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1.
J Gastroenterol Hepatol ; 36(7): 1803-1811, 2021 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-33150976

RESUMEN

BACKGROUND AND AIM: The goal of this study was to develop a preoperative nomogram for predicting the feasibility of trans-anal natural orifice specimen extraction (NOSE) for rectal cancer. METHODS: The analysis included 201 patients who underwent trans-anal NOSE and 457 patients who failed to undergo trans-anal NOSE in Shanghai East Hospital. The data collected included age, gender, body mass index, presence of tumor obstruction, distance from anal verge; maximum tumor diameter and anteroposterior thickness of mesorectum (AP) measured by magnetic resonance imaging; interspinous diameter, intertuberous diameter (IT), anteroposterior diameter of the inlet (API), anteroposterior diameter of the midplane, anteroposterior diameter of the outlet (APO), sacral length and pelvic depth (PD) measured by computed tomography. RESULTS: The multivariate analysis suggested that a lower body mass index (P < 0.001), no tumor obstruction (P = 0.005), a shorter distance from anal verge (P < 0.001), a smaller tumor size (P < 0.001), a thinner AP (P < 0.001), a wider and shallower bony pelvis (API/PD, P < 0.001), and a wider and shorter pelvic outlet (IT/APO, P < 0.001) were significantly associated with an increased probability of trans-anal NOSE. Successful NOSE patients had a decreased time to liquid intake (P < 0.001), a shorter postoperative hospital stay (P < 0.001), and fewer wound infections (P = 0.045). No significant difference in the rate of mortality or recurrence was observed. The nomogram model presented an area under the receiver operating characteristic curve of 0.81 (95% CI, 0.78 to 0.85) and good calibration. CONCLUSION: We developed a nomogram model that has some predicative value for the feasibility of laparoscopic rectal resection with trans-anal NOSE, utilizing clinical and radiologic parameters, available in most institutions.


Asunto(s)
Laparoscopía , Cirugía Endoscópica por Orificios Naturales , Nomogramas , Neoplasias del Recto/cirugía , Manejo de Especímenes , Canal Anal , China , Disección , Estudios de Factibilidad , Humanos , Selección de Paciente
2.
J Gastrointest Oncol ; 11(2): 260-268, 2020 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-32399267

RESUMEN

BACKGROUND: Laparoscopic anterior resection with natural orifice specimen extraction (NOSE) avoids extra abdominal extraction incision during colorectal surgery. Some surgeons realized the benefits of NOSE on clinical efficacy. We compared the clinical efficacy of laparoscopic NOSE, laparoscopic non-NOSE and open surgery (OS) for short-term recovery and quality of life (QoL). METHODS: A single randomized controlled trial of NOSE for middle and upper rectal cancer between April 2014 and February 2018. Preoperative and postoperative clinical variables were analyzed and compared between the groups. Preoperative and 6 months postoperative QoL was assessed with the SF-36 QoL questionnaire. RESULTS: A total of 378 patients were enrolled, 334 patients randomly divided into NOSE group (n=104), non-NOSE group (n=119), OS group (n=111). The NOSE group was superior to the other two groups on the QoL after surgery. The NOSE group had the lowest postoperative VAS score between three groups. The postoperative time for bowel function recovery and the length of hospital stay was statistically significantly different among the three groups, with the NOSE group having the shortest time. The incidence of postoperative complications was lower in the NOSE group (12/104, 11.5%) than in the non-NOSE group (20/119, 16.8%), the difference was statistically significant. The Kaplan-Meier (K-M) survival curve showed no statistically significant difference in the disease-free survival (DFS) rate between the three groups. CONCLUSIONS: Comparing NOSE to non-NOSE and OS, the NOSE had significantly better functional recovery and better QoL. The NOSE group had a significant lower surgical complication rate than the non-NOSE group.

3.
Cell Signal ; 26(1): 102-9, 2014 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-23899558

RESUMEN

The earlier studies have shown that Fascin1 (FSCN1), the actin bundling protein, is over-expressed in colorectal cancers, and is associated with cancer cell progression. Here, we aimed to understand the molecular mechanisms regulating FSCN1 expression by focusing on mammalian target of rapamycin (mTOR) signaling and its regulator microRNA-451. We found that microRNA-451 was over-expressed in multiple colorectal cancer tissues, and its expression was correlated with mTOR complex 1 (mTORC1) activity and FSCN1 expression. In cultured colorectal cancer HT-29 cells, knockdown of FSCN1 by RNAi inhibited cell migration and proliferation. Activation of mTORC1 was required for FSCN1 expression, HT-29 cell migration and proliferation, as RAD001 and rapamycin, two mTORC1 inhibitors, suppressed FSCN1 expression, HT-29 cell migration and proliferation. Meanwhile, forced activation of AMP-activated protein kinase (AMPK), the negative regulator of mTORC1, by its activators or by the genetic mutation, inhibited mTORC1 activation, FSCN1 expression, cell migration and proliferation. In HT-29 cells, we found that over-expression of microRNA-451 inhibited AMPK activation, causing mTORC1 over-activation and FSCN1 up-regulation, cells were with high migration ability and proliferation rate. Significantly, these effects by microRNA-451 were largely inhibited by mTORC1 inhibitors or the AMPK activator AICAR. On the other hand, knockdown of miRNA-451 by the treatment of HT-29 cells with miRNA-451 antagomir inhibited mTORC1 activation and FSCN1 expression. The proliferation and migration of HT-29 cells after miRNA-45 knockdown were also inhibited. Our results suggested that the over-expressed microRNA-451 in colon cancer cells might inhibit AMPK to activate mTORC1, which mediates FSCN1 expression and cancer cell progression.


Asunto(s)
Proteínas Quinasas Activadas por AMP/metabolismo , Proteínas Portadoras/genética , Regulación Neoplásica de la Expresión Génica , MicroARNs/metabolismo , Proteínas de Microfilamentos/genética , Complejos Multiproteicos/metabolismo , Serina-Treonina Quinasas TOR/metabolismo , Aminoimidazol Carboxamida/análogos & derivados , Aminoimidazol Carboxamida/farmacología , Proteínas Portadoras/metabolismo , Movimiento Celular/efectos de los fármacos , Movimiento Celular/genética , Proliferación Celular/efectos de los fármacos , Neoplasias Colorrectales/enzimología , Neoplasias Colorrectales/genética , Neoplasias Colorrectales/patología , Activación Enzimática/efectos de los fármacos , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Técnicas de Silenciamiento del Gen , Células HEK293 , Células HT29 , Humanos , Diana Mecanicista del Complejo 1 de la Rapamicina , MicroARNs/genética , Proteínas de Microfilamentos/metabolismo , Modelos Biológicos , Interferencia de ARN/efectos de los fármacos , Ribonucleótidos/farmacología , Transducción de Señal/efectos de los fármacos , Transducción de Señal/genética
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