MARIA MITZI BRENTANI

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

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Assunto: Oncology ×

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  • article
    Immunoexpression of claudins 4 and 7 among invasive breast carcinoma subtypes: A large diagnostic study using tissue microarray
    (2018) LOGULLO, Angela Flavia; PASINI, Fatima Solange; NONOGAKI, Suely; ROCHA, Rafael Malagoli; SOARES, Fernando Augusto; BRENTANI, Maria Mitzi
    Molecular phenotyping and tissue microarray (TMA) studies have identified distinct invasive breast carcinoma subtypes: Luminal A, luminal B, enriched with overexpressed human epidermal growth factor receptor 2 (HER-2) and triple-negative, i.e., negative for HER-2, as well as for estrogen and progesterone receptor (ER and PR, respectively) expression. These subtypes are useful in clinical management, since they bear distinct prognoses and predictive responses to targeted therapy. However, although molecular profiling provides important prognostic indicators, breast cancer risk stratification remains a challenge in triple-negative cases. What is referred to as claudin-low subtype was identified as a triple-negative subset that is associated with more aggressive tumor behavior and worse prognosis. However, the immunohistochemical expression of claudins has not yet been standardized. Our objective was to verify whether the immunoexpression of claudins 4 and 7 (the main claudins specifically expressed in human breast tissue) in TMA is associated with survival and prognosis in luminal A, HER-2 and triple-negative molecular subtypes. In this diagnostic study, we investigated ER/PR receptor status, HER-2, claudin 4 and 7 expression and stem cell CD44/24 profiles, and verified the association with prognosis and survival outcomes in 803 invasive breast carcinoma cases arranged in four TMAs. Among these, 503 (62.6%) were positive for claudin 4 and 369 (46.0%) for claudin 7. Claudin 4 exhibited the lowest expression in luminal A and triple-negative subtypes, and the highest frequency of expression in HER-2-enriched subtypes, whereas claudin 7 staining was not associated with any subtype. The stem cell phenotype was not associated with subgroups or claudins 4 and 7. Claudin immunoexpression profile was not able to distinguish between patients with better or worse prognosis, and it was not correlated to triple-negative cases. Therefore, it may be concluded that the immunoexpression of claudins 4 and 7, individually or within the usual immunohistochemical context (ER, PR and HER-2), does not provide additional prognostic information on breast cancer subtypes.
  • conferenceObject
    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.
  • article 13 Citação(ões) na Scopus
    Down-regulation of ANAPC13 and CLTCL1: Early Events in the Progression of Preinvasive Ductal Carcinoma of the Breast
    (2012) SENS-ABUAZAR, Carolina; FERREIRA, Elisa Napolitano e; OSORIO, Cynthia Aparecida Bueno Toledo; KREPISCHI, Ana Cristina Victorino; RICCA, Tatiana Iervolino; CASTRO, Nadia Pereira; CUNHA, Isabela Werneck da; MACIEL, Maria do Socorro; ROSENBERG, Carla; BRENTANI, Maria Mitzi; SOARES, Fernando Augusto; ROCHA, Rafael Malagoli; CARRARO, Dirce Maria
    Alterations in the gene expression profile in epithelial cells during breast ductal carcinoma (DC) progression have been shown to occur mainly between pure ductal carcinoma in situ (DCIS) to the in situ component of a lesion with coexisting invasive ductal carcinoma (DCIS-IDC) implying that the molecular program for invasion is already established in the preinvasive lesion. For assessing early molecular alterations in epithelial cells that trigger tumorigenesis and testing them as prognostic markers for breast ductal carcinoma progression, we analyzed, by reverse transcription-quantitative polymerase chain reaction, eight genes previously identified as differentially expressed between epithelial tumor cells populations captured from preinvasive lesions with distinct malignant potential, pure DCIS and the in situ component of DCIS-IDC. ANAPC13 and CLTCL1 down-regulation revealed to be early events of DC progression that anticipated the invasiveness manifestation. Further down-regulation of ANAPC13 also occurred after invasion appearance and the presence of the protein in invasive tumor samples was associated with higher rates of overall and disease-free survival in breast cancer patients. Furthermore, tumors with low levels of ANAPC13 displayed increased copy number alterations, with significant gains at 1q (1q23.1-1q32.1), 8q, and 17q (17q24.2), regions that display common imbalances in breast tumors, suggesting that down-regulation of ANAPC13 contributes to genomic instability in this disease.
  • article
    MYC is expressed in the stromal and epithelial cells of primary breast carcinoma and paired nodal metastases
    (2015) MUNDIM, Fiorita Gonzales Lopes; PASINI, Fatima Solange; BRENTANI, Maria Mitzi; SOARES, Fernando Augusto; NONOGAKI, Suely; WAITZBERG, Angela Flayia Logullo
    The MYC oncogene is directly involved in the proliferation, metabolism, progression and distant metastasis of breast cancer. Since metastatic spread to the lymph nodes is often the first indication of propensity for metastatic dissemination, the MYC status in nodal disease may represent a decision-making variable. However, the analysis of MYC expression in stromal cells, namely cancer-associated fibroblasts (CAFs), which are known to play a critical role in cancer progression, remains poorly reported. The aim of this study was to determine the expression of MYC and other markers, including estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2), p53, Ki67, epidermal growth factor receptor (EGFR), phosphorylated AKT (p-AKT) and phospho-mammalian target of rapamycin (p-mTOR) by immunohistochemistry in representative samples from 80 patients with ductal infiltrative breast cancer and 43 paired compromised axillary lymph nodes allocated in tissue microarrays (TMAs). The epithelial and stromal components of primary tumors and respective lymph node metastases were separately analyzed. MYC expression (cytoplasmic and nuclear) was a frequent event in the epithelial and stromal components of the primary tumors. The epithelial cells in the nodal metastases exhibited a trend for decreased MYC expression compared to that in the primary tumors (P=0.08) but retained the original status of the primary tumors for all other markers. The stromal cells were uniformly negative for ER, PR, HER2, p53, Ki67 and EGFR. Comparison of the stromas of primary tumors and respective lymph node metastases revealed a reduced frequency of nuclear MYC in 15% of the cases (P=0.003), whereas p-mTOR followed a similar trend (P=0.09). Analyses of the possible correlations among markers revealed that epithelial nuclear MYC was associated with p53 (P=0.048). This is an original study demonstrating a significant proportion of MYC expression (nuclear or cytoplasmic), as well p-mTOR and p-AKT expression, in the epithelial and stromal components of either the primary tumor or the nodal metastases. CAFs expressing MYC may establish an angiogenic microenvironment supporting cancer survival and facilitating colonization at the nodal metastatic site.
  • conferenceObject
    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.
  • conferenceObject
    Prognostic relevance of claudins 4 and 7 in invasive breast carcinoma (NOS) subtypes: A large tissue microarray study
    (2018) LOGULLO, Angela F.; ROCHA, Rafael M.; STIEPCICH, Monica; SOARES, Fernando A.; PASINI, Fatima S.; NONOGAKI, Sueli; BRENTANI, Maria M.
  • conferenceObject
    Metastatic lymph node fibroblasts maintain similar profile of stromal biomarkers registered in primary breast carcinomas
    (2015) MUNDIM, Fiorita G. L.; PASINI, Fatima S.; NONOGAKI, Suely; SOARES, Fernando A.; BRENTANI, M. Mitzi; LOGULLO, Angela F.
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    Ipsilateral breast cancer recurrence in conservative treatment for locally advanced breast cancer
    (2015) CARRARA, G. F. A.; NETO, C. S.; ABRAO-MACHADO, L. F.; NUNES, J. S.; FOLGUEIRA, M. A. A. K.; BRENTANI, M. M.; VIEIRA, R. A. C.
  • 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.
  • conferenceObject
    Fibroblast transcriptome sequencing reveals different gene expression profiles among distinct subtypes of breast cancer and normal mammary tissue
    (2012) BROMBERG, Natalia; FERREIRA, Elisa Napolitano; MOLINA, Gustavo Campos; PUGA, Renato David; CARRARO, Dirce Maria; BRENTANI, Maria Mitzi