Incorporation of circulating tumor cells and whole-body metabolic tumor volume of 18F-FDG PET/CT improves prediction of outcome inⅢB stage small-cell lung cancer

Objective: We investigated the correlation between the number of circulating tumor cells(CTCs) and wholebody metabolic tumor volume(WBMTV) measured by 18 F-fluorodeoxyglucose(FDG) positron emission tomography/computed tomography(PET/CT).The aim was to evaluate the value of the incorporation of CTC number and WBMTV in the prognostic prediction of stage III small-cell lung cancer(SCLC).Methods: One hundred and twenty-nine patients were enrolled in this study.All patients were treated with four cycles of a platinum-based regimen and concurrent chest irradiation,followed by prophylactic cranial irradiation.Blood samples for CTC analysis were obtained from 112 patients before the initiation of chemotherapy(as a baseline),after cycle 1 and after cycle 4.CTCs were measured using the CELLSEARCH? system.The patients underwent pretreatment FDG PET/CT WBMTV,which included all malignant lesions.The Spearman rank test was used to determine the correlation among CTC counts,WBMTV and disease stage.Overall survival(OS) and progression-free survival(PFS) curves were produced using the Kaplan-Meier method,and survival differences between groups were assessed by the log-rank test.Results: The number of CTCs at baseline did not correlate with WBMTV before the initiation of therapy(P=0.241).The number of CTCs at baseline and the WBMTV before the initiation of therapy were independent relevant factors for PFS and OS.The subgroup analysis(Group A: CTC count >19.5 and a WBMTV >266.5cm~3;Group B: CTC count >19.5 and a WBMTV ≤266.5cm~3; Group C: CTC count ≤19.5 and a WBMTV >266.5cm~3;Group D: CTC count ≤19.5 and a WBMTV ≤266.5cm~3) showed that the differences were statistically significant in the median PFS(Group A vs.D,P<0.001; Group B vs.D,P=0.018; Group C vs.D,P=0.029) and in the median OS(Group A vs.D,P<0.001; Group B vs.D,P=0.012).Conclusions: CTC number and WBMTV are related to progression and death in patients with SCLC.The incorporation of CTC number and WBMTV scans can provide a detailed prognostic prediction for SCLC.

Endostatin enhances antitumor effect of tumor antigen-pulsed dendritic cell therapy in mouse xenograft model of lung carcinoma

Objective： To investigate the antitumor effect of endostatin combined with tumor antigen-pulsed dendritic cell （DC）-T cell therapy on lung cancer. Methods： Transplanted Lewis lung cancer （LLC） models of C57BL/6 mice were established by subcutaneous injection of LLC cells in left extremity axillary. Tumor antigen-pulsed DC-T cells from spleen cells and bone of mice were cultured in vitro. Tumor-bearing mice were randomly divided into three groups, including DC- T＋endostatin group, DC-T group, and phosphate-buffered saline （PBS） control group. Microvessel density （MVD） of tumor tissue in tumor-bearing mice was determined by immunohistochemistry （IHC）. The expressions of vascular endothelial growth factor （VEGF） and hypoxia-inducible factor-1α （HIF-1α） were determined by Western blotting and IHC staining. The proportions of CD8＋ T cells, mature dendritic cells （mDC）, tumor-associated macrophages [TAM （M1/M2）], and myeloid-derived suppressor cells （MDSC） in suspended cells of tumor tissue were determined by flow cytometry. The expressions of inter｜eukin （IL）-6, IL-10, IL-17, transforming growth factor-β（TGF-β） and interferon-γ （IFN-γ） in suspended cells of tumor tissue were detected by enzyme-linked immune sorbent assay （ELISA）. Results： DC-T cells combined with endostatin remarkably suppressed tumor growth. MVD of mice in DC- T＋endostatin group was significantly lower than that of the control group and DC-T monotherapy group. The expressions of VEGF, IL-6 and IL-17 in tumors were markedly decreased, but IFN-γ, and HIF-1α increased after treating with DC-T cells combined with endostatin, compared to control group and DC-T group. In the DC- T＋endostatin group, the proportions of MDSC and TAM （M2 type） were significantly decreased, mDC and TAM （Nil type） were up-regulated, and CD8＋ T cells were recruited to infiltrate tumors, in contrast to PBS control and DC-T monotherapy. DC-T cells combined with endostatin potently reduced the expressions of IL-6, IL-10, TGF-β and IL-17 in tumor tissue, and enhanced the expression of IFN-γ. Conclusions： The study indicated the synergic antitumor effects between endostatin and tumor antigen-pulsed DC-T cells, which may be a prospective therapy strategy to achieve potent antitumor effects on lung cancer.

Implication of serum levels of interleukin-18 and nitric oxide in tumor growth and metastasis of non-small cell lung cancer

To study the effect of IL-18 and nitric oxide(NO) on the growth and metastasis of non-small cell lung cancer (NSCLC).Methods Serum IL-18 and nitrate and nitrite levels in 82 patients with NSCLC and 20 healthy control subjects were measured by using ELISA and Griess.Results The levels of serum IL-18 were (334.2±31.0)ng/L in NSCLC patients and (151.3±22.0)ng/L in control subjects,respectively.The levels of nitrate and nitrite were (237.1±21.0)μmol/L in NSCLC patients and (44.2±15.0)μmol/L in control subjects.The levels of serum IL-18 and nitrate and nitrite were not related with age,gender,histological types in patients with NSCLC.The levels of serum IL-18 was closely associated with TNM stage,lymph node metastasis and distal metastasis,but not with its degree and organ types of metastasis.There was a negative correlation between the levels of serum IL-18 and nitrate and nitrite.Conclusion Serum IL-18 and nitrate and nitrite levels may be useful to evaluate the prognosis of the patients with NSCLC.16 refs,2 tabs.

Tumor response assessment by the single-lesion measurement per organ in small cell lung cancer

Background： The criterion of two target lesions per organ in the Response Evaluation Criteria in Solid Tumors （RECIST） version I. 1 is an arbitrary one, being supported by no objective evidence. The optimal number of target lesions per organ still needs to be investigated. We compared tumor responses using the RECIST 1.1 （measuring two target lesions per organ） and modified RECIST I. 1 （measuring the single largest lesion in each organ） in patients with small cell lung cancer （SCLC）. Methods： We reviewed medical records of patients with SCLC who received first-line treatment between January 2004 and December 2014 and compared tumor responses according to the two criteria using computed tomography. Results： There were a total of 34 patients who had at least two target lesions in any organ according to the RECIST 1.1 during the study period. The differences in the percentage changes of the sum of tumor measurements between RECIST 1.1 and modified RECIST 1.1 were all within 13%. Seven patients showed complete response and fourteen showed partial response according to the RECIST I.I. The overall response rate was 61.8%. When assessing with the modified RECIST 1.1 instead of the RECIST 1.1, tumor responses showed perfect concordance between the two criteria （k= 1.0）. Conclusions： The modified RECIST 1.I showed perfect agreement with the original RECIST 1.I in the assessment of tumor response of SCLC. Our result suggests that it may be enough to measure the single largest target lesion per organ for evaluating tumor response.

DIAGNOSTIC VALUE OF SERUM PROGRP31-98 IN PATIENTS WITH SMALL-CELL LUNG CANCER

Objective To explore the clinical significance of serum level of pro gastrin releasing peptide 31 98 (ProGRP31 98) for small cell lung cancer (SCLC), in comparison with neuron specific enolase (NSE). Methods Serum level of ProGRP31 98 and NSE was measured by ELISA respectively in 30 patients with SCLC, 30 with non small cell lung cancer (NSCLC), 15 with benign lung diseases and 15 normal subjects, additionally, 10 SCLC patients after having treatment with chemotherapy were included. The receiver operating characteristic (ROC) curve was used to set the cut off value and evaluate the diagnostic accuracy. Results The serum level of ProGRP31 98 was higher in patients with SCLC than that in other groups. The SCLC patients with extensive disease had a higher value than the patients with limited disease. In SCLC patients with distant metastases, it was also higher than in those without. Increase in serum ProGRP31 98 and NSE was both seen in SCLC patients, but for the former one, the increase was of much greater compared to the normal controls. Given the cut off value for ProGRP31 98 was 40ng·L -1 and for NSE 8μg·L -1 , their sensitivity of diagnosis in SCLC was 73% and 60%, respectively. The area under ROC curve of ProGRP31 98 was significantly larger than that of NSE. All patients responded to chemotherapy showed marked decrease in ProGRP31 98. Conclusion ProGRP31 98 is a more specific and sensitive marker than NSE in the diagnosis of SCLC.

