ROGER CHAMMAS

(Fonte: Lattes)
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Departamento de Radiologia, Faculdade de Medicina - Docente
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/24 - Laboratório de Oncologia Experimental, Hospital das Clínicas, Faculdade de Medicina - Líder

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Autor: CHAMMAS, R. ×

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Agora exibindo 1 - 10 de 26
  • conferenceObject
    Melatonin treatment: A transcriptomic networks in a xenograft model of breast cancer
    (2017) JARDIM-PERASSI, B. V.; SONEHARA, N. M.; PAULA-JUNIOR, R. de; CHAMMAS, R.; COUTINHO, L. L.; REIS JUNIOR, O.; ALEXANDRE, P. A.; FUKUMASU, H.; ZUCCARI, D. A. P. C.
  • article 15 Citação(ões) na Scopus
    Endostatin gene therapy stimulates upregulation of ICAM-1 and VCAM-1 in a metastatic renal cell carcinoma model
    (2012) CHAVES, K. C. B.; PERON, J. P. S.; CHAMMAS, R.; TURACA, L. T.; PESQUERO, J. B.; BRAGA, M. S.; FOGUER, K.; SCHOR, N.; BELLINI, M. H.
    One of the greatest challenges in urological oncology is renal cell carcinoma (RCC), which is the third leading cause of death in genitourinary cancers. RCCs are highly vascularized and respond positively to antiangiogenic therapy. Endostatin (ES) is a fragment of collagen XVIII that possesses antiangiogenic activity. In this study, we examined the potential of ES-based antiangiogenic therapy to activate tumor-associated endothelial cells in metastatic RCC (mRCC). Balb/c-bearing Renca cells were treated with NIH/3T3-LendSN or, as a control, with NIH/3T3-LXSN cells. The T-cell subsets and lymphocyte populations of tumors, mediastinal lymph nodes and the spleen were assessed by flow cytometry. The expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) was assessed by real-time PCR, flow cytometry and immunohistochemistry analysis. ES gene therapy led to an increase in the percentage of infiltrating CD4-interferon (IFN)-gamma cells (P<0.05), CD8-IFN-gamma cells (P<0.01) and CD49b-tumor necrosis factor-alpha cells (P<0.01). In addition, ES therapy caused an increase at the mRNA level of ICAM-1 (1.4-fold; P<0.01) and VCAM-1 (1.5-fold) (control vs treated group; P<0.001). Through flow cytometry, we found a significant increase in the CD34/ICAM-1 cells (8.1-fold; P<0.001) and CD34/VCAM-1 cells (1.6-fold; P<0.05). ES gene therapy induced a significant increase in both T CD4 and CD8 cells in the lymph nodes and the spleen, suggesting that ES therapy may facilitate cell survival or clonal expansion. CD49b cells were also present in increased quantities in all of these organs. In this study, we demonstrate an antitumor inflammatory effect of ES in an mRCC model, and this effect is mediated by an increase in ICAM-1 and VCAM-1 expression in tumor-associated endothelial cells.
  • article 33 Citação(ões) na Scopus
    Platelet-activating factor (PAF) receptor as a promising target for cancer cell repopulation after radiotherapy
    (2017) SILVA JR., I. A. da; CHAMMAS, R.; LEPIQUE, A. P.; JANCAR, S.
    A major drawback of radiotherapy is the accelerated growth of the surviving tumor cells. Radiotherapy generates a variety of lipids that bind to the receptor for platelet-activating factor, expressed by cells in the tumor microenvironment. In the present study, using the TC-1 tumor cell line, we found that irradiation induced a twofold increase in receptor expression and generated agonists of receptor. Irradiated cells induced a 20-fold increase in live TC-1 proliferation in vitro. Furthermore, subcutaneous co-injection of irradiated TC-1 cells with TC-1 expressing luciferase (TC-1 fluc(+)) markedly increased TC-1 fluc(+) proliferation in a receptor-dependent way. Moreover we used a human carcinoma cell line not expressing the PAF receptor (KBM) and the same cell transfected with the receptor gene (KBP). Following co-injection of live KBP cells with irradiated KBM in RAG mice, the tumor growth was significantly increased compared with tumor formed following co-injection of live KBM with irradiated KBM. This tumor cell repopulation correlated with increased infiltration of tumor-promoting macrophages (CD206+). We propose that receptor represents a possible target for improving the efficacy of radiotherapy through inhibition of tumor repopulation.
