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1.
Arch. latinoam. nutr ; 64(1): 16-23, mar. 2014. ilus, tab
Artículo en Español | LILACS | ID: lil-752687

RESUMEN

La porción comestible del mango contiene ácido ascórbico, carotenoides, polifenoles, terpenoides y fibra que tienen efectos protectores para la salud, y posiblemente contra el desarrollo de cáncer de colon (CCO). El objetivo de este estudio fue evaluar la capacidad antiproliferativa en células de adenocarcinoma de colon (SW480) y preventiva en un modelo in vivo de CCO de un extracto acuoso de Mangifera indica cv. Azúcar. El contenido de fenoles totales, flavonoides y carotenoides también fue analizado. El extracto inhibió el crecimiento de las células SW480 en forma dosistiempo- dependiente hasta 22,3% luego de 72h de exposición al extracto (200 μg/mL). La carcinogénesis en el colon de ratones Balb/c fue inducida mediante dos inyecciones intraperitoneales de azoximetano (AOM) a la tercera y cuarta semana de haber iniciado el suministro de mango en el líquido de bebida (0,3%, 0,6%, 1,25%). Después de 10 semanas de tratamiento se observó inhibición dosis-dependiente de la formación de focos de criptas aberrantes (FCA); 0,3% de mango inhibió más del 60% de FCA (p=0,05) comparado con los controles que recibieron agua. Estos resultados muestran que la pulpa del mango de azúcar, un alimento natural, no tóxico, que forma parte de la dieta del ser humano contiene compuestos bioactivos capaces de reducir el crecimiento de células tumorales y prevenir la aparición de las lesiones precancerosas en colon durante el inicio de la carcinogénesis.


Mango pulp contains ascorbic acid, carotenoids, polyphenols, terpenoids and fiber which are healthy and could protect against colon cancer. The aim of this study was to evaluate the antiproliferative and preventive capacity of an aqueous extract of Mangifera indica cv. Azúcar on a human colon adenocarcinoma cell line (SW480) and in a rodent model of colorectal cancer, respectively. The content of total phenolics, flavonoids and carotenoids were also analyzed in the extract. SW480 cell growth was inhibited in a dose and time dependent manner by 22.3% after a 72h exposure to the extract (200 μg/ mL). Colon carcinogenesis was initiated in Balb/c mice by two intra-peritoneal injections of azoxymethane (AOM) at the third and fourth week of giving mango in drinking water (0.3%, 0.6%, 1.25%). After 10 weeks of treatment, in the colon of mice receiving 0.3% mango, aberrant crypt foci formation was inhibited more than 60% (p=0,05) and the inhibition was dose-dependent when compared with controls receiving water. These results show that mango pulp, a natural food, non toxic, part of human being diet, contains bioactive compounds able to reduce growth of tumor cells and to prevent the appearance of precancerous lesions in colon during carcinogenesis initiation.


Asunto(s)
Animales , Masculino , Anticarcinógenos/farmacología , Neoplasias del Colon/prevención & control , Mangifera/química , Extractos Vegetales/farmacología , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Transformación Celular Neoplásica/efectos de los fármacos , Neoplasias del Colon/inducido químicamente , Técnicas In Vitro , Ratones Endogámicos BALB C , Neoplasias Experimentales
2.
Experimental & Molecular Medicine ; : e10-2013.
Artículo en Inglés | WPRIM | ID: wpr-199830

RESUMEN

Human mesenchymal stem cells (MSCs) have emerged as attractive cellular vehicles to deliver therapeutic genes for ex-vivo therapy of diverse diseases; this is, in part, because they have the capability to migrate into tumor or lesion sites. Previously, we showed that MSCs could be utilized to deliver a bacterial cytosine deaminase (CD) suicide gene to brain tumors. Here we assessed whether transduction with a retroviral vector encoding CD gene altered the stem cell property of MSCs. MSCs were transduced at passage 1 and cultivated up to passage 11. We found that proliferation and differentiation potentials, chromosomal stability and surface antigenicity of MSCs were not altered by retroviral transduction. The results indicate that retroviral vectors can be safely utilized for delivery of suicide genes to MSCs for ex-vivo therapy. We also found that a single retroviral transduction was sufficient for sustainable expression up to passage 10. The persistent expression of the transduced gene indicates that transduced MSCs provide a tractable and manageable approach for potential use in allogeneic transplantation.


