LUCIANA NOGUEIRA DE SOUSA ANDRADE

(Fonte: Lattes)
Índice h a partir de 2011
10
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

Resultados de Busca

Agora exibindo 1 - 5 de 5
  • 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
  • article 1 Citação(ões) na Scopus
    Deciphering the Functional Status of Breast Cancers through the Analysis of Their Extracellular Vesicles
    (2023) CARRASCO, Alexis German Murillo; OTAKE, Andreia Hanada; MACEDO-DA-SILVA, Janaina; SANTIAGO, Veronica Feijoli; PALMISANO, Giuseppe; ANDRADE, Luciana Nogueira de Sousa; CHAMMAS, Roger
    Breast cancer (BC) accounts for the highest incidence of tumor-related mortality among women worldwide, justifying the growing search for molecular tools for the early diagnosis and follow-up of BC patients under treatment. Circulating extracellular vesicles (EVs) are membranous nanocompartments produced by all human cells, including tumor cells. Since minimally invasive methods collect EVs, which represent reservoirs of signals for cell communication, these particles have attracted the interest of many researchers aiming to improve BC screening and treatment. Here, we analyzed the cargoes of BC-derived EVs, both proteins and nucleic acids, which yielded a comprehensive list of potential markers divided into four distinct categories, namely, (i) modulation of aggressiveness and growth; (ii) preparation of the pre-metastatic niche; (iii) epithelial-to-mesenchymal transition; and (iv) drug resistance phenotype, further classified according to their specificity and sensitivity as vesicular BC biomarkers. We discuss the therapeutic potential of and barriers to the clinical implementation of EV-based tests, including the heterogeneity of EVs and the available technologies for analyzing their content, to present a consistent, reproducible, and affordable set of markers for further evaluation.
  • article 28 Citação(ões) na Scopus
    Extracellular Vesicles Shedding Promotes Melanoma Growth in Response to Chemotherapy
    (2019) ANDRADE, Luciana Nogueira de Sousa; OTAKE, Andreia Hanada; CARDIM, Silvia Guedes Braga; SILVA, Felipe I. Lelis da; SAKAMOTO, Mariana Mari Ikoma; FURUYA, Tatiane Katsue; UNO, Miyuki; PASINI, Fatima Solange; CHAMMAS, Roger
    Extracellular vesicles (EVs) are emerging as key players in intercellular communication. EVs can transfer biological macromolecules to recipient cells, modulating various physiological and pathological processes. It has been shown that tumor cells secrete large amounts of EVs that can be taken up by malignant and stromal cells, dictating tumor progression. In this study, we investigated whether EVs secreted by melanoma cells in response to chemotherapy modulate tumor response to alkylating drugs. Our findings showed that human and murine melanoma cells secrete more EVs after treatment with temozolomide and cisplatin. We observed that EVs shed by melanoma cells after temozolomide treatment modify macrophage phenotype by skewing macrophage activation towards the M2 phenotype through upregulation of M2-marker genes. Moreover, these EVs were able to favor melanoma re-growth in vivo, which was accompanied by an increase in Arginase 1 and IL10 gene expression levels by stromal cells and an increase in genes related to DNA repair, cell survival and stemness in tumor cells. Taken together, this study suggests that EVs shed by tumor cells in response to chemotherapy promote tumor repopulation and treatment failure through cellular reprogramming in melanoma cells.
  • article 1 Citação(ões) na Scopus
    Membrane-derived particles shed by PSMA-positive cells function as pro-angiogenic stimuli in tumors
    (2023) MACHADO, Camila M. L.; SKUBAL, Magdalena; HAEDICKE, Katja; SILVA, Fabio P.; STATER, Evan P.; SILVA, Thais L. A. de O.; COSTA, Erico T.; MASOTTI, Cibele; OTAKE, Andreia H.; ANDRADE, Luciana N. S.; JUNQUEIRA, Mara de S.; HSU, Hsiao-Ting; DAS, Sudeep; LARNEY, Benedict Mc; PRATT, Edwin C.; ROMIN, Yevgeniy; FAN, Ning; MANOVA-TODOROVA, Katia; POMPER, Martin; GRIMM, Jan
    Cell membrane-derived particles (Mp) are rounded membrane-enclosed particles that are shed from tumor cells. Mp are formed from tumor membranes and are capable of tumor targeting and immunotherapeutic agents because they share membrane homology with parental cells; thus, they are under consideration as a drug de-livery vehicle. Prostate-specific membrane antigen (PSMA), a transmembrane glycoprotein with enzymatic functionality, is highly expressed in Mp and extracellular vesicles (EV) from prostate cancer (PCa) with poor clinical prognosis. Although PSMA expression was previously shown in EV and Mp isolated from cell lines and from the blood of patients with high-grade PCa, no pathophysiological effects have been linked to PCa-derived Mp. Here, we compared Mp from PSMA-expressing (PSMA-Mp) and PSMA-non-expressing (WT-Mp) cells side by side in vitro and in vivo. PSMA-Mp can transfer PSMA and new phenotypic characteristics to the tumor micro -environment. The consequence of PSMA transfer to cells and increased secretion of vascular endothelial growth factor-A (VEGF-A), pro-angiogenic and pro-lymphangiogenic mediators, with increased 4E binding protein 1 (4EBP-1) phosphorylation.
  • conferenceObject
    Melanoma and breast adenocarcinoma growth inhibition by a 7-ketocholesterol loaded-phosphatidylserine liposome
    (2018) FAVERO, Giovani M.; TORTELLI, Tharcisio C.; OTAKE, Andreia H.; ANDRADE, Luciana N.; FARIA, Daniele P.; CARNEIRO, Camila G.; GARCEZ, Alexandre T.; MARQUES, Fabio L.; CHAMMAS, Roger