  • article 24 Citação(ões) na Scopus
    Somatic mutations in early onset luminal breast cancer
    (2018) ENCINAS, G.; SABELNYKOVA, V. Y.; LYRA, E. C. de; KATAYAMA, M. L. H.; MAISTRO, S.; VALLE, P. W. M. V.; PEREIRA, G. F. L.; RODRIGUES, L. M.; SERIO, P. A. M. P.; GOUVêA, A. C. R. C. de; GEYER, F. C.; BASSO, R. A.; PASINI, F. S.; DIZ, M. P. E.; BRENTANI, M. M.; GóES, J. C. G. S.; CHAMMAS, R.; BOUTROS, P. C.; FOLGUEIRA, M. A. A. K.
    Breast cancer arising in very young patients may be biologically distinct; however, these tumors have been less well studied. We characterized a group of very young patients (≤ 35 years) for BRCA germline mutation and for somatic mutations in luminal (HER2 negative) breast cancer. Thirteen of 79 unselected very young patients were BRCA1/2 germline mutation carriers. Of the non-BRCA tumors, eight with luminal subtype (HER2 negative) were submitted for whole exome sequencing and integrated with 29 luminal samples from the COSMIC database or previous literature for analysis. We identified C to T single nucleotide variants (SNVs) as the most common base-change. A median of six candidate driver genes was mutated by SNVs in each sample and the most frequently mutated genes were PIK3CA, GATA3, TP53 and MAP2K4. Potential cancer drivers affected in the present non-BRCA tumors include GRHL2, PIK3AP1, CACNA1E, SEMA6D, SMURF2, RSBN1 and MTHFD2. Sixteen out of 37 luminal tumors (43%) harbored SNVs in DNA repair genes, such as ATR, BAP1, ERCC6, FANCD2, FANCL, MLH1, MUTYH, PALB2, POLD1, POLE, RAD9A, RAD51 and TP53, and 54% presented pathogenic mutations (frameshift or nonsense) in at least one gene involved in gene transcription. The differential biology of luminal early-age onset breast cancer needs a deeper genomic investigation. © Encinas et al.
  • conferenceObject
    ERCC1 AND BETA-TUBULIN III IN ADVANCED NSCLC PATIENTS TREATED WITH CISPLATIN-VINORELBINE
    (2012) CASTRO JR., G. de; VICTOR, C. R.; BIGATON, F. J.; TAKAHASHI, T. K.; FEHER, O.; SABER, A. M. Ab'; TAKAGAKI, T. Y.; SIQUEIRA, S. A. C.; CHAMMAS, R.; HOFF, P. M. G.
    Background: Platinum-containing chemotherapy remains as the standard treatment in advanced/metastatic non-small-cell lung cancer (NSC LC) patients (pts). Increased ERCC 1 expression has been associated with resistance to platinum-based therapies, and beta-tubulin III (TUBB 3) was shown to be involved in resistance to antimicrotubule agents. Here we studied these tumor markers in NSC LC pts treated with cisplatin-vinorelbine and correlated their expression with survival. Methods: It is a retrospective study on pts diagnosed with advanced/metastatic NSC LC (TNM 6th ed), consecutively identified. All pts were treated with cisplatin 80 mg/m2 d1 and vinorelbine 30 mg/m2 d1, d8, d15, every 21 days, 4–6 cycles, in our Institution, between Sep/2002 and Oct/2008. ERCC 1 (clone 8F1) and TUBB 3 (clone TUJ1) expression were evaluated by immunohistochemistry, and biomarker expression was considered as high when more than 10% of tumor cells presented moderate to strong staining, nuclear or cytoplasmic, respectively. Overall survival (OS) was estimated by the Kaplan-Meier method and curves were compared with log-rank. Results: 142 pts were studied; median age 63 y (34-87), 67% male and 86% current smokers. Adenocarcinoma (ADC, 58 pts, 43%), followed by squamous cell carcinoma (SCC , 50 pts, 37%) were the most frequent histologic types. 100 pts (71%) were staged as IV and 34 pts (24%) as IIIB. The median number of cycles was 4 (1-7). Median OS was 7.9 mo. Overall, high ERCC 1 expression was observed in 61/104 pts (59%) and high TUBB 3 expression in 55/109 pts (51%). According to histologic types, low ERCC 1 expression was observed in 7/42 SCC pts (16%) and in 35/63 ADC pts (56%) (p=0.0004). Among ADC pts, 1-y OS rate was 28% and 47% in pts which tumors presented with high and low ERCC 1 expression, respectively (HR 1.57, 95% CI 0.9-2.7, p=0.08). TUBB 3 expression neither presented any difference between SCC and ADC types, nor any prognostic impact in terms of OS. Conclusions: Low ERCC 1 expression was observed more frequently in pts with advanced lung ADC and it was a favorable prognostic factor in ADC pts treated with cisplatin-vinorelbine.
