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[PMID]:29339738
[Au] Autor:Luo N; Nixon MJ; Gonzalez-Ericsson PI; Sanchez V; Opalenik SR; Li H; Zahnow CA; Nickels ML; Liu F; Tantawy MN; Sanders ME; Manning HC; Balko JM
[Ad] Endereço:Department of Anatomy and Histology, School of Medicine, Nankai University, Tianjin, 300071, China.
[Ti] Título:DNA methyltransferase inhibition upregulates MHC-I to potentiate cytotoxic T lymphocyte responses in breast cancer.
[So] Source:Nat Commun;9(1):248, 2018 01 16.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Potentiating anti-tumor immunity by inducing tumor inflammation and T cell-mediated responses are a promising area of cancer therapy. Immunomodulatory agents that promote these effects function via a wide variety of mechanisms, including upregulation of antigen presentation pathways. Here, we show that major histocompatibility class-I (MHC-I) genes are methylated in human breast cancers, suppressing their expression. Treatment of breast cancer cell lines with a next-generation hypomethylating agent, guadecitabine, upregulates MHC-I expression in response to interferon-γ. In murine tumor models of breast cancer, guadecitabine upregulates MHC-I in tumor cells promoting recruitment of CD8+ T cells to the microenvironment. Finally, we show that MHC-I genes are upregulated in breast cancer patients treated with hypomethylating agents. Thus, the immunomodulatory effects of hypomethylating agents likely involve upregulation of class-I antigen presentation to potentiate CD8+ T cell responses. These strategies may be useful to potentiate anti-tumor immunity and responses to checkpoint inhibition in immune-refractory breast cancers.
[Mh] Termos MeSH primário: Azacitidina/análogos & derivados
Neoplasias da Mama/metabolismo
DNA (Citosina-5-)-Metiltransferase 1/antagonistas & inibidores
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Genes MHC Classe I/fisiologia
Linfócitos T Citotóxicos/fisiologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Azacitidina/farmacologia
Linhagem Celular Tumoral
DNA (Citosina-5-)-Metiltransferase 1/genética
DNA (Citosina-5-)-Metiltransferase 1/metabolismo
Feminino
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Genes MHC Classe I/genética
Seres Humanos
Neoplasias Mamárias Experimentais
Camundongos
Regiões Promotoras Genéticas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 2KT4YN1DP7 (guadecitabine); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferase 1); EC 2.1.1.37 (DNMT1 protein, human); M801H13NRU (Azacitidine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02630-w


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[PMID]:29180866
[Au] Autor:Lapin NA; Vergara LA; Mackeyev Y; Newton JM; Dilliard SA; Wilson LJ; Curley SA; Serda RE
[Ad] Endereço:Michael E DeBakey Department of Surgery, Baylor College of Medicine.
[Ti] Título:Biotransport kinetics and intratumoral biodistribution of malonodiserinolamide-derivatized [60]fullerene in a murine model of breast adenocarcinoma.
[So] Source:Int J Nanomedicine;12:8289-8307, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:[60]Fullerene is a highly versatile nanoparticle (NP) platform for drug delivery to sites of pathology owing to its small size and both ease and versatility of chemical functionalization, facilitating multisite drug conjugation, drug targeting, and modulation of its physicochemical properties. The prominent and well-characterized role of the enhanced permeation and retention (EPR) effect in facilitating NP delivery to tumors motivated us to explore vascular transport kinetics of a water-soluble [60]fullerene derivatives using intravital microscopy in an immune competent murine model of breast adenocarcinoma. Herein, we present a novel local and global image analysis of vascular transport kinetics at the level of individual tumor blood vessels on the micron scale and across whole images, respectively. Similar to larger nanomaterials, [60]fullerenes displayed rapid extravasation from tumor vasculature, distinct from that in normal microvasculature. Temporal heterogeneity in fullerene delivery to tumors was observed, demonstrating the issue of nonuniform delivery beyond spatial dimensions. Trends in local region analysis of fullerene biokinetics by fluorescence quantification were in agreement with global image analysis. Further analysis of intratumoral vascular clearance rates suggested a possible enhanced penetration and retention effect of the fullerene compared to a 70 kDa vascular tracer. Overall, this study demonstrates the feasibility of tracking and quantifying the delivery kinetics and intratumoral biodistribution of fullerene-based drug delivery platforms, consistent with the EPR effect on short timescales and passive transport to tumors.
[Mh] Termos MeSH primário: Adenocarcinoma/tratamento farmacológico
Sistemas de Liberação de Medicamentos/métodos
Fulerenos/farmacocinética
Neoplasias Mamárias Experimentais/tratamento farmacológico
Nanopartículas/química
[Mh] Termos MeSH secundário: Animais
Difusão Dinâmica da Luz
Feminino
Fluorescência
Fulerenos/química
Microscopia Intravital/métodos
Cinética
Camundongos Endogâmicos BALB C
Microscopia Eletrônica de Varredura
Imagem Molecular/métodos
Solubilidade
Distribuição Tecidual
Água/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fullerenes); 059QF0KO0R (Water)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S138641


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[PMID]:28450564
[Au] Autor:Ahrens BJ; Li L; Ciminera AK; Chea J; Poku E; Bading JR; Weist MR; Miller MM; Colcher DM; Shively JE
[Ad] Endereço:Deparment of Molecular Immunology, Beckman Research Institute of the City of Hope, Duarte, California.
[Ti] Título:Diagnostic PET Imaging of Mammary Microcalcifications Using Cu-DOTA-Alendronate in a Rat Model of Breast Cancer.
[So] Source:J Nucl Med;58(9):1373-1379, 2017 Sep.
[Is] ISSN:1535-5667
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The development of improved breast cancer screening methods is hindered by a lack of cancer-specific imaging agents and effective small-animal models to test them. The purpose of this study was to evaluate Cu-DOTA-alendronate as a mammary microcalcification-targeting PET imaging agent, using an ideal rat model. Our long-term goal is to develop Cu-DOTA-alendronate for the detection and noninvasive differentiation of malignant versus benign breast tumors with PET. DOTA-alendronate was synthesized, radiolabeled with Cu, and administered to normal or tumor-bearing aged, female, retired breeder Sprague-Dawley rats for PET imaging. Mammary tissues were subsequently labeled and imaged with light, confocal, and electron microscopy to verify microcalcification targeting specificity of DOTA-alendronate and elucidate the histologic and ultrastructural characteristics of the microcalcifications in different mammary tumor types. Tumor uptake, biodistribution, and dosimetry studies were performed to evaluate the efficacy and safety of Cu-DOTA-alendronate. Cu-DOTA-alendronate was radiolabeled with a 98% yield. PET imaging using aged, female, retired breeder rats showed specific binding of Cu-DOTA-alendronate in mammary glands and mammary tumors. The highest uptake of Cu-DOTA-alendronate was in malignant tumors and the lowest uptake in benign tumors and normal mammary tissue. Confocal analysis with carboxyfluorescein-alendronate confirmed the microcalcification binding specificity of alendronate derivatives. Biodistribution studies revealed tissue alendronate concentrations peaking within the first hour, then decreasing over the next 48 h. Our dosimetric analysis demonstrated a Cu effective dose within the acceptable range for clinical PET imaging agents and the potential for translation into human patients. Cu-DOTA-alendronate is a promising PET imaging agent for the sensitive and specific detection of mammary tumors as well as the differentiation of malignant versus benign tumors based on absolute labeling uptake.
[Mh] Termos MeSH primário: Alendronato/química
Calcinose/diagnóstico por imagem
Radioisótopos de Cobre
Compostos Heterocíclicos com 1 Anel/química
Neoplasias Mamárias Experimentais/diagnóstico por imagem
Tomografia por Emissão de Pósitrons
[Mh] Termos MeSH secundário: Animais
Calcinose/metabolismo
Linhagem Celular Tumoral
Modelos Animais de Doenças
Feminino
Neoplasias Mamárias Experimentais/metabolismo
Ratos
Ratos Sprague-Dawley
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Copper Radioisotopes); 0 (Heterocyclic Compounds, 1-Ring); 1HTE449DGZ (1,4,7,10-tetraazacyclododecane- 1,4,7,10-tetraacetic acid); X1J18R4W8P (Alendronate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.2967/jnumed.117.190850


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[PMID]:29317633
[Au] Autor:Guo P; Liu D; Subramanyam K; Wang B; Yang J; Huang J; Auguste DT; Moses MA
[Ad] Endereço:Vascular Biology Program, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA, 02115, USA.
