Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 82
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Lung Cancer ; 139: 118-123, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31775086

RESUMO

OBJECTIVES: The 2015 World Health Organization classification defines pulmonary large-cell neuroendocrine carcinoma (LCNEC) as a high-grade neuroendocrine carcinoma. However, the clinical characteristics and prognostic factors of pure LCNEC and combined LCNEC remain unclear. Hence, we performed a multi-center retrospective study to compare the clinical outcomes of pure versus combined LCNEC. MATERIALS AND METHODS: Data from 381 patients with pulmonary LCNEC admitted to 17 Chinese institutes between 2009 and 2016 were collected retrospectively. Clinical characteristics and prognosis were analyzed among patients receiving adjuvant (adjuvant group; n = 56) and first-line (first-line group; n = 146) chemotherapy, as well as among patients receiving small cell lung cancer (SCLC) and non-SCLC (NSCLC) chemotherapy regimens. The Kaplan-Meier method and multivariable Cox regression were used to identify clinicopathological variables that might influence patient outcomes. RESULTS: Expression levels of neuroendocrine markers (synaptophysin, chromogranin-A, CD56) were associated with patients' prognosis in the total study cohort. In the adjuvant group, median disease-free survival was non-significantly longer for SCLC-based regimens than for NSCLC-based regimens (P = 0.112). In the first-line group, median progression-free survival was significantly longer for SCLC-based regimens than for NSCLC-based regimens (11.5 vs. 7.2 months, P = 0.003). Among patients with combined LCNEC, adenocarcinoma was the most common combined component, accounting for 70.0 % of cases. Additionally, median overall survival was non-significantly shorter for combined LCNEC than for pure LCNEC (P = 0.083). CONCLUSION: The SCLC regimen is a more effective choice, as either first-line or adjuvant chemotherapy, when compared to the NSCLC regimen for LCNEC treatment. Further studies are needed to clarify the survival differences between patients with pure-, and combined LCNEC.

2.
Cancer Med ; 9(1): 12-18, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31692291

RESUMO

The response to icotinib in advanced non-small cell lung cancers (NSCLC) with EGFR uncommon mutation (EGFRum) is unclear. Here we reported the efficacy and potential resistance mechanism of icotinib in Chinese EGFRum NSCLC patients. Between July 2013 and November 2016, 3117 NSCLC patients were screened for EGFRum in a multi-center study in China. Circulating tumor DNA (ctDNA) was detected and analyzed using next-generation sequencing (NGS) after progression from icotinib. The efficacy, safety and the potential resistance mechanism of icotinib were explored. After a median follow-up of 6.2 months, 69 patients (70.41%) developed disease progression, the objective rate (ORR) and disease control rate (DCR) were 13.27% and 29.59% respectively, and the median progression-free survival (PFS) was 5.5 months (95% CI: 1.2-13.0 months). Both complex-pattern with EGFR classical mutations (EGFRcm) and single-pattern have better PFS than complex-pattern without EGFRcm (median PFS was 7.2 (95% CI: 4.65-9.75), 5.2 (95% CI: 3.24-7.16) and 3.2 (95% CI: 2.97-3.44) months, respectively, P < .05); patients harboring S768I mutation had the worst PFS than others (2.0 months, P < .05). Diarrhea was the most frequent side effect (42.9%). Forty-eight (69.6%) patients developed drug resistance after 3.0 months and 81.2% of them acquired T790M mutation. Better response was observed in complex-pattern with the EGFRcm group. S768I mutation carriers may not benefit from icotinib. Acquired T790M mutation was common in icotinib-resistant EGFRum NSCLC patients.

