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1.
J Surg Oncol ; 127(6): 1028-1034, 2023 May.
Artículo en Inglés | MEDLINE | ID: mdl-36862078

RESUMEN

BACKGROUND OND OBJECTIVES: Complete cytoreductive surgery (CRS) may prolong survival for selected patients with peritoneal carcinomatosis from colorectal cancer (CRC). However, there is a paucity of data on outcomes following incomplete procedures. METHODS: Patients with incomplete CRS for well-differentiated (WD) and moderate/poorly-differentiated (M/PD) appendiceal cancer, right and left CRC were identified at a single tertiary center (2008-2021). RESULTS: Of 109 patients, 10% were WD and 51% M/PD appendiceal cancers, and 16% right and 23% left CRC. There were no differences in gender, BMI (mean = 27), ASA score, previous abdominal surgery (72%), and extent of CRS. The PC Index differed between appendiceal and colorectal cancers (mean = 27 vs. 17, p < 0.01). Overall, the perioperative outcomes were similar among the groups, with 15% experiencing complications. Postoperatively, 61% received chemotherapy, and 51% required ≥1 subsequent procedure. The 1 and 3-year survival for the WD, M/PD, right and left CRC subgroups were 100%, 67%, 44%, 51%, and 88%, 17%, 12%, and 23%, respectively (p = 0.02). CONCLUSIONS: Incomplete CRS was associated with significant morbidity and number of subsequent palliative procedures. Prognosis correlated with histologic subtype; WD appendiceal cancer patients having superior outcomes, while those with right sided CRC the worst survival. These data may help guiding expectations in the setting of incomplete procedures.


Asunto(s)
Neoplasias del Apéndice , Neoplasias Colorrectales , Hipertermia Inducida , Neoplasias Peritoneales , Humanos , Neoplasias Peritoneales/terapia , Neoplasias del Apéndice/patología , Procedimientos Quirúrgicos de Citorreducción , Pronóstico , Neoplasias Colorrectales/patología , Hipertermia Inducida/efectos adversos , Tasa de Supervivencia , Terapia Combinada , Estudios Retrospectivos
2.
J Surg Res ; 182(1): 85-93, 2013 Jun 01.
Artículo en Inglés | MEDLINE | ID: mdl-22998776

RESUMEN

BACKGROUND: The BRAF(V600E) mutation is present in 62% of radioactive iodine-resistant thyroid tumors and is associated with downregulation of the sodium-iodide symporter (NIS) and thyroid stimulating hormone receptor (TSHr). We sought to evaluate the combined effect of BRAF inhibition and TSH supplementation on (131)I uptake of BRAF(V600E)-mutant human thyroid cancer cells. MATERIALS AND METHODS: WRO cells (a BRAF(V600E)-mutant follicular-derived papillary thyroid carcinoma cell line) were transfected with small interfering RNA targeting BRAF for 72 h in a physiological TSH environment. NIS and TSHr expression were then evaluated at three levels: gene expression, protein levels, and (131)I uptake. These three main outcomes were then reassessed in TSH-depleted media and media supplemented with supratherapeutic concentrations of TSH. RESULTS: NIS gene expression increased 5.5-fold 36 h after transfection (P = 0.01), and TSHr gene expression increased 2.8-fold at 24 h (P = 0.02). NIS and TSHr protein levels were similarly increased 48 and 24 h after transfection, respectively. Seventy-two hours after BRAF inhibition, (131)I uptake was unchanged in TSH-depleted media, increased by 7.5-fold (P < 0.01) in physiological TSH media, and increased by 9.1-fold (P < 0.01) in supratherapeutic TSH media. CONCLUSIONS: The combined strategy of BRAF inhibition and TSH supplementation results in greater (131)I uptake than when either technique is used alone. This represents a simple and feasible approach that may improve outcomes in patients with radioactive iodine-resistant thyroid carcinomas for which current treatment algorithms are ineffective.


Asunto(s)
Adenocarcinoma Folicular/metabolismo , Silenciador del Gen , Yodo/metabolismo , Proteínas Proto-Oncogénicas B-raf/genética , Neoplasias de la Tiroides/metabolismo , Tirotropina/farmacología , Adenocarcinoma Folicular/patología , Línea Celular Tumoral , Silenciador del Gen/efectos de los fármacos , Humanos , Técnicas In Vitro , Radioisótopos de Yodo , Mutación/genética , ARN Interferente Pequeño/farmacología , Receptores de Tirotropina/metabolismo , Simportadores/metabolismo , Neoplasias de la Tiroides/patología , Transfección
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