[Ti] Título:Nanoparticle elasticity directs tumor uptake.
[So] Source:Nat Commun;9(1):130, 2018 01 09.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:To date, the role of elasticity in drug delivery remains elusive due to the inability to measure microscale mechanics and alter rheology without affecting chemistry. Herein, we describe the in vitro cellular uptake and in vivo tumor uptake of nanolipogels (NLGs). NLGs are composed of identical lipid bilayers encapsulating an alginate core, with tunable elasticity. The elasticity of NLGs was evaluated by atomic force microscopy, which demonstrated that they exhibit Young's moduli ranging from 45 ± 9 to 19,000 ± 5 kPa. Neoplastic and non-neoplastic cells exhibited significantly greater uptake of soft NLGs (Young's modulus <1.6 MPa) relative to their elastic counterparts (Young's modulus >13.8 MPa). In an orthotopic breast tumor model, soft NLGs accumulated significantly more in tumors, whereas elastic NLGs preferentially accumulated in the liver. Our findings demonstrate that particle elasticity directs tumor accumulation, suggesting that it may be a design parameter to enhance tumor delivery efficiency.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Módulo de Elasticidade
Nanopartículas/química
Nanopartículas/metabolismo
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/patologia
Linhagem Celular
Linhagem Celular Tumoral
Clorpromazina/farmacologia
Endocitose/efeitos dos fármacos
Filipina/farmacologia
Seres Humanos
Hidrazonas/farmacologia
Fígado/metabolismo
Células MCF-7
Neoplasias Mamárias Experimentais/metabolismo
Camundongos Endogâmicos BALB C
Microscopia de Força Atômica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hydrazones); 0 (N'-(3,4-dihydroxybenzylidene)-3-hydroxy-2-naphthahydrazide); 87Z59R7D14 (Filipin); U42B7VYA4P (Chlorpromazine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02588-9


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[PMID]:27775705
[Au] Autor:Horiuchi D; Camarda R; Zhou AY; Yau C; Momcilovic O; Balakrishnan S; Corella AN; Eyob H; Kessenbrock K; Lawson DA; Marsh LA; Anderton BN; Rohrberg J; Kunder R; Bazarov AV; Yaswen P; McManus MT; Rugo HS; Werb Z; Goga A
[Ad] Endereço:Department of Cell and Tissue Biology, University of California, San Francisco (UCSF), San Francisco, California, USA.
[Ti] Título:PIM1 kinase inhibition as a targeted therapy against triple-negative breast tumors with elevated MYC expression.
[So] Source:Nat Med;22(11):1321-1329, 2016 11.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Triple-negative breast cancer (TNBC), in which cells lack expression of the estrogen receptor (ER), the progesterone receptor (PR) and the ERBB2 (also known as HER2) receptor, is the breast cancer subtype with the poorest outcome. No targeted therapy is available against this subtype of cancer owing to a lack of validated molecular targets. We previously reported that signaling involving MYC-an essential, pleiotropic transcription factor that regulates the expression of hundreds of genes-is disproportionally higher in triple-negative (TN) tumors than in receptor-positive (RP) tumors. Direct inhibition of the oncogenic transcriptional activity of MYC has been challenging to achieve. Here, by conducting a shRNA screen targeting the kinome, we identified PIM1, a non-essential serine-threonine kinase, in a synthetic lethal interaction with MYC. PIM1 expression was higher in TN tumors than in RP tumors and was associated with poor prognosis in patients with hormone- and HER2-negative tumors. Small-molecule PIM kinase inhibitors halted the growth of human TN tumors with elevated MYC expression in patient-derived tumor xenograft (PDX) and MYC-driven transgenic mouse models of breast cancer by inhibiting the oncogenic transcriptional activity of MYC and restoring the function of the endogenous cell cycle inhibitor, p27. Our findings warrant clinical evaluation of PIM kinase inhibitors in patients with TN tumors that have elevated MYC expression.
[Mh] Termos MeSH primário: Carcinoma Ductal de Mama/metabolismo
Neoplasias Mamárias Experimentais/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-myc/metabolismo
Proteínas Proto-Oncogênicas c-pim-1/antagonistas & inibidores
Neoplasias de Mama Triplo Negativas/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Inibidor de Quinase Dependente de Ciclina p27/metabolismo
Feminino
Seres Humanos
Marcação In Situ das Extremidades Cortadas
Neoplasias Mamárias Experimentais/tratamento farmacológico
Neoplasias Mamárias Experimentais/genética
Camundongos Transgênicos
Microscopia de Fluorescência
Prognóstico
Proteínas Proto-Oncogênicas c-myc/genética
Proteínas Proto-Oncogênicas c-pim-1/metabolismo
RNA Interferente Pequeno
Reação em Cadeia da Polimerase em Tempo Real
Receptores Estrogênicos/metabolismo
Receptores de Progesterona/metabolismo
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cdkn1b protein, mouse); 0 (MYC protein, human); 0 (Myc protein, mouse); 0 (Protein Kinase Inhibitors); 0 (Proto-Oncogene Proteins c-myc); 0 (RNA, Small Interfering); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27); EC 2.7.11.1 (PIM1 protein, human); EC 2.7.11.1 (Pim1 protein, mouse); EC 2.7.11.1 (Proto-Oncogene Proteins c-pim-1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161108
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4213


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[PMID]:29348537
[Au] Autor:Kotagiri N; Cooper ML; Rettig M; Egbulefu C; Prior J; Cui G; Karmakar P; Zhou M; Yang X; Sudlow G; Marsala L; Chanswangphuwana C; Lu L; Habimana-Griffin L; Shokeen M; Xu X; Weilbaecher K; Tomasson M; Lanza G; DiPersio JF; Achilefu S
[Ad] Endereço:Department of Radiology, Washington University School of Medicine, St. Louis, MO, 63110, USA.
[Ti] Título:Radionuclides transform chemotherapeutics into phototherapeutics for precise treatment of disseminated cancer.
[So] Source:Nat Commun;9(1):275, 2018 01 18.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Most cancer patients succumb to disseminated disease because conventional systemic therapies lack spatiotemporal control of their toxic effects in vivo, particularly in a complicated milieu such as bone marrow where progenitor stem cells reside. Here, we demonstrate the treatment of disseminated cancer by photoactivatable drugs using radiopharmaceuticals. An orthogonal-targeting strategy and a contact-facilitated nanomicelle technology enabled highly selective delivery and co-localization of titanocene and radiolabelled fluorodeoxyglucose in disseminated multiple myeloma cells. Selective ablation of the cancer cells was achieved without significant off-target toxicity to the resident stem cells. Genomic, proteomic and multimodal imaging analyses revealed that the downregulation of CD49d, one of the dimeric protein targets of the nanomicelles, caused therapy resistance in small clusters of cancer cells. Similar treatment of a highly metastatic breast cancer model using human serum albumin-titanocene formulation significantly inhibited cancer growth. This strategy expands the use of phototherapy for treating previously inaccessible metastatic disease.
[Mh] Termos MeSH primário: Neoplasias Mamárias Experimentais/terapia
Mieloma Múltiplo/terapia
Compostos Organometálicos/administração & dosagem
Fotoquimioterapia
Compostos Radiofarmacêuticos/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Resistência a Medicamentos Antineoplásicos
Feminino
Integrina alfa4beta1
Camundongos Endogâmicos C57BL
Camundongos SCID
Micelas
Terapia de Alvo Molecular
Nanopartículas
Ratos
Albumina Sérica Humana
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Integrin alpha4beta1); 0 (Micelles); 0 (Organometallic Compounds); 0 (Radiopharmaceuticals); 1271-29-0 (titanocene); ZIF514RVZR (Serum Albumin, Human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02758-9


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[PMID]:29374685
[Au] Autor:Belkacemi L; Atkins JL; Yang LU; Gadgil P; Sater AK; Chow DS; Bose RN; Zhang SX
[Ad] Endereço:Department of Biology and Biochemistry, University of Houston, Houston, TX, U.S.A. lbelkace@uh.edu lbelkacemi1@gmail.com xzhang5@central.uh.edu.
[Ti] Título:Phosphaplatin Anti-tumor Effect Enhanced by Liposomes Partly an Up-regulation of PEDF in Breast Cancer.
[So] Source:Anticancer Res;38(2):623-646, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Phosphaplatin platinum (IV) (RRD4) complex has exceptional antitumor properties. The aim of this study was to investigate the effects and the mechanism of action of free and liposome-encapsulated RRD4 in breast cancer. MATERIALS AND METHODS: Liposome-encapsulated RRD4 prepared by thin-film dehydration: hydration and free RRD4 were tested in vivo and in vitro against 4T1 breast cancer cells. Cell proliferation, migration and viability were determined. Tissue and cell production and expression of pigment epithelium-derived factor (PEDF) were assessed by ELISA and western blot. 4T1 cells treated with PEDF siRNA were evaluated for viability and apoptosis. RESULTS: RRD4 inhibited tumor growth and prevented distant metastasis. Liposome formulation enhanced this therapeutic benefit without increasing toxicity and prolonged RRD4 retention in tumor tissues. In vitro, RRD4 induced 4T1 apoptosis through up-regulation of FAS, BAX, and PUMA, and down-regulation of BCL2. RRD4 facilitates a FAS-intrinsic signaling mechanism. PEDF up-regulation represents another antitumor mechanism associated with this phosphaplatin compound. DISCUSSION: Free RRD4 or formulated into liposomes, are excellent candidates for adjuvant therapy against breast tumor growth and metastasis.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Proteínas do Olho/metabolismo
Lipossomos/farmacologia
Neoplasias Mamárias Experimentais/tratamento farmacológico
Fatores de Crescimento Neural/metabolismo
Compostos Organoplatínicos/farmacologia
Serpinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/administração & dosagem
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Proteínas do Olho/genética
Feminino
Técnicas de Silenciamento de Genes
Lipossomos/administração & dosagem
Lipossomos/química
Neoplasias Mamárias Experimentais/metabolismo
Camundongos Endogâmicos BALB C
Fatores de Crescimento Neural/genética
Compostos Organoplatínicos/administração & dosagem
Serpinas/genética
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((1R,2R-diaminocyclohexane)(dihydropyrophosphato)(trans-dihydroxo)platinum(IV)); 0 (Antineoplastic Agents); 0 (Eye Proteins); 0 (Liposomes); 0 (Nerve Growth Factors); 0 (Organoplatinum Compounds); 0 (Serpins); 0 (pigment epithelium-derived factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE


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[PMID]:28459074
[Au] Autor:Rosenthal KS; Stone S; Koski G; Zimmerman DH
[Ad] Endereço:College of Medicine, Roseman University of Health Sciences, 10530 Discovery Drive, Las Vegas, NV 89135, USA.
[Ti] Título:LEAPS Vaccine Incorporating HER-2/neu Epitope Elicits Protection That Prevents and Limits Tumor Growth and Spread of Breast Cancer in a Mouse Model.
[So] Source:J Immunol Res;2017:3613505, 2017.
[Is] ISSN:2314-7156
[Cp] País de publicação:Egypt
[La] Idioma:eng
[Ab] Resumo:The prototype J-LEAPS T cell vaccine for HER-2/neu breast cancer (J-HER) consists of the murine HER-2/neu H-2 CD8 T cell epitope covalently attached through a triglycine linker to the J-immune cell binding ligand (ICBL) (human 2 microglobulin peptide). The J-ICBL was chosen for its potential to promote Th1/Tc1 responses. In this proof-of-concept study, the ability of J-HER to prevent or treat cancer was tested in the TUBO cell-challenged BALB/c mouse model for HER-2/neu-expressing tumors. The J-HER vaccine was administered as an emulsion in Montanide ISA-51 without the need for a more potent adjuvant. When administered as a prophylactic vaccination before tumor challenge, J-HER protected against tumor development for at least 48 days. Despite eliciting protection, antibody production in J-HER-immunized, TUBO-challenged mice was less than that in unimmunized mice. More importantly, therapeutic administration of J-HER one week after challenge with TUBO breast cancer cells limited the spread of the tumors and the morbidity and the mortality in the challenged mice. The ability to elicit responses that prevent spread of the TUBO tumor by J-HER suggests its utility as a neoimmunoadjuvant therapy to surgery. Individual or mixtures of J-LEAPS vaccines can be readily prepared to include different CD8 T cell epitopes to optimize tumor therapy and customize treatment for individuals with different HLA types.
[Mh] Termos MeSH primário: Vacinas Anticâncer
Neoplasias Mamárias Experimentais/prevenção & controle
Neoplasias Mamárias Experimentais/terapia
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/genética
Neoplasias da Mama/imunologia
Neoplasias da Mama/prevenção & controle
Neoplasias da Mama/terapia
Linfócitos T CD8-Positivos/imunologia
Vacinas Anticâncer/genética
Vacinas Anticâncer/imunologia
Vacinas Anticâncer/uso terapêutico
Linhagem Celular Tumoral
Modelos Animais de Doenças
Progressão da Doença
Epitopos de Linfócito T/imunologia
Feminino
Genes erbB-2
Imunoglobulina G/sangue
Neoplasias Mamárias Experimentais/imunologia
Neoplasias Mamárias Experimentais/patologia
Camundongos
Camundongos Endogâmicos BALB C
Metástase Neoplásica/prevenção & controle
Estudo de Prova de Conceito
Linfócitos T Citotóxicos/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cancer Vaccines); 0 (Epitopes, T-Lymphocyte); 0 (Immunoglobulin G)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1155/2017/3613505


  9 / 16850 MEDLINE  
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[PMID]:29244910
[Au] Autor:Poveshchenko AF; Kazakov OV; Orlov NB; Poveshchenko OV; Kim II; Bondarenko NA; Solovieva IG; Strunkin DN; Kabakov AV; Rayter TV; Lykov AP; Bogachev SS; Pokushalov EA; Konenkov VI
[Ti] Título:Lymph cytokines as markers oncogenesis and effective treatment of experimental breast cancer Wistar rat.
[So] Source:Patol Fiziol Eksp Ter;60(3):68-75, 2016 Jul-Sep.
[Is] ISSN:0031-2991
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng
[Ab] Resumo:The purpose of this paper is to examine the levels of cytokines in the lymph involved in the pathogenesis of breast cancer. Methods: Breast cancer was induced by introducing n-methyl-N-nitrosourea rats Wistar breed. Some of the animals subjected to surgery alone or chemotherapy alone (cyclophosphamide, methotrexate, 5-fluorouracil). Some animals combine both types of therapy, as well as a separate group to the administration of chemotherapy added Panagene drag presenting a fragmented DNA. To investigate the concentration of cytokines used in lymph test system Bio-Plex Pro Rat Cytokoness 24-Plex Assay (Bio-Rad, USA). Results: In rats with breast cancer content of most studied cytokines such as, IL-1b, IL-2, IL-4, IL-6, IL-7, IL-12, IL-13, IL-17A, MIP-1a, MIP-3a, RANTES, TNF-a, MCP-1 was significantly higher than in intact animals. Surgical removal of the tumor resulted in a significant decrease in the content in the lymph as a pro-inflammatory cytokine. Comparative performance study cytokine content in the lymph after tumor removal from intact animals showed that the content of cytokines such as IL-10, IL-18, GRO / KC, RANTES were significantly higher in the control animals group. Conducting chemotherapy has led to a significant decrease in the content of IL-1b, IL-4, IL-6, IL-7, IL-10, MIP-1a, MIP-3a, RANTES in rat breast cancer lymph. Comparative study of cytokine content in the lymph operated animals after the administration of chemotherapy and Panagene revealed that most of the content indicators cytokines such as IL-5, IL-6, IL-7, IL-10, IL-13, IL-17A, IL- 18, GRO / KC, IFNg, MIP-3a in the lymph was higher after administration of the drug Panagene. Conclusion: In a comparative study cytokine profile lymph Wistar rats found that cytokine content depended on the therapy in animals with induced breast cancer. Lymph cytokine levels may serve as a diagnostic criterion for tumor growth, as well as the predictor of the effectiveness of the therapy and the risk of metastasis of breast cancer.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Citocinas/metabolismo
Linfa/metabolismo
Neoplasias Mamárias Experimentais/metabolismo
[Mh] Termos MeSH secundário: Animais
Feminino
Neoplasias Mamárias Experimentais/patologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Cytokines)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE


  10 / 16850 MEDLINE  
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[PMID]:27773734
[Au] Autor:Deshantri AK; Kooijmans SA; Kuijpers SA; Coimbra M; Hoeppener A; Storm G; Fens MH; Schiffelers RM
[Ad] Endereço:Department of Clinical Chemistry and Haematology, University Medical Center Utrecht, Utrecht, The Netherlands.
[Ti] Título:Liposomal prednisolone inhibits tumor growth in a spontaneous mouse mammary carcinoma model.
[So] Source:J Control Release;243:243-249, 2016 12 10.
[Is] ISSN:1873-4995
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cancers are abundantly infiltrated by inflammatory cells that are modulated by tumor cells to secrete mediators fostering tumor cell survival and proliferation. Therefore, agents that interfere with inflammatory signaling molecules or specific immune cell populations have been investigated as anticancer drugs. Corticosteroids are highly potent anti-inflammatory drugs, whose activity is intensified when targeted by nanocarrier systems. Liposome-targeted corticosteroids have been shown to inhibit tumor growth in different syngeneic murine tumor models as well as human xenograft mouse models, which is attributed to a switch in the tumor microenvironment from a pro-inflammatory to an anti-inflammatory state. Despite the recognized value of implantation tumor models in preclinical research, the "acute" inflammation induced by inoculation of tumor cells together with the exponential tumor growth in a relatively short period of time does not resemble slow progressive human disease that develops in situ. Therefore, in this study, the antitumor effect of liposomal corticosteroids was investigated in a clinically more relevant setting of transgenic mice developing spontaneous breast carcinomas. Here we show that liposomal prednisolone phosphate inhibits the growth of spontaneous breast carcinoma. Interestingly, the liposomal prednisolone was significantly more active than free drug. At 72h after injection of the liposomal formulation, 3µg prednisolone per gram of tumor tissue was recovered whereas no drug could be recovered after injection of the free agent. This indicates that, despite etiological and morphological differences between implanted and spontaneous tumor models, EPR-mediated accumulation of drug occurs to similar extent in this spontaneous mammary carcinoma model as in the syngeneic tumor models. Finally, we analyzed miRNA profiles in the MMTV/neu model and showed that the top 10 of miRNAs in the MMTV/neu tumor consisted of miRNAs with a known involvement in breast carcinoma proliferation and metastasis. The only exception was the appearance of miR-146b, a known inflammation-regulating miRNA species, after liposomal prednisolone treatment.
[Mh] Termos MeSH primário: Antineoplásicos Hormonais/administração & dosagem
Glucocorticoides/administração & dosagem
Neoplasias Mamárias Experimentais/tratamento farmacológico
Prednisolona/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Antineoplásicos Hormonais/farmacologia
Feminino
Glucocorticoides/farmacologia
Seres Humanos
Lipossomos
Neoplasias Mamárias Experimentais/patologia
Camundongos
Camundongos Transgênicos
MicroRNAs/metabolismo
Prednisolona/administração & dosagem
Prednisolona/farmacologia
Fatores de Tempo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (Glucocorticoids); 0 (Liposomes); 0 (MIRN146 microRNA, human); 0 (MicroRNAs); 752SY38R6C (prednisolone phosphate); 9PHQ9Y1OLM (Prednisolone)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180117
[Lr] Data última revisão:
180117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE



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