HYPERMETHYLATION OF p14^(ARF) PROMOTER REGION AND EXPRESION OF p14^(ARF) GENE PRODUCT IN NON-SMALL CELL LUNG CANCER

Objective： This study was designed to investigate promoter methylation status and protein expression of p14^ARF gene in non-small cell lung cancer, and value the role of p14^ARF promoter methylation in carcinogenesis of non-small cell lung cancer. Methods： Promoter methylation status and protein expression of p14^ARF gene in 40 cases of non-small cell lung cancer were analyzed by methylation specific polymerase china reaction （MSP）, restriction enzyme-related polymerase chain reaction （RE-PCR） and immunohistochemistry （IHC）. Results： The positive rates of p14^ARF promoter methylation in tumor tissues and normal tissues adjacent to cancer were 17.5% （7/40） and 2.5% （1/40） respectively. There were statistically significant differences between them, P〈0.05. The results of RE-PCR were consistent with that of MSP. The expression rate of p14^ARF protein in tumor tissues was significantly lower than that in normal tissues adjacent to cancer, p〈0.01. Promoter methylation status and protein expression of p14^ARF gene in non-small cell lung cancer showed significantly an inverse correlation （r=-0.56, P〈0.01）, and both of them did not relate statistically with the clinicopathologic characteristics of patients such as histological classification, clinical stage, differentiation grade and lymph node involvement. Conclusion： Promoter methylation is a crucial mechanism of inactivation of p14^ARF gene. Promoter methylation of p14^ARF gene might he involved in carcinogenesis of non-small cell lung cancer, and is an early event in development process of non-small cell lung cancer. It might be used as a new target in gene treatments in the future.

Immunity of Unloaded Dendritic Cells in Lung Melanoma of Mice

In order to investigate the immunity of unloaded dendritic cells （DCs） derived from murine bone marrow to preexisting lung melanoma metastases of mice, MO5 were intravenously injected to induce lung metastases in syngeneic C57BI-/6 mice. Unloaded GM-CSF DCs, PBS and DCs＋SIINFEKEL were subcutaneously injected into the mice, which were divided as experimental group, negative control group and positive control group respectively. Monoclonal antibody was used to deplete NK or T cells separately. The immunity-inhibitory effects on the lung melanoma were observed and the corresponding effector cells were examined. It was found that in the experimental and positive groups, the regression was induced in metastatic nodules in the lungs of tumor-bearing mice, but abrogated by treatment with anti-asialo-GM1 but not anti-CD8. It was concluded that the unloaded DCs could suppress the lung melanoma metastases to some extent, which was mediated by NK cells, and could be used as a potent therapeutic agents for lung tumor.

Antineoplastic effects of deoxyelephantopin,a sesquiterpene lactone from Elephantopusscaber, on lung adenocarcinoma (A549) cells

OBJECTIVE： Deoxyelephantopin, a sesquiterpene lactone from Elephantopus scaber, showed inhibition of the growth of various tumor cells in vitro. In the present study, we investigated the cytotoxicity and apoptosis-inducing capacity of deoxyelephantopin on lung adenocarcinoma （A549） cells. METHODS： The cytotoxic effect of deoxyelephantopin on A549 cells and normal lymphocytes was evaluated using 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay and 50% inhibitory concentration （IC50） value was determined. The self-renewal and proliferating potential of A549 cells after treatment with deoxyelephantopin were examined by colony formation assay. Cellular morphology of deoxyelephantopin-treated cells was observed using phase- contrast microscopy. The induction of apoptosis was evaluated using acddine orange and ethidium bromide staining, Hoechst 33342 staining, terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end-labeling （TUNEL） assay, DNA fragmentation analysis and Annexin V-fluorescein isothiocyanate staining by flow cytometry. Activation of caspases was detected using fluorogenic substrate specific to caspases 2, 3, 8 and 9 and flow cytometric analysis. The total cellular DNA content and expression of cleaved poly （ADP-ribose） polymerase was also analyzed. RESULTS： Deoxyelephantopin exhibited cytotoxicity to A549 cells （IC50 = 12.287 μg/mL）, however, there was no toxicity towards normal human lymphocytes. Deoxyelephantopin suppressed the colony-forming ability of A549 cells in a dose-dependent manner. Acridine orange, ethidium bromide and Hoechst 33342 staining showed cell shrinkage, chromosomal condensation and nuclear fragmentation, indicating induction of apoptosis. Deoxyelephantopin increased apoptosis of A549 cells, as evidenced by more TUNEL-positive cells. DNA fragmentation and Annexin V staining revealed late-stage apoptotic cell population. Deoxyelephantopin inhibited A549 cell growth by cell cycle arrest at G2/M phase and induced apoptosis through both extrinsic and intrinsic pathways. CONCLUSION： These results suggest that deoxyelephantopin has great potential as a new chemotherapeutic agent to be developed further for the treatment of lung cancer.

Significance of Multimodality Therapy in Patients with a Superior Sulcus Tumor of the Lung: A Review Article

Despite the aggressive pursuit of diagnostic and treatment modalities for lung cancer, the treatment outcomes are still not satisfactory, and even patients with surgically resectable non-small cell lung cancer (NSCLC) are often at considerable risk of suffering recurrence and/or death from lung cancer. Regarding the treatment of patients with locally advanced, resectable NSCLC, several retrospective and prospective studies have shown the significance of multimodality treatments with preoperative chemoradiotherapy and surgical treatment. However, no definitive treatment strategies for locally advanced NSCLC patients have yet been established. One of the reasons for the lack of established treatment strategies for patients with locally advanced NSCLC is considered to be the heterogeneity of the population, i.e., cT4N0, cT3-4N1 and cT1a-3N2 tumors are included in stage IIIA disease, and superior sulcus tumors (SSTs) are also included in this classification. With regard to SST, two representative prospective phase II trials indicated the efficacy of surgical treatment following concurrent radiation and chemotherapy. In a study conducted by the Southwest Oncology Group, 110 patients with superior sulcus NSCLC were treated with two cycles of cisplatin and etoposide concurrently with 45 gray (Gy) of radiation, followed by surgical treatment and two additional cycles of chemotherapy postoperatively. The response rate (RR) to the preoperative chemoradiotherapy was 86%, and 83 patients (76%) were able to undergo complete resection. A pathological complete response (CR) was observed in 61 patients (56%), and the five-year survival of all patients and those undergoing complete resection was 44% and 54%, respectively. A phase II study conducted by the Japan Clinical Oncology Group examined the safety and efficacy of preoperative concurrent chemoradiotherapy using mitomycin, vinblastin and cisplatin followed by surgical treatment. Seventy-six patients with SST were enrolled in this study, and all received chemotherapy using two cycles of MVP concurrently with 45 Gy of radiation, followed by surgery. Neoadjuvant chemoradiotherapy resulted in a 61% RR, and pathological complete resection was successfully achieved in 51 patients (68%). A pathological CR was observed in 12 patients (16%), and the disease-free and overall survival rates at five years were 45% and 56%, respectively. Both studies showed the efficacy and tolerability of the multimodality treatment for SST, thus suggesting that multimodality treatment with preoperative chemoradiotherapy followed by surgery may therefore be an effective treatment for resectable SST. We herein review the results of retrospective and prospective studies while assessing the treatment outcomes of NSCLC patients with SST.

Transfection of Nm23-H1 Gene Inhibited the Metastatic Potential of Human High-metastatic Large Cell Lung Cancer L9981

Background and objective Invasion and metastasis is not only the malignant phenotypes of lung cancer but also the main cause of death. Elucidating the molecular mechanism of

Expression of STAT3 in non-small cell lung cancer and its clinical significance

Signal transducer and activator of transcription 3(STAT3) plays an important role in tumor occurrence and development. Here we attempt to evaluate the clinical diagnostic value of STAT3 as a potential tumor marker by detecting the expression of STAT3 in blood of non-small cell lung cancer (NSCLC) patients. Immunohistochemistry was applied to detect STAT3 protein in A549 cells and MRC-5 cell, real time PCR was applied to detect STAT3 mRNA and ELISA was applied to detect the expression of STAT3 protein in NSCLC patients, benign lung disease group and healthy controls. The expression levels of STAT3 mRNA and STAT3 protein in A549 cells and NSCLC patients were significantly higher (P < 0.01). The areas under ROC curves (Az) of STAT3 mRNA and STAT3 protein were 0.870 and 0.860 respectively, which had no significant difference (P > 0.05). When comparing the Az of STAT3 protein with CEA, CA125 and CYFRA21-1 respectively, there was no significant difference (P > 0.05). And we compared the Az of the four joint detection (STAT3 + CEA + CA125 + CYFRA21-1) with the three joint detection (CEA + CA125 + CYFRA21-1), 0.930 and 0.841, respectively, P < 0.05. It appears that the diagnostic value and accuracy of STAT3 is equivalent with CEA, CA125, and CYFRA21-1 in NSCLC, and to joint with other three can achieve higher diagnosis value.

