Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 39
Filtrar
Mais filtros

Base de dados
País/Região como assunto
Tipo de documento
Intervalo de ano de publicação
1.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao ; 45(4): 689-694, 2023 Aug.
Artigo em Zh | MEDLINE | ID: mdl-37654151

RESUMO

Cold agglutinins(CA),autoantibodies against the antigen I or i on the surface of red blood cells,are mainly of IgM class,and the majority have κ light chains.They can lead to red blood cell agglutination at decreased body temperature and are usually associated with infections,drug reactions,autoimmune diseases,and hematological malignancies.However,solid tumors with CA are rare.We reported two cases of CA in the peripheral blood of patients with solid tumors.Peripheral complete blood cell count of the patients at admission showed reduced erythrocyte count and hematocrit,mismatching between erythrocyte count and hemoglobin,abnormally elevated levels of mean corpuscular hemoglobin and mean cell hemoglobin concentration.Peripheral blood smear showed erythrocyte aggregation.After the sample was preheated at 37 ℃ for 30 min,the reversibility of red blood cell aggregation was observed,and the erythrocyte parameters were corrected.


Assuntos
Autoanticorpos , Neoplasias da Mama , Neoplasias Ovarianas , Humanos , Autoanticorpos/isolamento & purificação , Feminino , Neoplasias da Mama/imunologia , Neoplasias Ovarianas/imunologia
2.
J Clin Lab Anal ; 32(3)2018 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-28643351

RESUMO

INTRODUCTION: Sigma metrics were applied to evaluate the performance of 20 routine chemistry assays, and individual quality control criteria were established based on the sigma values of different assays. METHODS: Precisions were expressed as the average coefficient variations (CVs) of long-term two-level chemistry controls. The biases of the 20 assays were obtained from the results of trueness programs organized by National Center for Clinical Laboratories (NCCL, China) in 2016. Four different allowable total error (TEa) targets were chosen from biological variation (minimum, desirable, optimal), Clinical Laboratory Improvements Amendments (CLIA, US), Analytical Quality Specification for Routine Analytes in Clinical Chemistry (WS/T 403-2012, China) and the National Cholesterol Education Program (NECP). RESULTS: The sigma values from different TEa targets varied. The TEa targets for ALT, AMY, Ca, CHOL, CK, Crea, GGT, K, LDH, Mg, Na, TG, TP, UA and Urea were chosen from WS/T 403-2012; the targets for ALP, AST and GLU were chosen from CLIA; the target for K was chosen from desirable biological variation; and the targets for HDL and LDL were chosen from the NECP. Individual quality criteria were established based on different sigma values. CONCLUSIONS: Sigma metrics are an optimal tool to evaluate the performance of different assays. An assay with a high value could use a simple internal quality control rule, while an assay with a low value should be monitored strictly.


Assuntos
Testes de Química Clínica/normas , Controle de Qualidade , Humanos , Modelos Estatísticos , Reprodutibilidade dos Testes
3.
Histopathology ; 64(5): 713-21, 2014 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-24117943

RESUMO

AIMS: In order to determine whether the expression of tumour-associated carbohydrate antigens (Tn/sTn) and a representative inflammation marker, nuclear factor-κB (NF-κB), is associated with the invasiveness of oral squamous cell carcinoma (OSCC), this study has attempted to investigate the correlation of the aforementioned markers with the well-established invasive pattern grading score (IPGS) and clinicopathological parameters. METHODS AND RESULTS: Specimens from 143 OSCC patients with classified clinicopathological parameters and IPGS were stained immunohistochemically using anti-Tn, sTn and NF-κB antibodies. Our results showed that the expression of both Tn and NF-κB was correlated positively with staging (P = 0.036; P = 0.015), recurrence (P < 0.001; P < 0.001) and distant metastasis (P = 0.005; P = 0.009), as well as with IPGS, while the expression of sTn was correlated inversely. In addition, poor survival was associated with overexpression of Tn and NF-κB but not with expression of sTn. CONCLUSIONS: Our results indicate that a reciprocal relationship between Tn and sTn expression may serve as a reliable indicator for OSCC prognostic evaluation. In addition, expression of Tn rather than sTn may play an important role in deeply invasive OSCC via regulation of NF-κB signalling.


Assuntos
Antígenos Glicosídicos Associados a Tumores/metabolismo , Carcinoma de Células Escamosas/metabolismo , Carcinoma de Células Escamosas/patologia , Neoplasias Bucais/metabolismo , Neoplasias Bucais/patologia , NF-kappa B/metabolismo , Feminino , Humanos , Imuno-Histoquímica , Estimativa de Kaplan-Meier , Masculino , Pessoa de Meia-Idade , Invasividade Neoplásica , Prognóstico , Transdução de Sinais
4.
J Pathol ; 231(2): 180-9, 2013 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-23775566