3.
J Craniomaxillofac Surg ; 48(1): 1-8, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31884028

RESUMO

PURPOSE: The treatment of hemimandibular hyperplasia (HH) is difficult by performing condylectomy and orthognathic surgery in one stage. This study investigated the clinical feasibility of treating HH with computer-aided design and computer-aided manufacturing (CAD/CAM) cutting and drilling guides and the pre-bent titanium plates to improve the accuracy of operation to avoid condyle reconstruction. METHODS: 12 patients diagnosed with HH were included in this study from 2014 to 2018. Conservative condylectomy and bimaxillary orthognathic surgery were performed in all patients. The CAD/CAM cutting and drilling guides and the pre-bent titanium plates were used to guide surgeries. Follow-up and radiographic examinations were performed. The difference between virtually simulated and postoperative models was measured. RESULTS: All patients got satisfactory and stable results, without complications or obvious relapse during follow-up. Occlusion relationship, temporomandibular joint function and facial symmetry were improved obviously after surgery. Comparison between simulated plans and actual postoperative outcomes showed that the surgical plans were transferred accurately. CONCLUSIONS: CAD/CAM cutting and drilling guides and the pre-bent titanium plates described in this paper can help transferring the results from computer simulation to the operating room accurately. Conservative condylectomy can be operated exactly matching bimaxillary orthognathic surgery for treating HH, avoiding condyle reconstruction.


Assuntos
Placas Ósseas , Cirurgia Assistida por Computador , Simulação por Computador , Projeto Auxiliado por Computador , Humanos , Hiperplasia , Titânio
4.
Onco Targets Ther ; 12: 9303-9307, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31807010

RESUMO

Fibroblast growth factor receptor (FGFR) family includes four highly conserved receptor tyrosine kinases. Particularly, FGFR2 has been identified as a potential target for tyrosine kinase inhibitor (TKI) treatment. Except for immunohistochemistry and fluorescence in situ hybridization, next-generation sequencing (NGS) technology represents a novel tool for FGFR2 detection that covers a wide range of fusion genes. In the present work, we present a case of cholangiocarcinoma who had FGFR2-BICC1 rearrangement detected by NGS. A 76-year-old female diagnosed with cholangiocarcinoma underwent four cycles of chemotherapy. The NGS assay showed that the tumor had a FGFR2-BICC1 rearrangement. The patient had a favorable tumor response to sorafenib. Herein, we report the first case with cholangiocarcinoma harboring FGFR2-BICC1 who is sensitive to sorafenib therapy.

6.
Cancer Sci ; 2019 Dec 11.
Artigo em Inglês | MEDLINE | ID: mdl-31828849

RESUMO

The incidence of epidermal growth factor receptor uncommon mutation (EGFRum) is relatively low and patients harboring EGFRum are resistant to the first-generation tyrosine kinase inhibitors (TKI). However, the mechanism of primary resistance remains unclear. Medical records of 98 patients who had never been treated by TKI and who accepted icotinib treatment were collected and followed. The circulating tumor DNA (ctDNA) were detected and analyzed using the next-generation sequencing (NGS) platform after progression on icotinib. The potential primary resistance mechanism of icotinib was explored. A total of 21 (21.4%) and 48 (49%) patients developed primary and acquired resistance to icotinib, respectively. The median progression-free survival (PFS) of primary resistance patients was 1.8 months (0.5-2.3, 95% CI = 1.50-2.10). Before treatment, 52.4% (11/21) of patients carried S768I, 23.8% (5/21) L861Q, 14.3% (3/21) G719X and 14.3% (3/21) exon 20-ins mutations. Approximately 23.8% (5/21) of patients harbored the combined pattern mutations and 76.2% (16/21) of patients harbored the single pattern mutations. The combined pattern with EGFR classical mutation (EGFRcm) had worse PFS than the combined with EGFRum and single pattern (P < .05). There were 6 (28.57%) patients with acquired EGFR extracellular domain mutation, 5 (23.81%) with BCL2L11 loss (BIM deletion polymorphism), 3 (14.29%) with MET amplification, 1 (4.76%) with ERBB2 amplification, 1 (4.76%) with MYC amplification, 1 (4.76%) with PTEN mutation, 1 (4.76%) with PIK3CA mutation and 3 (14.29%) with unknown status. EGFR extracellular domain mutation, BCL2L11 loss, PI3K-AKT-mTOR signaling pathway (PTEN and PIK3CA mutations), MET amplification, ERBB2 amplification or MYC amplification might contribute to molecular mechanisms of primary resistance to icotinib in patients with advanced non-small cell lung cancer harboring uncommon mutant epidermal growth factor receptor. Combined targeted therapy or chemotherapy should be considered in this population.

7.
Clin Chem ; 2019 Dec 06.
Artigo em Inglês | MEDLINE | ID: mdl-31810998

RESUMO

BACKGROUND: Targeted next-generation sequencing is a powerful method to comprehensively identify biomarkers for cancer. Starting material is currently either DNA or RNA for different variations, but splitting to 2 assays is burdensome and sometimes unpractical, causing delay or complete lack of detection of critical events, in particular, potent and targetable fusion events. An assay that analyzes both templates in a streamlined process is eagerly needed. METHODS: We developed a single-tube, dual-template assay and an integrated bioinformatics pipeline for relevant variant calling. RNA was used for fusion detection, whereas DNA was used for single-nucleotide variations (SNVs) and insertion and deletions (indels). The reaction chemistry featured barcoded adaptor ligation, multiplexed linear amplification, and multiplexed PCR for noise reduction and novel fusion detection. An auxiliary quality control assay was also developed. RESULTS: In a 1000-sample lung tumor cohort, we identified all major SNV/indel hotspots and fusions, as well as MET exon 14 skipping and several novel or rare fusions. The occurrence frequencies were in line with previous reports and were verified by Sanger sequencing. One noteworthy fusion event was HLA-DRB1-MET that constituted the second intergenic MET fusion ever detected in lung cancer. CONCLUSIONS: This method should benefit not only a majority of patients carrying core actionable targets but also those with rare variations. Future extension of this assay to RNA expression and DNA copy number profiling of target genes such as programmed death-ligand 1 may provide additional biomarkers for immune checkpoint therapies.

8.
Transl Oncol ; 13(2): 329-335, 2019 Dec 24.
Artigo em Inglês | MEDLINE | ID: mdl-31881505

RESUMO

BACKGROUND: KRAS gene mutations are well known as a key driver of advanced non-small cell lung cancer (NSCLC). The impact of KRAS-mutant subtypes on the survival benefit from salvage chemotherapy is controversial. Here, we present a real-world study in patients across China with advanced NSCLC with KRAS mutations using a website-based patient self-report system. METHODS: We identified a total of 75 patients diagnosed with KRAS-mutant (determined by molecular sequencing) advanced NSCLC between 2014/5/9 and 2019/5/30. KRAS mutation subtypes were divided into G12C and non-G12C groups for statistical analysis. The clinicopathological characteristics and treatment survival benefit in all patients with a KRAS mutation were evaluated. Programmed death-ligand 1 (PD-L1) expression data were collected from 30 patients in the same cohort. RESULTS: In this study, 23 patients with stage IIIB NSCLC and 52 patients with stage IV NSCLC were enrolled with 58 men and 17 women; the median age was 60 years (39-84). All patients received regular chemotherapy/radiotherapy/targeted therapy/immune therapy as per the disease condition. Four main KRAS mutation subtypes were detected: G12C (33%), G12V (19%), G12A (12%), and G12D (12%). Three predominant KRAS comutations were detected: TP53-KRAS (31%), EGFR-KRAS (11%), and STK11-KRAS (8%). Compared with the KRAS non-G12C mutation subtype, patients with the KRAS G12C mutation had potentially longer progression-free survival (PFS) after first-line chemotherapy (4.7 vs. 2.5 months, p < 0.05). Pemetrexed-based chemotherapy appeared to be superior to taxanes- and gemcitabine-based chemotherapies in all patients (PFS: 5.0 vs. 1.5 and 2.3 months, respectively, p > 0.05). Cox regression analysis showed that the KRAS G12C mutation and pemetrexed-based first-line chemotherapy were positive influencers for PFS after first-line (hazard ratios = 0.31 and 0.55, respectively, P < 0.05), but not second-line chemotherapies. CONCLUSION: The KRAS G12C mutation could be a predictive biomarker for better survival benefit from first-line chemotherapy in patients with advanced NSCLC and KRAS mutations. The first-line chemotherapy regimen could possibly influence the outcome in patients with KRAS mutations. Larger and prospective clinical trials are warranted to confirm our conclusions.

9.
J Thorac Oncol ; 2019 Dec 12.
Artigo em Inglês | MEDLINE | ID: mdl-31843683

RESUMO

INTRODUCTION: Blood-based tumor mutational burden (bTMB) has been studied to differentiate non-small cell lung cancer (NSCLC) patients who would benefit from anti-programmed cell death protein 1 (PD-1)/programmed death ligand 1 (PD-L1) therapies. However, it failed to predict overall survival (OS) benefits, which warrants further exploration. METHODS: Three independent cohorts of NSCLC patients treated with immunotherapy were used in this study. A new bTMB algorithm was first developed in the two independent cohorts (POPLAR, N=211 and OAK, N=462) and further validated in the third National Cancer Center cohort (NCC, N=64). RESULTS: bTMB-H (bTMB≥cut-off point) was not associated with favorable OS following immunotherapy regardless of the cut-off points in either the POPLAR and OAK or the NCC cohorts (P>0.05) due to its correlation with the circulating tumor DNA (ctDNA) amount, which was associated with poor OS. In the POPLAR and OAK cohorts, upon allele frequency (AF) adjustment, a high allele frequency bTMB (HAF-bTMB, mutation counts with an AF>5%) was strongly correlated with the ctDNA amount (Pearson's r=0.65), while a low allele frequency bTMB (LAF-bTMB, mutation counts with an AF≤5%) was not (Pearson's r=0.09). LAF-bTMB-H was associated with favorable OS (hazard ratio [[HR], 0.70; 95% confidence interval [CI], 0.52-0.95; P=0.02), progression-free survival (PFS) (HR, 0.62; 95% CI, 0.47-0.80; P<0.001), and the objective response rate (ORR) (P<0.001) following immunotherapy but not chemotherapy, with a cut-off point of 12 trained in the POPLAR cohort and validated in the OAK cohort. The LAF-bTMB algorithm was further validated in the NCC cohort in which LAF-bTMB-H was associated with OS (HR, 0.20; 95% CI, 0.05-0.84; P=0.02), PFS (HR, 0.30; 95% CI, 0.13-0.70; P=0.003), and the ORR (P=0.001). CONCLUSIONS: We developed and validated a new LAF-bTMB algorithm as a feasible predictor of OS, PFS, and the ORR following anti-PD-1/PD-L1 therapies in NSCLC patients, which needs to be prospectively validated.

11.
BMC Cancer ; 19(1): 769, 2019 Aug 05.
Artigo em Inglês | MEDLINE | ID: mdl-31382924

RESUMO

BACKGROUND: ROS1 rearrangements are validated drivers in lung cancer, which have been identified in a small subset (1-2%) of patients with non-small cell lung cancer (NSCLC). To date, 18 fusion genes of ROS1 have been identified in NSCLC. The ALK inhibitor (crizotinib) exhibits therapeutic effect against ROS1-rearranged NSCLC. Next-generation sequencing (NGS) technology represents a novel tool for ROS1 detection that covers many fusion genes. CASE PRESENTATION: A 55-year-old female with EGFR mutation (L858R) was diagnosed with lung adenocarcinoma, who was responsive to first-generation EGFR-tyrosine kinase inhibitor (TKI). Afterwards, she developed acquired resistance accompanied with a ROS1 rearrangement. A NGS assay showed that the tumor had a novel ROS1-ADGRG6 rearrangement generated by the fusion of exons of 1-33 of ROS1 on chr6: q22.1 to exons of 2-26 of ADGRG6 on chr6: q24.2. The patient was obviously responsive to crizotinib. CONCLUSION: We firstly identified ROS1-ADGRG6 fusion variant in NSCLC by NGS, which should be considered in further ROS1 detecting assays.


Assuntos
Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Carcinoma Pulmonar de Células não Pequenas/genética , Crizotinibe/uso terapêutico , Neoplasias Pulmonares/tratamento farmacológico , Neoplasias Pulmonares/genética , Proteínas de Fusão Oncogênica/genética , Inibidores de Proteínas Quinases/uso terapêutico , Proteínas Tirosina Quinases/genética , Proteínas Proto-Oncogênicas/genética , Cromossomos Humanos Par 6/genética , Crizotinibe/farmacologia , Resistencia a Medicamentos Antineoplásicos/genética , Receptores ErbB/antagonistas & inibidores , Receptores ErbB/genética , Éxons/genética , Feminino , Seguimentos , Rearranjo Gênico/genética , Sequenciamento de Nucleotídeos em Larga Escala , Humanos , Pessoa de Meia-Idade , Mutação , Medicina de Precisão , Inibidores de Proteínas Quinases/farmacologia , Proteínas Tirosina Quinases/antagonistas & inibidores , Proteínas Proto-Oncogênicas/antagonistas & inibidores , Resultado do Tratamento
12.
Cancer Sci ; 110(10): 3382-3390, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31444835

RESUMO

Anaplastic lymphoma kinase (ALK) fusions have been recognized as a therapeutic target in non-small cell lung cancer (NSCLC). However, molecular signatures and clinical characteristics of the Chinese population with ALK-rearranged NSCLC are not well elucidated. In the present study, we carried out targeted next-generation sequencing on tissue and plasma ctDNA samples in 1688 patients with NSCLC. Overall, ALK fusions were detected in 70 patients (4.1%), and the frequencies of ALK fusions detected in tissue and plasma samples were 5.1% and 3.3%, respectively. Additionally, the prevalence of breakpoint locations for EML4-ALK fusions in ctDNA was significantly correlated with that in tumor tissues (R2  = .91, P = .045). According to age, the incidence rates of ALK fusions among young (age <45 years), middle-aged (between 45 and 70 years) and elderly (>70 years) patients were significantly different (P < .001). In 70 ALK-rearranged cases, coexistence of epidermal growth factor receptor (EGFR) alterations and ALK fusions was detected in 12 cases (17.1%) and EGFR mutations tended to coexist with non-EML4-ALK rearrangements. Notably, novel ALK fusion partners, including TRIM66, SWAP70, WNK3, ERC1, TCF12 and FBN1 were identified in the present study. Among EML4-ALK fusion variants, patients with variant V1 were younger than patients with variant V3 (P = .023), and TP53 mutations were more frequently concurrent with variant V3 compared with variant V1 (P = .009). In conclusion, these findings provide new insights into the molecular-clinical profiles of patients with ALK-rearranged NSCLC that may improve the treatment strategy of this population.


Assuntos
Quinase do Linfoma Anaplásico/genética , Grupo com Ancestrais do Continente Asiático/genética , Carcinoma Pulmonar de Células não Pequenas/genética , Rearranjo Gênico , Sequenciamento de Nucleotídeos em Larga Escala/métodos , Neoplasias Pulmonares/genética , Adulto , Distribuição por Idade , Idoso , Idoso de 80 Anos ou mais , Feminino , Frequência do Gene , Humanos , Masculino , Pessoa de Meia-Idade , Proteínas de Fusão Oncogênica/genética , Estudos Prospectivos , Análise de Sequência de DNA , Translocação Genética
14.
J Craniofac Surg ; 30(7): 2144-2148, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31232991

RESUMO

Facial asymmetry is a common maxillofacial deformity which requires surgery to recover the 3-dimensional relationship of bones. The computer-aided design and computer-aided manufacturing (CAD/CAM) has been developed and applied to improve orthognathic analysis and surgery design. How to accurately realize the preoperative design of orthognathic surgery with CAD/CAM occlusal splints during operation remains a big problem. In this study, 24 consecutive patients with facial asymmetry were recruited and assigned to 2 groups. For Group A, CAD/CAM was applied to designing and producing not only the occlusal splints, but also the drilling guiding templates and pre-bent titanium plates, and for Group B CAD/CAM was applied for occlusal splints only. Postoperative clinical examinations, symmetry evaluation through 3D cephalometric analysis, accuracy comparison using color distance maps and quantitative accuracy analysis were performed. Symmetry evaluation showed that patients of both groups achieved improved facial symmetry after surgery. The color distance maps and quantitative accuracy analysis together demonstrated significantly less difference found between virtual simulated surgery and postoperative CT scan data in Group A than in Group B. In conclusion, by navigation with the drilling guiding templates and pre-bent titanium plates, the facial symmetry for patients with facial asymmetry was successfully restored after orthognathic surgery, same as applying CAD/CAM occlusal splints only. However, the drilling guiding templates and pre-bent titanium plates would provide a more accurate performance according to preoperative simulation, especially for proximal mandibular segments.


Assuntos
Assimetria Facial/cirurgia , Placas Oclusais , Procedimentos Cirúrgicos Ortognáticos/métodos , Titânio , Adolescente , Adulto , Cefalometria/métodos , Projeto Auxiliado por Computador , Humanos , Mandíbula , Procedimentos Cirúrgicos Ortognáticos/instrumentação , Cirurgia Assistida por Computador/métodos , Tomografia Computadorizada por Raios X/métodos , Adulto Jovem
15.
Biosci Rep ; 39(7)2019 Jul 31.
Artigo em Inglês | MEDLINE | ID: mdl-31221814

RESUMO

Osteosarcoma (OS), the most common malignant bone tumor, is the main cause of cancer-related deaths in children and young adults. Despite the combination of surgery and multi-agent chemotherapy, patients with OS who develop resistance to chemotherapy or experience recurrence have a dismal prognosis. MicroRNAs (miRNAs) are a class of small noncoding RNAs that repress their targets by binding to the 3'-UTR and/or coding sequences, leading to the inhibition of gene expression. miR-221 is found to be up-regulated in tumors when compared with their matched normal osteoblast tissues. We also observed significant miR-221 up-regulation in the OS cell lines, MG-63, SaoS-2, and U2OS, when compared with the normal osteoblast cell line, HOb. Overexpression of miR-221 promoted OS cell invasion, migration, proliferation, and cisplatin resistance. MG-63 and SaoS-2 cells transfected with miR-221 mimics were more resistant to cisplatin. The IC50 of MG-63 cells transfected with control mimics was 1.24 µM. However, the IC50 of MG-63 cells overexpressing miR-221 increased to 7.65 µM. Similar results were found in SaoS-2 cells, where the IC50 for cisplatin increased from 3.65 to 8.73 µM. Thus, we report that miR-221 directly targets PP2A subunit B (PPP2R2A) in OS by binding to the 3'-UTR of the PPP2R2A mRNA. Restoration of PPP2R2A in miR-221-overexpressing OS cells recovers the cisplatin sensitivity of OS cells. Therefore, the present study suggests a new therapeutic approach by inhibiting miR-221 for anti-chemoresistance in OS.

16.
Cell Mol Biol (Noisy-le-grand) ; 65(4): 48-52, 2019 Apr 30.
Artigo em Inglês | MEDLINE | ID: mdl-31078152

RESUMO

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related deaths. Compound K, an active metabolite of ginsenosides, is reported to exhibit anti-cancer property in various types of human malignancies. The present study investigated the role of compound K on glucose metabolism in NSCLC cells and its underlying mechanism. Our study found that compound K dose-dependently inhibited the cell viability of NSCLC cells. Moreover, administration with compound K decreased glucose uptake and lactate secretion under normoxic and hypoxic conditions. Consistently, the expression of key enzymes (HK II, PDK1 and LDHA) involved in glucose metabolism were inhibited in compound K-treated tumor cells. In addition, compound K inhibited the expression of HIF-1α and its downstream gene GLUT1. On the contrary, overexpression of HIF-1α elevated metabolic reactions and partly attenuated the inhibitory role of compound K on NSCLC cell growth. These results demonstrate that compound K suppresses NSCLC cell growth via HIF-1α mediated metabolic alteration, contributing to novel anticancer therapy by targeting glucose metabolism.


Assuntos
Ginsenosídeos/farmacologia , Glucose/metabolismo , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patologia , Morte Celular/efeitos dos fármacos , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Humanos , Subunidade alfa do Fator 1 Induzível por Hipóxia/genética , Neoplasias Pulmonares/enzimologia , Neoplasias Pulmonares/genética
17.
J Craniomaxillofac Surg ; 47(7): 1007-1014, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-30929993

RESUMO

BACKGROUND: Orthognathic surgery is a surgical procedure for the correction of maxillofacial deformities. The existence of condylar resorption before orthognathic surgery affects the selection of surgery time and plan. Besides, condylar resorption after orthognathic surgery often leads to the recurrence of deformities and affects the long-term effect of surgery. The purpose of this study was to perform a systematic review of the management of condylar resorption before or after orthognathic surgery. METHODS: A systematic review of the scientific literature listed on PubMed, Embase, and Cochrane Controlled Trials Register was performed, up to October 2018. The outcome of the search was reviewed with a chart. RESULTS: Ten articles with 180 patients were included in this study based on inclusion and exclusion criteria. We compared these studies to examine the effectiveness of the management of condylar resorption. CONCLUSION: The occurrence of condylar resorption can be influenced by complex factors. The management of condylar resorption before or after orthognathic surgery should base on the severity of condylar resorption. As the eligible studies with small sample sizes, heterogeneity in management method and outcome, high-quality clinical study concerning condylar resorption treatment is needed.


Assuntos
Reabsorção Óssea , Cirurgia Ortognática , Procedimentos Cirúrgicos Ortognáticos , Humanos , Côndilo Mandibular , Duração da Cirurgia
18.
Oncol Lett ; 17(3): 3466-3474, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30867785

RESUMO

C-ros oncogene 1 receptor tyrosine kinase (ROS1) rearrangement forms a novel molecular subgroup of non-small cell lung cancer (NSCLC). The present study explored the clinicopathological features and clinical efficacy of crizotinib in patients with ROS1-positive NSCLC. A retrospective analysis of 2,617 cases of NSCLC diagnosed between January 2013 and December 2016 was performed. ROS1 fusion genes were detected by reverse transcription-quantitative polymerase chain reaction, fluorescence in situ hybridization or next-generation sequencing techniques, and patients positive for the ROS1 fusion gene received oral treatment with crizotinib. The ROS1 fusion was identified in 67 out of 2,617 cases (2.56%), including 21 cases that were male and 46 cases that were female. The median age was 68 years. Among these cases, 59 (88.06%) were adenocarcinoma and 8 were non-adenocarcinoma. According to Tumor-Node-Metastasis (TNM) staging, 4 cases were stage I-IIIa and 63 (94.02%) were stage IIIb-IV. The epidermal growth factor receptor (EGFR) gene status included 60 cases of wild-type, 1 case of co-mutation and 6 unknown cases. Statistically significant differences were identified for sex, TNM staging and EGFR gene status between ROS1 fusion gene-positive and -negative patients (P<0.001). A total of 23 patients received oral treatment with crizotinib, of which 13 (56.52%), 5 (21.74%) and 5 (21.74%) patients demonstrated a partial response, stable disease and progressive disease, respectively. The objective response rate was 56.52% and the disease control rate was 78.26%. Among all patients, the median progression-free survival (mPFS) time was 14.5 months. No differences were revealed in the mPFS time with regard to age, sex, smoking history, performance status score, histopathological type, TNM staging, tumor protein p53 gene status, EGFR gene status and first-line crizotinib treatment, whether by single or multiple factor analysis. The grade 3/4 treatment-associated adverse events included gastrointestinal disturbance, followed by increased transaminase concentration. In conclusion, the rate of ROS1 fusion in NSCLC among the patients is low, and crizotinib is an effective and safe drug for the treatment of ROS1-positive advanced NSCLC.

20.
J Craniofac Surg ; 30(2): 541-547, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30730510

RESUMO

OBJECTIVE: Temporomandibular joint (TMJ) dislocation means the condyle moves out of the normal position. There are several treatments for TMJ dislocation, including conservative treatment, injection treatment, minimally invasive treatment, and open surgical treatment. In this study, we tried to review the literature related to the augmentation of the articular eminence and proposed a modified eminoplasty technique of TMJ dislocation by computer-aided design and computer-aided manufacturing (CAD/CAM) cutting guides. METHODS: The literature on eminoplasty for TMJ was reviewed with 3 charts. Besides, 2 (67 and 69 years old) patients with chronic recurrent dislocation were treated by the CAD/CAM-guided surgical technique in our study, and postoperative measures were recorded to verify the safety and effectiveness regarding this technique. RESULTS: A total of 28 studies (including 268 patients) of the augmentation of the articular eminence have been reported since 1967, including the 2 present patients. According to the analysis of the recurrence and complications in the review, we found the modified technique had an obvious advantage. The technique with cutting guides was also found having higher accuracy. CONCLUSION: The modified technique was a reliable method when treating the TMJ dislocation, and the combination of CAD/CAM cutting guides was useful for more accuracy, even reduced the operation difficulty.


Assuntos
Projeto Auxiliado por Computador , Luxações Articulares/cirurgia , Procedimentos Cirúrgicos Bucais/métodos , Osteotomia/métodos , Articulação Temporomandibular/lesões , Idoso , Humanos , Modelos Anatômicos , Recidiva , Articulação Temporomandibular/diagnóstico por imagem , Articulação Temporomandibular/cirurgia , Zigoma/diagnóstico por imagem , Zigoma/cirurgia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA