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1.
Anticancer Res ; 39(10): 5261-5284, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31570422

RESUMO

Natural products (NPs) are useful sources of bioactive compounds and play important roles in the development and discovery of new drugs for diverse human diseases. Most natural products originate from terrestrial species, but diverse marine organisms are another source of new agents for cancer therapy. Natural products derived from marine organisms show diverse pharmacological activities via bioactive secondary metabolites. They regulate biological activities, such as cell proliferation, cell viability, induction of ROS production, ER stress, and apoptosis via modulation of cellular mechanisms in many cancers. Many natural products isolated from marine species require further study to elucidate the efficacy of their biological activity and anticancer effects. In this review, we summarize the biological properties and anticancer effects of diverse natural products extracted from marine organisms and their roles in tumor therapy.


Assuntos
Antineoplásicos/farmacologia , Antineoplásicos/uso terapêutico , Organismos Aquáticos/química , Produtos Biológicos/farmacologia , Produtos Biológicos/uso terapêutico , Neoplasias/tratamento farmacológico , Animais , Humanos
2.
Lancet ; 394(10200): 793-804, 2019 08 31.
Artigo em Inglês | MEDLINE | ID: mdl-31478503

RESUMO

Antibody-drug conjugates (ADCs) are immunoconjugates comprised of a monoclonal antibody tethered to a cytotoxic drug (known as the payload) via a chemical linker. The ADC is designed to selectively deliver the ultratoxic payload directly to the target cancer cells. To date, five ADCs have received market approval and over 100 are being investigated in various stages of clinical development. In this Therapeutics paper, we review recent clinical experience with the approved ADCs and other promising late-stage candidates on the horizon, following an overview of the biology and chemistry of ADCs and how the individual components of an ADC (antibody [or target], linker and conjugation chemistry, and cytotoxic payload) influence its activity. We briefly discuss opportunities for enhancing ADC efficacy, drug resistance, and future perspectives for this novel antibody-based molecular platform, which has great potential to make a paradigm shift in cancer chemotherapy.


Assuntos
Anticorpos Monoclonais , Antineoplásicos Imunológicos , Imunoconjugados , Neoplasias/tratamento farmacológico , Anticorpos Monoclonais/administração & dosagem , Anticorpos Monoclonais/efeitos adversos , Anticorpos Monoclonais/farmacocinética , Anticorpos Monoclonais/farmacologia , Antineoplásicos Imunológicos/administração & dosagem , Antineoplásicos Imunológicos/efeitos adversos , Antineoplásicos Imunológicos/farmacocinética , Antineoplásicos Imunológicos/farmacologia , Ensaios Clínicos como Assunto , Humanos , Imunoconjugados/administração & dosagem , Imunoconjugados/efeitos adversos , Imunoconjugados/farmacocinética , Imunoconjugados/farmacologia
3.
Adv Exp Med Biol ; 1167: 237-248, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31520359

RESUMO

In recent years, there has been growing interest in using Drosophila for drug discovery as it provides a unique opportunity to screen small molecules against complex disease phenotypes in a whole animal setting. Furthermore, gene-compound interaction experiments that combine compound feeding with complex genetic manipulations enable exploration of compound mechanisms of response and resistance to an extent that is difficult to achieve in other experimental models. Here, I discuss how compound screening and testing approaches reported in Drosophila fit into the current cancer drug discovery pipeline. I then propose a framework for a Drosophila-based cancer drug discovery strategy which would allow the Drosophila research community to effectively leverage the power of Drosophila to identify candidate therapeutics and push our discoveries into the clinic.


Assuntos
Antineoplásicos/farmacologia , Drosophila , Descoberta de Drogas , Neoplasias/tratamento farmacológico , Animais , Modelos Animais de Doenças , Técnicas Genéticas , Fenótipo
4.
J Cancer Res Clin Oncol ; 145(10): 2413-2422, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31492983

RESUMO

PURPOSE: Polo-like kinase 4 (PLK4) is a serine/threonine protein kinase that regulates centriole duplication. PLK4 deregulation causes centrosome number abnormalities, mitotic defects, chromosomal instability and, consequently, tumorigenesis. Therefore, PLK4 has emerged as a therapeutic target for the treatment of multiple cancers. In this review, we summarize the critical role of centrosome amplification and PLK4 in cancer. We also highlight recent advances in the development of PLK4 inhibitors and discuss potential combination therapies for cancer. METHODS: The relevant literature from PubMed is reviewed in this article. The ClinicalTrials.gov database was searched for clinical trials related to the specific topic. RESULTS: PLK4 is aberrantly expressed in multiple cancers and has prognostic value. Targeting PLK4 with inhibitors suppresses tumor growth in vitro and in vivo. CONCLUSIONS: PLK4 plays an important role in centrosome amplification and tumor progression. PLK4 inhibitors used alone or in combination with other drugs have shown significant anticancer efficacy, suggesting a potential therapeutic strategy for cancer. The results of relevant clinical trials await evaluation.


Assuntos
Biomarcadores Tumorais , Neoplasias/etiologia , Neoplasias/metabolismo , Proteínas Serina-Treonina Quinases/metabolismo , Animais , Antineoplásicos/farmacologia , Antineoplásicos/uso terapêutico , Transformação Celular Neoplásica/genética , Transformação Celular Neoplásica/metabolismo , Centrossomo/metabolismo , Regulação Neoplásica da Expressão Gênica , Humanos , Terapia de Alvo Molecular , Metástase Neoplásica , Neoplasias/tratamento farmacológico , Neoplasias/patologia , Especificidade de Órgãos/genética , Inibidores de Proteínas Quinases/farmacologia , Inibidores de Proteínas Quinases/uso terapêutico , Proteínas Serina-Treonina Quinases/antagonistas & inibidores , Proteínas Serina-Treonina Quinases/química , Proteínas Serina-Treonina Quinases/genética , Relação Estrutura-Atividade , Proteína Supressora de Tumor p53/genética , Proteína Supressora de Tumor p53/metabolismo
5.
J Cancer Res Clin Oncol ; 145(10): 2625-2631, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31492984

RESUMO

PURPOSE: Immune checkpoint inhibitors (ICIs) are effective against a wide variety of cancers. However, they also induce a plethora of unique immune-related adverse events (irAEs). Since for many organ systems symptoms can be unspecific, differential diagnosis with progression of disease or infection may be difficult. C-reactive protein (CRP) has been suggested as a marker for infection. The purpose of this study was to evaluate the diagnostic value of CRP in differentiating infectious causes from autoimmune side effects induced by ICIs. METHODS: In order to investigate the role of CRP in irAEs, we screened our patient data base. Only events with full infectious workup were included. In total 88 events of irAEs in 37 melanoma patients were analyzed. CRP levels before and during irAEs were evaluated. Statistical analyses were conducted using the Chi-square test for categorical variables. RESULTS: At the onset of irAE, CRP rose in 93% of cases to a mean of 52.7 mg/L (CI 35.1-70.3) from 8.4 mg/L at baseline (normal < 5 mg/L) (P < 0.0001). Other causes of CRP elevation including infectious diseases were excluded, and procalcitonin (PCT) levels were normal in 92% of events. Importantly, in 42% of cases CRP elevations preceded clinical symptoms. CONCLUSION: CRP elevation can predict the onset of irAEs in patients treated with ICIs in the absence of infectious disease.


Assuntos
Antineoplásicos Imunológicos/farmacologia , Biomarcadores , Proteína C-Reativa , Imunomodulação , Adulto , Antineoplásicos Imunológicos/uso terapêutico , Biomarcadores Tumorais , Feminino , Humanos , Imunomodulação/efeitos dos fármacos , Masculino , Pessoa de Meia-Idade , Gradação de Tumores , Estadiamento de Neoplasias , Neoplasias/diagnóstico , Neoplasias/tratamento farmacológico , Neoplasias/imunologia , Neoplasias/metabolismo , Adulto Jovem
6.
Bull Cancer ; 106(10): 847-859, 2019 Oct.
Artigo em Francês | MEDLINE | ID: mdl-31521255

RESUMO

INTRODUCTION: The Cancer Observatory, from the OMEDITs (Observatory for Medicines and Medical Devices and Treatment Innovations) of Bretagne and Pays de la Loire areas has conducted a survey aiming to know and map the current practices of management of patients by Oral Anti-cancer Drug (OAD) in inter-region. METHODS: Forty eight cancer centers received by e-mail in July and October 2016 a questionnaire concerning the management of OADs : from prescription by the specialist of oncology, to the intervention of the pharmacist (analysis and pharmaceutical consulting), to follow-up by nurse, as well as the financing of this activity and the feelings of the actors about this organizational set up. RESULTS: Fifty-seven professionals from 31 centers, including the most important ones, responded to the survey. As a result, half of the establishments carry out a pharmaceutical analysis for some or all of the OAD prescriptions and only 30% carry out a pharmaceutical consulting. The nurse consultation is, on the other hand, more largely implanted (74% of the centers) as well as the telephone follow-up (6%). More than 90% of professionals believe that the organizational set up could be improved and more secure by, at least, the stronger involvement of pharmacists, the development of tools for nurse (for monitoring, therapeutic education…) and by improving the city-hospital link. CONCLUSION: This survey shows the variability in the management of patients under OAD because of the lack of resources to ensure the fairness and sustainability of the organizational set up. The hospital/city link could still be optimized to secure patient care.


Assuntos
Antineoplásicos/administração & dosagem , Pesquisas sobre Serviços de Saúde/estatística & dados numéricos , Neoplasias/tratamento farmacológico , Administração Oral , Institutos de Câncer/estatística & dados numéricos , Continuidade da Assistência ao Paciente/estatística & dados numéricos , Prescrições de Medicamentos , França , Humanos , Papel do Profissional de Enfermagem , Objetivos Organizacionais , Satisfação do Paciente , Farmacêuticos , Padrões de Prática em Enfermagem/estatística & dados numéricos , Telefone
8.
Tumour Biol ; 41(9): 1010428319873749, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31496424

RESUMO

Differentiation therapy is directed to the self-renewing cancer stem cells, as well as their progeny transit amplifying cells, to force them to mature to terminal differentiation. Differentiation therapy is effective in treatment of neuroblastomas and myeloid leukemias. Checkpoint inhibition therapy removes blocks to cancer reactive T-killer cells and allows them to react to malignant cells and limit the growth of cancer. The percentage of patients with a given cancer that responds to either therapy is less than hoped for, and the duration of response is variable. Multiplying the response rate (percentage of patients responding to therapy) by the duration of response may be used to derive a survival score for patients treated with differentiation therapy or checkpoint inhibition. By this criterion, differentiation therapy gives better survival scores than checkpoint inhibition. Yet, checkpoint inhibition is considered a great success, mostly because it may be applied to many different types of cancer, and differentiation therapy is considered relatively ineffective because it is limited to a few specific cancers. On the other hand, the cost of checkpoint inhibition treatment is 10-20 times more per patient than that of differentiation therapy. Hopefully, future combined treatments and advances in both approaches will increase the effectiveness of these cancer treatments.


Assuntos
Antineoplásicos/uso terapêutico , Sobreviventes de Câncer/estatística & dados numéricos , Pontos de Checagem do Ciclo Celular/efeitos dos fármacos , Diferenciação Celular/efeitos dos fármacos , Neoplasias/mortalidade , Células-Tronco Neoplásicas/efeitos dos fármacos , Linfócitos T/efeitos dos fármacos , Humanos , Neoplasias/tratamento farmacológico , Neoplasias/patologia , Prognóstico , Taxa de Sobrevida
9.
Chem Biol Interact ; 312: 108814, 2019 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-31509734

RESUMO

Nanotechnology is a growing science that may provide several new applications for medicine, food preservation, diagnostic technologies, and sanitation. Despite its beneficial applications, there are several questions related to the safety of nanomaterials for human use. The development of nanotechnology is associated with some concerns because of the increased risk of carcinogenesis following exposure to nanomaterials. The increased levels of reactive oxygen species (ROS) that are due to exposure to nanoparticles (NPs) are primarily responsible for the genotoxicity of metal NPs. Not all, but most metal NPs are able to directly produce free radicals through the release of metal ions and through interactions with water molecules. Furthermore, the increased production of free radicals and the cell death caused by metal NPs can stimulate reduction/oxidation (redox) reactions, leading to the continuous endogenous production of ROS in a positive feedback loop. The overexpression of inflammatory mediators, such as NF-kB and STATs, the mitochondrial malfunction and the increased intracellular calcium levels mediate the chronic oxidative stress that occurs after exposure to metal NPs. In this paper, we review the genotoxicity of different types of metal NPs and the redox mechanisms that amplify the toxicity of these NPs.


Assuntos
Nanopartículas Metálicas/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Animais , Cálcio/metabolismo , Dano ao DNA/efeitos dos fármacos , Aditivos Alimentares/química , Humanos , Nanopartículas Metálicas/química , Nanopartículas Metálicas/uso terapêutico , Neoplasias/tratamento farmacológico , Oxirredução , Espécies Reativas de Oxigênio/metabolismo
11.
Anticancer Res ; 39(9): 4687-4698, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31519568

RESUMO

BACKGROUND/AIM: Propagermanium (PG) inhibits the CCL2/CCR2 axis, and has been shown to function as an immune modulator. This study investigated its anti-tumor mechanism in patients with refractory cancers. MATERIALS AND METHODS: Five healthy volunteers and 23 patients with refractory oral (n=8) or gastric (n=15) cancer received PG (30 mg/day). We performed flow cytometry (FCM) of peripheral blood mononuclear cells and in vitro killing assays. RESULTS: FCM revealed that CD16+/CD56Dim NK cells (i.e., mature, cytolytic subset) increased, and the apoptosis induction rate of cancer cells increased after PG administration. Among gastric cancer patients, median OS was 172.0 days. Two patients showed complete remission of lung or liver metastasis. Survival of patients with oral cancer also tended to be prolonged. CONCLUSION: PG induces NK cell maturation, and may potentiate anti-tumor activity.


Assuntos
Antineoplásicos/farmacologia , Diferenciação Celular/efeitos dos fármacos , Diferenciação Celular/imunologia , Células Matadoras Naturais/efeitos dos fármacos , Células Matadoras Naturais/imunologia , Neoplasias/imunologia , Neoplasias/mortalidade , Compostos Organometálicos/farmacologia , Linhagem Celular Tumoral , Resistencia a Medicamentos Antineoplásicos , Humanos , Estimativa de Kaplan-Meier , Leucócitos Mononucleares/efeitos dos fármacos , Leucócitos Mononucleares/imunologia , Leucócitos Mononucleares/metabolismo , Subpopulações de Linfócitos/imunologia , Subpopulações de Linfócitos/metabolismo , Neoplasias/diagnóstico , Neoplasias/tratamento farmacológico , Tomografia Computadorizada por Raios X
12.
BMJ ; 366: l5221, 2019 09 18.
Artigo em Inglês | MEDLINE | ID: mdl-31533922