  • article 20 Citação(ões) na Scopus
    Galectin-3 sensitized melanoma cell lines to vemurafenib (PLX4032) induced cell death through prevention of autophagy
    (2018) BUSTOS, S. O.; PEREIRA, G. J. S.; SAITO, R. F.; GIL, C. D.; ZANATTA, D. B.; SMAILI, S. S.; CHAMMAS, R.
    Melanoma is a current worldwide problem, as its incidence is increasing. In the last years, several studies have shown that melanoma cells display high levels of autophagy, a self-degradative process that can promote survival leading to drug resistance. Consequently, autophagy regulation represents a challenge for cancer therapy. Herein, we showed that galectin-3 (Gal-3), a β-galactoside binding lectin which is often lost along melanoma progression, is a negative regulator of autophagy in melanoma cells. Our data demonstrated that Gal-3low/negative cells were more resistant to the inhibition of the activity of the cancer driver gene BRAFV600E by vemurafenib (PLX4032). Interestingly, in these cells, starvation caused further LC3-II accumulation in cells exposed to chloroquine, which inhibits the degradative step in autophagy. In addition, Gal-3 low/negative tumor cells accumulated more LC3-II than Gal-3 high tumor cells in vivo. Resistance of Gal-3low/negative cells was associated with increased production of superoxide and activation of the Endoplasmic Reticulum (ER) stress response, as evaluated by accumulation of GRP78. Pharmacological inhibition of autophagy with bafilomycin A reversed the relative resistance of Gal-3low/negative cells to vemurafenib treatment. Taken together, these results show that the autophagic flux is dependent on Gal-3 levels, which attenuate the prosurvival role of autophagy. © Bustos et al.
  • article 29 Citação(ões) na Scopus
    Safe therapeutics of murine melanoma model using a novel antineoplasic, the partially methylated mannogalactan from Pleurotus eryngii
    (2017) BISCAIA, S. M. P.; CARBONERO, E. R.; BELLAN, D. L.; BORGES, B. S.; COSTA, C. R.; ROSSI, G. R.; GONCALVES, J. P.; MELO, C. M.; LIVERO, F. A. R.; RUTHES, A. C.; ZOTZ, R.; SILVA, E. V.; OLIVEIRA, C. C.; ACCO, A.; NADER, H. B.; CHAMMAS, R.; IACOMINI, M.; FRANCO, C. R. C.; TRINDADE, E. S.
    A heteropolysaccharide was isolated by cold aqueous extraction from edible mushroom Pleurotus eryngii (""King Oyster"") basidiocarps and its biological properties were evaluated. Structural assignments were carried out using mono-and bidimensional NMR spectroscopy, monosaccharide composition, and methylation analyses. A man-nogalactan having a main chain of (1 -> 6)-linked alpha-D-galactopyranosyl and 3-O-methyl-alpha-D-galactopyranosyl residues, both partially substituted at OH-2 by beta-D-Manp (MG-Pe) single-unit was found. Biological effects of mannogalactan from P. eryngii (MG-Pe) were tested against murine melanoma cells. MG-Pe was non-cytotoxic, but reduced in vitro melanoma cells invasion. Also, 50 mg/kg MG-Pe administration to melanoma-bearing C57BL/6 mice up to 10 days decreased in 60% the tumor volume compared to control. Additionally, no changes were observed when biochemical profile, complete blood cells count (CBC), organs, and body weight were analyzed. Mg-Pe was shown to be a promising anti-melanoma molecule capable of switching melanoma cells to a non-invasive phenotype with no toxicity to melanoma-bearing mice.
  • conferenceObject
    Radioactive and near-infrared fluorescence in vivo imaging of Non-Hodgkin Lymphoma using 99mTc/Cy7-Fab(Bevacizumab)
    (2021) CAMACHO, X.; PERRONI, C.; CARNEIRO, C.; JUNQUEIRA, M.; FARIA, D.; GARCIA, M.; FERNANDEZ, M.; BUCHPIGUEL, C.; CERECETTO, H.; CHAMMAS, R.; RIVA, E.; CABRAL, P.; GAMBINI, J.
  • conferenceObject
    COMPARATIVE EFFECTIVENESS OF SURGICAL VERSUS NONSURGICAL THERAPY FOR LARYNGEAL AND OROPHARYNGEAL CANCER
    (2017) CAMPOLINA, A. G.; V, R. Lopez; LOPES, E. F.; HOFF, P. M.; CHAMMAS, R.
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