Asunto(s)
Adolescente , Animales , Niño , Humanos , Ratones , Muerte Celular/efectos de los fármacos , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Transformación Celular Neoplásica/efectos de los fármacos , Citosina Desaminasa/genética , Fluorouracilo/farmacología , Terapia Genética , Inestabilidad Genómica/efectos de los fármacos , Cariotipo , Células Madre Mesenquimatosas/citología , Células Madre Multipotentes/citología , Neoplasias/terapia , Retroviridae/metabolismo , Factores de Tiempo , Transducción Genética
3.
Experimental & Molecular Medicine ; : 109-120, 2012.
Artículo en Inglés | WPRIM | ID: wpr-93419

RESUMEN

Basal autophagy plays a critical role in maintaining cellular homeostasis and genomic integrity by degrading aged or malfunctioning organelles and damaged or misfolded proteins. However, autophagy also plays a complicated role in tumorigenesis and treatment responsiveness. It can be tumor-suppressing during the early stages of tumorigenesis (i.e., it is an anti-tumor mechanism), as reduced autophagy is found in tumor cells and may be associated with malignant transformation. In this case, induction of autophagy would seem to be beneficial for cancer prevention. In established tumors, however, autophagy can be tumor-promoting (i.e., it is a pro-tumor mechanism), and cancer cells can use enhanced autophagy to survive under metabolic and therapeutic stress. The pharmacological and/or genetic inhibition of autophagy was recently shown to sensitize cancer cells to the lethal effects of various cancer therapies, including chemotherapy, radiotherapy and targeted therapies, suggesting that suppression of the autophagic pathway may represent a valuable sensitizing strategy for cancer treatments. In contrast, excessive stimulation of autophagy may also provide a therapeutic strategy for treating resistant cancer cells having high apoptotic thresholds. In order for us to develop successful autophagy-modulating strategies against cancer, we need to better understand how the roles of autophagy differ depending on the tumor stage, cell type and/or genetic factors, and we need to determine how specific pathways of autophagy are activated or inhibited by the various anti-cancer therapies.


Asunto(s)
Humanos , Anticarcinógenos/uso terapéutico , Autofagia/fisiología , Transformación Celular Neoplásica/efectos de los fármacos , Neoplasias/tratamiento farmacológico
4.
Experimental & Molecular Medicine ; : 759-767, 2010.
Artículo en Inglés | WPRIM | ID: wpr-122640

RESUMEN

The abnormality of serine/threonine kinase Aurora-A is seen in many types of cancers. Although in physiological context it has been shown to play a vital role in cellular mitosis, how this oncogene contributes to tumorigenesis remains unclear. Here we demonstrate that Aurora-A overexpression enhances both the expression level and transcriptional activity of c-Myc. The inhibition of c-Myc expression by RNA interference significantly impaired the oncogenic potential of Aurora-A, resulting in attenuated cellular proliferation and transformation rates as well as fewer centrosomal aberrations. Furthermore, downregulation of c-Myc effectively overcame Aurora-A-induced resistance to cisplatin in esophageal cancer cells. Taken together, our results suggest an important role for c-Myc in mediating the oncogenic activity of Aurora-A, which may in turn allow for future targeting of c-Myc as a potential therapeutic strategy for tumors with Aurora-A overexpression.


Asunto(s)
Humanos , Línea Celular Transformada , Proliferación Celular/efectos de los fármacos , Transformación Celular Neoplásica/efectos de los fármacos , Cisplatino/farmacología , Regulación hacia Abajo , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Proteínas Serina-Treonina Quinasas/genética , Proteínas Proto-Oncogénicas c-myc/genética , ARN Interferente Pequeño/genética , Activación Transcripcional , Transgenes/genética
5.
Experimental & Molecular Medicine ; : 717-727, 2009.
Artículo en Inglés | WPRIM | ID: wpr-71511

