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[PMID]:29368833
[Au] Autor:Abholz EV; Adonyeva NV; Gruntenko NE; Rauschenbach IY
[Ti] Título:[Gene dilp6 regulates octopamine metabolism in Drosophila melanogaster].
[So] Source:Genetika;52(6):718-22, 2016 Jun.
[Is] ISSN:0016-6758
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The effect of strong hypomorphic mutation of the insulin-like protein gene (dilp6) on metabolism of octopamine (one of the main biogenic amines in insects) was studied in Drosophila melanogaster males and females. The activity of tyrosine decarboxylase (the key enzyme of octopamine synthesis) and the activity of octopamine-dependent N-acetyltransferase (the enzyme of its degradation) were measured. It was demonstrated that the activity of both studied enzymes is decreased under normal conditions in the dilp6 41 mutants (as we previously demonstrated, this is correlated with an increased level of octopamine). It was also found that hypomorphic mutation of the dilp6 gene decreases the intensity of tyrosine decarboxylase response to heat stress. Thus, it was demonstrated for the first time that insulin-like DILP6 protein in drosophila influences the level of octopamine (regulating the activity of the enzyme degrading octopamine).
[Mh] Termos MeSH primário: Proteínas de Drosophila
Resposta ao Choque Térmico/fisiologia
Octopamina
Somatomedinas
[Mh] Termos MeSH secundário: Animais
Proteínas de Drosophila/genética
Proteínas de Drosophila/metabolismo
Drosophila melanogaster
Octopamina/genética
Octopamina/metabolismo
Somatomedinas/genética
Somatomedinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dilp6 protein, Drosophila); 0 (Drosophila Proteins); 0 (Somatomedins); 14O50WS8JD (Octopamine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE


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[PMID]:27779364
[Au] Autor:van Beijnum JR; Pieters W; Nowak-Sliwinska P; Griffioen AW
[Ad] Endereço:Department of Medical Oncology, Angiogenesis Laboratory, VU University Medical Center, PO box 7057, 1007 MB, Amsterdam, The Netherlands.
[Ti] Título:Insulin-like growth factor axis targeting in cancer and tumour angiogenesis - the missing link.
[So] Source:Biol Rev Camb Philos Soc;92(3):1755-1768, 2017 Aug.
[Is] ISSN:1469-185X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Numerous molecular players in the process of tumour angiogenesis have been shown to offer potential for therapeutic targeting. Initially denoted to be involved in malignant transformation and tumour progression, the insulin-like growth factor (IGF) signalling axis has been subject to therapeutic interference, albeit with limited clinical success. More recently, IGFs and their receptors have received attention for their contribution to tumour angiogenesis, which offers novel therapeutic opportunities. Here we review the contribution of this signalling axis to tumour angiogenesis, the mechanisms of resistance to therapy and the interplay with other pro-angiogenic pathways, to offer insight in the renewed interest in the application of IGF axis targeting agents in anti-cancer combination therapies.
[Mh] Termos MeSH primário: Neoplasias/terapia
Neovascularização Patológica
Transdução de Sinais
Somatomedinas/metabolismo
[Mh] Termos MeSH secundário: Sistemas de Liberação de Medicamentos
Seres Humanos
Neoplasias/fisiopatologia
Ligação Proteica
Somatomedinas/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Somatomedins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1111/brv.12306


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[PMID]:28939196
[Au] Autor:Zhang H; Shi Y; He M
[Ad] Endereço:CAS Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong Provincial Key Laboratory of Applied Marine Biology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou 510301, China; University of Chinese Academy of Sciences, Beijing 100049, China.
[Ti] Título:Molecular identification of an insulin growth factor binding protein (IGFBP) and its potential role in an insulin-like peptide system of the pearl oyster, Pinctada fucata.
[So] Source:Comp Biochem Physiol B Biochem Mol Biol;214:27-35, 2017 Dec.
[Is] ISSN:1879-1107
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Insulin-like growth factors (IGFs) play critical roles in regulating metabolism, growth, and reproduction in invertebrates. IGF binding proteins (IGFBPs) serve as major regulators of IGF activity and regulate endocrine system. In the present study, the full-length cDNA of an igfbp was identified from the pearl oyster, Pinctada fucata, using expressed sequence tag (EST) sequence. The 1124bp Pfigfbp cDNA contains a 465bp open reading frame (ORF) encoding a putative protein of 154 amino acids, a 5'-untranslated region (UTR) of 238bp, and a 3'-UTR of 394bp (not including polyA+). Multiple sequence alignment of the deduced IB domain sequences revealed that twelve conserved Cys and ILP binding site in PfIGFBP were well aligned with human IGFBPs1-7, Mizuhopecten yessoensis IGFBP5 and Eriocheir sinensis IGFBP7. Gene expression analysis indicated that Pfigfbp mRNA was expressed in all the tissues and developmental stages examined, with a higher level in the foot than in other tissues and a higher level in the polar body stage and 32-cell stage than in the other stages. Pfigfbp and PfILP (insulin-like peptide) mRNA levels significantly increased in the digestive gland after feeding, while levels were dramatically reduced during a week of food deprivation and increased upon refeeding. In vitro experiments indicated that Pfigfbp mRNA expression in mantle cells was affected by insulin/IGFs (IGF-I, IGF-II). Our data suggests that Pfigfbp may be involved in endocrine signaling in P. fucata via the regulation of insulin-like peptide signaling.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica no Desenvolvimento
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/genética
Insulina/genética
Fases de Leitura Aberta
Pinctada/genética
Somatomedinas/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sítios de Ligação
Clonagem Molecular
Ingestão de Alimentos/genética
Escherichia coli/genética
Escherichia coli/metabolismo
Etiquetas de Sequências Expressas/química
Seres Humanos
Insulina/metabolismo
Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/metabolismo
Especificidade de Órgãos
Pectinidae
Filogenia
Pinctada/classificação
Pinctada/crescimento & desenvolvimento
Pinctada/metabolismo
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
Transdução de Sinais
Somatomedinas/metabolismo
Inanição/genética
Inanição/metabolismo
Regiões não Traduzidas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (Insulin-Like Growth Factor Binding Proteins); 0 (Recombinant Proteins); 0 (Somatomedins); 0 (Untranslated Regions)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170924
[St] Status:MEDLINE


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[PMID]:28902870
[Au] Autor:Augustin H; McGourty K; Allen MJ; Madem SK; Adcott J; Kerr F; Wong CT; Vincent A; Godenschwege T; Boucrot E; Partridge L
[Ad] Endereço:Max Planck Institute for Biology of Aging, Köln, Germany.
[Ti] Título:Reduced insulin signaling maintains electrical transmission in a neural circuit in aging flies.
[So] Source:PLoS Biol;15(9):e2001655, 2017 Sep.
[Is] ISSN:1545-7885
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lowered insulin/insulin-like growth factor (IGF) signaling (IIS) can extend healthy lifespan in worms, flies, and mice, but it can also have adverse effects (the "insulin paradox"). Chronic, moderately lowered IIS rescues age-related decline in neurotransmission through the Drosophila giant fiber system (GFS), a simple escape response neuronal circuit, by increasing targeting of the gap junctional protein innexin shaking-B to gap junctions (GJs). Endosomal recycling of GJs was also stimulated in cultured human cells when IIS was reduced. Furthermore, increasing the activity of the recycling small guanosine triphosphatases (GTPases) Rab4 or Rab11 was sufficient to maintain GJs upon elevated IIS in cultured human cells and in flies, and to rescue age-related loss of GJs and of GFS function. Lowered IIS thus elevates endosomal recycling of GJs in neurons and other cell types, pointing to a cellular mechanism for therapeutic intervention into aging-related neuronal disorders.
[Mh] Termos MeSH primário: Envelhecimento/fisiologia
Drosophila/fisiologia
Insulina/metabolismo
Somatomedinas/metabolismo
Transmissão Sináptica
[Mh] Termos MeSH secundário: Animais
Conexinas/metabolismo
Reação de Fuga/fisiologia
Feminino
Junções Comunicantes/fisiologia
Masculino
Proteínas rab de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexins); 0 (Insulin); 0 (Somatomedins); EC 3.6.5.2 (rab GTP-Binding Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pbio.2001655


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[PMID]:28806748
[Au] Autor:Politis SN; Mazurais D; Servili A; Zambonino-Infante JL; Miest JJ; Sørensen SR; Tomkiewicz J; Butts IAE
[Ad] Endereço:National Institute of Aquatic Resources, Technical University of Denmark, DTU, Lyngby, Denmark.
[Ti] Título:Temperature effects on gene expression and morphological development of European eel, Anguilla anguilla larvae.
[So] Source:PLoS One;12(8):e0182726, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Temperature is important for optimization of rearing conditions in aquaculture, especially during the critical early life history stages of fish. Here, we experimentally investigated the impact of temperature (16, 18, 20, 22 and 24°C) on thermally induced phenotypic variability, from larval hatch to first-feeding, and the linked expression of targeted genes [heat shock proteins (hsp), growth hormone (gh) and insulin-like growth factors (igf)] associated to larval performance of European eel, Anguilla anguilla. Temperature effects on larval morphology and gene expression were investigated throughout early larval development (in real time from 0 to 18 days post hatch) and at specific developmental stages (hatch, jaw/teeth formation, and first-feeding). Results showed that hatch success, yolk utilization efficiency, survival, deformities, yolk utilization, and growth rates were all significantly affected by temperature. In real time, increasing temperature from 16 to 22°C accelerated larval development, while larval gene expression patterns (hsp70, hsp90, gh and igf-1) were delayed at cold temperatures (16°C) or accelerated at warm temperatures (20-22°C). All targeted genes (hsp70, hsp90, gh, igf-1, igf-2a, igf-2b) were differentially expressed during larval development. Moreover, expression of gh was highest at 16°C during the jaw/teeth formation, and the first-feeding developmental stages, while expression of hsp90 was highest at 22°C, suggesting thermal stress. Furthermore, 24°C was shown to be deleterious (resulting in 100% mortality), while 16°C and 22°C (~50 and 90% deformities respectively) represent the lower and upper thermal tolerance limits. In conclusion, the high survival, lowest incidence of deformities at hatch, high yolk utilization efficiency, high gh and low hsp expression, suggest 18°C as the optimal temperature for offspring of European eel. Furthermore, our results suggest that the still enigmatic early life history stages of European eel may inhabit the deeper layer of the Sargasso Sea and indicate vulnerability of this critically endangered species to increasing ocean temperature.
[Mh] Termos MeSH primário: Anguilla/crescimento & desenvolvimento
Anguilla/genética
Regulação da Expressão Gênica no Desenvolvimento
Temperatura Ambiente
[Mh] Termos MeSH secundário: Anguilla/anatomia & histologia
Animais
Gema de Ovo/metabolismo
Feminino
Hormônio do Crescimento/metabolismo
Larva/anatomia & histologia
Larva/genética
Larva/crescimento & desenvolvimento
Masculino
Reação em Cadeia da Polimerase em Tempo Real
Somatomedinas/metabolismo
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Somatomedins); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182726


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[PMID]:28724578
[Au] Autor:Miyagawa I; Nakayamada S; Nakano K; Yamagata K; Sakata K; Yamaoka K; Tanaka Y
[Ad] Endereço:First Department of Internal Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.
[Ti] Título:Induction of Regulatory T Cells and Its Regulation with Insulin-like Growth Factor/Insulin-like Growth Factor Binding Protein-4 by Human Mesenchymal Stem Cells.
[So] Source:J Immunol;199(5):1616-1625, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human mesenchymal stem cells (MSCs) are multipotent and exert anti-inflammatory effects, but the underlying mechanism remains to be elucidated. In the current study, we investigated the regulatory mechanism of regulatory T cell (Treg) induction through the growth factors released by human MSCs. Human naive CD4 T cells were stimulated with anti-CD3/28 Abs and cocultured with human MSC culture supernatant for 48 h. The proliferation and cytokine production of CD4 T cells and surface molecule expression on CD4 T cells were evaluated. The proliferation of anti-CD3/28 Abs-stimulated CD4 T cells was suppressed by the addition of human MSC culture supernatant; in addition, the production of IL-10 and IL-4 increased. The human MSC culture supernatant induced CD4 FOXP3 Tregs that expressed CD25, CTLA-4, glucocorticoid-induced TNFR-related protein, insulin-like growth factor (IGF)-1R, and IGF-2R, showing antiproliferative activity against CD4 T cells. In addition, the induction of Tregs by human MSC culture supernatant was enhanced by the addition of IGF and suppressed by the inhibition of IGF-1R. In contrast, a significant amount of IGF binding protein (IGFBP)-4, an inhibitor of IGF action, was detected in the human MSC culture supernatant. After neutralization of IGFBP-4 in the human MSC culture supernatant by anti-IGFBP-4 Ab, Treg numbers increased significantly. Thus, our results raise the possibility that human MSC actions also involve a negative-regulatory mechanism that suppresses Treg proliferation by releasing IGFBP-4. The results of this study suggest that regulation of IGF may be important for treatments using human MSCs.
[Mh] Termos MeSH primário: Tolerância Imunológica
Proteína 4 de Ligação a Fator de Crescimento Semelhante à Insulina/metabolismo
Células Mesenquimais Estromais/fisiologia
Somatomedinas/metabolismo
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Anticorpos Neutralizantes/farmacologia
Antígeno CTLA-4/metabolismo
Proliferação Celular
Células Cultivadas
Técnicas de Cocultura
Fatores de Transcrição Forkhead/metabolismo
Proteína Relacionada a TNFR Induzida por Glucocorticoide/metabolismo
Seres Humanos
Proteína 4 de Ligação a Fator de Crescimento Semelhante à Insulina/imunologia
Subunidade alfa de Receptor de Interleucina-2/metabolismo
Receptor IGF Tipo 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (CTLA-4 Antigen); 0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); 0 (Glucocorticoid-Induced TNFR-Related Protein); 0 (Insulin-Like Growth Factor Binding Protein 4); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Somatomedins); EC 2.7.10.1 (Receptor, IGF Type 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600230


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[PMID]:28528691
[Au] Autor:Pickard A; Durzynska J; McCance DJ; Barton ER
[Ad] Endereço:Centre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast, BT9 7AE, UK; Wellcome Centre for Cell Matrix Research, University of Manchester, M13 9PL, UK. Electronic address: adam.pickard@manchester.ac.uk.
[Ti] Título:The IGF axis in HPV associated cancers.
[So] Source:Mutat Res Rev Mutat Res;772:67-77, 2017 Apr - Jun.
[Is] ISSN:1388-2139
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Human papillomaviruses (HPV) infect and replicate in stratified epithelium at cutaneous and mucosal surfaces. The proliferation and maintenance of keratinocytes, the cells which make up this epithelium, are controlled by a number of growth factor receptors such as the keratinocyte growth factor receptor (KGFR, also called fibroblast growth factor receptor 2b (FGFR2b)), the epithelial growth factor receptor (EGFR) and the insulin-like growth factor receptors 1 and 2 (IGF1R and IGF2R). In this review, we will delineate the mutation, gene transcription, translation and processing of the IGF axis within HPV associated cancers. The IGFs are key for developmental and postnatal growth of almost all tissues; we explore whether this crucial axis has been hijacked by HPV.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
Neoplasias/genética
Neoplasias/virologia
Papillomaviridae/patogenicidade
Somatomedinas/genética
[Mh] Termos MeSH secundário: Proliferação Celular
Seres Humanos
Queratinócitos/citologia
Queratinócitos/virologia
Receptor do Fator de Crescimento Epidérmico/genética
Receptor do Fator de Crescimento Epidérmico/metabolismo
Receptor Tipo 2 de Fator de Crescimento de Fibroblastos/genética
Receptor Tipo 2 de Fator de Crescimento de Fibroblastos/metabolismo
Receptor IGF Tipo 2/genética
Receptor IGF Tipo 2/metabolismo
Receptores de Somatomedina/genética
Receptores de Somatomedina/metabolismo
Somatomedinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (IGF1R protein, human); 0 (Receptor, IGF Type 2); 0 (Receptors, Somatomedin); 0 (Somatomedins); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (FGFR2 protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170523
[St] Status:MEDLINE


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[PMID]:28528683
[Au] Autor:Durzynska J
[Ad] Endereço:Department of Molecular Virology, Institute of Experimental Biology, Faculty of Biology, Adam Mickiewicz University, Ul. Umultowska 89, 61-614 Poznan, Poland. Electronic address: juliadur@amu.edu.pl.
[Ti] Título:Special Issue " HPV and IGF axis in carcinogenesis".
[So] Source:Mutat Res Rev Mutat Res;772:1-2, 2017 Apr - Jun.
[Is] ISSN:1388-2139
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Mh] Termos MeSH primário: Carcinogênese/genética
Neoplasias/virologia
Papillomaviridae/genética
Somatomedinas/genética
[Mh] Termos MeSH secundário: Carcinogênese/patologia
Epigênese Genética
Seres Humanos
Publicações Periódicas como Assunto
Somatomedinas/metabolismo
[Pt] Tipo de publicação:EDITORIAL; INTRODUCTORY JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Somatomedins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170523
[St] Status:MEDLINE


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[PMID]:28431247
[Au] Autor:Tawo R; Pokrzywa W; Kevei É; Akyuz ME; Balaji V; Adrian S; Höhfeld J; Hoppe T
[Ad] Endereço:Institute for Cell Biology, University of Bonn, Ulrich-Haberland Str. 61a, 53121 Bonn, Germany.
[Ti] Título:The Ubiquitin Ligase CHIP Integrates Proteostasis and Aging by Regulation of Insulin Receptor Turnover.
[So] Source:Cell;169(3):470-482.e13, 2017 Apr 20.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aging is attended by a progressive decline in protein homeostasis (proteostasis), aggravating the risk for protein aggregation diseases. To understand the coordination between proteome imbalance and longevity, we addressed the mechanistic role of the quality-control ubiquitin ligase CHIP, which is a key regulator of proteostasis. We observed that CHIP deficiency leads to increased levels of the insulin receptor (INSR) and reduced lifespan of worms and flies. The membrane-bound INSR regulates the insulin and IGF1 signaling (IIS) pathway and thereby defines metabolism and aging. INSR is a direct target of CHIP, which triggers receptor monoubiquitylation and endocytic-lysosomal turnover to promote longevity. However, upon proteotoxic stress conditions and during aging, CHIP is recruited toward disposal of misfolded proteins, reducing its capacity to degrade the INSR. Our study indicates a competitive relationship between proteostasis and longevity regulation through CHIP-assisted proteolysis, providing a mechanistic concept for understanding the impact of proteome imbalance on aging.
[Mh] Termos MeSH primário: Envelhecimento
Antígenos CD/metabolismo
Receptor de Insulina/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Animais
Caenorhabditis elegans
Drosophila melanogaster
Endocitose
Seres Humanos
Longevidade
Lisossomos/metabolismo
Proteólise
Proteoma
Transdução de Sinais
Somatomedinas
Ubiquitinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Proteome); 0 (Somatomedins); EC 2.3.2.27 (STUB1 protein, human); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.10.1 (INSR protein, human); EC 2.7.10.1 (Receptor, Insulin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171001
[Lr] Data última revisão:
171001
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170422
[St] Status:MEDLINE


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[PMID]:28369940
[Au] Autor:Schirripa M; Zhang W; Heinemann V; Cao S; Okazaki S; Yang D; Loupakis F; Berger MD; Ning Y; Miyamoto Y; Suenaga M; Gopez RF; West JD; Hanna D; Barzi A; Falcone A; Stintzing S; Lenz HJ
[Ad] Endereço:Medical Oncology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, 90033.
[Ti] Título:Single nucleotide polymorphisms in the IGF-IRS pathway are associated with outcome in mCRC patients enrolled in the FIRE-3 trial.
[So] Source:Int J Cancer;141(2):383-392, 2017 Jul 15.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Insulin-like growth factor (IGF)/IGF-receptor pathway with its scaffolding proteins Insulin Receptor Substrate (IRS)1 and IRS2 are crucial regulators of metabolism and progression in metastatic colorectal cancer (mCRC). The goal of the study was the identification of predictive and prognostic markers among IRS1, IRS2, IGF1 and IGF-1R SNPs in mCRC patients enrolled in the FIRE-3 trial. Four SNPs of IRS (IRS1 rs1801278, rs1801123; IRS2 rs1805097, rs2289046) and four SNPs of IGF1-IGFR1 (rs6214, rs6220, rs2946834, rs2016347) were analyzed by PCR/direct-sequencing in the FIRE-3 trial. The relation of SNPs with PFS and OS was evaluated through Kaplan-Meier method and log-rank test in the overall population and in subgroup according to RAS status and treatment arm. In the overall population IRS1 rs1801123 C/- carriers (N= 105) achieved significantly worse OS compared to T/T (N = 464) in univariate (HR = 1.32 [95%CI 1.03-1.70], p = 0.029) and in multivariable. Similar results were observed among RAS wild type. Patients with IGF1 rs2946834 T/- variant (N= 280) achieved improved PFS compared to C/C (N = 257) in univariate (HR = 0.77 [95%CI 0.64-0.92], p = 0.004) and in multivariable. In the RAS wild-type subgroup IGF1 rs2946834 T/- carriers showed better PFS and OS compared to C/C (univariate HR for PFS = 0.65 [95%CI 0.51-0.81], p < 0.001; multivariable HR for PFS = 0.63 [95%CI 0.50-0.81], p < 0.001). IRS1 rs1801123 SNP was identified as a new prognostic marker for mCRC. IGF1 rs2946834 was confirmed as prognostic factor in the overall population and in RAS wild type patients. Our findings underline the importance of IGF downstream signaling pathway in RAS wild-type mCRC patient.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Neoplasias Colorretais/tratamento farmacológico
Proteínas Substratos do Receptor de Insulina/genética
Polimorfismo de Nucleotídeo Único
Somatomedinas/genética
[Mh] Termos MeSH secundário: Bevacizumab/uso terapêutico
Camptotecina/análogos & derivados
Camptotecina/uso terapêutico
Cetuximab/uso terapêutico
Neoplasias Colorretais/genética
Feminino
Fluoruracila/uso terapêutico
Estudos de Associação Genética/métodos
Seres Humanos
Leucovorina/uso terapêutico
Masculino
Metástase Neoplásica
Prognóstico
Análise de Sequência de DNA
Transdução de Sinais
Análise de Sobrevida
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Insulin Receptor Substrate Proteins); 0 (Somatomedins); 2S9ZZM9Q9V (Bevacizumab); PQX0D8J21J (Cetuximab); Q573I9DVLP (Leucovorin); U3P01618RT (Fluorouracil); XT3Z54Z28A (Camptothecin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.30715



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