RESUMO

OBJECTIVE: To examine the design characteristics, risk of bias, and reporting adequacy of pivotal randomised controlled trials of cancer drugs approved by the European Medicines Agency (EMA). DESIGN: Cross sectional analysis. SETTING: European regulatory documents, clinical trial registry records, protocols, journal publications, and supplementary appendices. ELIGIBILITY CRITERIA: Pivotal randomised controlled trials of new cancer drugs approved by the EMA between 2014 and 2016. MAIN OUTCOME MEASURES: Study design characteristics (randomisation, comparators, and endpoints); risk of bias using the revised Cochrane tool (bias arising from the randomisation process, deviations from intended interventions, missing outcome data, measurement of the outcome, and selection of the reported result); and reporting adequacy (completeness and consistency of information in trial protocols, publications, supplementary appendices, clinical trial registry records, and regulatory documents). RESULTS: Between 2014 and 2016, the EMA approved 32 new cancer drugs on the basis of 54 pivotal studies. Of these, 41 (76%) were randomised controlled trials and 13 (24%) were either non-randomised studies or single arm studies. 39/41 randomised controlled trials had available publications and were included in our study. Only 10 randomised controlled trials (26%) measured overall survival as either a primary or coprimary endpoint, with the remaining trials evaluating surrogate measures such as progression free survival and response rates. Overall, 19 randomised controlled trials (49%) were judged to be at high risk of bias for their primary outcome. Concerns about missing outcome data (n=10) and measurement of the outcome (n=7) were the most common domains leading to high risk of bias judgments. Fewer randomised controlled trials that evaluated overall survival as the primary endpoint were at high risk of bias than those that evaluated surrogate efficacy endpoints (2/10 (20%) v 16/29 (55%), respectively). When information available in regulatory documents and the scientific literature was considered separately, overall risk of bias judgments differed for eight randomised controlled trials (21%), which reflects reporting inadequacies in both sources of information. Regulators identified additional deficits beyond the domains captured in risk of bias assessments for 10 drugs (31%). These deficits included magnitude of clinical benefit, inappropriate comparators, and non-preferred study endpoints, which were not disclosed as limitations in scientific publications. CONCLUSIONS: Most pivotal studies forming the basis of EMA approval of new cancer drugs between 2014 and 2016 were randomised controlled trials. However, almost half of these were judged to be at high risk of bias based on their design, conduct, or analysis, some of which might be unavoidable because of the complexity of cancer trials. Regulatory documents and the scientific literature had gaps in their reporting. Journal publications did not acknowledge the key limitations of the available evidence identified in regulatory documents.


Assuntos
Antineoplásicos/uso terapêutico , Aprovação de Drogas/métodos , Neoplasias/tratamento farmacológico , Ensaios Clínicos Controlados Aleatórios como Assunto/métodos , Viés , Estudos Transversais , Controle de Medicamentos e Entorpecentes , Humanos , Projetos de Pesquisa , Relatório de Pesquisa
13.
Adv Exp Med Biol ; 1152: 173-215, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31456184

RESUMO

Cancer is the result of a cell's acquisition of a variety of biological capabilities or 'hallmarks' as outlined by Hanahan and Weinberg. These include sustained proliferative signalling, the ability to evade growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and the ability to invade other tissue and metastasize. More recently, the ability to escape immune destruction has been recognized as another important hallmark of tumours. It is suggested that genome instability and inflammation accelerates the acquisition of a variety of the above hallmarks. Inflammation, is a product of the body's response to tissue damage or pathogen invasion. It is required for tissue repair and host defense, but prolonged inflammation can often be the cause for disease. In a cancer patient, it is often unclear whether inflammation plays a protective or deleterious role in disease progression. Chemotherapy drugs can suppress tumour growth but also induce pathways in tumour cells that have been shown experimentally to support tumour progression or, in other cases, encourage an anti-tumour immune response. Thus, with the goal of better understanding the context under which each of these possible outcomes occurs, recent progress exploring chemotherapy-induced inflammatory cytokine production and the effects of cytokines on drug efficacy in the tumour microenvironment will be reviewed. The implications of chemotherapy on host and tumour cytokine pathways and their effect on the treatment of cancer patients will also be discussed.


Assuntos
Citocinas/metabolismo , Neoplasias/tratamento farmacológico , Neoplasias/metabolismo , Microambiente Tumoral , Humanos , Neovascularização Patológica , Transdução de Sinais
14.
J Cancer Res Clin Oncol ; 145(9): 2303-2311, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31396700

RESUMO

BACKGROUND: Since 1997, several monoclonal antibodies (mAbs) targeting the same receptor or its ligand have been approved for use in oncology. However, no studies have summarized head-to-head trials of these mAbs. METHODS: Systematic search of the biomedical literature and ClinicalTrials.gov for randomized studies comparing mAbs targeting the same receptor or its ligand that have been completed and published, completed and unpublished, or ongoing. We extracted trial characteristics including phase, indication, enrollment or target enrollment, randomization, primary endpoint and sponsor. RESULTS: Twenty-two approved cancer mAbs had at least one other approved mAb targeting the same receptor or its ligand, totaling 41 different oncology indications. These include 5 anti-CD20 mAbs, 5 anti-PD1/PDL1 mAbs, 4 anti-HER2 mAbs, 3 anti-EGFR mAbs, 3 anti-VEGF mAbs and 2 anti-IL6/IL6R mAbs. Seventeen were completed and published and 14 were unpublished or ongoing trials. The completed and published trials enrolled 11,373 patients and tested 13 mAbs (13/22, 59%). Additionally, 13 (76%) contained drugs manufactured by the same company and 13 (76%) reached conclusions felt to be favorable to the sponsor. Of the 14 ongoing/completed unpublished trials, there is a total target enrollment of 3404 patients with 9 mAbs tested. Of these, 86% (12/14) are testing mAbs manufactured by the same company and 71% (10/14) are sponsored by the company that made the drug being tested. CONCLUSIONS: Most trials test drugs manufactured or sponsored by the same company. An overview of clinical trials agenda may lead to more uniform testing, helping clinicians make better evidence-informed prescribing decisions.


Assuntos
Anticorpos Monoclonais/uso terapêutico , Antineoplásicos Imunológicos/uso terapêutico , Ensaios Clínicos como Assunto/estatística & dados numéricos , Neoplasias/tratamento farmacológico , Ensaios Clínicos como Assunto/métodos , Aprovação de Drogas , Humanos , Neoplasias/epidemiologia , Estados Unidos/epidemiologia , United States Food and Drug Administration
16.
Gene ; 715: 144005, 2019 Oct 05.
Artigo em Inglês | MEDLINE | ID: mdl-31376410

RESUMO

Members of the highly conserved pleiotropic CK1 family of serine/threonine-specific kinases are tightly regulated in the cell and play crucial regulatory roles in multiple cellular processes from protozoa to human. Since their dysregulation as well as mutations within their coding regions contribute to the development of various different pathologies, including cancer and neurodegenerative diseases, they have become interesting new drug targets within the last decade. However, to develop optimized CK1 isoform-specific therapeutics in personalized therapy concepts, a detailed knowledge of the regulation and functions of the different CK1 isoforms, their various splice variants and orthologs is mandatory. In this review we will focus on the stress-induced CK1 isoform delta (CK1δ), thereby addressing its regulation, physiological functions, the consequences of its deregulation for the development and progression of diseases, and its potential as therapeutic drug target.


Assuntos
Caseína Quinase Idelta/química , Caseína Quinase Idelta/metabolismo , Proteínas de Neoplasias/metabolismo , Neoplasias/enzimologia , Transdução de Sinais , Animais , Caseína Quinase Idelta/antagonistas & inibidores , Caseína Quinase Idelta/genética , Sistemas de Liberação de Medicamentos/métodos , Humanos , Isoenzimas/antagonistas & inibidores , Isoenzimas/química , Isoenzimas/genética , Isoenzimas/metabolismo , Proteínas de Neoplasias/antagonistas & inibidores , Proteínas de Neoplasias/genética , Neoplasias/tratamento farmacológico , Neoplasias/genética , Neoplasias/patologia , Relação Estrutura-Atividade
17.
Anticancer Res ; 39(8): 4455-4462, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31366544

RESUMO

BACKGROUND/AIM: Platinum-based chemotherapy often fails due to its severe adverse effects. The aim of this study was to examine the adverse effects profile and efficacy of dicycloplatin and compare them to those of cisplatin and carboplatin. MATERIALS AND METHODS: Cystoscopy surveillance of the first American cancer patient treated with dicycloplatin was performed quarterly. In vitro and in vivo studies were conducted using immunoblotting and flow cytometry to assess immune status of spleen and bone marrow of mice treated with dicycloplatin, cisplatin and carboplatin. RESULTS: The American patient did not suffer clinically significant myelosuppression; dicycloplatin has sustained remission in this patient to date. Experimental studies showed that dicycloplatin is less toxic to bone marrow and spleen of mice than cisplatin and carboplatin. CONCLUSION: Dicycloplatin is a promising drug in cancer chemotherapy with less aggressive side-effects than those typically associated with cisplatin and carboplatin. This is an important therapeutic advantage in cancer chemotherapy. Clinical investigation of dicycloplatin as an alternative to cisplatin or carboplatin is warranted.


Assuntos
Medula Óssea/efeitos dos fármacos , Glutamatos/administração & dosagem , Neoplasias/tratamento farmacológico , Compostos Organoplatínicos/administração & dosagem , Baço/efeitos dos fármacos , Animais , Medula Óssea/patologia , Carboplatina/administração & dosagem , Carboplatina/efeitos adversos , Cisplatino/administração & dosagem , Cisplatino/efeitos adversos , Cistoscopia , Modelos Animais de Doenças , Combinação de Medicamentos , Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos , Feminino , Glutamatos/efeitos adversos , Humanos , Camundongos , Compostos Organoplatínicos/efeitos adversos , Baço/patologia
18.
Anticancer Res ; 39(8): 4475-4478, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31366547

RESUMO

Chronic inflammation is involved in the development of cancer, lifestyle-related diseases, and autoimmune diseases. It also influences the severity of these diseases. Macrophages that accumulate in tumor tissues and adipose tissues of obesity have been shown to increase expression of inflammatory cytokines, thereby inducing inflammatory changes in these tissues. The macrophage phenotype is believed to be important in mediating inflammatory changes in tissues. Recently, monocytes/macrophages activated with low-dose lipopolysaccharide (LPS) were demonstrated to suppress increased expression of monocyte chemotactic protein (MCP)-1 and inflammatory cytokines (interleukin (IL)-1 ß, IL-8, and tumor necrosis factor (TNF)-α). By suppressing the increased expression of chemotaxis-related and inflammation-related factors, monocytes/macrophages activated with low-dose LPS are considered to suppress the migration of macrophages into tissues and to regulate inflammatory changes in these tissues, respectively. The effects of macrophages activated with low-dose LPS were different from those of macrophages activated with high-dose LPS. In this review, we discuss the usefulness of monocytes/macrophages activation by low-dose LPS.


Assuntos
Inflamação/tratamento farmacológico , Lipopolissacarídeos/uso terapêutico , Neoplasias/tratamento farmacológico , Obesidade/genética , Tecido Adiposo/metabolismo , Tecido Adiposo/patologia , Quimiocina CCL2/genética , Relação Dose-Resposta a Droga , Regulação da Expressão Gênica/efeitos dos fármacos , Humanos , Inflamação/genética , Interleucina-1beta/genética , Interleucina-8/genética , Macrófagos/efeitos dos fármacos , Monócitos/efeitos dos fármacos , Neoplasias/genética , Obesidade/patologia , Fator de Necrose Tumoral alfa/genética
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