RESUMEN

Triptolide, a diterpenoid triepoxide from the traditional Chinese medicinal herb Tripterygium wilfordii Hook. f., is a potential treatment for autoimmune diseases as well a possible anti-tumor agent. It inhibits proliferation of coloretal cancer cells in vitro and in vivo. In this study, its ability to block progress of colitis to colon cancer, and its molecular mechanism of action are investigated. A mouse model for colitis-induced colorectal cancer was used to test the effect of triptolide on cancer progression. Treatment of mice with triptolide decreased the incidence of colon cancer formation, and increased survival rate. Moreover, triptolide decreased the incidence of tumors in nude mice inoculated with cultured colon cancer cells dose-dependently. In vitro, triptolide inhibited the proliferation, migration and colony formation of colon cancer cells. Secretion of IL6 and levels of JAK1, IL6R and phosphorylated STAT3 were all reduced by triptolide treatment. Triptolide prohibited Rac1 activity and blocked cyclin D1 and CDK4 expression, leading to G1 arrest. Triptolide interrupted the IL6R-JAK/STAT pathway that is crucial for cell proliferation, survival, and inflammation. This suggests that triptolide might be a candidate for prevention of colitis induced colon cancer because it reduces inflammation and prevents tumor formation and development.


Asunto(s)
Animales , Humanos , Masculino , Ratones , Transformación Celular Neoplásica/efectos de los fármacos , Colitis/complicaciones , Neoplasias del Colon/inducido químicamente , Sulfato de Dextran/toxicidad , Dimetilhidrazinas/toxicidad , Diterpenos/administración & dosificación , Compuestos Epoxi/administración & dosificación , Interleucina-6/biosíntesis , Quinasas Janus/metabolismo , Ratones Endogámicos BALB C , Ratones Endogámicos ICR , Ratones Desnudos , Trasplante de Neoplasias , Fenantrenos/administración & dosificación , Factor de Transcripción STAT3/metabolismo , Transducción de Señal/efectos de los fármacos , Carga Tumoral/efectos de los fármacos , Proteína de Unión al GTP rac1/biosíntesis
6.
Artículo en Inglés | IMSEAR | ID: sea-37512

RESUMEN

Aberrant crypt foci (ACF) are recognized as preneoplastic lesions for colon cancer, and ACF in rodents are widely used as an intermediate biomarker to predict tumorigenicity in the colon. However, a lack of correlations between the formation of ACF and the development of colonic tumors has been reported in several studies. For example, 2-(carboxyphenyl) retinamide (2-CPR) and genistein were reported to inhibit the carcinogen-induced formation of ACF, whereas both of them were later found to enhance colon tumorigenesis in rats treated with azoxymethane (AOM). Recently, we have identified b-catenin-accumulated crypts (BCAC) in the colon of rats shortly after administration of AOM, and provided evidence that these are independent early lesions of classical ACF, and BCAC might be direct precursors for colon cancers. In the present study, we performed a comparative analysis of the modifying effects of 2-CPR and genistein on 1,2-dimethylhydrazine (DMH)-induced BCAC and ACF in male F344 rats. Dietary administration of 2-CPR (315 ppm) significantly reduced the total number, multiplicity and size of ACF in DMH-exposed colonic mucosa, while genistein (250 ppm) had no significant effects on DMH-induced ACF formation. In contrast, both of 2-CPR and genistein significantly enhanced the multiplicity and size of DMH-induced BCAC when compared with DMH alone group. In addition, both 2-CPR and genistein significantly increased the proliferating cell nuclear antigen (PCNA) index preferentially in BCAC. Together with previous findings that 2-CPR and genistein are tumor promoters in the colon, our results support the concept that BCAC are precursors of colon tumors and suggest that these lesions are more reliable short-term biomarkers for colon carcinogenesis in rodents than ACF.


Asunto(s)
1,2-Dimetilhidrazina/toxicidad , Animales , Anticarcinógenos/uso terapéutico , Carcinógenos/toxicidad , Transformación Celular Neoplásica/efectos de los fármacos , Neoplasias del Colon/inducido químicamente , Genisteína/uso terapéutico , Masculino , Lesiones Precancerosas/inducido químicamente , Ratas , Ratas Endogámicas F344 , Tretinoina/análogos & derivados
7.
Artículo en Inglés | IMSEAR | ID: sea-37307

RESUMEN

The preventive effect of dietary exposure to a flavonoid myricitrin of azoxymethane (AOM)-induced aberrant crypt foci (ACF) and beta-catenin-accumulated crypts (BCAC) formation was investigated in male F344 rats. Thirty-four rats were divided randomly into five experimental groups. Rats in groups 1-3 were given subcutaneous injections of AOM (15 mg/kg body weight) once a week for 3 weeks. Starting 1 week before the first injection of AOM, rats in groups 2 and 3 were fed a diet containing 500 or 1000 ppm myricitrin, respectively, for 11 weeks. Rats in group 4 were fed a diet containing 1000 ppm myricitrin. Rats in groups 1 and 5 were given the basal diet alone during the study. The experiment was terminated 11 weeks after the start. The frequency of ACF per colon in group 3 treated with AOM and 1000 ppm myricitrin was significantly lower than that in group 1 treated with AOM alone (p<0.01). Furthermore, dietary myricitrin at both doses (groups 2 and 3) significantly inhibited the formation of BCAC when compared to group 1 (p<0.05). These results indicate that myricitrin had possible chemopreventive effects in the present short-term colon carcinogenesis bioassays and suggest that longer exposure may cause suppression of tumor development.


