MARIANA FURIERI GUZZO
Projetos de Pesquisa
Unidades Organizacionais
LIM/42 - Laboratório de Hormônios e Genética Molecular, Hospital das Clínicas, Faculdade de Medicina
9 resultados
Resultados de Busca
Agora exibindo 1 - 9 de 9
conferenceObject Congenital Hypopituitarism: Stem Cell Accumulation in Mutants with Developmental Arrest and Depletion in Mutants with Hyperplasia(2014) CHANG, Claudia Veiga; ARAUJO, Ricardo Viera; CIRQUEIRA, Cinthya Santos; PARFIENIUK, Agata; GUZZO, Mariana F.; BENEDETTI, Anna Flavia F.; SOARES, Ibere C.; MILLAN, Maria Ines Perez; CAMPER, Sally Ann; CARVALHO, Luciani R. S.- Ketoconazole Treatment Decreases the Viability of Immortalized Pituitary Cell Lines Associated with an Increased Expression of Apoptosis-Related Genes and Cell Cycle Inhibitors(2015) GUZZO, M. F.; CARVALHO, L. R.; BRONSTEIN, M. D.Ketoconazole, which was initially developed as an antifungal agent, is a potent inhibitor of adrenal steroidogenesis and has therefore been used in the management of Cushing's disease. Surprisingly, the reduction of cortisol levels during ketoconazole treatment is not accompanied by the expected elevation in plasma adrenocorticotrophic hormone (ACTH) at the loss of negative cortisol feedback from corticotrophic cells, suggesting a direct effect of ketoconazole on these cells. To characterize the direct effects of ketoconazole, we evaluated its invitro effect on cell viability using the pituitary tumoural cell lines AtT-20 (which secretes ACTH), GH3 (which secretes growth hormone and prolactin) and T3.1 (which secretes -subunit) and we also determined the expression levels of genes involved in apoptosis and DNA replication by the quantitative reverse transcription polymerase chain reaction (qRT-PCR). We also evaluated ACTH levels in AtT-20 cells during ketoconazole treatment. We observed a ketoconazole concentration-dependent decrease in pituitary cell viability and reduced ACTH levels in AtT-20 cells after removal of the drug. We also observed increased expression of cell death receptors (e.g. Fas, tumour necrosis factor receptor) and caspases (e.g., caspase-6, caspase-7, caspase-9), suggesting activation of the apoptosis pathway. In addition, we observed increased gene expression of the cell cycle inhibitors p21 and p27 in GH3 cells and increased expression of p21 in T3.1 cells. In conclusion, our findings suggest that ketoconazole significantly reduces cell viability in a concentration-dependent manner in pituitary tumour cell lines and is associated with an increase in apoptosis- and cell cycle regulation-related gene expression.
bookPart Adenomas Hipofisários Clinicamente não funcionantes(2016) GUZZO, Mariana Furieri; BRONSTEIN, Marcello DelanoconferenceObject The Inhibitory Effects of Ketoconazole in Immortalized Pituitary Cell Lines Leading to Decreased Cell Viability Are Due to an Increase of Apoptosis Markers and Cell Cycle Inhibitors(2014) GUZZO, Mariana F.; CARVALHO, Luciani R. S.; BRONSTEIN, Marcello D.- An intrasellar germinoma with normal tumor marker concentrations mimicking primary lymphocytic hypophysitis(2013) GUZZO, Mariana F.; BUENO, Cristina B. Formiga; AMANCIO, Thiago T.; ROSEMBERG, Sergio; BUENO, Cleonice; ARIOLI, Edson L.; GLEZER, Andrea; BRONSTEIN, Marcello D.Intracranial germinomas (GE) are malignant neoplasms most commonly found in the suprasellar region, which may cause anterior and particularly posterior pituitary hormone deficits with central diabetes insipidus (DI). Differential diagnosis of pituitary stalk thickening includes granulomatous, inflammatory, infectious, and neoplastic lesions. Although careful analysis of clinical, laboratory, and imaging findings may facilitate the diagnosis, transsphenoidal biopsy is indicated to confirm the disease, as the correct diagnosis directs the appropriate treatment.
- Apoptosis: its role in pituitary development and neoplastic pituitary tissue(2014) GUZZO, M. F.; CARVALHO, L. R. S.; BRONSTEIN, M. D.Apoptosis, also known as programmed cell death, is a phenomenon in which different stimuli trigger cellular mechanisms that culminate in death, in the absence of inflammatory cell response. Two different activation pathways are known, the intrinsic pathway (or mitochondrial) and extrinsic (or death-receptor pathway), both pathways trigger enzymatic reactions that lead cells to break up and be phagocytized by neighboring cells. This process is a common occurrence in physiological and pathological states, participating in the control of cell proliferation, differentiation and remodeling of organs. In the early steps of pituitary gland formation, numerous apoptotic cells are detected in the separation of Rathke's pouch from the roof of oral ectoderm. In the distal part of the gland, which will form the adenohypophysis, the ratio of apoptosis was significantly lower. However, there is evidence that neoplastic pituitary cells undergo unbalance in genes that control apoptosis leading to uncontrolled cell growth. No direct evidence of apoptosis was found in the drugs used for tumors producing prolactin and growth hormone. In conclusion, an unbalancing in the apoptosis process is the boundary between development and tumor growth.
conferenceObject Congenital Hypopituitarism: Stem Cell Accumulation in Mutants with Developmental Arrest and Depletion in Mutants with Hyperplasia(2014) CHANG, Claudia Veiga; ARAUJO, Ricardo Viera; CIRQUEIRA, Cinthya Santos; PARFIENIUK, Agata; GUZZO, Mariana F.; BENEDETTI, Anna Flavia F.; SOARES, Ibere C.; MILLAN, Maria Ines Perez; CAMPER, Sally Ann; CARVALHO, Luciani R. S.conferenceObject Evaluation of SSTR2, SSTR3 and SSTR5 and DRD2-Long and Short Isoforms Gene Expression in Nonfunctioning Pituitary Adenomas(2014) AMORIM, Paulo Vinicius Goncalves Holanda; TRARBACH, Ericka Barbosa; FORMIGA, Cristina B.; GUZZO, Mariana F.; CESCATO, Valter Angelo Sperling; GLEZER, Andrea; BRONSTEIN, Marcello D.conferenceObject Recovery of Hypopituitarism after Surgical or Medical Therapy for Pituitary Adenoma(2014) BRONSTEIN, Marcello D.; BUENO, Cristina B. F.; CACCELLI, Milena; GUZZO, Mariana F.; SICKLER, Thais P.; DUARTE, Felipe H. G.; GLEZER, Andrea; JALLAD, Raquel S.