RESUMEN
In view of the controversial findings on the utility of D-dimer and carcinoembryonic antigen (CEA) as biomarkers in advanced colorectal cancer (CRC), we evaluated the predictive and prognostic value of the D-dimer and CEA levels in unresectable advanced CRC patients treated with first-line chemotherapy. A total of 57 previously untreated patients with advanced CRC were enrolled. We assessed both plasma D-dimer and CEA levels at the start (D1 and CEA1) and after two cycles (D2 and CEA2) of chemotherapy. Based on the respective optimal cut-off values of 0.8 and 5.0 ng/mL for D1 and CEA1, respectively, patients were divided into low and high D-dimer or CEA groups. The results show that D1 and CEA1 levels were correlated (r = 0.392, P = 0.003). Mean CEA2 was reduced by 26.24 ng/mL in patients with partial response and stable disease and increased by 165.95 ng/mL in patients with progressive disease relative to the CEA1 level (P < 0.001). However, no correlation was evident between changes in the D-dimer levels and chemotherapy response (P = 0.441). The overall survival (OS) of patients with high D1 was shorter than that of patients with low D1 (median OS, 16 vs 29 months, P = 0.009). Multivariate analyses further demonstrated that D1 (P = 0.042) and chemotherapy response (P = 0.016), but not CEA, were independent prognostic factors for OS in advanced CRC. Taken together, our result found that changes in CEA levels may serve as a predictive biomarker of the chemotherapy response and baseline D-dimer levels as a prognostic biomarker of OS in patients with advanced CRC.
RESUMEN
Knowledge of the molecular mechanisms on malignant tumors is very critical for the development of new treatment strategies like molecularly targeted therapies. In last 5 years, many investigations suggest that stathmin is over-expressed in a variety of human malignant tumors, and potentially promotes the occurrence and development of tumors. Rather, down-regulation of stathmin can reduce cell proliferation, motility and metastasis and induce apoptosis of malignant tumors. Thus, a stathmin antagonist, such as a specific inhibitor (antibody, small molecule compound, peptide, or siRNA), may be a novel strategy of molecular targeted therapy. This review summarizes the research progress of recent 5 years on the role of stathmin in tumorigenesis, the molecular mechanisms and development of anti-stathmin treatment, which suggest that continued investigations into the function of stathmin in the tumorigenesis could lead to more rationally designed therapeutics targeting stathmin for treating human malignant tumors.
RESUMEN
BACKGROUND: Endostar is a new endogenous angiogenic inhibitor with implicated anti-tumor activity. This study was to investigate whether thoracic perfusion of Endostar could be used to control malignant pleural effusions (MPE). METHODS: We searched the databases of MEDLINE, Web of Science, EMBASE, Goggle, Cochrance Library and CNKI to select the studies regarding the efficacy of Endostar to treat MPE. A total of 13 randomised controlled trials (RCTs) with 1066 patients were included. RESULTS: The overall response rate (ORR) (P < 0.001; odds ratio = 3.58) and disease control rate (DCR) (P < 0.001; odds ratio = 2.97) of Endostar combined with chemotherapeutic agents were significantly higher than those of chemotherapeutic agents alone. In addition, Endostar combined treatment remarkably promoted quality of life (QOL) of patients (P < 0.001; odds ratio = 3.04) compared with that of chemotherapeutic agents alone. Moreover, Endostar combined treatment did not have an impact on the incidence of adverse reactions (AEs) (P < 0.05). CONCLUSIONS: The efficacy of Endostar combined chemotherapeutic agents was superior to chemotherapeutic agents alone through thoracic perfusion in treating MPE, which indicated that Endostar could be an effective agent for controlling MPE.
Asunto(s)
Inhibidores de la Angiogénesis/administración & dosificación , Antineoplásicos/administración & dosificación , Endostatinas/administración & dosificación , Derrame Pleural Maligno/tratamiento farmacológico , Proteínas Recombinantes/administración & dosificación , Antineoplásicos/efectos adversos , Protocolos de Quimioterapia Combinada Antineoplásica/efectos adversos , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapéutico , Quimioterapia del Cáncer por Perfusión Regional , Endostatinas/efectos adversos , Humanos , Oportunidad Relativa , Derrame Pleural Maligno/patología , Sesgo de Publicación , Calidad de Vida , Ensayos Clínicos Controlados Aleatorios como Asunto , Proteínas Recombinantes/efectos adversos , Resultado del TratamientoRESUMEN
BACKGROUND: Previous studies have disclosed that serum amyloid A (SAA) is likely involved in the lung cancer pathogenesis and progression. We performed a systematic evaluation and meta-analysis to disclose the correlation between the expression of SAA and lung cancer and to evaluate its value for lung cancer diagnosis. METHODS: We searched the relevant articles from the databases of Medline, Embase, Cochrance Library and Web of Science and calculated the standardized mean difference (SMD) with 95 % confidence interval (CI) to assess the expression difference of SAA between lung cancer and normal patients. Moreover, we counted the positive rate, sensitivity and specificity and drew a summary receiver operating characteristic curve (SROC) to evaluate the diagnostic value of SAA for lung cancer. RESULTS: A total of nine studies with 1392 individuals were included in this analysis. The results showed an increased SAA was correlated with the incidence of lung cancer (P < 0.001), especially with the lung squamous cell carcinoma (LSCC) (p = 0.012). The overall sensitivity and specificity of SAA for discerning lung cancer was 0.59 (95 % CI: 0.54-0.63) and 0.92 (95 % CI: 0.88-0.95), respectively. The area under the SROC curve was 0.9066 (SE = 0.0437). CONCLUSIONS: Increased SAA in lung cancer was intimately correlated with the development and progression of lung cancer. A higher specificity of SAA suggested that it should be a significant biomarker for discerning lung cancer from normal individuals, especially for LSCC (p = 0.012).
Asunto(s)
Biomarcadores de Tumor/sangre , Neoplasias Pulmonares/diagnóstico , Proteína Amiloide A Sérica/metabolismo , Progresión de la Enfermedad , Humanos , Neoplasias Pulmonares/sangre , PronósticoRESUMEN
BACKGROUND: Many studies have investigated the efficacy and safety of matrine in treating malignant pleural effusion by thoracic perfusion. This study is an analytic value of available evidence. METHODS: Twelve studies were analyzed in this study. Pooled odds ratios and hazard ratio with 95 % confidence intervals were calculated using the fixed effects model. RESULTS: Overall response rate of matrine combined with other medications in treating malignant pleural effusion (MPE) was significantly higher than those of other medications alone (p < 0.05). Time to pleural effusion relief and quality of life were improved after the treatment of matrine combined with other medications (p < 0.05). Moreover, matrine combined with other medications had a lower incidence of adverse reactions (p < 0.05). CONCLUSIONS: Matrine combined with other medications improves the control of the malignant pleural effusions and decreases the incidence of adverse reactions.
Asunto(s)
Alcaloides/uso terapéutico , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapéutico , Neoplasias Pulmonares/prevención & control , Derrame Pleural Maligno/prevención & control , Calidad de Vida , Quinolizinas/uso terapéutico , Quimioterapia Adyuvante , Humanos , Metaanálisis como Asunto , Perfusión , Pronóstico , MatrinasRESUMEN
BACKGROUND AND OBJECTIVE: Interstitial lung disease with lung cancer (ILD-LC) is rare and its management has not been fully described. This study aimed to investigate the management and prognosis of ILD-LC patients in China. METHODS: The present analysis is a retrospective real-world cohort study. Clinical data of ILD-LC patients were obtained from 3 hospitals in China. The overall survival (OS) of patients was analyzed. Univariate and multivariate regression analyses were performed. RESULTS: One hundred eighty-four ILD-LC patients included were biased toward male (85.3%), smokers (75.5%), idiopathic pulmonary fibrosis (IPF) (58.2%) patients with comorbidities (67.9%) and ECOG-PS score of 1 (65.2%). Most patients were advanced peripheral non-small cell lung cancer. The initial anti-cancer regimen for ILD-LC is mainly chemotherapy, and patients with early-stage LC prefer surgery. In the anti-cancer cohort, the number of ILD-LC patients who underwent the 2nd and 3rd or more anti-cancer regimens were 78 (55.7%) and 32 (22.8%), respectively. In the non-anticancer cohort, the median OS was 3.5 months. In the early-stage cohort, the median OS was 14.2 months in the systematic therapy group; however, the median OS was not reached in the surgery group. In the advanced-stage cohort with systematic therapy, the median OS was 7.2 months. Interstitial pneumonia (IIP) and anti-angiogenesis were associated with OS in the univariate analysis, whereas anti-angiogenesis was an independent protective factor for advanced LC with ILD. CONCLUSION: Patients with ILD-LC have very poor prognosis. Appropriate anti-tumor treatment can prolong the survival time of patients who can tolerate it. Targeted therapy and immunotherapy are alternative treatments for LC patients with mild ILD. For ILD patients with advanced LC, antiangiogenic regimens significantly improve the prognosis of the disease.