Asunto(s)
Animales , Azoximetano/toxicidad , Carcinógenos/toxicidad , Transformación Celular Neoplásica/efectos de los fármacos , Neoplasias del Colon/inducido químicamente , Dieta , Flavonoides/farmacología , Masculino , Lesiones Precancerosas/inducido químicamente , Ratas , Ratas Endogámicas F344 , beta Catenina/farmacología
8.
Artículo en Inglés | IMSEAR | ID: sea-38067

RESUMEN

Spices and flavouring agents are now receiving increasing attention as many of them have been shown to have anticarcinogenic properties. Cloves, sun-dried unopened flower buds from the plant Syzygium aromaticum L, are commonly used as a spice and food flavour. The present study was designed to investigate the chemopreventive action of aqueous infusion of cloves on 9,10-dimethyl benz(a)anthracene (DMBA) and croton oil induced skin carcinogenesis in Swiss mice. The results indicate protection against skin papilloma formation in a dose dependent manner. It has been shown that oral administration of aqueous infusions of clove at a dose of 100 microl/mouse/day not only delays the formation of papilloma but also reduces the incidence of papilloma as well as the cumulative number of papillomas per papilloma bearing mouse. Our observations suggest a promising role for cloves in restriction of the carcinogenesis process.


Asunto(s)
9,10-Dimetil-1,2-benzantraceno , Administración Oral , Animales , Carcinógenos , Transformación Celular Neoplásica/efectos de los fármacos , Quimioprevención , Eugenia/química , Ratones , Neoplasias Experimentales , Papiloma/fisiopatología , Extractos Vegetales/farmacología , Neoplasias Cutáneas/fisiopatología
9.
West Indian med. j ; 52(1): 10-13, Mar. 2003.
Artículo en Inglés | LILACS | ID: lil-410842

RESUMEN

The anti-cancer therapeutic promise of cantharidin is limited because of its high mammalian toxicity. In order to find new anti-cancer lead compounds with reduced toxicity of the cantharidin prototype, the following seven derivatives were screened against the human SH-SY5Y neuroblastoma and MCF-7 breast cancer cells in vitro: 2,3-dimethyl-7-oxabicylo-[2.2.1]heptane-2,3-dicarboxylic anhydride (cantharidin) [1], 1-cyclohexen-1,2-dicarboxylic anhydride [2], cis-4-cyclohexen-1,2-dicarboxylic anhydride [3], cis-1, 2-cyclohexanedicarboxylic anhydride [4], exo-7-oxabicyclo[2.2.1]hept-5-ene-2-3 dicarboxylic anhydride [5], exo-7-oxabicyclo[2.2.1]heptane-2,3-dicarboxylic anhydride (norcantharidin) [6], and (S)-(-)-O-acetylmalic anhydride [7]. Cantharidin, was found to be the most effective anti-proliferative compound on both cell lines. However, on the human neuroblastoma cells cantharidin was of equal toxicity to compound [6]. Mode of action studies revealed that cantharidin inhibited growth factor-mediated activation of mitogen activated protein kinase (MAPkinase) and attenuated the de-phosphorylation of the extracellular regulated kinases 1 and 2 (erk1 and erk2)


Asunto(s)
Humanos , Anhídridos/toxicidad , Cantaridina/toxicidad , Inhibidores Enzimáticos/toxicidad , Activación Enzimática/efectos de los fármacos , Células Tumorales Cultivadas , /farmacología , Matriz Extracelular/efectos de los fármacos , Matriz Extracelular/enzimología , Neoplasias de la Mama/tratamiento farmacológico , Neuroblastoma/tratamiento farmacológico , Proteínas Quinasas Activadas por Mitógenos/efectos de los fármacos , Transformación Celular Neoplásica/efectos de los fármacos
10.
Experimental & Molecular Medicine ; : 371-378, 2003.
Artículo en Inglés | WPRIM | ID: wpr-171364

RESUMEN

This study was conducted to examine the effects of dietary grape extracts on preneoplastic foci formation in rat hepatocarcinogenesis, and related hepatic enzymes. Male Sprague-Dawley rats were fed basal diet or grape diet containing 15% concentrated grape extracts (68 bricks). The grape diet groups were divided into whole-period grape diet group (DEN-GW; grape diet group fed throughout experimental period) and postinitiation grape diet group (DEN-GP; grape diet group fed from post initiation stage) according to the starting time point of the grape diet. Hepatocarcinogenesis was induced by diethylnitrosamine (DEN; 200 mg/kg bw) and 2/3 partial hepatectomy (DEN-B; DEN-treated basal diet group, DEN-GW, and DEN-GP groups), while the control group treated with saline and sham operation (Control group). The formation of placental glutathione (GSH) S-transferase positive (GST-P(+)) foci in DEN-GW group was moderately but significantly suppressed, however, not in DEN- GP group. Thiobarbituric acid reactive substances content of DEN-GW group was significantly lower than that of DEN-B group. The activity of fatty acid synthase (FAS) in the grape diet groups was decreased about 1/2 of the DEN-B group. The content of GSH and GSH peroxidase activity were increased by carcinogen treatment, but not modulated by grape diet. The activities of GSH S-transferase, p-nitrophenol hydroxylase, and catalase were not affected by diet or treatment. Conclusively, the grape diet-induced reduction of FAS activity that was expressed highly in neoplastic tissues, might be one of the contributing mechanisms of hepatic cancer prevention.


Asunto(s)
Animales , Masculino , Ratas , Administración Oral , Peso Corporal/efectos de los fármacos , Catalasa/metabolismo , Transformación Celular Neoplásica/efectos de los fármacos , Dieta , Suplementos Dietéticos , Ácido Graso Sintasas/metabolismo , Glutatión/metabolismo , Glutatión Peroxidasa/metabolismo , Hígado/efectos de los fármacos , Neoplasias Hepáticas/dietoterapia , Tamaño de los Órganos/efectos de los fármacos , Extractos Vegetales , Ratas Sprague-Dawley , Vitis/química
11.
Indian J Exp Biol ; 1999 Sep; 37(9): 904-18
Artículo en Inglés | IMSEAR | ID: sea-59006

RESUMEN

Malachite green (MG), consisting of green crystals with a metallic lustre, is very soluble in water and is highly cytotoxic to mammalian cells in culture and also acts as a liver tumour promoter. In view of its industrial importance and possible exposure to human beings, MG poses a potential environmental health hazard. Accordingly, we have studied the effect of MG on the formation of free radicals using Electron Spin Resonance (ESR) analysis with 5,5-dimethyl-1-pyrroline N-oxide (DMPO) as a spin trapping agent. ESR analysis showed formation of reactive free radicals during exposure of MG to Syrian hamster embryo (SHE) cells. As per mechanism-based toxicology in cancer risk assessment, the chemicals that have the potential to be metabolized to active free radical species could be human cancer hazards. So, we have investigated the effect of MG on the formation of Type II and Type III morphologically transformed foci using SHE cell transformation assay. MG induced dose related transformed foci. Some of these transformed foci were taken out using selective trypsinisation and established immortal cell lines. One of these immortal cell lines was characterized extensively. This immortal cell line showed enhanced DNA synthesis in the form of BrdU incorporation, increased presence of proliferating cell nuclear antigen (PCNA), bcl-2 and p53 proteins by immunohistochemistry. When these immortal cells were injected subcutaneously into nude mice, they developed tumors which were transplantable and histopathologically sarcomas. The present studies indicate that MG could be a potential candidate for two year chemical carcinogenesis rodent bioassays.