RESUMO

Head and neck squamous cell carcinoma (HNSCC) is one of the leading causes of cancer-related death worldwide. The prognosis of HNSCC is usually poor because of its propensity for extensive invasion, local recurrence and frequent regional lymph node metastasis, even at initial diagnosis. Carcinoma-associated fibroblasts (CAFs), a major type of tumour-surrounding stromal cell, generate mediators through which they interact with tumours and contribute to cancer progression. The orchestration between CAFs and cancer cells is complex. Despite recent studies demonstrating the paracrine effect of stromal cells in the tumour microenvironment on initiation and progression of cancer cells, the major mediator related to CAFs and its underlying mechanism remain unknown. In the present study, we used organotypic culture to investigate CAFs that promote aggressive behaviour of HNSCC cells. Using microarray analysis, we detected abundant expression of interleukin-33 (IL-33) in CAFs and identified IL-33 as a critical mediator in CAF-induced invasiveness. Counteracting IL-33 activity diminished the aggressive phenotype of cancer cells induced by CAFs. Administration of IL-33 promoted cancer cell migration and invasion through induction of epithelial-to-mesenchymal transdifferentiation and increased IL-33 gene expression in cancer cells. In 40 patients with HNSCC, IL-33 expression in CAFs correlated with IL-33 expression in cancer cells. Most cases with a low invasion pattern grading score (IPGS) showed low or no expression of IL-33, whereas most HNSCC cases with high IPGS displayed over-expression of IL-33 in CAFs and cancer cells. High IL-33 expression associated with poor prognosis in terms of nodal metastasis-free survival. These results indicate that CAFs promote cancer invasiveness via paracrine and autocrine effects on microenvironmental IL-33 signalling, and suggest that IL-33 is a potential prognostic biomarker that could be considered in therapeutic strategies for the treatment of patients with HNSCC.


Assuntos
Carcinoma de Células Escamosas/metabolismo , Carcinoma de Células Escamosas/patologia , Fibroblastos/metabolismo , Neoplasias de Cabeça e Pescoço/metabolismo , Neoplasias de Cabeça e Pescoço/patologia , Interleucinas/metabolismo , Comunicação Parácrina/fisiologia , Western Blotting , Carcinoma de Células Escamosas/mortalidade , Linhagem Celular Tumoral , Ensaio de Imunoadsorção Enzimática , Neoplasias de Cabeça e Pescoço/mortalidade , Humanos , Imuno-Histoquímica , Interleucina-33 , Estimativa de Kaplan-Meier , Invasividade Neoplásica , Análise de Sequência com Séries de Oligonucleotídeos , Prognóstico , Reação em Cadeia da Polimerase em Tempo Real , Carcinoma de Células Escamosas de Cabeça e Pescoço , Microambiente Tumoral/fisiologia
5.
J Dent Sci ; 19(4): 2045-2056, 2024 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-39347094

RESUMO

Background/purpose: The incidence of human papillomavirus (HPV)-related oropharyngeal cancer (OPC) is increasing worldwide. HPV vaccines have shown efficacy in preventing diseases in both males and females. Therefore, there is a need to develop cost-effective strategies for HPV vaccines to prevent HPV-related OPC. This meta-analysis aimed to evaluate cost-effectiveness using the global mean of incremental cost-effectiveness ratios compared to the willingness-to-pay threshold and incremental net benefits (INBs) of HPV vaccination strategies between boys' extension vaccine and girls only. These recommendations will be useful for countries that have not implemented universal HPV vaccines in national programs, such as Taiwan. Materials and methods: Studies evaluating the cost-effectiveness of HPV vaccination strategies in the prevention of OPC that included both sexes versus girls only were identified through the Cochrane Library, EMBASE, PubMed, ScienceDirect, and Web of Science databases on February 05, 2024, and a meta-analysis of pooled INBs was performed using a random-effects model. The outcome was an effective measurement of the OPC burden. The results are represented in USD (2024). Results: Fifteen model analyses were included. All the studies were conducted in high-income countries. The global mean of incremental cost-effectiveness ratio was $39,553 (95% CI, $27,008-66,641) per quality-adjusted life years gained, which was below the global mean of the willingness-to-pay threshold of $65,473 (95% CI, $52,138-83,755). Pooled INBs of $9370 (95% CI, $5046-13,695; P < 0.001) favored the extended HPV in boys. Conclusion: HPV vaccination strategies that include boys are cost-effective compared to those with girls only in preventing OPC burden. By implementing a universal HPV vaccination program, countries can receive $9370 in additional monetary benefits per patient. Given its relevance to high-income countries, this study offers key insights that can aid policymakers in Taiwan.

6.
Cells ; 13(16)2024 Aug 12.
Artigo em Inglês | MEDLINE | ID: mdl-39195225

RESUMO

Colorectal cancer (CRC) is a leading cause of cancer mortality worldwide, and cancer-associated fibroblasts (CAFs) play a major role in the tumor microenvironment (TME), which facilitates the progression of CRC. It is critical to understand how CAFs promote the progression of CRC for the development of novel therapeutic approaches. The purpose of this study was to understand how CAF-derived stromal-derived factor-1 (SDF-1) and its interactions with the corresponding C-X-C motif chemokine receptor 4 (CXCR4) promote CRC progression. Our study focused on their roles in promoting tumor cell migration and invasion and their effects on the characteristics of cancer stem cells (CSCs), which ultimately impact patient outcomes. Here, using in vivo approaches and clinical histological samples, we analyzed the influence of secreted SDF-1 on CRC progression, especially in terms of tumor cell behavior and stemness. We demonstrated that CAF-secreted SDF-1 significantly enhanced CRC cell migration and invasion through paracrine signaling. In addition, the overexpression of SDF-1 in CRC cell lines HT29 and HCT-116 triggered these cells to generate autocrine SDF-1 signaling, which further enhanced their CSC characteristics, including those of migration, invasion, and spheroid formation. An immunohistochemical study showed a close relationship between SDF-1 and CXCR4 expression in CRC tissue, and this significantly affected patient outcomes. The administration of AMD3100, an inhibitor of CXCR4, reversed the entire phenomenon. Our results strongly suggest that targeting this signaling axis in CRC is a feasible approach to attenuating tumor progression, and it may, therefore, serve as an alternative treatment method to improve the prognosis of patients with CRC, especially those with advanced, recurrent, or metastatic CRC following standard therapy.


Assuntos
Comunicação Autócrina , Fibroblastos Associados a Câncer , Movimento Celular , Quimiocina CXCL12 , Neoplasias Colorretais , Células-Tronco Neoplásicas , Comunicação Parácrina , Receptores CXCR4 , Transdução de Sinais , Humanos , Neoplasias Colorretais/patologia , Neoplasias Colorretais/metabolismo , Neoplasias Colorretais/genética , Quimiocina CXCL12/metabolismo , Receptores CXCR4/metabolismo , Fibroblastos Associados a Câncer/metabolismo , Fibroblastos Associados a Câncer/patologia , Células-Tronco Neoplásicas/metabolismo , Células-Tronco Neoplásicas/patologia , Animais , Invasividade Neoplásica , Camundongos , Microambiente Tumoral , Linhagem Celular Tumoral , Células HCT116 , Masculino , Feminino , Células HT29
7.
Cells ; 13(11)2024 Jun 03.
Artigo em Inglês | MEDLINE | ID: mdl-38891100

RESUMO

Pulmonary adenocarcinoma (PADC) treatment limited efficacy in preventing tumor progression, often resulting in malignant pleural effusion (MPE). MPE is filled with various mediators, especially interleukin-8 (IL-8). However, the role of IL-8 and its signaling mechanism within the fluid microenvironment (FME) implicated in tumor progression warrants further investigation. Primary cultured cells from samples of patients with MPE from PADC, along with a commonly utilized lung cancer cell line, were employed to examine the role of IL-8 and its receptor, CXCR1, through comparative analysis. Our study primarily assessed migration and invasion capabilities, epithelial-mesenchymal transition (EMT), and cancer stem cell (CSC) properties. Additionally, IL-8 levels in MPE fluid versus serum, along with immunohistochemical expression of IL-8/CXCR1 signaling in tumor tissue and cell blocks were analyzed. IL-8/CXCR1 overexpression enhanced EMT and CSC properties. Furthermore, the immunocytochemical examination of 17 cell blocks from patients with PADC and MPE corroborated the significant correlation between upregulated IL-8 and CXCR1 expression and the co-expression of IL-8 and CXCR1 in MPE with distant metastasis. In summary, the IL-8/ CXCR1 axis in FME is pivotal to tumor promotion via paracrine and autocrine signaling. Our study provides a therapeutic avenue for improving the prognosis of PADC patients with MPE.


Assuntos
Adenocarcinoma de Pulmão , Transição Epitelial-Mesenquimal , Interleucina-8 , Neoplasias Pulmonares , Derrame Pleural Maligno , Receptores de Interleucina-8A , Transdução de Sinais , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adenocarcinoma de Pulmão/patologia , Adenocarcinoma de Pulmão/metabolismo , Adenocarcinoma de Pulmão/genética , Adenocarcinoma de Pulmão/complicações , Linhagem Celular Tumoral , Movimento Celular , Progressão da Doença , Interleucina-8/metabolismo , Neoplasias Pulmonares/patologia , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/genética , Células-Tronco Neoplásicas/metabolismo , Células-Tronco Neoplásicas/patologia , Derrame Pleural Maligno/patologia , Derrame Pleural Maligno/metabolismo , Receptores de Interleucina-8A/metabolismo , Receptores de Interleucina-8A/genética , Microambiente Tumoral
8.
Polymers (Basel) ; 15(9)2023 Apr 28.
Artigo em Inglês | MEDLINE | ID: mdl-37177258

RESUMO

The effects of alumina particle size and jet pressure on the bond strength of polyetheretherketone (PEEK) were examined to determine the airborne particle abrasion parameters with minimal effects on PEEK and to achieve optimal bond strength, as a reference for future clinical use. An alumina particle with four particle sizes and three jet pressures was used to air-abrade PEEK. Surface roughness (Ra), morphology, chemical structure, and wettability were analyzed using a stylus profilometer, scanning electron microscope, X-ray diffractometer, and contact angle analyzer, respectively. The shear bond strength (SBS) of PEEK and dental resin cement was analyzed using a universal testing machine (n = 10). The failure modes and debonded fracture surfaces were observed using optical microscopy. Airborne particle abrasion increased the Ra and hydrophobicity of PEEK and deposited alumina residues. The SBS generally decreased after thermal cycling. A large particle size damaged the PEEK surface. The effects of different particle sizes and jet pressures on the SBS were only significant in certain groups. Adhesive failure was the main mode for all groups. Within the limitations of this study, 110 µm grain-sized alumina particles combined with a jet pressure of 2 bar prevented damage to PEEK, providing sufficient SBS and bonding durability between PEEK and dental resin cement.

9.
Ann Surg Oncol ; 19(11): 3432-40, 2012 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-22739652

RESUMO

BACKGROUND: Despite development in therapeutic strategies, such as neoadjuvant concurrent chemoradiotherapy (CCRT), the prognosis of colorectal cancer remains relatively poor. Cancer stem cells (CSC) with several characteristics can lead to therapeutic resistance. CD133 has been identified as a putative CSC marker in colorectal cancer; however, its functional role still needs elucidation. We verified the role of CD133 with emphasis on expression location and correlated the results of CD133 with clinical outcome in colorectal cancer. METHODS: We used immunohistochemistry to investigate the expression of CD133 in samples from 157 patients with colonic adenocarcinoma and from 76 patients with rectal adenocarcinoma who received neoadjuvant CCRT. We also correlated the expression location of CD133 with the clinicopathological parameters and prognosis. RESULTS: CD133 protein was variably overexpressed in colorectal cancer tissues and was present in three locations: apical and/or endoluminal surfaces, cytoplasm, and lumen. Cytoplasmic CD133 expression level correlated significantly with tumor local recurrence (P = 0.025) and survival of patients with colorectal cancer (P = 0.002), and correlated inversely with tumor regression grading (P = 0.021) after CCRT in patients with rectal cancer. CONCLUSIONS: The expression of CD133 in the cytoplasm is closely associated with local recurrence and patient survival, and may provide a reliable prognostic indicator of tumor regression grading in patients with rectal cancer after CCRT. Cytoplasmic CD133 expression may also help identify the surviving cancer cells in areas with nearly total regression after CCRT.


Assuntos
Adenocarcinoma/metabolismo , Adenocarcinoma/patologia , Antígenos CD/metabolismo , Neoplasias do Colo/metabolismo , Neoplasias do Colo/patologia , Glicoproteínas/metabolismo , Recidiva Local de Neoplasia/metabolismo , Peptídeos/metabolismo , Neoplasias Retais/metabolismo , Neoplasias Retais/patologia , Antígeno AC133 , Adenocarcinoma/terapia , Idoso , Quimiorradioterapia Adjuvante , Neoplasias do Colo/terapia , Citoplasma/metabolismo , Feminino , Humanos , Imuno-Histoquímica , Estimativa de Kaplan-Meier , Masculino , Pessoa de Meia-Idade , Terapia Neoadjuvante , Gradação de Tumores , Prognóstico , Neoplasias Retais/terapia , Indução de Remissão , Estatísticas não Paramétricas
10.
J Oral Pathol Med ; 41(4): 322-31, 2012 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-22103929

RESUMO

BACKGROUND: To clarify the efficacy of grape seed procyanidin (GSP) on antiproliferative effects related to p53 functional status of oral squamous cell carcinoma (OSCC) for its chemoadjuvant potential. METHODS: We used GSP to investigate SCC-25 cells with wild-type p53 gene and OEC-M1 cells with mutant p53 gene for the assessment of antiproliferative effects including cell viability, cell cycle, apoptosis, migration and invasion potential, and alterations of associated oncoproteins involved in cellular and molecular events. RESULTS: The findings suggest that GSP on OEC-M1 cells leads to cell cycle arrest by increasing the expression of p21(Cip1) /p27(Kip1) protein without functioning mitochondria-mediated apoptosis, whereas GSP on SCC-25 cells inhibits cell proliferation via both G1-phase arrest and mitochondria-mediated apoptosis in a dose-dependent manner as a result of alterations of Bcl-2. GSP also inhibits the migration and invasion of both cells, which are associated with the suppression of matrix metalloproteinases (MMPs), MMP-2 and MMP-9. CONCLUSION: Antiproliferative effectiveness of GSP is closely associated with the p53 status of OSCC cells. GSP displays chemoadjuvant potential via cell cycle blockage and apoptotic induction. Our findings clearly suggest that GSP may play a role as a novel chemopreventive or therapeutic agent for OSCC.


Assuntos
Antineoplásicos/farmacologia , Carcinoma de Células Escamosas/patologia , Extrato de Sementes de Uva/farmacologia , Neoplasias Bucais/patologia , Preparações de Plantas/farmacologia , Proantocianidinas/farmacologia , Proteína Supressora de Tumor p53/efeitos dos fármacos , Vitis , Anticarcinógenos/farmacologia , Apoptose/efeitos dos fármacos , Ciclo Celular/efeitos dos fármacos , Morte Celular/efeitos dos fármacos , Linhagem Celular Tumoral , Movimento Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Inibidor de Quinase Dependente de Ciclina p21/efeitos dos fármacos , Inibidor de Quinase Dependente de Ciclina p27/efeitos dos fármacos , Relação Dose-Resposta a Droga , Fase G1/efeitos dos fármacos , Humanos , Metaloproteinase 2 da Matriz/efeitos dos fármacos , Metaloproteinase 9 da Matriz/efeitos dos fármacos , Mitocôndrias/efeitos dos fármacos , Invasividade Neoplásica , Proteínas Oncogênicas/efeitos dos fármacos , Mutação Puntual/genética , Inibidores de Proteínas Quinases/análise , Proteínas Proto-Oncogênicas c-bcl-2/efeitos dos fármacos , Proteína Supressora de Tumor p53/genética
11.
J Oral Pathol Med ; 41(1): 9-15, 2012 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-21595750

RESUMO

BACKGROUND: Betel nut chewing, cigarette smoking and alcohol drinking are thought to be major environmental risk factors responsible for the development of oral squamous cell carcinomas. Oncogenic human papillomavirus infections have a well-established association with uterine cervical carcinoma. However, little is known about the exact role of human papillomavirus infections in oral squamous cell carcinomas. This study is designed to elucidate the role of human papillomavirus infections in cancer development and prognosis of oral squamous cell carcinomas. METHODS: Molecular techniques including in situ hybridization and immunohistochemistry of p16(INK4A) and p53 for evidences of human papillomavirus in tissue micro-arrays were investigated. RESULTS: Twenty-four of 65 cases of oral squamous cell carcinomas were found positive for in situ hybridization and 14 were found positive for p16(INK4A). The majority of cases without the evidence of human papillomavirus were related to p53 over-expression. There were statistically significant correlations between the results of human papillomavirus test and size or extent of the tumor (P = 0.003) or the stage of oral squamous cell carcinomas (P = 0.015). Kaplan-Meier plot analysis demonstrated a tendency of longer survival in cases of oral squamous cell carcinomas with the evidence of human papillomavirus or positive p16 (INK4A). CONCLUSIONS: Human papillomavirus infections may play a unique role in oral carcinogenesis. Our data strongly suggest that human papillomavirus-positive oral squamous cell carcinomas comprise a distinct clinical and pathological disease entity that appears related to a better outcome with longer survival and bears a causally associated relationship different from other carcinogenic mechanisms.


Assuntos
Alphapapillomavirus/classificação , Carcinoma de Células Escamosas/virologia , Neoplasias Bucais/virologia , Infecções por Papillomavirus/virologia , Alphapapillomavirus/genética , Inibidor p16 de Quinase Dependente de Ciclina/análise , DNA Viral/análise , Feminino , Seguimentos , Regulação Neoplásica da Expressão Gênica/genética , Papillomavirus Humano 11/isolamento & purificação , Papillomavirus Humano 16/isolamento & purificação , Papillomavirus Humano 18/isolamento & purificação , Papillomavirus Humano 31/isolamento & purificação , Papillomavirus Humano 6/isolamento & purificação , Humanos , Imuno-Histoquímica , Hibridização In Situ , Masculino , Análise em Microsséries , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Prognóstico , Taxa de Sobrevida , Proteína Supressora de Tumor p53/análise
12.
Polymers (Basel) ; 14(12)2022 Jun 08.
Artigo em Inglês | MEDLINE | ID: mdl-35745899

RESUMO

With increasing aesthetic awareness and emphasis on time costs in today's society, monolithic multilayer precolored zirconia ceramics (M-Zr) facilitate aesthetic restorations in a convenient and straightforward manner without the need for veneering porcelain to modify the color. However, the effect of abutment materials on the final color of M-Zr remains unclear. Herein, we placed Vita A1 Shade M-Zr on six different abutment materials, zirconia (Y-TZP), 3D printed composite resin (CR), dental model resin (MR), polyetheretherketone (PEEK), polyetherketoneketone (PEKK), and cobalt−chromium alloy (Co−Cr), to evaluate their effect on the color accuracy of M-Zr. The color attributes (L*, a*, and b*) were measured using a dental spectrophotometer. The translucency parameter (TP), contrast ratio, color difference (ΔE) between each background substrate and the Vita A1 Shade Guide, and chroma values (C) were calculated to evaluate the color accuracy of M-Zr. A statistical analysis was performed using one-way analysis of variance and post hoc Tukey's HSD tests (α = 0.05). The experimental results indicate that the TP values and contrast ratio of the M-Zr samples were 14.85 and 0.83, respectively. Co−Cr had the highest ΔE (6.08) and lowest C value (7.52); PEKK had the lowest ΔE (2.60), and PEEK had the highest C value (12.23) (p < 0.05). Notably, the ΔE values of CR (3.13), PEEK (2.86), and PEKK were within clinical indicators (ΔE < 3.7). Based on these results, it can be concluded that the abutment material has a significant effect on the final color of the M-Zr, and PEEK or PEKK resulted in good color accuracy. When choosing the dental MR, traditional zirconia, or metals as abutment materials, colored or opaque cement might be required to eliminate color distortion and achieve desirable optical properties.

13.
Cancers (Basel) ; 14(13)2022 Jun 27.
Artigo em Inglês | MEDLINE | ID: mdl-35804913

RESUMO

The tumor microenvironment (TME) plays a crucial role in tumor progression. One of its key stromal components, cancer-associated fibroblasts (CAFs), may crosstalk with cancer cells by secreting certain cytokines or chemokines. However, which important mediator(s) are released by CAFs, and the underlying molecular mechanism, remain largely unknown. In the present study, we isolated patient-derived CAFs and normal fibroblasts (NFs). Using microarray analysis, we detected chemokine ligand 11 (CCL11) overexpression in CAFs compared to NFs. CCL11 administration promoted the migration and invasion of head and neck cancer (HNC) cells with enhanced cancer stem cell-like properties and induction of epithelial-to-mesenchymal transition. Furthermore, neutralization of CCL11 activity reversed the aggressive phenotype of CAF-induced cancer cells. Confocal microscopy showed colocalization of CCL11 and CC chemokine receptor 3 (CCR3) on HNC cells. Moreover, immunohistochemical analysis of clinical samples from 104 patients with HNC showed that expression of CCL11 and CCR3 were significantly correlated with poor overall survival (p = 0.003 and 0.044, respectively). Collectively, CCL11 expressed on CAFs promotes HNC invasiveness, and neutralization of CCL11 reverses this effect. We propose that the CCL11/CCR3 signaling circuit is a potential target for optimizing therapeutic strategies against HNC.

14.
Cancers (Basel) ; 13(14)2021 Jul 09.
Artigo em Inglês | MEDLINE | ID: mdl-34298657

RESUMO

Despite recent advances, treatment for head and neck squamous cell carcinoma (HNSCC) has limited efficacy in preventing tumor progression. We confirmed previously that carcinoma-associated fibroblasts (CAF)-induced interleukin-33 (IL-33) contributed to cancer progression. However, the molecular mechanisms underlying the complex communication network of the tumor microenvironment merited further evaluation. To simulate the IL-33-induced autocrine signaling, stable clones of IL-33-overexpressing HNSCC cells were established. Besides well-established IL-33/ST2 and SDF1/CXCR4 (stromal-derived factor 1/C-X-C motif chemokine receptor 4) signaling, the CAF-induced IL-33 upregulated CXCR4 via cancer cell induction of IL-33 self-production. The IL-33-enhanced-CXCR4 regulatory circuit involves SDF1/CXCR4 signaling activation and modulates tumor behavior. An in vivo study confirmed the functional role of IL-33/CXCR4 in tumor initiation and metastasis. The CXCR4 and/or IL-33 blockade reduced HNSCC cell aggressiveness, with attenuated invasions and metastases. Immunohistochemistry confirmed that IL-33 and CXCR4 expression correlated significantly with disease-free survival and IL-33-CXCR4 co-expression predicted a poor outcome. Besides paracrine signaling, the CAF-induced IL-33 reciprocally enhanced the autocrine cancer-cell self-production of IL-33 and the corresponding CXCR4 upregulation, leading to the activation of SDF1/CXCR4 signaling subsequent to cancer progression. Thus, targeting the IL-33-enhanced-CXCR4 regulatory circuit attenuates tumor aggressiveness and provides a potential therapeutic option for improving the prognosis in HNSCC patients.

15.
Histopathology ; 57(2): 295-303, 2010 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-20659175

RESUMO

AIMS: To test the validity of an invasive pattern grading score (IPGS) developed for oral squamous cell carcinoma (OSCC) as a prognostic indicator and to elucidate the relationship between the IPGS and clinical parameters. METHODS AND RESULTS: The IPGS was applied to a total of 153 cases of OSCC. There were significant correlations between IPGS and distant metastasis (P = 0.01) or recurrence (P = 0.001). However, there were no significant correlations between IPGS and gender, age, size or extent, location, status of lymph node metastasis, clinical staging, or histological grading. Cases of OSCC with higher IPGS were associated with poor patient survival (P < 0.001) and higher probability of tumour recurrence (P = 0.001). Intraobserver (kappa = 0.74) and interobserver agreement (kappa = 0.67) were very satisfactory. CONCLUSIONS: Our study confirms the validity of the IPGS, an indicator that is simple and easy to use. IPGS not only provides histological assessment of biological behaviour, but also offers an independent prognostic factor that may influence the treatment of OSCC.


Assuntos
Carcinoma de Células Escamosas/patologia , Neoplasias Bucais/patologia , Carcinoma de Células Escamosas/mortalidade , Carcinoma de Células Escamosas/secundário , Feminino , Humanos , Estimativa de Kaplan-Meier , Metástase Linfática , Masculino , Pessoa de Meia-Idade , Neoplasias Bucais/mortalidade , Invasividade Neoplásica , Estadiamento de Neoplasias , Prognóstico
16.
J Oral Pathol Med ; 38(9): 722-30, 2009 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-19473443

RESUMO

BACKGROUND: Oral squamous cell carcinoma (OSCC) is one of the most common head and neck cancers. The prognosis of OSCC is usually poor because of extensive local invasion at initial diagnosis. In the literature, Fascin has been reported responsible for cell motility and over-expression of Fascin contributes to an unfavorable clinical course. Nevertheless, the roles of Fascin protein playing in aggressiveness of OSCC and their potential mechanisms need to be elucidated. METHODS: Two cell lines of OSCC (OECM-1 and SCC-25) via the vector-based small interfering RNA (siRNA) to suppress the expression of the Fascin gene were used. Subsequent analyses and observation regarding the expression of Fascin protein and cyto-morphological alterations were detected by Western blot and immunofluorescent microscopy. Boyden chamber invasion assay, cell migration assay and adhesion assay were also applied to investigate the functional changes of OSCC. RESULTS: There were statistically significant differences (P < 0.05) of Fascin expression before and after silencing. Down-regulation of Fascin protein directly led to changes of cell surface protrusions under immunofluorescent microscopy and resulted in suppression of migration, invasion and increase of adhesion in both cell lines (P < 0.05). Furthermore, down-regulation of Fascin expression also resulted in alterations of E-cadherin, beta-catenin and TWIST at certain level, implicative of an association with epithelial-mesenchymal transition (EMT). CONCLUSIONS: Our results suggest that expression of Fascin protein may play an essential role in regulation of progression of OSCC and contributes to the event of EMT in the early aggressiveness of OSCC.


Assuntos
Carcinoma de Células Escamosas/genética , Proteínas de Transporte/genética , Proteínas de Transporte/fisiologia , Proteínas dos Microfilamentos/genética , Proteínas dos Microfilamentos/fisiologia , Neoplasias Bucais/genética , Invasividade Neoplásica/genética , Western Blotting , Caderinas/biossíntese , Carcinoma de Células Escamosas/metabolismo , Proteínas de Transporte/biossíntese , Adesão Celular , Linhagem Celular Tumoral , Ensaios de Migração Celular , Transformação Celular Neoplásica/genética , Regulação para Baixo , Células Epiteliais/patologia , Regulação Neoplásica da Expressão Gênica , Técnicas de Silenciamento de Genes , Humanos , Mesoderma/patologia , Proteínas dos Microfilamentos/biossíntese , Neoplasias Bucais/metabolismo , RNA Interferente Pequeno/fisiologia , Transfecção , Proteína 1 Relacionada a Twist/biossíntese , beta Catenina/biossíntese
17.
PLoS One ; 13(8): e0201267, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30148841

RESUMO

Long-term nicotine-derived nitrosamine ketone (NNK) and arecoline exposure promotes carcinogenesis and head and neck squamous cell carcinoma (HNSCC) progression, although most associated data on the two were analyzed individually. The molecular mechanisms underlying tumor progression associated with the synergistic effects of NNK and arecoline remain unclear. We treated SCC-25 and FaDu cells with NNK and arecoline (separately or in combination) for 3 months. Comparative analysis was performed to investigate the mechanism underlying the acquisition of properties related to tumor promotion, including stemness, anti-apoptosis, and resistance to HNSCC therapeutics. Long-term exposure to NNK and arecoline resulted in an increase in cancer stem cell properties, anti-apoptosis, and the resistance to cisplatin in HNSCC. We detected abundant epidermal growth factor receptor (EGFR) expression in HNSCC cells after combined treatment with NNK and arecoline. EGFR was pivotal in inducing tumor promotion and anti-apoptosis in cancer cells by inducing pAKT and NFκB. Combined treatment with NNK and arecoline synergistically facilitated tumor aggressiveness via EGFR-AKT signaling. Targeting EGFR-AKT signaling may be a feasible strategy for treating HNSCC.


Assuntos
Arecolina/farmacologia , Carcinoma de Células Escamosas/metabolismo , Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Neoplasias de Cabeça e Pescoço/metabolismo , Nicotina/química , Nitrosaminas/farmacologia , Transdução de Sinais/efeitos dos fármacos , Arecolina/agonistas , Carcinoma de Células Escamosas/patologia , Linhagem Celular Tumoral , Receptores ErbB/biossíntese , Neoplasias de Cabeça e Pescoço/patologia , Humanos , Nitrosaminas/agonistas , Nitrosaminas/química , Proteínas Proto-Oncogênicas c-akt/metabolismo
18.
PLoS One ; 12(1): e0169550, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28081258

RESUMO

PURPOSE: Diabetes mellitus (DM) is a global pandemic metabolic disorder. In recent years, the amount of medical resources required for the treatment of diabetes has increased as diabetes rates have gradually risen. The combined effects of individual and neighbourhood socio-economic status (SES) on DM survival rates are still not clear, especially in patients of working age. In this paper, we aim to analyze the combined effects of neighbourhood and individual SES on DM survival rates in patients of working age in Taiwan. METHODS: The study of 23,781 people who were diagnosed with DM by using population-based study between 2002 and 2006. Each sample was followed up for 4 years or as a sensor case. We defined Individual SES and neighbourhood SES by each patient's job category and household income which characterized as advantaged or disadvantaged. Then we compared the survival rates by SES group used Cox proportional hazards model for adjust risk factors. RESULTS: The 4-year overall survival rates of diabetic patients were worst for those with low individual SES who living in advantaged neighbourhoods. After adjustment for patient characteristics, DM patients with high individual SES living in disadvantaged neighbourhoods had the same risk of mortality as those patients with high individual SES living in advantaged neighbourhoods (hazard ratio: 1.11; 95% confidence interval [CI]: 0.81-1.51). The study found that DM patients with low individual SES who live in disadvantaged areas had a greater risk of mortality than those with high SES (odds ratio: 2.57; 95% CI: 2.04-3.24). There were significant differences in survival rates between patients with high individual SES and patients with low individual SES. In contrast, the results did not statistically significant differences in survival rates between advantaged and disadvantaged neighbourhood SES groups. CONCLUSION: DM patients with low individual SES had the worst survival rate, regardless of whether they were living in a high or low SES neighbourhood area. The competitive cause of death, i.e., the fact that complications, rather than DM itself, are often the cause of death, may be the reason for the inverse relationship found between the effects of individual SES and neighbourhood SES on DM survival. We conclude that the socio-economic gradient in survival among DM patients may be the result of differences in access to medical treatment and attributes related to individual SES.


Assuntos
Diabetes Mellitus/mortalidade , Fatores Etários , Idoso , Diabetes Mellitus/terapia , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Modelos de Riscos Proporcionais , Fatores Socioeconômicos , Taxa de Sobrevida , Taiwan/epidemiologia
19.
Nat Cell Biol ; 19(10): 1286-1296, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-28920955

RESUMO

The mechanisms by which hypoxic tumours evade immunological pressure and anti-tumour immunity remain elusive. Here, we report that two hypoxia-responsive microRNAs, miR-25 and miR-93, are important for establishing an immunosuppressive tumour microenvironment by downregulating expression of the DNA sensor cGAS. Mechanistically, miR-25/93 targets NCOA3, an epigenetic factor that maintains basal levels of cGAS expression, leading to repression of cGAS during hypoxia. This allows hypoxic tumour cells to escape immunological responses induced by damage-associated molecular pattern molecules, specifically the release of mitochondrial DNA. Moreover, restoring cGAS expression results in an anti-tumour immune response. Clinically, decreased levels of cGAS are associated with poor prognosis for patients with breast cancer harbouring high levels of miR-25/93. Together, these data suggest that inactivation of the cGAS pathway plays a critical role in tumour progression, and reveal a direct link between hypoxia-responsive miRNAs and adaptive immune responses to the hypoxic tumour microenvironment, thus unveiling potential new therapeutic strategies.


Assuntos
Neoplasias da Mama/enzimologia , MicroRNAs/metabolismo , Nucleotidiltransferases/metabolismo , Evasão Tumoral , Imunidade Adaptativa , Animais , Neoplasias da Mama/genética , Neoplasias da Mama/imunologia , Neoplasias da Mama/patologia , DNA Mitocondrial/genética , DNA Mitocondrial/metabolismo , Proteínas de Ligação a DNA/genética , Proteínas de Ligação a DNA/metabolismo , Progressão da Doença , Epigênese Genética , Feminino , Regulação Enzimológica da Expressão Gênica , Regulação Neoplásica da Expressão Gênica , Humanos , Células MCF-7 , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , MicroRNAs/genética , Oxigenases de Função Mista/genética , Oxigenases de Função Mista/metabolismo , Coativador 3 de Receptor Nuclear/genética , Coativador 3 de Receptor Nuclear/metabolismo , Nucleotidiltransferases/genética , Proteínas Proto-Oncogênicas/genética , Proteínas Proto-Oncogênicas/metabolismo , Interferência de RNA , Receptor de Interferon alfa e beta/deficiência , Receptor de Interferon alfa e beta/genética , Transdução de Sinais , Fatores de Tempo , Transfecção , Hipóxia Tumoral , Microambiente Tumoral
20.
Oncotarget ; 7(17): 23512-20, 2016 Apr 26.
Artigo em Inglês | MEDLINE | ID: mdl-26992205

RESUMO

A tobacco-specific component, 4-methylnitrosamino-1-3-pyridyl-1-butanone (NNK), is a major risk factor for many cancers. Recent reports have demonstrated that NNK exposure may be associated with tumor progression and chemoresistance in certain cancers. However, the underlying NNK-induced mechanism contributing to the aggressiveness of colorectal cancer (CRC) has not been thoroughly studied. In this study, we used HT29 cells treated with NNK to simulate the long-term exposure of cigarette smoke. A comparative analysis was performed to evaluate cell proliferation, migration, and invasion as well as epithelial-mesenchymal transition (EMT) markers and drug-resistance genes expression, cancer stem cell (CSC) properties, and anti-apoptotic activity. Signaling pathways related to chemoresistance were also investigated. As a result, NNK exposure dose-dependently stimulates cell proliferation, enhance abilities of migration and invasion, induce EMT phenomenon, and attenuate apoptosis. Furthermore, NNK exposure also promotes the capabilities of sphere formation, upregulation of Snail, and overexpression of CD133, Nanog, OCT4, and the drug-resistant genes. Knockdown of Snail results in upregulation of Raf kinase inhibitor protein (RKIP), increased apoptosis, reversal of EMT phenomenon, and reducation of expression of CSC markers, all of which contribute to a decrease of chemoresistance. Our study demonstrates a number of related mechanisms that mediate the effect of NNK exposure on increasing CRC therapeutic resistance via the Snail signaling pathway. Targeting Snail may provide a feasible strategy for the treatment of CRC.


Assuntos
Neoplasias Colorretais/patologia , Resistencia a Medicamentos Antineoplásicos , Nitrosaminas/farmacologia , Compostos Organoplatínicos/farmacologia , Proteína de Ligação a Fosfatidiletanolamina/antagonistas & inibidores , Fatores de Transcrição da Família Snail/antagonistas & inibidores , Antineoplásicos/farmacologia , Apoptose/efeitos dos fármacos , Biomarcadores Tumorais/metabolismo , Carcinógenos/farmacologia , Movimento Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Neoplasias Colorretais/tratamento farmacológico , Neoplasias Colorretais/metabolismo , Transição Epitelial-Mesenquimal/efeitos dos fármacos , Humanos , Oxaliplatina , Transdução de Sinais , Células Tumorais Cultivadas
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA