Cachexia induced by Walker 256 tumor growth causes rat lymphocyte death

Lima, Thaís Martins de; Lima, Manuela Maria Ramos; Almeida, Débora Cristina Gonçalves de; Mendonça, J. R.; Curi, Rui

doi:10.1007/s00262-004-0570-4

Cited by 11 publications

(9 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, very few data are available on the inflammatory cell response in cachexia. In two different rat models of cancer cachexia, an overall immunosuppression has been actually reported 30,42 . In particular, Vannucci et al report a significant decrease in circulating NK, B and T lymphocytes in tumorbearing animals 42 .…”

Section: Discussionmentioning

confidence: 97%

See 1 more Smart Citation

Skeletal muscle is enriched in hematopoietic stem cells and not inflammatory cells in cachectic mice

Berardi

Aulino

Murfuni

et al. 2008

Neurological Research

View full text Add to dashboard Cite

The elevated levels of cytokines which characterize cachexia may represent a trigger for inflammatory cell activation. However, we find that in cachexia, inflammatory cells in muscle are not increased while muscle tissue nuclei decline. Our data suggest that the inflammatory cell-mediated stress is not an etiologic component of muscle wasting in cachexia. The relative increase in HSCs in cachectic skeletal muscle suggests an attempt to maintain muscle homeostasis by recruitment and/or activation of stem cells.

show abstract

Section: Discussionmentioning

confidence: 97%

“…Hampered levels of enzymes involved in antitumor T-cell signal transduction have also been reported 25,26 . Other works showed high levels of apoptosis in T lymphocytes localized both to the tumor mass [27][28][29] and the lymph nodes 30 .…”

Section: Introductionmentioning

confidence: 93%

Skeletal muscle is enriched in hematopoietic stem cells and not inflammatory cells in cachectic mice

Berardi

Aulino

Murfuni

et al. 2008

Neurological Research

View full text Add to dashboard Cite

show abstract

“…Moreover, W256-induced cachexia is associated with immunosuppression caused by lymphocyte apoptosis. 22 These metabolic effects of W256 tumor could have contributed to the cachexia presented by the animals of the control group. As far as we are concerned, this is the first experimental account of intracerebral W256 induced cachexia and one of the first experimental brain tumor animal models to show significant cachexia so far.…”

Section: Discussionmentioning

confidence: 99%

Cyclosporin safety in a simplified rat brain tumor implantation model

Félix

Fontenele

Teles

et al. 2012

Arq. Neuro-Psiquiatr.

View full text Add to dashboard Cite

There is a continuing need for experimental neuro-oncology for animal models that can be used to assess the efficacy of innovative approaches for the treatment of brain tumors. The rat has been one of the most widely used of all experimental animals, and rat brain tumor models have been used extensively ABStrActBrain cancer is the second neurological cause of death. A simplified animal brain tumor model using W256 (carcinoma 256, Walker) cell line was developed to permit the testing of novel treatment modalities. Wistar rats had a cell tumor solution inoculated stereotactically in the basal ganglia (right subfrontal caudate). This model yielded tumor growth in 95% of the animals, and showed absence of extracranial metastasis and systemic infection. Survival median was 10 days. Estimated tumor volume was 17.08±6.7 mm 3 on the 7 th day and 67.25±19.8 mm 3 on 9 th day post-inoculation. Doubling time was 24.25 h. Tumor growth induced cachexia, but no hematological or biochemical alterations. This model behaved as an undifferentiated tumor and can be promising for studying tumor cell migration in the central nervous system. Dexamethasone 3.0 mg/kg/day diminished significantly survival in this model. Cyclosporine 10 mg/kg/day administration was safely tolerated.Key words: brain neoplasms, neoplasms, experimental, carcinoma 256, Walker, cachexia, cell movement, immunosuppressive agents.reSUMO Neoplasias encefálicas constituem a segunda causa neurológica de morte. Foi desenvolvido um modelo animal simplificado de tumor cerebral em ratos utilizando a linhagem celular W256 (carcinoma 256 de Walker) para permitir teste de novos tratamentos. Ratos Wistar foram inoculados nos gânglios da base (caudato subfrontal direito) com uma solução celular tumoral, por via estereotáxica. Este modelo demonstrou crescimento tumoral em 95% dos animais inoculados com sucesso, além de mostrar ausência de metástases extracranianas e infecção sistêmica. A mediana de sobrevida dos animais foi de 10 dias. O volume tumoral estimado foi de 17,08±6,7 mm 3 no sétimo dia e de 67,25±19,8 mm 3 no nono dia após a inoculação. O tempo de duplicação foi estimado em 24,25 h. O crescimento tumoral induziu a caquexia, mas não houve alterações bioquímicas ou hematológicas. Esse modelo permite fácil reprodução e comporta-se como um tumor indiferenciado, mostrando potencial para estudar migração celular tumoral no sistema nervoso central. Dexametasona 3,0 mg/kg/dia reduziu significantemente a sobrevida dos animais inoculados com tumor nesse modelo. Ciclosporina 10 mg/kg/dia não teve efeito na sobrevida, sendo sua administração bem tolerada.Palavras-Chave: neoplasias encefálicas, neoplasias experimentais, carcinoma 256 de Walker, caquexia, movimento celular, imunossupressores.since the mid 1970s. Rat tumor models have a series of advantages when compared to mouse models despite the recent and frequent use of knockout genetic mice models.It was first reported in the early 1970s that central nervous system (CNS) tumors could be reproducibly and

show abstract

“…Walker 256 tumor is a carcinosarcoma that has been maintained in our Laboratory. The tumor cells were obtained from a rat ascitic fluid by intraperitoneal passages as described elsewhere [ 8 ]. The percentage of viable cells was established by trypan blue solution (1 %) using a Neubauer chamber.…”

Section: Methodsmentioning

confidence: 99%

Fish oil administration mediates apoptosis of Walker 256 tumor cells by modulation of p53, Bcl-2, caspase-7 and caspase-3 protein expression

et al. 2015

View full text Add to dashboard Cite

BackgroundSeveral studies have been shown pro-apoptotic effects of fish oil (FO), rich in n-3 polyunsaturated fatty acids (n-3 PUFA) on cancer cells. Nevertheless, few in vivo experiments have provided data of its ability on apoptosis protein expression in tumor tissue. Thus, in this study we investigate the effect of FO supplementation on apoptosis protein expression in Walker 256 tumor bearing rats. Male Wistar rats were randomly assigned to three groups: fed with regular chow (W); fed regular chow supplemented with FO (WFO) or coconut fat (WCO) (1 g/kg body weight/daily). After thirty days, all animals were inoculated subcutaneously with Walker 256 tumor cells.FindingsProtein expression was done by western blotting in Walker 256 tumor tissue samples. FO decreased the Bcl-2/Bax ratio (p < 0.05) and increased the p53 (p < 0.05), cleaved caspase-7 (p < 0.05) and cleaved caspase-3 (p < 0.05) in Walker 256 tumor tissue.ConclusionsOur data suggest that the pro-apoptotic effect of FO in Walker 256 tumor is related with specifics cleaved caspases.

show abstract

Cachexia induced by Walker 256 tumor growth causes rat lymphocyte death

Cited by 11 publications

References 33 publications

Skeletal muscle is enriched in hematopoietic stem cells and not inflammatory cells in cachectic mice

Skeletal muscle is enriched in hematopoietic stem cells and not inflammatory cells in cachectic mice

Cyclosporin safety in a simplified rat brain tumor implantation model

Fish oil administration mediates apoptosis of Walker 256 tumor cells by modulation of p53, Bcl-2, caspase-7 and caspase-3 protein expression

Contact Info

Product

Resources

About