Asunto(s)
Animales , Transformación Celular Neoplásica/efectos de los fármacos , Células Cultivadas , Cricetinae , Humanos , Mesocricetus , Ratones , Colorantes de Rosanilina/toxicidad
12.
Braz. j. med. biol. res ; 32(7): 821-5, July 1999.
Artículo en Inglés | LILACS | ID: lil-234886

RESUMEN

TGF-ß1 regulates both cellular growth and phenotypic plasticity important for maintaining a growth advantage and increased invasiveness in progressively malignant cells. Recent studies indicate that TGF-ß-1 stimulates the conversion of epitheliod to fibroblastoid phenotype which presumably leads to the inactivation of growth-inhibitory effects by TGF-ß1 (Portella et al. (1998) Cell Growth and Differentiation, 9: 393-404). Therefore, the investigation of TGF-ß1 signaling that leads to altered growth and migration may provide novel targets for the prevention of increased cell growth and invasion. Although much attention has been paid to TGF-ß1 responses in epithelial cells, the above studies suggest that examination of signal transduction pathways in fibroblasts are important as well. Data from our laboratory are consistent with the concept that TGF-ß1 can act as a regulatory switch in density-dependent C3H 10T1/2 fibroblasts capable of either promoting or delaying G1 traverse. The regulation of this switch is proposed to occur prior to pRb phosphorylation, namely prior to activation of cyclin-dependent kinases. The current study is concerned with the evaluation of a key cyclin (cyclin D1) which activates cdk4 and p27KIP1 which in turn inhibit cdk2 in the proliferative responses of epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) and their modulation by TGF-ß1. Although the molecular events that lead to elevation of cyclin D1 are not completely understood, it appears likely that activation of p42/p44MAPK kinases is involved in its transcriptional regulation. TGF-ß1 delayed EGF- or PDGF-induced cyclin D1 expression and blocked the induction of active p42/p44MAPK. The mechanism by which TGF-ß1 induces a block in p42/p44MAPK activation is being examined and the possibility that TGF-ß1 regulates phosphatase activity is being tested


Asunto(s)
Humanos , Proteínas Quinasas Dependientes de Calcio-Calmodulina/metabolismo , Transformación Celular Neoplásica/efectos de los fármacos , Ciclina D1/farmacología , Factor de Crecimiento Epidérmico/farmacología , Factor de Crecimiento Transformador beta/farmacología , Activación Enzimática/efectos de los fármacos
13.
Braz. j. med. biol. res ; 32(7): 841-3, July 1999.
Artículo en Inglés | LILACS | ID: lil-234889

RESUMEN

FGF2 elicits a strong mitogenic response in the mouse Y-1 adrenocortical tumor cell line, that includes a rapid and transient activation of the ERK-MAPK cascade and induction of the c-Fos protein. ACTH, itself a very weak mitogen, blocks the mitogenic response effect of FGF2 in the early and middle G1 phase, keeping both ERK-MAPK activation and c-Fos induction at maximal levels. Probing the mitogenic response of Y-1 cells to FGF2 with ACTH is likely to uncover reactions underlying the effects of this hormone on adrenocortical cell growth


Asunto(s)
Animales , Ratones , Neoplasias de la Corteza Suprarrenal , Hormona Adrenocorticotrópica/farmacología , Proteína Quinasa 1 Activada por Mitógenos/farmacología , Proteínas Proto-Oncogénicas c-fos/farmacología , Receptores de Factores de Crecimiento de Fibroblastos/efectos de los fármacos , Transformación Celular Neoplásica/efectos de los fármacos , Interacciones Farmacológicas
14.
Indian J Pediatr ; 1992 Jul-Aug; 59(4): 443-8
Artículo en Inglés | IMSEAR | ID: sea-80201

RESUMEN

Sixteen children with myelodysplastic syndrome as defined by the French-American-British co-operative group are presented. The mean age was 10.5 (2.5 to 16) years, with a male predominance. All patients belonged to the more aggressive subtypes of myelodysplastic syndromes. Seven patients presented with refractory anaemia with excess blasts, six had refractory anemia with excess blasts in transformation, and three had chronic myelomonocytic leukemia. Cytogenetic analysis done in 7 of the 16 patients, revealed karyotype abnormalities involving chromosomes 7, 8 and 17. One patient with Down's syndrome had karyotype of 47, XY, +21 (major clone) and 46, XY (minor clone). Five of these patients evolved to acute leukemia. The mean duration of survival was 5.5 months. Aggressive chemotherapy as a primary line of treatment induced remission in five out of six patients. Predominance of aggressive types of myelodysplastic syndromes in children and their good but short-lived response to aggressive chemotherapy suggests the need for early bone marrow transplantation following chemotherapy.


