ROSIMEIRE APARECIDA ROELA

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Lattes
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Unidades Organizacionais
Departamento de Radiologia, Faculdade de Medicina
LIM/24 - Laboratório de Oncologia Experimental, Hospital das Clínicas, Faculdade de Medicina

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Agora exibindo 1 - 10 de 23
  • conferenceObject
    Evaluation of an AI system for breast cancer screening in mammograms of young women.
    (2020) PETRINI, Daniel Gustavo Pellacani; VALENTE, Gabriel Vansuita; SHIMIZU, Carlos; ROELA, Rosimeire Aparecida; ARAUJO, Gabriel Miranda de; TUCUNDUVA, Tatiana Cardoso de Mello; FOLGUEIRA, Maria A. A. Koike; KIM, Hae Yong
  • article 23 Citação(ões) na Scopus
    Melatonin Regulates Angiogenic and Inflammatory Proteins in MDA-MB-231 Cell Line and in Co-culture with Cancer-associated Fibroblasts
    (2016) MASCHIO-SIGNORINI, Larissa B.; GELALETI, Gabriela B.; MOSCHETTA, Marina G.; BORIN, Thaiz F.; JARDIM-PERASSI, Bruna V.; LOPES, Juliana R.; LACERDA, Jessica Z.; ROELA, Rosimeire A.; BORDIN, Newton A.; CORREA, Lizandra A.; CARDOSO, Jessica P.; ZUCCARI, Debora Aparecida Pires de Campos
    Background: Cancer-associated fibroblast (CAFs) are the most abundant cells in the tumor microenvironment, able to secrete growth factors and act on tumor progression. Melatonin is associated with several mechanisms of action with oncostatics and oncoprotectors effects, and also participate in the reduction of synthesis of surrounding fibroblasts and endothelial cells in breast cancer. Objective: The objectives of this study were to determine the effectiveness of melatonin in cell viability and expression of proteins involved in angiogenesis and inflammation in triplenegative mammary tumor cell line (MDA-MB-231) and in co-culture with CAFs. Method: Cell viability was measured by MTT assay and the protein expression was evaluated by Membrane Antibody Array after melatonin treatment. Results: Melatonin treatment (1 mM) for 48 hours reduced the cell viability of MDA-MB-231, CAFs and co-culture (p < 0.05). The semi-quantitative protein analysis showed that when monoculture of tumor cells were compared with co-culture of CAFs, there was a regulation of angiogenic and inflammatory proteins (p < 0.05). Melatonin treatment also leads a differential expression of angiogenic and inflammatory proteins in both monoculture and co-culture of tumor cells and CAFs (p < 0.05). Conclusion: The influence of CAFs under the tumor microenvironment was confirmed, increasing the malignancy of the tumor. In addition, melatonin is effective in both monoculture and co-culture, regulating angiogenic and inflammatory proteins that contribute to tumor progression. This study show an overview of melatonin ability in regulating angiogenic and inflammatory proteins, and opens the way for exploration of each individual protein in further studies.
  • conferenceObject
    Profile of somatic mutations in young adults with pancreatic cancer.
    (2019) RODRIGUES, Livia Munhoz; MAISTRO, Simone; KATAYAMA, Maria Lucia Hirata; ROELA, Rosimeire Aparecida; FOLGUEIRA, Maria A. A. Koike
  • conferenceObject
    End-to-end training of convolutional network for breast cancer detection in two-view mammography.
    (2021) PETRINI, Daniel G.; SHIMIZU, Carlos; VALENTE, Gabriel V.; FOLGUEIRA, Guilherme; NOVAES, Guilherme A.; KATAYAMA, Maria L.; SERIO, Pedro; ROELA, Rosimeire A.; TUCUNDUVA, Tatiana C.; FOLGUEIRA, Maria Aparecida A.; KIM, Hae Y.
  • conferenceObject
    Pathogenic Copy Number Variants are Frequently Identified in Children with Short Stature of Unknown Etiology
    (2016) CANTON, Ana; HOMMA, Thais; FURUYA, Tatiane; ROELA, Rosimeire; ARNHOLD, Ivo; JORGE, Alexander
  • bookPart
    Uma breve história do câncer
    (2022) MUNHOZ, Rodrigo Ramella; ROELA, Rosimeire Aparecida; BRENTANI, Maria Mitzi
  • article 36 Citação(ões) na Scopus
    A gene expression profile related to immune dampening in the tumor microenvironment is associated with poor prognosis in gastric adenocarcinoma
    (2014) PASINI, Fatima Solange; ZILBERSTEIN, Bruno; SNITCOVSKY, Igor; ROELA, Rosimeire Aparecida; MANGONE, Flavia R. Rotea; RIBEIRO JR., Ulysses; NONOGAKI, Suely; BRITO, Glauber Costa; CALLEGARI, Giovanna D.; CECCONELLO, Ivan; ALVES, Venancio Avancini Ferreira; ELUF-NETO, Jose; CHAMMAS, Roger; FEDERICO, Miriam Hatsue Honda
    The TNM Classification of Malignant Tumours (TNM) staging system is the primary means of determining a prognosis for gastric adenocarcinoma (GC). However, tumor behavior in the individual patient is unpredictable and in spite of treatment advances, a classification of 'advanced stage' still portends a poor prognosis. Thus, further insights from molecular analyses are needed for better prognostic stratification and determination of new therapeutic targets. A total of fifty-one fresh frozen tumor samples from patients with histopathologically confirmed diagnoses of GC, submitted to surgery with curative intent, were included in the study. Total RNA was extracted from an initial group of fifteen samples matched for known prognostic factors, categorized into two subgroups, according to patient overall survival: poor (< 24 months) or favorable (at or above 24 months), and hybridized to Affymetrix Genechip human genome U133 plus 2.0 for genes associated with prognosis selection. Thirteen genes were selected for qPCR validation using those initial fifteen samples plus additional thirty-six samples. A total of 108 genes were associated with poor prognosis, independent of tumor staging. Using systems biology, we suggest that this panel reflects the dampening of immune/inflammatory response in the tumor microenvironment level and a shift to Th2/M2 activity. A gene trio (OLR1, CXCL11 and ADAMDEC1) was identified as an independent marker of prognosis, being the last two markers validated in an independent patient cohort. We determined a panel of three genes with prognostic value in gastric cancer, which should be further investigated. A gene expression profile suggestive of a dysfunctional inflammatory response was associated with unfavorable prognosis.
  • article 5 Citação(ões) na Scopus
    Gene Expression Profile in Response to Doxorubicin-Rapamycin Combined Treatment of HER-2-Overexpressing Human Mammary Epithelial Cell Lines
    (2012) TRAPE, Adriana Priscila; KATAYAMA, Maria Lucia Hirata; ROELA, Rosimeire Aparecida; BRENTANI, Helena; RAVACCI, Graziela Rosa; LIMA, Leandro de Araujo; BRENTANI, Maria Mitzi
    HER-2-positive breast cancers frequently sustain elevated AKT/mTOR signaling, which has been associated with resistance to doxorubicin treatment. Here, we investigated whether rapamycin, an mTOR inhibitor, increased the sensitivity to doxorubicin therapy in two HER-2-overexpressing cell lines: C5.2, which was derived from the parental HB4a by transfection with HER-2 and SKBR3, which exhibits HER-2 amplification. The epithelial mammary cell line HB4a was also analyzed. The combined treatment using 20 nmol/L of rapamycin and 30 nmol/L of doxorubicin arrested HB4a and C5.2 cells in S to G(2)-M, whereas SKBR3 cells showed an increase in the G(0)-G(1) phase. Rapamycin increased the sensitivity to doxorubicin in HER-2-overexpressing cells by approximately 2-fold, suggesting that the combination displayed a more effective antiproliferative action. Gene expression profiling showed that these results might reflect alterations in genes involved in canonical pathways related to purine metabolism, oxidative phosphorylation, protein ubiquitination, and mitochondrial dysfunction. A set of 122 genes modulated by the combined treatment and specifically related to HER-2 overexpression was determined by finding genes commonly regulated in both C5.2 and SKBR3 that were not affected in HB4a cells. Network analysis of this particular set showed a smaller subgroup of genes in which coexpression pattern in HB4a cells was disrupted in C5.2 and SKBR3. Altogether, our data showed a subset of genes that might be more robust than individual markers in predicting the response of HER-2-overexpressing breast cancers to doxorubicin and rapamycin combination.