RESUMEN
BACKGROUND: Many studies have evaluated the accuracy of EGFR mutation status in blood against that in tumor tissues as the reference. We conducted this systematic review and meta-analysis to assess whether blood can be used as a substitute for tumor tissue in detecting EGFR mutations. METHODS: Investigations that provided data on EGFR mutation status in blood were searched in the databases of Medline, Embase, Ovid Technologies and Web of Science. The detect efficiency of EGFR mutations in paired blood and tissues was compared using a random-effects model of meta-analysis. Pooled sensitivity and specificity and diagnostic accuracy were calculated by receiver operating characteristic curve. RESULTS: A total of 19 studies with 2,922 individuals were involved in this meta-analysis. The pooled results showed the positive detection rate of EGFR mutations in lung cancer tissues was remarkably higher than that of paired blood samples (odds ratio [OR] = 1.47, p<0.001). The pooled sensitivity and specificity of blood were 0.65 and 0.91, respectively, and the area under the receiver operating characteristic curve was 0.89. CONCLUSIONS: Although blood had a better specificity for detecting EGFR mutations, the absence of blood positivity should not necessarily be construed as confirmed negativity. Patients with negative results for blood should decidedly undergo further biopsies to ascertain EGFR mutations.
Asunto(s)
Biomarcadores de Tumor/genética , Carcinoma de Pulmón de Células no Pequeñas/genética , Receptores ErbB/genética , Biomarcadores de Tumor/sangre , Carcinoma de Pulmón de Células no Pequeñas/sangre , Carcinoma de Pulmón de Células no Pequeñas/patología , Receptores ErbB/sangre , Humanos , Mutación , Inhibidores de Proteínas Quinasas/uso terapéuticoRESUMEN
BACKGROUND: Many studies have evaluated the accuracy of EGFR mutation status in blood against that in tumor tissues as the reference. We conducted this systematic review and meta-analysis to assess whether blood can be used as a substitute for tumor tissue in detecting EGFR mutations. METHODS: Investigations that provided data on EGFR mutation status in blood were searched in the databases of Medline, Embase, Ovid Technologies and Web of Science. The detect efficiency of EGFR mutations in paired blood and tissues was compared using a random-effects model of meta-analysis. Pooled sensitivity and specificity and diagnostic accuracy were calculated by receiver operating characteristic curve. RESULTS: A total of 19 studies with 2,922 individuals were involved in this meta-analysis. The pooled results showed the positive detection rate of EGFR mutations in lung cancer tissues was remarkably higher than that of paired blood samples (odds ratio [OR] = 1.47, p<0.001). The pooled sensitivity and specificity of blood were 0.65 and 0.91, respectively, and the area under the receiver operating characteristic curve was 0.89. CONCLUSIONS: Although blood had a better specificity for detecting EGFR mutations, the absence of blood positivity should not necessarily be construed as confirmed negativity. Patients with negative results for blood should decidedly undergo further biopsies to ascertain EGFR mutations.
RESUMEN
Stathmin has been investigated as a tumor biomarker because it appear to be associated with tumorigenesis; however, the effect of stathmin in lung adenocarcinoma (LAC) remains poorly understood. The purpose of this study was to examine the expression of stathmin in lung adenocarcinoma, and to disclose the relationship between them. The expression of stathmin was examined by RT-PCR, IHC and Western blot. Furthermore, small interfering RNA (shRNA)-mediated silencing of stathmin was employed in LAC cells to investigate cell proliferation, invasion and apoptosis. In this study, we showed that overexpression of stathmin was significantly associated with poorly differentiated, lymph node metastasis and advance TNM stages of lung adenocarcinoma. And silencing of stathmin expression inhibited the proliferation, migration and invasion of lung adenocarcinoma PC-9 cells, and retarded the growth of PC-9 cells xenografts in nude mice. Additionally, the anticarcinogenic efficacy of stathmin silencing might be involved in P38 and MMP2 signaling pathways. In conclusion, these results showed that stathmin expression was significantly up-regulated in LAC, which may act as a biomarker for LAC. Furthermore, silence of stathmin inhibiting LAC cell growth indicated that stathmin may be a promising molecular target for LAC therapy.
Asunto(s)
Adenocarcinoma/genética , Adenocarcinoma/patología , Expresión Génica , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/patología , Estatmina/genética , Adenocarcinoma/metabolismo , Adenocarcinoma del Pulmón , Adulto , Anciano , Animales , Apoptosis/genética , Biomarcadores de Tumor , Línea Celular Tumoral , Movimiento Celular/genética , Proliferación Celular , Modelos Animales de Enfermedad , Femenino , Silenciador del Gen , Xenoinjertos , Humanos , Neoplasias Pulmonares/metabolismo , Masculino , Metaloproteinasa 2 de la Matriz/metabolismo , Ratones , Persona de Mediana Edad , Clasificación del Tumor , Estadificación de Neoplasias , ARN Interferente Pequeño/genética , Transducción de Señal , Estatmina/metabolismo , Proteínas Quinasas p38 Activadas por Mitógenos/metabolismoRESUMEN
BACKGROUND@#A lack of effective treatment for lung squamous cell carcinoma (LUSC) makes it an important factor restricting the 5-year survival rate of non-small cell lung cancer (NSCLC). Long non-coding RNA 00668 (LINC00668) was reported to play crucial regulatory roles in the tumorigenesis and progression of various cancers; however, its role in LUSC is unclear. The aim of this study was to investigate the prognosis value and biological function of LINC00668 in NSCLC, especially in LUSC.@*METHODS@#The expression pattern of LINC00668 and its relationship with clinical characteristics and prognosis of patients were investigated in the NSCLC especially LUSC based on The Cancer Genome Altas (TCGA) database. Its function in LUSC cells was explored in vitro.@*RESULTS@#LINC00668 expression was significantly up-regulated in LUSC patients and high expression level of LINC00668 was associated with advanced tumor-node-metastasis (TMN) stage. Moreover, the expression of LINC00668 significantly increased in smoking patients, and was a prognostic indicator for overall survival (OS) of smoking patients with LUSC. In vitro experiments showed that LINC00668 has significantly higher expression level in LUSC cell lines and tissues compared to normal bronchial epithelial cell and para-tumor tissues; meanwhile, functional assay indicated knockdown of LINC00668 effectively inhibited the migration and invasion of LUSC cells.@*CONCLUSIONS@#LINC00668 might closely relate to the development of LUSC, and inhibition of LINC00668 may reduce the metastasis of LUSC.
Asunto(s)
Humanos , Carcinoma de Pulmón de Células no Pequeñas , Carcinoma de Células Escamosas/genética , Movimiento Celular/genética , Pulmón , Neoplasias Pulmonares/genética , ARN Largo no Codificante/genéticaRESUMEN
Icotinib is a new epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that developed and used in China; this work was to evaluate its efficacy and safety in treating non-small cell lung cancer (NSCLC). Clinical studies evaluating the efficacy and safety of icotinib in treating NSCLC were identified from the databases of Medline, Web of Science, Embase and Cochrance Library. Pooled efficacy and safety of icotinib were calculated through a series of predefined search strategies. A total of 15 studies with 2,304 patients were involved in this study. The overall response rate (ORR) and disease control rate (DCR) of icotinib were 40.99% (95% CI: 33.77% to 48.22%) and 77.16% (95% CI: 51.43% to 82.31%). The pooled progression-free survival (PFS) and overall survival (OS) were 7.34 months (95% CI: 5.60 to 9.07) and 14.98 months (95% CI: 9.78 to 20.18). Patients with EGFR mutations exhibited better ORR (OR = 3.67, p < 0.001), DCR (OR = 1.39, p = 0.001) and PFS (11.0 ± 0.76 vs. 1.97 ± 0.82 months). Moreover, patients with rash had a higher ORR (OR = 2.14, p = 0.001) than those without rash. The common adverse effects (AEs) included skin rash (31.4%), diarrhea (14.2%), pruritus (6.7%) and hepatic toxicity (3.8%) and most of them were well tolerated. In conclusion, Icotinib is an effective and well tolerated regimen for Chinese patients with advanced NSCLC. Further randomized trials with large population are required to provide stronger evidence for icotinib in treating NSCLC.
Asunto(s)
Carcinoma de Pulmón de Células no Pequeñas/tratamiento farmacológico , Éteres Corona/uso terapéutico , Neoplasias Pulmonares/tratamiento farmacológico , Quinazolinas/uso terapéutico , Carcinoma de Pulmón de Células no Pequeñas/genética , Éteres Corona/efectos adversos , Diarrea/inducido químicamente , Supervivencia sin Enfermedad , Receptores ErbB/genética , Exantema/inducido químicamente , Humanos , Neoplasias Pulmonares/genética , Mutación , Inhibidores de Proteínas Quinasas/efectos adversos , Inhibidores de Proteínas Quinasas/uso terapéutico , Prurito/inducido químicamente , Quinazolinas/efectos adversos , Resultado del TratamientoRESUMEN
A certain number of studies have showed that p53 gene transfer has an anti-tumor activity in vitro and in vivo. This study was to evaluate the efficacy and safety of thoracic perfusion of recombinant human adenovirus p53 (rAd-p53, Gendicine) for controlling malignant pleural effusion (MPE). We searched for the relevant studies from the database of MEDLINE, Web of Science, EMBASE, Cochrance Library and CNKI to collect the trials concerning the efficacy and safety of rAd-p53 to treat MPE. Fourteen randomised controlled trials (RCTs) with 879 patients were involved in this analysis. The rAd-p53 combined with chemotherapeutic agents significantly improved the overall response rate (ORR) (P < 0.001; odds ratio = 3.73) and disease control rate (DCR) (P < 0.001; odds ratio = 2.32) of patients with MPE as well as the quality of life (QOL) of patients (P < 0.001; odds ratio = 4.27), compared with that of chemotherapeutic agents alone. In addition, the participation of rAd-p53 did not have an obvious impact on the most of incidence of adverse reactions (AEs) (P < 0.05) except the fever (P < 0.001). However, the fever was self-limited and could be tolerated well. The application of rAd-p53 through thoracic perfusion for treating MPE had a better efficacy and safety, which could be a potential choice for controlling MPE.
Asunto(s)
Antineoplásicos/administración & dosificación , Productos Biológicos/administración & dosificación , Terapia Genética/métodos , Derrame Pleural Maligno/tratamiento farmacológico , Proteínas Recombinantes/administración & dosificación , Proteína p53 Supresora de Tumor/administración & dosificación , Adenovirus Humanos/genética , Adulto , Anciano , Anciano de 80 o más Años , Antineoplásicos/efectos adversos , Productos Biológicos/efectos adversos , Portadores de Fármacos , Femenino , Terapia Genética/efectos adversos , Vectores Genéticos , Humanos , Masculino , Persona de Mediana Edad , Ensayos Clínicos Controlados Aleatorios como Asunto , Proteínas Recombinantes/efectos adversos , Resultado del Tratamiento , Proteína p53 Supresora de Tumor/efectos adversosRESUMEN
Stathmin has been investigated to be involved in development and progress of malignant tumors. This study was to clarify the relationship between expression of stathmin and tumors and assess its clinical significance. We identified 25 studies with a total of 3,571 individuals from the electronic bibliographic databases and strictly evaluated the quality and heterogeneity of included studies. We analysed the relationship between expression of stathmin and clinical characteristics by the fixed-effects and random-effects of meta-analysis and constructed a summary receiver-operator characteristic curve to estimate the test characteristics. The results showed that patients with cancer displayed a higher stathmin expression than those of non-cancer individuals (OR, 0.31), and overexpression of stathmin correlated with tumor cell differentiation (OR, 0.73), lymph node invasion (OR, 0.80) and high TNM stage (OR, 0.67). The pooled sensitivity of stathmin for distinguishing malignant tumors was 0.73 and the specificity was 0.77. The maximum balance joint for sensitivity and specificity (the Q-value) was 0.7566 and the area under the curve (AUC) was 0.8234. In conclusion, these results showed that overexpression of stathmin intimately correlated with malignant behavior of tumors, suggesting it could be a risk factor of malignant tumors. Stathmin had great sensitivity and specificity indicated it should be a significant molecular biomarker for malignant tumors.
Asunto(s)
Neoplasias/patología , Estatmina/metabolismo , Regulación hacia Arriba , Anciano , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , Masculino , Persona de Mediana Edad , Metástasis de la Neoplasia , Estadificación de Neoplasias , Neoplasias/metabolismo , Curva ROC , Análisis de SupervivenciaRESUMEN
The invasion and metastasis of malignant tumor cells lead to normal tissue destruction and are major prognostic factors for many malignant cancers. Long non-coding RNA (LncRNA) is associated with occurrence, development and prognoses of non-small cell lung cancer (NSCLC), but its mechanisms of action involved in tumor invasion and metastasis are not clear. In this study, we screened and detected the expression of LncRNA in two NSCLC lines 95D and 95C by using high throughput LncRNA chip. We found that TATDN1 (Homo sapiens TatD DNase domain containing 1, TATDN1), one of LncRNAs, was highly expressed in 95D cells and NSCLC tumor tissues compared to 95C cells. Knockdown of TATDN1-1 by shRNA significantly inhibited cell proliferation, adhesion, migration and invasion in 95D cells. Further mechanism study showed that TATDN1 knockdown suppressed the expression of E-cadherin, HER2, ß-catenin and Ezrin. Moreover, knockdown TATDN1 also inhibited tumor growth and metastasis in a 95D mouse model in vivo by inhibiting ß-catenin and Ezrin. These data indicate that TATDN1 expression is associated with 95D cells' higher potential of invasion and metastasis, and suggest that TATDN1 may be a potential prognostic factor and therapeutic target for NSCLCs.
Asunto(s)
Carcinoma de Pulmón de Células no Pequeñas/genética , Carcinoma de Pulmón de Células no Pequeñas/patología , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/patología , ARN Largo no Codificante/genética , Animales , Cadherinas/metabolismo , Línea Celular Tumoral , Proteínas del Citoesqueleto/metabolismo , Humanos , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Desnudos , Invasividad Neoplásica/genética , Interferencia de ARN , ARN Largo no Codificante/metabolismo , ARN Interferente Pequeño/genética , Receptor ErbB-2/metabolismo , beta Catenina/metabolismoRESUMEN
BACKGROUND@#Solitary pulmonary nodule has received increasing attention in recent years. A couple of lung nodules have been recognized as primary malignant tumors, which leads to an urgent need in enhancing the diagnosis of benign/malignant lung nodules at clinical settings. This study aims to explore the value of the combined detection of cytokines and tumor markers in differencing benign and malignant solitary pulmonary nodules in diagnose.@*METHODS@#With 81 solitary pulmonary nodules cases with a clear diagnosis, the general clinical data, nodule imaging features, pathological diagnosis data, serological index cytokine series and tumor marker expression levels were collected in groups. Both single factor and multi-factors analysis were conducted to screen out the serum influence indexes that can predict the malignant probability of lung nodules, and mean while binary logistic regression analysis was used to construct joint indexes; After receiver operating characteristic curve (ROC) was drawn, the area under the curve and the corresponding sensitivity, specificity and positive of each index predicted value, negative predicted value and accuracy could be calculated with a view to determine the statistical significance of area under the curve (AUC).@*RESULTS@#There are differences in the distribution of malignant solitary pulmonary nodules at different locations, with the highest proportion of the right upper lobe (40.4%). The serum levels of carcinoembryonic antigen (CEA), cytokeratin 19 fragment 21-1 (CYFRA21-1), interleukin-6 (IL-6), interleukin-8 (IL-8) in the malignant nodule group were higher than those in the benign nodule group. Logistic regression analysis suggests that CEA, IL-6 and IL-8 are independent risk factors for predicting malignant nodules. ROC curve analysis shows that the areas under the curve of the individual indicators CEA, IL-6 and IL-8 are 0.642, 0.684 and 0.749. The comparison result of the test efficiency of the area under the curve suggests that CEA+IL-6+IL-8 has a larger area under the curve and higher detection efficiency.@*CONCLUSIONS@#CEA, IL-6 and IL-8 are independent risk factors for malignant solitary pulmonary nodules. The combined detection of cytokines and tumor markers has played a role in the differential diagnosis of benign and malignant lung nodules. The diagnostic value of the combined detection of CEA+IL-6+IL-8 is the highest.
RESUMEN
Since mid-December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has outbroken in Wuhan, Hubei Province, China, and spread rapidly to other provinces in China and dozens of countries and regions around the world, becoming the Public Health Emergency of International Concern (Public Health Emergency of International Concern). SARS-CoV-2 can mainly transmit by droplets or close contact, and is generally susceptible in the crowd. Tumor patients are at high risk of this pathogen because of their impaired immune function. Identifying tumor patients with 2019 novel coronavirus disease (COVID-19) early, and understanding its distribution characteristics can help to improve the cure rate of patients, and better control the epidemic and development of SARS-CoV-2 much better. With comprehensive analysis of relevant literature, this paper reviews the clinical characteristics of neoplastic patients with COVID-19, and puts forward some suggestions on how to deal with this epidemic.
Asunto(s)
Humanos , Betacoronavirus , Infecciones por Coronavirus , Epidemiología , Epidemias , Neoplasias , Pandemias , Neumonía Viral , EpidemiologíaRESUMEN
Annexin A1 is a 37 kDa calcium and phospholipid-binding protein that participates in several biological processes, such as inflammatory reactions, modulation of cell proliferation, regulation of cell death signaling, apoptosis, and, most importantly, tumor formation and development. Although annexin A1 has been implicated in the biology of various tumors, the findings are highly controversial and information regarding the underlying mechanism remains limited. Moreover, the mechanism by which annexin A1 participates in carcinogenesis and tumor progression is rather unclear. In the current study, we review the important biological functions of annexin A1 in different tumors. This work indicates that annexin A1 is a possible target for novel therapeutic intervention and that it is a potential biomarker for tumor diagnosis and screening.
Asunto(s)
Anexina A1/genética , Neoplasias/genética , Transducción de Señal/genética , Apoptosis/genética , Regulación Neoplásica de la Expresión Génica , Humanos , Neoplasias/diagnóstico , Neoplasias/patologíaRESUMEN
AIM: Hsp90-ß and annexin A1 have been demonstrated to be associated with tumorigenesis. However, the effect of Hsp90-ß and annexin A1 in lung cancer remains poorly understood. In this research, the correlation of Hsp90-ß and annexin A1 in lung cancer patients were analyzed. METHODS: The expression levels of Hsp90-ß and annexin A1 were examined by immunohistochemistry and ELISA. RESULTS: Lung cancer tissues and serum exhibited higher co-expression of Hsp90-ß and annexin A1 than control groups (p < 0.05). Hsp90-ß and annexin A1 could discriminate lung cancer from the control groups (sensitivity of Hsp90-ß was 80.2% in tissues and 96% in serum; specificity of Hsp90-ß was 80% in tissues and 83.33% in serum; sensitivity of annexin A1 was 68.76% in tissues and 95.23% in serum; specificity of annexin A1 was 75% in tissues and 85.7% in serum) and multi-index combined detection had a better diagnostic value. CONCLUSION: The expression levels of Hsp90-ß and annexin A1 positively correlated and such co-overexpression of Hsp90-ß and annexin A1 contributed to lung cancer diagnosis.
Asunto(s)
Anexina A1/genética , Regulación Neoplásica de la Expresión Génica , Proteínas HSP90 de Choque Térmico/genética , Neoplasias Pulmonares/diagnóstico , Neoplasias Pulmonares/genética , Adulto , Anciano , Anexina A1/sangre , Anexina A1/metabolismo , Biomarcadores de Tumor , Estudios de Casos y Controles , Femenino , Proteínas HSP90 de Choque Térmico/sangre , Proteínas HSP90 de Choque Térmico/metabolismo , Humanos , Neoplasias Pulmonares/metabolismo , Masculino , Persona de Mediana Edad , Clasificación del Tumor , Metástasis de la Neoplasia , Estadificación de Neoplasias , Pronóstico , Curva ROC , Reproducibilidad de los Resultados , Factores de RiesgoRESUMEN
INTRODUCTION: Many studies have investigated the usefulness of cytokeratin 19 fragments (CYFRA 21-1) in pleural fluid for the differential diagnosis of benign (BPE) and malignant pleural (MPE) effusions. In the present meta-analysis, the reported studies on the diagnosis between CYFRA 21-1 and pleural effusion were assessed to summarize the diagnostic characteristics of CYFRA 21-1 in Chinese patients. MATERIAL AND METHODS: The data sources from the creation of each database up to January 2011 included Medline, Chinese National Knowledge Infrastructure, EMBASE, Cochrane Library, and bibliographies of review and original articles. Through a systematic literature search for publications, the data from 22 studies were summarized based on their discussions on the result of the CYFRA 21-1 assay in pleural effusion and differential diagnosis evaluation in the Chinese population. RESULTS: A total of 22 studies were available for analysis, and the high CYFRA 21-1 level in MPE was significantly associated with risk for lung cancer (standardized mean difference [SMD] = 1.65, 95% confidence interval [CI] = 1.48-1.82, Z = 18.97, p < 0.00001) compared with BPE. The CYFRA 21-1 level in pleural effusion (13 studies) was significantly higher than that in serum (SMD = 1.10, 95% CI = 0.71-1.48, Z = 5.59, p < 0.00001). The risk for squamous cell carcinoma (SCC) for CYFRA 21-1 was 1.03 (95% CI = 0.64-1.42, Z = 5.15, p < 0.00001) compared with that of adenocarcinoma (8 studies). The sensitivity of CYFRA 21-1 reported in the articles ranged from 46% to 94%, and the specificity ranged from 57% to 100%. The summary measure of the test characteristics derived from the summary receiver operating characteristic curve was 81% for both sensitivity and specificity (17 studies). CONCLUSIONS: The measurement of pleural CYFRA 21-1 is likely to be a useful diagnostic tool for the confirmation of MPE.
RESUMEN
PURPOSE: Gefitinib is a well known therapy for non-small-cell lung cancer (NSCLC). The purpose of this study was to review clinical reports of gefitinib as maintenance therapy after first-line chemotherapy regardless of epidermal growth factor receptor (EGFR) mutation, and assess its efficacy and safety in Chinese patients. MATERIALS AND METHODS: Systematic computerized searches of the following databases were conducted from the start of each database up to July 2012; these include Medline, EMBASE, CNKI and www.clinicaltrials.gov. Terms searched include 'non-small-cell lung cancer', 'NSCLC', 'lung cancer', 'lung tumor', 'gefitinib', 'Iressa', 'EGFR' and 'epidermal growth factor receptor tyrosine kinase inhibitors'. A total of 22 studies were reviewed. RESULTS: In general, the overall response rate (ORR), disease control rate (DCR) and one year survival (OYS) of gefitinib maintenance therapy were 30.89%, 67.5% and 50.6% respectively, in addition, the median overall survival (OS) and median progression free survival (PFS) were 13.09 and 7.88 months respectively. Moreover, ORR, DCR, median survival time (MST) and PFS of female, nonsmoking, lung adenocarcinoma (LAC) patients and patients with rash had higher performance than male, smoking, non-LAC patients and patients without rash (p < 0.05). The adverse events (AEs) were mainly skin rashes and diarrhea, most of which were grades 1 or 2 and were well tolerated. CONCLUSION: Gefitinib produced encouraging efficacy, safety and survival when delivered as maintenance therapy for NSCLC in Chinese patients after first-line chemotherapy regardless of EGFR mutation, especially for the patients who were female, non-smokers, LAC and with rash. Key limitations of this review include limited subgroup data, small sample sizes, and the lack of EGFR/KRAS data.