometry. RESULTS: After RNAi targeting PLK1, PLK1 mRNA and protein level decreased obviously, the cell microtubules became obscure and lost cohesiveness, the mitosis phenotype also varied substantially (P < 0.05), more gastric cancer cells became rounded and showed G(2) phase cell DNA content (P < 0.05). CONCLUSION: PLK1 gene plays a key role in mitosis and its inhibition can lead to mitosis arrest in MKN45 cells.
Asunto(s)
Proteínas de Ciclo Celular/biosíntesis , Mitosis/efectos de los fármacos , Proteínas Serina-Treonina Quinasas/biosíntesis , Proteínas Proto-Oncogénicas/biosíntesis , Interferencia de ARN , ARN Interferente Pequeño/farmacología , Neoplasias Gástricas/metabolismo , Adenocarcinoma/enzimología , Adenocarcinoma/metabolismo , Adenocarcinoma/patología , Proteínas de Ciclo Celular/genética , Línea Celular Tumoral , Fase G2/efectos de los fármacos , Humanos , Proteínas Serina-Treonina Quinasas/genética , Proteínas Proto-Oncogénicas/genética , ARN Mensajero/biosíntesis , ARN Mensajero/genética , ARN Interferente Pequeño/genética , Neoplasias Gástricas/enzimología , Neoplasias Gástricas/patología , Transfección , Quinasa Tipo Polo 1RESUMEN
OBJECTIVE: To investigate the role of STK15 in regulating mitosis of gastric cancer cells (MKN45) by gene silencing through RNA interference mechanism. METHODS: RNA interference technique was used to inhibit STK15 expression in MKN45 cells. The expression levels of STK15 mRNA and protein were measured by real-time quantitative RT-PCR and Western blot respectively and cell morphological changes were investigated by reverse microscopy. In addition, cell cycle distribution and cellular proliferation were determined by flow-cytometry and MTT assay respectively. Finally, the mitotic phenotype of MKN45 cells was studied by immunofluorescence staining and confocal microscopy. RESULTS: Silencing of STK15 gene by RNA interference was confirmed by marked decrease of STK15 mRNA and protein levels in the treated MKN45 cells. This silencing correlated with rounding of the cells, decreasing of DNA content in G(2) phase (P < 0.05) and a lowered proliferation index (P < 0.05), along with alterations of mitotic phenotype of MKN45 (P < 0.05). CONCLUSION: STK15 gene may play a key role in regulating cellular mitosis and its inhibition by RNA interference leading to mitosis arrest in MKN45 cells.
Asunto(s)
Silenciador del Gen , Mitosis/efectos de los fármacos , Proteínas Serina-Treonina Quinasas/biosíntesis , ARN Interferente Pequeño/farmacología , Neoplasias Gástricas/metabolismo , Adenocarcinoma/metabolismo , Adenocarcinoma/patología , Aurora Quinasa A , Aurora Quinasas , Ciclo Celular/efectos de los fármacos , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , ADN de Neoplasias/metabolismo , Humanos , Proteínas Serina-Treonina Quinasas/genética , Interferencia de ARN , ARN Mensajero/biosíntesis , ARN Mensajero/genética , Neoplasias Gástricas/patologíaRESUMEN
OBJECTIVE: To observe the effect of polo like kinase 1 (plk1) gene depletion on the growth of gastric cancer cell line-MKN45 cells in vitro and vivo and discuss the feasibility and effectiveness of arranging plk1 as gene therapeutic target for gastric cancer. METHODS: The plk1 expression of MKN45 cells was inhibited by RNA interference (RNAi). The plk1 mRNA and protein level were measured by real-time quantitative PCR and western blotting, and the change of cell cycle distribution and apoptosis rate were detected by flow-cytometry, and the MKN45 cells proliferation was measured by MTT method. MKN45 cells treated with plk1 siRNA were transplanted subcutaneously in nude mice and their tumorgenesis ability were observed, the plk1 protein levels of the samples from nude mice in different groups were compared. RESULTS: After treatment with plk1 siRNA, plk1 mRNA and protein level decreased obviously in certain time, more MKN45 cells accumulated at G(2)/M (P < 0.05). Apoptosis rate of MKN45 cells treated with plk1 siRNA was higher than that of control cells at 48 h and 72 h (P < 0.05), and MKN45 cells proliferated slowly than control groups (P < 0.05), while the tumorgenesis ability obviously decreased, but the plk1 protein levels of the samples from nude mice in different groups were not different. CONCLUSIONS: siRNA targeting plk1 can inhibit the proliferation of MKN45 cells in vitro and vivo. Plk1 may be a novel therapeutic target for gastric cancer.