RESUMO
Cachexia is a common cancer complication and is associated with weight loss and anorexia. In this study, we investigated the ameliorating effects of cystine and theanine on cancer cachexia using a mouse model. In mice carrying the colon cancer cell line C-26, there was a suppression of body weight increase and reduction in both internal fat and lower limb muscles. Repeated cystine and theanine administration significantly prevented weight loss, internal fat loss, lower limb muscle loss, and serum IL-6 increase in the cachexia model. These results suggested that cystine and theanine may be effective in ameliorating cancer cachexia.
Assuntos
Caquexia , Neoplasias , Humanos , Caquexia/tratamento farmacológico , Caquexia/etiologia , Cistina/farmacologia , Neoplasias/complicações , Redução de PesoRESUMO
BACKGROUND: Prostate cancer is often multifocal and shows histological heterogeneity among different tumor foci within the same prostate. We analyzed the origin and molecular basis of multifocal prostate cancer and genomic alterations associated with tumor progression. METHODS: We examined 45 multifocal prostate cancer foci from 22 radical prostatectomy specimens by comparative genomic hybridization (CGH). Laser capture microdissection (LCM) was used to gather cancer cells from frozen prostate specimens. RESULTS: Frequent chromosomal alternations were losses of 2q21-24 (22.2%), 6q14-22 (60.0%), 8p12-22 (35.6%), 13q14-31 (44.4%) and 16q13-24 (24.4%) and gains of 8q21.3-24.3 (37.8%) and 7q21-33 (20.0%). Frequency of losses of 8p12-22 and 16q13-24 and gains of 8q21.3-24.3 were significantly higher in tumors with high Gleason score (GS) than in those with low GS (P < 0.01, P < 0.05, and P < 0.01, respectively). Tumors with losses of 8p12-22 or 13q14-31 displayed larger volume than those without such losses (P < 0.05 and P < 0.01, respectively). In comparison between different tumor foci within the same prostate, chromosomal alterations did not show completely the same pattern between any tumor foci, except for one case in which two of the three foci displayed no chromosomal abnormalities. More malignant tumors (high GS or extracapsular invasion) displayed significantly higher frequency of losses of 8p12-22 (P < 0.05). CONCLUSIONS: These results suggest that tumor foci within the same prostate represent independent tumors with differing clonal origin and that loss of 8p12-22 represents an important determinant of prostate cancer progression.
Assuntos
Aberrações Cromossômicas , Hibridização de Ácido Nucleico/métodos , Neoplasias da Próstata/genética , Cromossomos Humanos Par 13/genética , Cromossomos Humanos Par 16/genética , Cromossomos Humanos Par 2/genética , Cromossomos Humanos Par 6/genética , Cromossomos Humanos Par 8/genética , Interpretação Estatística de Dados , Progressão da Doença , Humanos , Masculino , Prostatectomia , Neoplasias da Próstata/cirurgia , Estudos RetrospectivosRESUMO
The present study demonstrates the estrogenic effects of fluorotelomer alcohols (FTOHs). In a yeast two-hybrid assay, treatment with 1H,1H,2H,2H-perfluorooctan-1-ol (6:2 FTOH), 1H,1H,2H,2H-perfluoro-decan-1-ol (8:2 FTOH) and 2,2,3,3,4,4,5,5,6,6,7,7,8,8,9,9,10,10,10-nonadecafluoro-1-decanol (NFDH) showed a dose-dependent interaction between the human estrogen receptor (hER) isoforms hERalpha or hERbeta ligand-binding domain and coactivator TIF2, whereas there were no estrogenic effects of perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) for these hERs. The estrogenic effects of FTOHs on hERalpha were higher than those on hERbeta, indicating a differential responsiveness of hERs to FTOHs. The relative ranks of tested chemicals on the estrogenic effects for hERalpha and hERbeta descended in the order of estradiol-17beta>>>6:2 FTOH>NFDH>8:2 FTOH. These results suggest that certain FTOHs including 6:2 FTOH, 8:2 FTOH and NFDH interact with hER isoforms alpha and beta in vitro. Further studies are necessary to investigate contamination levels, potential biological effects and the risks of these compounds on human health.