  • article 18 Citação(ões) na Scopus
    Breast cancer tissue slices as a model for evaluation of response to rapamycin
    (2013) GROSSO, Stana Helena Giorgi; KATAYAMA, Maria Lucia Hirata; ROELA, Rosimeire Aparecida; NONOGAKI, Suely; SOARES, Fernando Augusto; BRENTANI, Helena; LIMA, Leandro; FOLGUEIRA, Maria Aparecida Azevedo Koike; WAITZBERG, Angela Flavia Logullo; PASINI, Faima Solange; GOES, Joao Carlos Guedes Sampaio; BRENTANI, M. Mitzi
    Rapamycin is a selective inhibitor of the mammalian target of rapamycin (mTOR), a regulator kinase that integrates growth factors signaling via the phosphoinositide-3-kinase pathway and that has emerged as a novel therapeutic modality in breast cancer (BC). We propose a pre-clinical ""ex-vivo"" personalized organotypic culture of BC that preserves the microenvironment to evaluate rapamycin-mediated gene expression changes. Freshly excised ductal invasive BC slices, 400 mu m thick (n=30), were cultured in the presence or absence (control) of rapamycin (20 nM) for 24 h. Some slices were formalin-fixed for immunohistochemical determinations and some were processed for microarray analysis. Control slices in culture retained their tissue morphology and tissue viability (detected by BrdU uptake). The percentage of proliferating cells (assessed by Ki67) did not change up to 24 h of treatment. Immunohistochemical evaluation of p-AKT, p-mTOR, p-4EBP1 and p-S6K1 indicated that AKT/mTOR pathway activation was maintained during cultivation. For microarray analysis, slices were divided into two groups, according to the presence/absence of epidermal growth factor receptor-type 2 and analyzed separately. Limited overlap was seen among differentially expressed genes after treatment (P < 0.01) in both groups suggesting different responses to rapamycin between these BC subtypes. Ontology analysis indicated that genes involved in biosynthetic processes were commonly reduced by rapamycin. Our network analysis suggested that concerted expression of these genes might distinguish controls from treated slices. Thus, breast carcinoma slices constitute a suitable physiological tool to evaluate the short-term effects of rapamycin on the gene profile of individual BC samples.
  • article 19 Citação(ões) na Scopus
    Specific upregulation of RHOA and RAC1 in cancer-associated fibroblasts found at primary tumor and lymph node metastatic sites in breast cancer
    (2015) ROZENCHAN, Patricia Bortman; PASINI, Fatima Solange; ROELA, Rosimeire A.; KATAYAMA, Maria Lucia Hirata; MUNDIM, Fiorita Gonzales Lopes; BRENTANI, Helena; LYRA, Eduardo C.; BRENTANI, Maria Mitzi
    The importance of tumor-stromal cell interactions in breast tumor progression and invasion is well established. Here, an evaluation of differential genomic profiles of carcinoma-associated fibroblasts (CAFs) compared to fibroblasts derived from tissues adjacent to fibroadenomas (NAFs) revealed altered focal adhesion pathways. These data were validated through confocal assays. To verify the possible role of fibroblasts in lymph node invasion, we constructed a tissue microarray consisting of primary breast cancer samples and corresponding lymph node metastasis and compared the expression of adhesion markers RhoA and Rac1 in fibroblasts located at these different locations. Two distinct tissue microarrays were constructed from the stromal component of 43 primary tumors and matched lymph node samples, respectively. Fibroblasts were characterized for their expression of alpha-smooth muscle actin (alpha-SMA) and vimentin. Moreover, we verified the level of these proteins in the stromal compartment from normal adjacent tissue and in non-compromised lymph nodes. Our immunohistochemistry revealed that 59 % of fibroblasts associated with primary tumors and 41 % of the respective metastatic lymph nodes (p = 0.271) displayed positive staining for RhoA. In line with this, 57.1 % of fibroblasts associated with primary tumors presented Rac1-positive staining, and the frequency of co-positivity within the lymph nodes was 42.9 % (p = 0.16). Expression of RhoA and Rac1 was absent in fibroblasts of adjacent normal tissue and in compromised lymph nodes. Based on our findings that no significant changes were observed between primary and metastatic lymph nodes, we suggest that fibroblasts are active participants in the invasion of cancer cells to lymph nodes and support the hypothesis that metastatic tumor cells continue to depend on their microenvironment.