THARCISIO CITRANGULO TORTELLI JUNIOR
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Câncer do Estado de São Paulo, Hospital das Clínicas, Faculdade de Medicina
LIM/24 - Laboratório de Oncologia Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/24 - Laboratório de Oncologia Experimental, Hospital das Clínicas, Faculdade de Medicina
14 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 14
- Metabolomic profiling of breast cancer and adjacent tissue(2017) SANTOS, J. R.; BRENTANNI, M. M.; TORTELLI, T.; DALE, I.; WAITZBERG, A.; WAITZBERG, D.; RAVACCI, G.
conferenceObject Stochastic model of contact inhibition and the proliferation of melanoma in situ.(2018) MORAIS, Mauro Cesar C.; STUHL, Izabella; SABINO, Alan U.; LAUTENSCHLAGER, Willian W.; QUEIROGA, Alexandre S.; TORTELLI JR., Tharcisio C.; CHAMMAS, Roger; SUHOV, Yuri; RAMOS, Alexandre F.- HER2-associated lipogenic phenotype as a potential therapeutical target in breast cancer patients(2017) RAVACCI, G. R.; SANTOS, J. R.; BRENTANI, M. M.; TORTELLI, T.; DALE, I.; LOGULLO, A. F.; WAITZBERG, D. L.
- Emerging targets for combination therapy in melanomas(2015) SAITO, Renata de Freitas; TORTELLI JR., Tharcisio Citrangulo; JACOMASSI, Mayara D'Auria; OTAKE, Andreia Hanada; CHAMMAS, RogerCutaneous melanomas are often difficult to treat when diagnosed in advanced stages. Melanoma cells adapt to survive in extreme environmental conditions and are among the tumors with larger genomic instability. Here we discuss some intrinsic and extrinsic mechanisms of resistance of melanoma cells to both conventional and target therapies, such as autophagy, adaptation to endoplasmic reticulum stress, metabolic reprogramming, mechanisms of tumor repopulation and the role of extracellular vesicles in this later phenomenon. These biological processes are potentially targetable and thus provide a platform for research and discovery of new drugs for combination therapy to manage melanoma patient treatment.
conferenceObject 7-Ketocholesterol loaded-phosphatidylserine liposome induces cell death, autophagy, and growth inhibition of melanoma and breast adenocarcinoma.(2018) FAVERO, Giovani Marino; TORTELLI JR., Tharcisio Citrangulo; FERNANDES, Daniel; PRESTES, Ana Paula; KMETIUK, Louise N. B.; OTAKE, Andreia Hanada; ANDRADE, Luciana N. S.; FARIA, Daniele de Paula; CARNEIRO, Camila de Godoi; GARCEZ, Alexandre Teles; MARQUES, Fabio L. N.; CHAMMAS, Roger- Role of galectin-3 in the elastic response of radial growth phase melanoma cancer cells(2023) HERRERA-REINOZA, Nataly; TORTELLI JUNIOR, Tharcisio Citrangulo; TEIXEIRA, Fernanda de Sa; CHAMMAS, Roger; SALVADORI, Maria CeciliaMelanoma is originated from the malignant transformation of the melanocytes and is characterized by a high rate of invasion, the more serious stage compromising deeper layers of the skin and eventually leading to the metastasis. A high mortality due to melanoma lesion persists because most of melanoma lesions are detected in advanced stages, which decreases the chances of survival. The identification of the principal mechanics implicated in the development and progression of melanoma is essential to devise new early diagnosis strategies. Cell mechanics is related with a lot of cellular functions and processes, for instance motility, differentiation, migration and invasion. In particular, the elastic modulus (Young's modulus) is a very explored parameter to describe the cell mechanical properties; most cancer cells reported in the literature smaller elasticity modulus. In this work, we show that the elastic modulus of melanoma cells lacking galectin-3 is significantly lower than those of melanoma cells expressing galectin-3. More interestingly, the gradient of elastic modulus in cells from the nuclear region towards the cell periphery is more pronounced in shGal3 cells.
- Accumulation of prohibitin is a common cellular response to different stressing stimuli and protects melanoma cells from ER stress and chemotherapy-induced cell death(2017) TORTELLI JUNIOR, Tharcisio Citrangulo; GODOY, Lyris Martins Franco de; SOUZA, Gustavo Antonio de; BONATTO, Diego; OTAKE, Andreia Hanada; SAITO, Renata de Freitas; ROSA, Jose Cesar; GREENE, Lewis Joel; CHAMMAS, RogerMelanoma is responsible for most deaths among skin cancers and conventional and palliative care chemotherapy are limited due to the development of chemoresistance. We used proteomic analysis to identify cellular responses that lead to chemoresistance of human melanoma cell lines to cisplatin. A systems approach to the proteomic data indicated the participation of specific cellular processes such as oxidative phosphorylation, mitochondrial organization and homeostasis, as well as the unfolded protein response (UPR) to be required for the survival of cells treated with cisplatin. Prohibitin (PHB) was among the proteins consistently accumulated, interacting with the functional clusters associated with resistance to cisplatin. We showed PHB accumulated at different levels in melanoma cell lines under stressing stimuli, such as (i) treatment with temozolomide (TMZ), dacarbazine (DTIC) and cisplatin; (ii) serum deprivation; (iii) tunicamycin, an UPR inducer. Prohibitin accumulated in the mitochondria of melanoma cells after cisplatin and tunicamycin treatment and its de novo accumulation led to chemoresistance melanoma cell lines. In contrast, PHB knockdown sensitized melanoma cells to cisplatin and tunicamycin treatment. We conclude that PHB participates in the survival of cells exposed to different stress stimuli, and can therefore serve as a target for the sensitization of melanoma cells to chemotherapy.
conferenceObject Effects of sulforaphane association to conventional therapy for treating triple-negative breast cancer(2023) COUTINHO, L. L.; CHENG, R.; RIDNOUR, L.; JUNQUEIRA, M. S.; CHAMMAS, R.; WINK, D.; TORTELLI, T. C.; RANGEL, M.- Reduction of HER2-associated lipogenic phenotype by docosahexaenoic acid (DHA) induces apoptosis in breast tumor cells harboring HER2 overexpression(2015) RAVACCI, Graziela R.; BRENTANI, Maria M.; FESTUCCIA, William; TORTELLI, Tharcisio; WAITZBERG, Angela F.; WAITZBERG, Dan L.
- Polymorphisms in the p27(kip-1) and prohibitin genes denote novel genes associated with melanoma risk in Brazil, a high ultraviolet index region(2013) FRANCISCO, Guilherme; GONCALVES, Fernanda T.; LUIZ, Olinda C.; SAITO, Renata F.; TOLEDO, Rodrigo A.; SEKIYA, Tomoko; TORTELLI JR., Tharcisio C.; VIOLLA, Esther D. V. B.; MAZZOTTI, Tatiane K. Furuya; CIRILO, Priscila D. R.; FESTA-NETO, Cyro; SANCHES, Jose A.; GATTAS, Gilka J. F.; ELUF-NETO, Jose; CHAMMAS, RogerUltraviolet (UV) radiation is a major environmental risk factor to the development of cutaneous melanoma as it induces pyrimidine dimers in DNA. Genes that exert their function by arresting the cell cycle are critical to avoid carcinogenic mutations, allowing the processing of DNA repair systems. This study was carried out to evaluate the role of polymorphisms in cell cycle genes such as TP53, p27(kip-1), CDKN2A, prohibitin, and GADD153 in melanoma risk as well as their influence on known risk factors in a high UV index region. A hospital-based case-control study was carried out in Brazil to evaluate the contribution of polymorphisms in cell cycle genes toward melanoma risk. The study comprised 202 melanoma patients and 210 controls. The polymorphisms analyzed were TP53 Arg72Pro, p27(kip-1) Val109Gly, GADD153 Phe10Phe (rs697221), CDKN2A 3 ' UTR C540G, and prohibitin 3 ' UTR C1703T. As regards, p27(kip-1) Val109Gly, both heterozygous and homozygous Gly genotypes were shown to be protective genotypes on calculating both crude and adjusted odds ratios (ORs) for age, sex, and educational level [OR 0.37; 95% confidence interval (CI) 0.16-0.87; P < 0.05]. Similarly, the prohibitin TT genotype increased melanoma risk in the crude and adjusted analyses (OR 2.40; 95% CI 1.10-5.26; P < 0.05). The p27(kip-1) Gly protective genotype decreased the risk for melanoma in a stratified analysis of the known risk factors such as hair and eye color, sunburns, pigmented lesions, and European ancestry. The prohibitin TT genotype increased the risk of melanoma by such host factors. Our results showed for the first time that polymorphisms in p27(kip-1) Val109Gly and in prohibitin 3 ' UTR C1703T genotypes modulate the risk to melanoma in a high UV index region. Melanoma Res 23: 231-236 (C) 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins.