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[PMID]:28301514
[Au] Autor:Klebaner D; Hamilton-Dutoit S; Ahern T; Crawford A; Jakobsen T; Cronin-Fenton DP; Damkier P; Janssen E; Kjaersgaard A; Ording AG; Søiland H; Sørensen HT; Lash TL; Hellberg Y
[Ad] Endereço:Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia, United States of America.
[Ti] Título:Apolipoprotein D expression does not predict breast cancer recurrence among tamoxifen-treated patients.
[So] Source:PLoS One;12(3):e0171453, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Apolipoprotein D (ApoD) has been proposed as a predictor of breast cancer recurrence among estrogen receptor-positive (ER+), tamoxifen-treated patients. METHODS: We conducted a population-based case-control study nested in a population of 11,251 women aged 35-69 years at diagnosis with Stage I-III breast cancer between 1985 and 2001 on Denmark's Jutland Peninsula and registered with the Danish Breast Cancer Cooperative Group. We identified 541 recurrent or contralateral breast cancers cases among women with ER+ disease treated with tamoxifen for at least 1 year and 300 cases in women with ER- disease never treated with tamoxifen. We matched one control subject per case and assessed ApoD expression in the tumor cell nucleus and cytoplasm using tissue microarray immunohistochemistry. We computed the odds ratio (OR) associating ApoD expression with recurrence and adjusted for potential confounding using logistic regression. RESULTS: Cytoplasmic ApoD expression was seen in 68% of ER+ tumors, in 66% of ER- tumors, and in 66% of controls across both groups. In women with ER+ tumors, the associations of cytoplasmic ApoD expression with recurrence (OR = 1.0; 95% CI = 0.7 to 1.4) and increasing cytoplasmic expression with recurrence (OR = 1.0; 95% CI = 0.996 to 1.003) were null, as were those for women with ER- tumors. Associations for nuclear ApoD expression and combined nuclear and cytoplasmic expression were similarly near-null. CONCLUSION: ApoD expression is likely not a predictor of recurrence in tamoxifen-treated patients. IMPACT: This study eliminates the previously suggested marker ApoD as a predictor of recurrence among tamoxifen-treated women.
[Mh] Termos MeSH primário: Antineoplásicos Hormonais/uso terapêutico
Apolipoproteínas D/metabolismo
Biomarcadores Tumorais/metabolismo
Neoplasias da Mama/tratamento farmacológico
Neoplasias da Mama/metabolismo
Recidiva Local de Neoplasia
Tamoxifeno/uso terapêutico
[Mh] Termos MeSH secundário: Adolescente
Idoso
Neoplasias da Mama/patologia
Feminino
Seres Humanos
Meia-Idade
Modelos Teóricos
Receptores Estrogênicos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (Apolipoproteins D); 0 (Biomarkers, Tumor); 0 (Receptors, Estrogen); 094ZI81Y45 (Tamoxifen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170317
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0171453


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[PMID]:28182653
[Au] Autor:Pascua-Maestro R; Diez-Hermano S; Lillo C; Ganfornina MD; Sanchez D
[Ad] Endereço:Instituto de Biología y Genética Molecular-Departamento de Bioquímica y Biología Molecular y Fisiología, Universidad de Valladolid-CSIC, Valladolid, Spain.
[Ti] Título:Protecting cells by protecting their vulnerable lysosomes: Identification of a new mechanism for preserving lysosomal functional integrity upon oxidative stress.
[So] Source:PLoS Genet;13(2):e1006603, 2017 Feb.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Environmental insults such as oxidative stress can damage cell membranes. Lysosomes are particularly sensitive to membrane permeabilization since their function depends on intraluminal acidic pH and requires stable membrane-dependent proton gradients. Among the catalog of oxidative stress-responsive genes is the Lipocalin Apolipoprotein D (ApoD), an extracellular lipid binding protein endowed with antioxidant capacity. Within the nervous system, cell types in the defense frontline, such as astrocytes, secrete ApoD to help neurons cope with the challenge. The protecting role of ApoD is known from cellular to organism level, and many of its downstream effects, including optimization of autophagy upon neurodegeneration, have been described. However, we still cannot assign a cellular mechanism to ApoD gene that explains how this protection is accomplished. Here we perform a comprehensive analysis of ApoD intracellular traffic and demonstrate its role in lysosomal pH homeostasis upon paraquat-induced oxidative stress. By combining single-lysosome in vivo pH measurements with immunodetection, we demonstrate that ApoD is endocytosed and targeted to a subset of vulnerable lysosomes in a stress-dependent manner. ApoD is functionally stable in this acidic environment, and its presence is sufficient and necessary for lysosomes to recover from oxidation-induced alkalinization, both in astrocytes and neurons. This function is accomplished by preventing lysosomal membrane permeabilization. Two lysosomal-dependent biological processes, myelin phagocytosis by astrocytes and optimization of neurodegeneration-triggered autophagy in a Drosophila in vivo model, require ApoD-related Lipocalins. Our results uncover a previously unknown biological function of ApoD, member of the finely regulated and evolutionary conserved gene family of extracellular Lipocalins. They set a lipoprotein-mediated regulation of lysosomal membrane integrity as a new mechanism at the hub of many cellular functions, critical for the outcome of a wide variety of neurodegenerative diseases. These results open therapeutic opportunities by providing a route of entry and a repair mechanism for lysosomes in pathological situations.
[Mh] Termos MeSH primário: Astrócitos/metabolismo
Lisossomos/metabolismo
Neurônios/metabolismo
Estresse Oxidativo
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Animais Recém-Nascidos
Apolipoproteínas D/genética
Apolipoproteínas D/metabolismo
Apolipoproteínas D/farmacologia
Astrócitos/efeitos dos fármacos
Astrócitos/ultraestrutura
Autofagia/efeitos dos fármacos
Autofagia/genética
Linhagem Celular Tumoral
Células Cultivadas
Drosophila
Células HEK293
Herbicidas/farmacologia
Seres Humanos
Concentração de Íons de Hidrogênio
Immunoblotting
Lipocalinas/farmacologia
Lisossomos/química
Camundongos Knockout
Microscopia Confocal
Microscopia Eletrônica
Modelos Biológicos
Doenças Neurodegenerativas/genética
Doenças Neurodegenerativas/metabolismo
Doenças Neurodegenerativas/prevenção & controle
Neurônios/efeitos dos fármacos
Paraquat/farmacologia
Fagossomos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins D); 0 (Herbicides); 0 (Lipocalins); PLG39H7695 (Paraquat)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170607
[Lr] Data última revisão:
170607
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170210
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006603


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[PMID]:27804940
[Au] Autor:Allina DO; Andreeva YY; Zavalishina LE; Moskvina LV; Frank GA
[Ad] Endereço:Russian Medical Academy of Postgraduate Education, Moscow, Russia.
[Ti] Título:[Estimation of the diagnostic potential of APOD, PTOV1, and EPHA4 for prostatic neoplasms].
[Ti] Título:Otsenka diagnosticheskogo potentsiala APOD, PTOV1 i EPHA4 dlya novoobrazovanii predstatel'noi zhelezy..
[So] Source:Arkh Patol;78(5):9-14, 2016.
[Is] ISSN:0004-1955
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Prostate cancer is one of the most frequently detected malignancies in men. The gold standard for its diagnosis is morphological examination; at the same time the differential diagnosis of adenocarcinoma, high-grade prostatic intraepithelial neoplasia (HGPIN), and benign conditions that are able to mimic the malignancies is tremendously difficult in a number of cases, this being so, the hyperdiagnosis rate of HGPIN requiring mandatory repeat biopsy is as high as 24%. The currently available differential diagnostic panel of antibodies is imperfect, which necessitates a search for novel markers. AIM: to estimate the diagnostic and prognostic value of the expression of PTOV1, APOD, and EPHA4 in prostatic neoplasias. MATERIAL AND METHODS: A total of 90 samples from prostate cancer patients who had undergone radical prostatectomy were examined. The presence of adenocarcinoma and HGPIN was verified by immunohistochemical tests using antibodies to AMACR (P504S) and high molecular weight cytokeratin 34ßE12 in serial sections. The latter were also used to immunohistochemically analyze the expression of PTOV1, APOD, and EPHA4. RESULTS: APOD expression was noted in 76% of cases of both adenocarcinomas and HGPIN, in 4% in only cancer, and in 7% in only HGPIN. All the study samples showed a considerable decrease in PTOV1 expression in cancer and HGPIN compared to morphologically normal glands. Three samples also exhibited no PTOV1 expression in a number of morphologically normal glands. No difference was found in the expression of EPHA4 in morphologically normal glands, HGPIN, or cancer. CONCLUSION: The high rate of APOD expression in HGPIN and cancer, as well as the absence of its expression in the vast majority of morphologically normal glands allows the use of this protein as an additional marker in the differential diagnosis of prostatic neoplasms. The emerging trends in the difference of PTOV1 expression in morphologically normal prostate tissue, HGPIN, and cancer call for further investigations with a larger sample.
[Mh] Termos MeSH primário: Adenocarcinoma/metabolismo
Apolipoproteínas D/metabolismo
Biomarcadores Tumorais/metabolismo
Carcinoma in Situ/metabolismo
Proteínas de Neoplasias/metabolismo
Neoplasias da Próstata/metabolismo
Receptor EphA4/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/patologia
Adulto
Idoso
Apolipoproteínas D/genética
Biomarcadores Tumorais/genética
Carcinoma in Situ/patologia
Estudos de Casos e Controles
Seres Humanos
Masculino
Meia-Idade
Proteínas de Neoplasias/genética
Neoplasias da Próstata/patologia
Receptor EphA4/genética
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOD protein, human); 0 (Apolipoproteins D); 0 (Biomarkers, Tumor); 0 (Neoplasm Proteins); 0 (PTOV1 protein, human); EC 2.7.10.1 (Receptor, EphA4)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161103
[St] Status:MEDLINE
[do] DOI:10.17116/patol20167859-14


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[PMID]:27583472
[Au] Autor:Hornig NC; Ukat M; Schweikert HU; Hiort O; Werner R; Drop SL; Cools M; Hughes IA; Audi L; Ahmed SF; Demiri J; Rodens P; Worch L; Wehner G; Kulle AE; Dunstheimer D; Müller-Roßberg E; Reinehr T; Hadidi AT; Eckstein AK; van der Horst C; Seif C; Siebert R; Ammerpohl O; Holterhus PM
[Ad] Endereço:Department of Pediatrics (N.C.H., M.U., J.D., P.R., A.E.K., P.-M.H.), Division of Pediatric Endocrinology and Diabetes, and Institute of Human Genetics (L.W., R.S., O.A.), Christian-Albrechts-University Kiel and University Hospital Schleswig-Holstein, Campus Kiel, Schwanenweg 20, 24105 Kiel, Germany
[Ti] Título:Identification of an AR Mutation-Negative Class of Androgen Insensitivity by Determining Endogenous AR Activity.
[So] Source:J Clin Endocrinol Metab;101(11):4468-4477, 2016 Nov.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CONTEXT: Only approximately 85% of patients with a clinical diagnosis complete androgen insensitivity syndrome and less than 30% with partial androgen insensitivity syndrome can be explained by inactivating mutations in the androgen receptor (AR) gene. OBJECTIVE: The objective of the study was to clarify this discrepancy by in vitro determination of AR transcriptional activity in individuals with disorders of sex development (DSD) and male controls. DESIGN: Quantification of DHT-dependent transcriptional induction of the AR target gene apolipoprotein D (APOD) in cultured genital fibroblasts (GFs) (APOD assay) and next-generation sequencing of the complete coding and noncoding AR locus. SETTING: The study was conducted at a university hospital endocrine research laboratory. PATIENTS: GFs from 169 individuals were studied encompassing control males (n = 68), molecular defined DSD other than androgen insensitivity syndrome (AIS; n = 18), AR mutation-positive AIS (n = 37), and previously undiagnosed DSD including patients with a clinical suspicion of AIS (n = 46). INTERVENTION(S): There were no interventions. MAIN OUTCOME MEASURE(S): DHT-dependent APOD expression in cultured GF and AR mutation status in 169 individuals was measured. RESULTS: The APOD assay clearly separated control individuals (healthy males and molecular defined DSD patients other than AIS) from genetically proven AIS (cutoff < 2.3-fold APOD-induction; 100% sensitivity, 93.3% specificity, P < .0001). Of 46 DSD individuals with no AR mutation, 17 (37%) fell below the cutoff, indicating disrupted androgen signaling. CONCLUSIONS: AR mutation-positive AIS can be reliably identified by the APOD assay. Its combination with next-generation sequencing of the AR locus uncovered an AR mutation-negative, new class of androgen resistance, which we propose to name AIS type II. Our data support the existence of cellular components outside the AR affecting androgen signaling during sexual differentiation with high clinical relevance.
[Mh] Termos MeSH primário: Síndrome de Resistência a Andrógenos/diagnóstico
Apolipoproteínas D
Bioensaio/normas
Transtornos do Desenvolvimento Sexual/diagnóstico
Receptores Androgênicos/metabolismo
Testosterona/análogos & derivados
[Mh] Termos MeSH secundário: Adulto
Síndrome de Resistência a Andrógenos/genética
Síndrome de Resistência a Andrógenos/metabolismo
Células Cultivadas
Transtornos do Desenvolvimento Sexual/genética
Transtornos do Desenvolvimento Sexual/metabolismo
Fibroblastos
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Masculino
Mutação
Receptores Androgênicos/genética
Sensibilidade e Especificidade
Testosterona/metabolismo
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APOD protein, human); 0 (AR protein, human); 0 (Apolipoproteins D); 0 (Receptors, Androgen); 3XMK78S47O (Testosterone); 5H7I2IP58X (boldenone)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160902
[St] Status:MEDLINE


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[PMID]:27506732
[Au] Autor:Martineau C; Najyb O; Signor C; Rassart É; Moreau R
[Ad] Endereço:Laboratoire du Métabolisme Osseux, Centre BioMed, Département des Sciences Biologiques, Université du Québec à Montréal, Montréal, Québec, Canada. Electronic address: cmartineau@shriners.mcgill.ca.
[Ti] Título:Apolipoprotein D deficiency is associated to high bone turnover, low bone mass and impaired osteoblastic function in aged female mice.
[So] Source:Metabolism;65(9):1247-58, 2016 Sep.
[Is] ISSN:1532-8600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Apolipoprotein D (ApoD) is a member of the lipocalin family known to transport small hydrophobic ligands. A major site of ApoD expression in mice is the central nervous system where evidence suggests that it plays a protective role. Gene expression of ApoD was reported in bone-forming osteoblasts but its impact on bone metabolism remains undocumented. METHODS: We compared basic bone parameters of ApoD(-/-) (null) and transgenic (tg) mice to wild-type (wt) littermates through microCT and histochemistry, as well as ApoD expression and secretion in osteoblasts under various culture conditions through real-time PCR and immunoblotting. RESULTS: ApoD-null females displayed progressive bone loss with aging, resulting in a 50% reduction in trabecular bone volume and a 23% reduction in cortical bone volume by 9months of age. Only cortical bone volume was significantly reduced in ApoD-null males by an average of 24%. Histochemistry indicated significantly higher osteoblast surface and number of osteoclasts in femora from ApoD-null females. ApoD gene expression was confirmed in primary cultures of bone marrow mesenchymal cells (MSC), with higher expression levels in MSC from females compared to males. ApoD-null MSC exhibited impaired proliferation and differentiation potentials. Moreover, exogenous ApoD partially rescued the osteogenic potential of null MSC, which were shown to readily uptake the protein from media. ApoD expression was upregulated under low proliferation conditions, by contact inhibition and osteoblastic differentiation in MC3T3-E1 osteoblast-like cells. CONCLUSION: Our results indicate that ApoD influences bone metabolism in mice in a gender-specific manner, potentially through an auto-/paracrine pathway.
[Mh] Termos MeSH primário: Envelhecimento/genética
Apolipoproteínas D/deficiência
Desenvolvimento Ósseo/genética
Remodelação Óssea/genética
Osteoblastos
[Mh] Termos MeSH secundário: Células 3T3
Animais
Apolipoproteínas D/genética
Apolipoproteínas D/metabolismo
Células da Medula Óssea/metabolismo
Ciclo Celular/genética
Diferenciação Celular
Proliferação Celular
Feminino
Fêmur/citologia
Fêmur/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Osteoblastos/metabolismo
Cultura Primária de Células
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins D)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170523
[Lr] Data última revisão:
170523
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160811
[St] Status:MEDLINE


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[PMID]:27265652
[Au] Autor:Gao GQ; Song LS; Tong B; Li GP
[Ad] Endereço:Research Center for Laboratory of Animal Science, Inner Mongolia University, Hohhot 010070, China.
[Ti] Título:Expression levels of GSTA2 and APOD genes might be associated with carotenoid coloration in golden pheasant (Chrysolophus pictus) plumage.
[So] Source:Dongwuxue Yanjiu;37(3):144-50, 2016 May 18.
[Is] ISSN:0254-5853
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:Carotenoids, which generate yellow, orange, and red colors, are crucial pigments in avian plumage. Investigations into genes associated with carotenoidbased coloration in avian species are important; however, such research is difficult because carotenoids cannot be synthetized in vertebrates as they are only derived from dietary sources. Here, the golden pheasant (Chrysolophus pictus) was used as a model in analysis of candidate gene expression profiles implicated in carotenoid binding and deposition. Using mass and Raman spectrometry to confirm the presence of carotenoids in golden pheasant feathers, we found C40H54O and C40H56O2 in feathers with yellow to red colors, and in the rachis of iridescent feathers. The global gene expression profiles in golden pheasant skins were analyzed by RNA-seq and all six carotenoid binding candidate genes sequenced were studied by realtime PCR. StAR4, GSTA2, Scarb1, and APOD in feather follicles showed different expressions in red breast and orange nape feathers compared with that of iridescent mantle feathers. Further comparison of golden pheasant yellow rump and Lady Amherst's pheasant (Chrysolophus amherstiae) white nape feathers suggested that GSTA2 and APOD played a potential role in carotenoid-based coloration in golden pheasant.
[Mh] Termos MeSH primário: Apolipoproteínas D/genética
Carotenoides/metabolismo
Plumas/metabolismo
Galliformes/genética
Regulação Enzimológica da Expressão Gênica
Glutationa Transferase/genética
Isoenzimas/genética
Pigmentação/genética
[Mh] Termos MeSH secundário: Animais
Galliformes/anatomia & histologia
Galliformes/metabolismo
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins D); 0 (Isoenzymes); 36-88-4 (Carotenoids); EC 2.5.1.18 (Glutathione Transferase); EC 2.5.1.18 (glutathione S-transferase alpha)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170330
[Lr] Data última revisão:
170330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160607
[St] Status:MEDLINE


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[PMID]:27193151
[Au] Autor:Kliuchnikova AA; Samokhina NI; Ilina IY; Karpov DS; Pyatnitskiy MA; Kuznetsova KG; Toropygin IY; Kochergin SA; Alekseev IB; Zgoda VG; Archakov AI; Moshkovskii SA
[Ad] Endereço:Institute of Biomedical Chemistry, Moscow, Russia.
[Ti] Título:Human aqueous humor proteome in cataract, glaucoma, and pseudoexfoliation syndrome.
[So] Source:Proteomics;16(13):1938-46, 2016 Jul.
[Is] ISSN:1615-9861
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Twenty-nine human aqueous humor samples from patients with eye diseases such as cataract and glaucoma with and without pseudoexfoliation syndrome were characterized by LC-high resolution MS analysis. In total, 269 protein groups were identified with 1% false discovery rate including 32 groups that were not reported previously for this biological fluid. Since the samples were analyzed individually, but not pooled, 36 proteins were identified in all samples, comprising the constitutive proteome of the fluid. The most dominant molecular function of aqueous humor proteins as determined by GO analysis is endopeptidase inhibitor activity. Label-free protein quantification showed no significant difference between glaucoma and cataract aqueous humor proteomes. At the same time, we found decrease in the level of apolipoprotein D as a marker of the pseudoexfoliation syndrome. The data are available from ProteomeXchange repository (PXD002623).
[Mh] Termos MeSH primário: Humor Aquoso/química
Catarata/diagnóstico
Síndrome de Exfoliação/diagnóstico
Glaucoma/diagnóstico
Proteoma/análise
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Apolipoproteínas D/análise
Biomarcadores/análise
Cromatografia Líquida
Seres Humanos
Meia-Idade
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins D); 0 (Biomarkers); 0 (Proteome)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170823
[Lr] Data última revisão:
170823
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160520
[St] Status:MEDLINE
[do] DOI:10.1002/pmic.201500423


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[PMID]:27105922
[Au] Autor:Lee MY; Kim EY; Kim SH; Cho KC; Ha K; Kim KP; Ahn YM
[Ad] Endereço:Institute for Systems Biology, Seattle, WA, United States; Department of Applied Chemistry, College of Applied Science, Kyung Hee University, Yongin, Republic of Korea.
[Ti] Título:Discovery of serum protein biomarkers in drug-free patients with major depressive disorder.
[So] Source:Prog Neuropsychopharmacol Biol Psychiatry;69:60-8, 2016 08 01.
[Is] ISSN:1878-4216
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Major depressive disorder (MDD) is a systemic and multifactorial disorder involving complex interactions between genetic predisposition and disturbances of various molecular pathways. Its underlying molecular pathophysiology remains unclear, and no valid and objective diagnostic tools for the condition are available. METHODS: We performed large-scale proteomic profiling to identify novel peripheral biomarkers implicated in the pathophysiology of MDD in 25 drug-free female MDD patients and 25 healthy controls. First, quantitative serum proteome profiles were obtained and analyzed by liquid chromatography-tandem mass spectrometry using serum samples from 10 MDD patients and 10 healthy controls. Next, candidate biomarker sets, including differentially expressed proteins from the profiling experiment and those identified in the literature, were verified using multiple-reaction monitoring in 25 patients and 25 healthy controls. The final panel of potential biomarkers was selected using multiparametric statistical analysis. RESULTS: We identified a serum biomarker panel consisting of six proteins: apolipoprotein D, apolipoprotein B, vitamin D-binding protein, ceruloplasmin, hornerin, and profilin 1, which could be used to distinguish MDD patients from controls with 68% diagnostic accuracy. Our results suggest that modulation of the immune and inflammatory systems and lipid metabolism are involved in the pathophysiology of MDD. CONCLUSIONS: Our findings of functional proteomic changes in the peripheral blood of patients with MDD further clarify the molecular biological pathway underlying depression. Further studies using larger, independent cohorts are needed to verify the role of these candidate biomarkers for the diagnosis of MDD.
[Mh] Termos MeSH primário: Transtorno Depressivo Maior/sangue
[Mh] Termos MeSH secundário: Adulto
Apolipoproteína B-100/sangue
Apolipoproteínas D/sangue
Biomarcadores/sangue
Análise Química do Sangue
Proteínas de Ligação ao Cálcio/sangue
Ceruloplasmina/metabolismo
Cromatografia Líquida de Alta Pressão
Estudos de Coortes
Feminino
Perfilação da Expressão Gênica
Seres Humanos
Proteínas de Filamentos Intermediários/sangue
Profilinas/sangue
Proteoma
Escalas de Graduação Psiquiátrica
Espectrometria de Massas em Tandem
Proteína de Ligação a Vitamina D/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (APOB protein, human); 0 (APOD protein, human); 0 (Apolipoprotein B-100); 0 (Apolipoproteins D); 0 (Biomarkers); 0 (Calcium-Binding Proteins); 0 (HRNR protein, human); 0 (Intermediate Filament Proteins); 0 (PFN1 protein, human); 0 (Profilins); 0 (Proteome); 0 (Vitamin D-Binding Protein); EC 1.16.3.1 (Ceruloplasmin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170410
[Lr] Data última revisão:
170410
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160424
[St] Status:MEDLINE


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[PMID]:26961242
[Au] Autor:Tan WJ; Cima I; Choudhury Y; Wei X; Lim JC; Thike AA; Tan MH; Tan PH
[Ad] Endereço:Division of Biodevices and Diagnostics, Institute of Bioengineering and Nanotechnology, 31 Biopolis Way, The Nanos, #04-01, Singapore, 138669, Republic of Singapore. wjtan@ibn.a-star.edu.sg.
[Ti] Título:A five-gene reverse transcription-PCR assay for pre-operative classification of breast fibroepithelial lesions.
[So] Source:Breast Cancer Res;18(1):31, 2016 Mar 09.
[Is] ISSN:1465-542X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Breast fibroepithelial lesions are biphasic tumors and include fibroadenomas and phyllodes tumors. Preoperative distinction between fibroadenomas and phyllodes tumors is pivotal to clinical management. Fibroadenomas are clinically benign while phyllodes tumors are more unpredictable in biological behavior, with potential for recurrence. Differentiating the tumors may be challenging when they have overlapping clinical and histological features especially on core biopsies. Current molecular and immunohistochemical techniques have a limited role in the diagnosis of breast fibroepithelial lesions. We aimed to develop a practical molecular test to aid in distinguishing fibroadenomas from phyllodes tumors in the pre-operative setting. METHODS: We profiled the transcriptome of a training set of 48 formalin-fixed, paraffin-embedded fibroadenomas and phyllodes tumors and further designed 43 quantitative polymerase chain reaction (qPCR) assays to verify differentially expressed genes. Using machine learning to build predictive regression models, we selected a five-gene transcript set (ABCA8, APOD, CCL19, FN1, and PRAME) to discriminate between fibroadenomas and phyllodes tumors. We validated our assay in an independent cohort of 230 core biopsies obtained pre-operatively. RESULTS: Overall, the assay accurately classified 92.6 % of the samples (AUC = 0.948, 95 % CI 0.913-0.983, p = 2.51E-19), with a sensitivity of 82.9 % and specificity of 94.7 %. CONCLUSIONS: We provide a robust assay for classifying breast fibroepithelial lesions into fibroadenomas and phyllodes tumors, which could be a valuable tool in assisting pathologists in differential diagnosis of breast fibroepithelial lesions.
[Mh] Termos MeSH primário: Neoplasias da Mama/diagnóstico
Diagnóstico Diferencial
Fibroadenoma/diagnóstico
Tumor Filoide/diagnóstico
Reação em Cadeia da Polimerase Via Transcriptase Reversa/métodos
[Mh] Termos MeSH secundário: Transportadores de Cassetes de Ligação de ATP/biossíntese
Transportadores de Cassetes de Ligação de ATP/genética
Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Antígenos de Neoplasias/biossíntese
Antígenos de Neoplasias/genética
Apolipoproteínas D/biossíntese
Apolipoproteínas D/genética
Biópsia
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Quimiocina CCL19/biossíntese
Quimiocina CCL19/genética
Feminino
Fibroadenoma/genética
Fibroadenoma/patologia
Fibronectinas/biossíntese
Fibronectinas/genética
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Meia-Idade
Tumor Filoide/genética
Tumor Filoide/patologia
Período Pré-Operatório
Transcriptoma/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ABCA8 protein, human); 0 (APOD protein, human); 0 (Antigens, Neoplasm); 0 (Apolipoproteins D); 0 (CCL19 protein, human); 0 (Chemokine CCL19); 0 (FN1 protein, human); 0 (Fibronectins); 0 (PRAME protein, human)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160311
[St] Status:MEDLINE
[do] DOI:10.1186/s13058-016-0692-6


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[PMID]:26829325
[Au] Autor:Li H; Ruberu K; Karl T; Garner B
[Ad] Endereço:Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, NSW 2522, Australia.
[Ti] Título:Cerebral Apolipoprotein-D Is Hypoglycosylated Compared to Peripheral Tissues and Is Variably Expressed in Mouse and Human Brain Regions.
[So] Source:PLoS One;11(2):e0148238, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent studies have shown that cerebral apoD levels increase with age and in Alzheimer's disease (AD). In addition, loss of cerebral apoD in the mouse increases sensitivity to lipid peroxidation and accelerates AD pathology. Very little data are available, however, regarding the expression of apoD protein levels in different brain regions. This is important as both brain lipid peroxidation and neurodegeneration occur in a region-specific manner. Here we addressed this using western blotting of seven different regions (olfactory bulb, hippocampus, frontal cortex, striatum, cerebellum, thalamus and brain stem) of the mouse brain. Our data indicate that compared to most brain regions, the hippocampus is deficient in apoD. In comparison to other major organs and tissues (liver, spleen, kidney, adrenal gland, heart and skeletal muscle), brain apoD was approximately 10-fold higher (corrected for total protein levels). Our analysis also revealed that brain apoD was present at a lower apparent molecular weight than tissue and plasma apoD. Utilising peptide N-glycosidase-F and neuraminidase to remove N-glycans and sialic acids, respectively, we found that N-glycan composition (but not sialylation alone) were responsible for this reduction in molecular weight. We extended the studies to an analysis of human brain regions (hippocampus, frontal cortex, temporal cortex and cerebellum) where we found that the hippocampus had the lowest levels of apoD. We also confirmed that human brain apoD was present at a lower molecular weight than in plasma. In conclusion, we demonstrate apoD protein levels are variable across different brain regions, that apoD levels are much higher in the brain compared to other tissues and organs, and that cerebral apoD has a lower molecular weight than peripheral apoD; a phenomenon that is due to the N-glycan content of the protein.
[Mh] Termos MeSH primário: Apolipoproteínas D/metabolismo
Cérebro/metabolismo
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas E/metabolismo
Biomarcadores/metabolismo
Feminino
Glicosilação
Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
Peso Molecular
Ácido N-Acetilneuramínico/metabolismo
Polissacarídeos/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apolipoproteins D); 0 (Apolipoproteins E); 0 (Biomarkers); 0 (Polysaccharides); GZP2782OP0 (N-Acetylneuraminic Acid)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160202
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0148238



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