ESS - CQB - Comunicações em eventos científicos
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Browsing ESS - CQB - Comunicações em eventos científicos by Author "Almeida, Joana"
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- Adipocyte-released factors enhance melanocyte’s proliferation and motilityPublication . Fernandes, Rúben; Coelho, Pedro; Almeida, Joana; Prudêncio, Cristina; Soares, RaquelObesity, favored by the modern lifestyle, acquired epidemic proportions nowadays. Obesity has been associated with various major causes of death and morbidity including malignant neoplasms. Cutaneous melanoma incidence rates have also been increasing uring the last four decades in several countries. Obesity involvement in melanoma etiology has been recognized, but the implicated mechanisms remain unclear. We propose to address the above relationship and investigate the mechanism interplaying between obesity and an increased risk of melanoma onset.
- Biomolecules in the relationship of cancer and obesityPublication . Almeida, Joana; Coelho, Pedro; Prudêncio, Cristina; Vieira, Mónica; Fernandes, Rúben; Fonseca, Magda; Soares, Raquel; Silva, Liliana; Faria, Isabel; Monteiro, Armanda; Pinto, Gabriela; Cea, V.; Galesio, M.; Noronha, J. P.; Diniz, M. S.; Sala, C.Obesity has been associated with various major causes of death and morbidity including malignant neoplasms. This increased prevalence has been accompanied by a worldwide increase in cutaneous melanoma incidence rates during the last decades, as well as gliomas, the most common primary malignant brain tumors in adults (Almeida et al., 2019). Although obesity aetiology is established, the implicated mechanisms remain unclear (Coelho et al., 2016). Melanoma is refractory to conventional therapies, and radiotherapy usage as an adjuvant therapy in cutaneous melanoma patients is ineffective, so it is extremely important to understand the antioxidant modulation of melanoma under an environment of obesity (Coelho et al., 2017; Oliveira et al., 2016). Moreover, the metastatic potential of some types of cancer is reduced or inhibited by obesity, which drives major concerns on the prognosis of metastasized patients (Fonseca et al., 2021). All of the studies disclose interesting models for the study of these tumors’ biology under an obese environment, that can be explored for the search of biomarkers, prognostic markers and therapeutic approaches.
- Linfangiogénese no tecido adiposo em ratinhos e sua relação com a obesidade: Avaliação histoquímica e metabolómica (lipidómica) mediante UPLC-MS/MSPublication . Fernandes, Rúben; Soares, Raquel; Prudêncio, Cristina; Macedo, Bárbara; Ramalho, Renata; Almeida, JoanaIntrodução: O tecido adiposo é um órgão endócrino dinâmico, secretando factores importantes na regulação do metabolismo lipídico, do fluxo vascular sanguíneo e linfático e função imunológica, entre outros. Em caso de acumulação de tecido adiposo por ingestão de uma dieta gorda, ou por disfunção metabólica, os adipócitos podem desencadear uma reacção inflamatória por falha na drenagem linfática, acumulando-se mediadores inflamatórios, os quais potenciam a propagação da reacção. Assim, questiona-se uma potencial associação entre o aumento de tecido adiposo na obesidade, hipoxia adipocitária e estimulação da linfangiogénese. Além disso, a expressão de adipocinas varia de acordo com a distribuição do tecido adiposo (subcutâneo, TAS e visceral, TAV). Métodos: Ensaios com ratinhos da estirpe C57Bl/6J, divididos em grupos submetidos a dieta normal (ND) e dieta rica em gordura (HFD). Avaliação semi-quantitativa da expressão tecidular de LYVE-1 (marcador da linfangiogénese) por imunohistoquímica em material embebido em parafina, no TAS e TAV, e cromatografia líquida de ultra-performance acoplada de espectrometria de massa (UPLC-MS) para análise da expressão plasmática de ceramida e esfingosina-1-fosfato (S1P). Resultados: Observou-se diminuição do número de vasos linfáticos e intensidade de sinal correspondente ao LYVE-1 ao longo do tempo em TAV, e aumento de ambos os parâmetros em TAS e hipertrofia adipocitária. As concentrações de ceramida e S1P corroboram a existência de um processo inflamatório nos ratinhos em estudo, ainda que numa fase muito inicial. Conclusão: A resposta inflamatória avaliada através dos diferentes parâmetros permite afirmar que num estado inicial de obesidade a proliferação linfática poderá estar a ser retardada pela hipertrofia adipocitária. A libertação de adipocinas será observada apenas numa fase posterior, desencadeando todo o processo inflamatório que incrementará a proliferação linfática. Adicionalmente, é possível sugerir que a maior pressão à qual o TAV se encontra sujeito não favorece a proliferação linfática, pelo menos num estadio incial.
- Potentional radiosensitizer effect of TUDCA in a obesity model of brain tumor cellsPublication . Silva, Liliana; Almeida, Joana; Coelho, Pedro; Faria, Isabel; Monteiro, Armanda; Soares, Raquel; Vieira, Mónica; Prudêncio, Cristina; Fernandes, RúbenObesity may play an important role in the biology of seve ral types of cancer, but the correlation with glioma Is still not very well defined. Former studies indicated that obesity may be related with an decreased resistance to radiation and increased redox status in brain tumors. Since radiothetapy is the most commonly treatment modality used in this type of tumor, we creale a new model of experiments to determinate the influence of obesity in glioma cells [n the presence of radiation with an imbalance of redox status, BC3H1 glioma cells were treated with t-BOOH (150~M), TUDCA (25~M) and a mix of t-BOOH and TUOCA{150~M and 25~M respectively) in serum-free OMEM or conditioned media (CM) from differentiated 3T3-L 1 adj pocytes. Afterwards the cells were irradiated with a total dose of 2 Gy. Subsequently BC3H1 viability was evaluated, by MTT assay, after 4 and 12 hours. We observed an increase in viability In all cells treated solely with 3T3-L 1 eM. Interestingly, in the presence of CM plus TUDCA or t-BOOH, the viability of 6C3H1 was inferior of TUOCA or t~BOOH treatments alone, this effect was independent of irradia tion. After 12 hours the I/iability of the glioma cells was significantly higher on irradiated ceUs treated only with eM, this effect was not yet observed at the 4 hours time point But, in the presence of mix of t~BOOH and TUDCA, with eM and irradiation the cells viability decrea se significanUy. The 3T3-L 1 Me increase (he cell viabrlity in the presence of radiation or not, after 12 hours expose" But in the presence of oxidatIve inducer and, In specially, with the antioxidant TUDCA, the BC3Hi viability significantly decrease. So, we observed a potential radiosensitfzer effect of TUDCA in BC3H1 in the presence of 3T3-L1 adipocytes.