PAULO FRANCISCO RAMOS MARGARIDO

(Fonte: Lattes)
Índice h a partir de 2011
6
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Obstetrícia e Ginecologia, Faculdade de Medicina - Docente
SCGINEC-62, Hospital Universitário
LIM/58 - Laboratório de Ginecologia Estrutural e Molecular, Hospital das Clínicas, Faculdade de Medicina

Resultados de Busca

Agora exibindo 1 - 2 de 2
  • article 2 Citação(ões) na Scopus
    Abnormal uterine bleeding and chronic iron deficiency Number 11-December 2022
    (2022) BARROS, Venina Viana de; HASE, Eliane Azeka; SALAZAR, Cristiano Caetano; IGAI, Ana Maria Kondo; ORSI, Fernanda Andrade; MARGARIDO, Paulo Francisco Ramos
  • article 4 Citação(ões) na Scopus
    Local and Systemic STAT3 and p65 NF-KappaB Expression as Progression Markers and Functional Targets for Patients With Cervical Cancer
    (2020) ROSSETTI, Renata A. M.; SILVA-JUNIOR, Ildefonso A. da; RODRIGUEZ, Gretel R; ALVAREZ, Karla L. F.; STONE, Simone C.; CIPELLI, Marcella; SILVEIRA, Caio R. F.; BELDI, Mariana Carmezim; MOTA, Giana R.; MARGARIDO, Paulo F. R.; BARACAT, Edmund C.; UNO, Miyuki; VILLA, Luisa L.; CARVALHO, Jesus P.; YOKOCHI, Kaori; ROSA, Maria Beatriz S. F.; LORENZI, Noely P.; LEPIQUE, Ana Paula
    Cervical cancer, which main etiologic factor is Human Papillomavirus (HPV) infection, continues to be a burden for public health systems in developing countries. Our laboratory has been working with the hypothesis that signals generated in the tumor microenvironment can modulate local and systemic immune responses. In this context, it would be reasonable to think that tumors create pro-tumoral bias in immune cells, even before they are recruited to the tumor microenvironment. To understand if and how signaling started in the tumor microenvironment can influence cells within the tumor and systemically, we investigated the expression of key proteins in signaling pathways important for cell proliferation, viability, immune responses and tolerance. Besides, we used detection of specific phosphorylated residues, which are indicative of activation for Akt, CREB, p65 NF kappa B, and STAT3. Our findings included the observation of a significant STAT3 expression increase and p65 NF kappa B decrease in circulating leukocytes in correlation with lesion grade. In light of those observations, we started investigating the result of the inhibition of STAT3 in a tumor experimental model. STAT3 inhibition impaired tumor growth, increased anti-tumor T cell responses and decreased the accumulation of myeloid cells in the spleen. The concomitant inhibition of NF kappa B partially reversed these effects. This study indicates that STAT3 and NF kappa B are involved in immunomodulatory tumor effects and STAT3 inhibition could be considered as therapy for patients with cervical cancer.