Asunto(s)
Adolescente , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapéutico , Biopsia con Aguja , Médula Ósea/patología , Transformación Celular Neoplásica/efectos de los fármacos , Niño , Preescolar , Aberraciones Cromosómicas/genética , Femenino , Humanos , Leucemia Mieloide Aguda/diagnóstico , Masculino , Síndromes Mielodisplásicos/diagnóstico , Pronóstico
15.
Indian J Exp Biol ; 1991 Sep; 29(9): 813-7
Artículo en Inglés | IMSEAR | ID: sea-58964

RESUMEN

Subacute doses (1/20 LD50) of aflatoxin B1 and ochratoxin A were fed to weanling albino rats individually and in combination for 36 weeks and then rats were maintained on toxin free normal diet for a period of 24 weeks. Livers of rats were fatty, wherever aflatoxin was administered but the enzyme activity did not show significant differences among various groups. However, in a few individuals whose livers were severely affected, higher concentrations of urine creatinine, liver RNA and DNA, and ALT enzyme activity were recorded. Histopathological examination showed various stages of hepatoma and hepatocarcinoma including nodular hyperplasia, hypertrophy, vacuolisation, degeneration, pseudolobulation, cellular infiltration and fibrosis of liver of rats fed with aflatoxin individually and in combination. Few anaplastic cells in the corticomedullary region and nuclear enlargement of proximal tubular epithelium of kidney were found wherever combined toxin and ochratoxin alone were administered. Liver tumor expression was time dependent.


Asunto(s)
Administración Oral , Aflatoxina B1/administración & dosificación , Animales , Carcinógenos/administración & dosificación , Transformación Celular Neoplásica/efectos de los fármacos , Riñón/citología , Masculino , Ocratoxinas/administración & dosificación , Ratas , Ratas Endogámicas
16.
Indian J Cancer ; 1989 Jun; 26(2): 92-8
Artículo en Inglés | IMSEAR | ID: sea-51218

RESUMEN

The extract of black and green tea (Camellia sp.) which are widely consumed as commonest beverage, decreased the 12-O-Tetradecanoylphorbol-13 acetate (TPA) induced promotion of transformation in dose dependent manner in JB6 mouse epidermal cell system. The probable mechanisms have been discussed.


Asunto(s)
Animales , Antioxidantes/administración & dosificación , Línea Celular Transformada/efectos de los fármacos , Transformación Celular Neoplásica/efectos de los fármacos , Relación Dosis-Respuesta a Droga , Ratones , , Acetato de Tetradecanoilforbol
17.
Medicina (B.Aires) ; 45(1): 35-41, 1985. tab, ilus
Artículo en Español | LILACS | ID: lil-27731

RESUMEN

El compuesto difluormetilornitina (DFMO) es un inhibidor irreversible de la enzima ornitina decarboxilasa de células animales y provoca una marcada disminución de los niveles endógenos de putrescina y espermidina. El agregado de esta droga a cultivos de fibroblastos de ratón (células A-31) y a células derivadas de las anteriores y transformadas con el agente químico benzopireno (células BP-A-31) detiene la multiplicación celular después de 3 a 6 días de cultivo. Cuando se elimina el inhibidor del medio de cultivo después de 6 días de tratamiento, las células A-31 pueden reiniciar su proliferación después de un período de varios días, mientras las células transformadas BP-A-31 no se recuperan. El DFMO provoca la disminución de la síntesis de ARN y de proteínas tanto en células A-31 como en BP-A-31, pero en estas últimas la inhibición es mayor. Por otra parte, cuando se elimina la droga después de 72h de tratamiento y se continúa el cultivo, la sintesis de proteínas en células BP-A-31 sigue estando inhibida, mientras en células A-31 aumenta rápidamente hasta niveles cercanos a los de los cultivos controles realizados en ausencia de DFMO. La marcación de las proteínas con metionina radioactiva en cultivos de células A-31 y BP-A-31 en presencia o ausencia de DFMO indica que la droga inhibe específicamente la biosíntesis de algunas proteínas cuyos pesos moleculares son aproximadamente 50 000, 70 000, 90 000 y 180 000 daltons. El tratamiento combinado de los cultivos con DFMO y Ara C sugiere que el inhibidor de la biosíntesis de poliaminas detiene el crecimiento de las células A-31 y BP-A-31 en la fase G1 del ciclo


Asunto(s)
Células/crecimiento & desarrollo , Técnicas In Vitro , Ornitina/farmacología , Poliaminas/farmacología , Transformación Celular Neoplásica/efectos de los fármacos
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