RESUMEN
BACKGROUND: Postdiagnosis weight gain in patients with breast cancer has been associated with increased cancer recurrence and mortality. This study was designed to identify risk factors for weight gain and create a predictive model to identify a high-risk population for targeted interventions. METHODS: The weight of 393 patients with breast cancer from the Northwestern Robert H. Lurie Cancer Center was measured over a 2-year period from diagnosis, with body mass index (BMI) change over 18 months as the primary endpoint. Demographics, clinical factors, treatment methods, as well as tumor characteristics were also recorded; and a lifestyle questionnaire was conducted. Blood samples were genotyped for 16 single nucleotide polymorphisms in FTO, adiponectin pathway genes (ADIPOQ, ADIPOR1), and FNDC5. Serum leptin, adiponectin, and irisin levels also were measured. RESULTS: Mean ± standard deviation 18-month BMI changes were 0.68 ± 1.42, 0.98 ± 1.62, 0.79 ± 1.74, and -0.44 ± 1.58 kg/m2 for patients ages <40, 40 to 49, 50 to 59, and ≥60 years, respectively. The optimal multivariable model for 18-month BMI change contained the predictors age, height, and endocrine therapy, but only age was statistically significant, with a 0.04 kg/m2 increase in 18-month BMI change per younger year of age. Single nucleotide polymorphisms in ADIPOR1, FTO, and FNDC5 were associated with 18-month BMI change, and the first 2 remained significant after adjusting for the optimal clinical model (all P < .05). CONCLUSIONS: Women age 60 years and younger at the time of breast cancer diagnosis who have an obesity genetic risk model are at increased risk for weight gain after treatment and should be targeted for weight-maintenance interventions. Cancer 2017;123:2413-21. © 2017 American Cancer Society.
Asunto(s)
Antineoplásicos Hormonales/uso terapéutico , Neoplasias de la Mama/terapia , Obesidad/genética , Radioterapia , Sobrevivientes , Aumento de Peso/genética , Adiponectina/sangre , Adiponectina/genética , Adulto , Anciano , Anciano de 80 o más Años , Dioxigenasa FTO Dependiente de Alfa-Cetoglutarato/genética , Antraciclinas/uso terapéutico , Antineoplásicos/uso terapéutico , Índice de Masa Corporal , Neoplasias de la Mama/patología , Femenino , Fibronectinas/sangre , Fibronectinas/genética , Genotipo , Humanos , Leptina/sangre , Persona de Mediana Edad , Estadificación de Neoplasias , Polimorfismo de Nucleótido Simple , Estudios Prospectivos , Receptores de Adiponectina/genética , Factores de RiesgoRESUMEN
PURPOSE: To evaluate the effect of autologous platelet-rich plasma (PRP) on the early phases of osteoinduction by allogenic demineralized bone matrix (DBM) in rabbit intramuscular positions. MATERIALS AND METHODS: Allogenic DBM was produced from bones of 3 healthy rabbits. In each of 6 experimental animals, 0.3 mL autologous PRP was prepared and 2 muscle pouches were created, where 250 mg DBM + PRP (experimental sites) and 250 mg DBM without PRP (control sites) were randomly implanted. Animals were euthanized 3 weeks postoperatively. RESULTS: Histologic examination revealed uneventful healing in all cases, whereas remineralization of the periphery of the bone graft particles was a constant finding. In both control and experimental sites, fibroblasts and other mesenchymal cells (probably osteoprogenitor cells and preosteoblasts) were observed. The main histological difference was the recolonization of the empty lacunae of the bone graft particles by osteocytes at the control sites. The degradation of the graft at the control sites was statistically significantly quicker, although a statistically significant difference regarding the amount of the newly formed fibrous connective tissue was not observed. CONCLUSION: The present study demonstrated that in this experimental model, the addition of PRP to DBM had a negative effect on the early phases of osteoinduction at 3 weeks of observation.
Asunto(s)
Regeneración Ósea , Sustitutos de Huesos , Trasplante Óseo/efectos adversos , Rechazo de Injerto , Plasma Rico en Plaquetas , Animales , Matriz Ósea/trasplante , Regeneración Ósea/efectos de los fármacos , Masculino , Conejos , Distribución AleatoriaRESUMEN
MYCN is a well-known oncogene overexpressed in different human malignancies including neuroblastoma, rhabdomyosarcoma, medulloblastoma, astrocytoma, Wilms' tumor, and small cell lung cancer. While neuroblastoma is one of the most common childhood malignancies, in adults it is extremely rare and its treatment is based on pediatric protocols that take into consideration stage and genotypic features, such as MYCN amplification. Although neuroblastoma therapy has evolved, identification of early stage patients who need chemotherapy continues to pose a therapeutic challenge. The emerging prognostic role of MYCN phenotype of this disease is currently under investigation as it may redefine MYCN amplified subgroups. We describe an unusual case of adult neuroblastoma with MYCN amplification diagnosed incidentally and discuss possible therapeutic dilemmas.