POST-OPERATIVE STAGING AND SURVIVAL BASED ON THE REVISED TNM STAGING SYSTEM FOR NON-SMALL CELL LUNG CANCER

Objective: To study the factors affecting post-operative staging and survival in non-small cell lung cancer (NSCLC) patients based on the revised TNM staging system adopted by the UICC in 1977. Methods: Data were collected from 1757 consecutively operated NSCLC patients, including those receiving complete tumor excision, tumor debulking and exploratory thoractomy from April 1969 through Dec. 1993. the end point of follow-up was Nov. 30, 1998. Cumulative survival and its influencing factors were analyzed by Kaplan-Meier and Cox model of SPSS software. Results: In this series, 30 patients (1.7%) were lost from follow-up. The 5-year cumulative survival was 88.0% for patients in stage I A, and 53.9% in stage IB, 33.5% in stage II, 14.7% in stage III A, 5.5% in stage IIIB and 7.0% in stage IV. The overall 5-year survival rate was 28.2%. The 5-year survivals were 39.8%, 14.4% and 4.2% in patients treated with completely tumor resection, tumor debulking and explorative thoractomy, respectively. The 10-year survival rate was 31.4%, 9.5% and 0, respectively. Factors affecting long-term cumulative survival, in the order of decreasing significance, were the type of operation, lymph node status, staging, size and pathological type of the primary tumor. Conclusion: the revised staging system for NSCLC is superior to that used since 1986 as far as the end results of treatment in patients in different stage and the staging specificity are concerned. The T3N1M0 classification and the definition of Ml need to be further studied.

Influence of Nm23-H1 Gene Site Mutagenesis on Invasive And Metastatic Phenotype in Human High-Metastatic Large Cell Lung Cancer Cell Line L9981

Background and Objective Invasion and metastasis is not only the malignant phenotypes of lung cancer but also the main cause of death. To study and elucidate the molecular mechanism

影像组学在非小细胞肺癌肿瘤微环境及免疫治疗中的研究进展

非小细胞肺癌是肺癌中最常见的组织学类型。近年来,随着免疫治疗的兴起,部分无法手术或靶向治疗无效的非小细胞肺癌病人获得了延长生存时间的机会。但是,由于肿瘤微环境的影响,免疫治疗的效果存在不确定性。因此,急需一种新的方式来监测肿瘤微环境的变化和免疫治疗效果。影像组学可以无创、实时和定量地分析医学图像,反映疾病更深层次的信息,已广泛应用于疾病诊断和鉴别诊断、肿瘤分期分级、疗效评价和预后预测等领域。现围绕影像组学在非小细胞肺癌肿瘤微环境及免疫治疗方面的研究进展进行综述。

肿瘤标志物在非小细胞肺癌复发检验中的应用效果分析

目的分析肿瘤标志物在非小细胞肺癌复发检验中的应用效果。方法纳入永煤集团总医院2022年3月至2024年6月的72例非小细胞肺癌患者为研究样本。根据病理分型将患者分为42例肺腺癌患者与30例肺鳞癌患者。所有患者入院后均接受血清肿瘤标志物检查,检查标志物包括鳞状细胞癌相关抗原(SCCA)、细胞角蛋白19片段(CYFRA21-1)、癌胚抗原(CEA)。所有患者均接受临床对症治疗,对比42例肺腺癌患者与30例肺鳞癌患者治疗前、治疗1月后上述指标变化情况。后对患者进行随访,根据疾病复发情况将患者分为肺腺癌复发组(20例)、肺腺癌未复发组(22例)、肺鳞癌复发组(18例)、肺鳞癌未复发组(12例),对比复发患者、未复发患者SCCA、CYFRA21-1、CEA测值。结果肺腺癌治疗1月后CYFRA21-1、CEA测值均低于治疗前,差异均有统计学意义(P<0.05),SCCA对比差异无统计学意义(P>0.05);肺鳞癌治疗1月后SCCA、CYFRA21-1测值均低于治疗前,差异均有统计学意义(P<0.05),CEA对比差异无统计学意义(P>0.05);肺腺癌复发组CYFRA21-1、CEA测值均高于肺腺癌未复发组,差异均有统计学意义(P<0.05),SCCA对比差异无统计学意义(P>0.05);肺鳞癌复发组SCCA、CYFRA21-1测值均高于肺鳞癌未复发组,差异均有统计学意义(P<0.05),CEA对比差异无统计学意义(P>0.05)。结论肿瘤标志物在非小细胞肺癌复发检验中具有较高的应用价值,可为疾病是否复发提供一定参考依据。

The Inhibitory Effects of Rh-endostatin(YH-16) in Combination with Radiotherapy on Lung Adenocarcinoma A549 in Mice and the Underlying Mechanisms

In order to investigate the inhibitory effects of Endostar(rh-endostatin,YH-16)in combination with radiotherapy on lung adenocarcinoma A549 in mice and the interaction mechanisms of combined therapy,the transplantation tumor models of A549 lung adenocarcinoma were established.When the largest diameter of tumor reached 1.0cm,all nude mice were randomly divided into 4 groups:Endostar group,radiotherapy group,radiotherapy plus Endostar(combined treatment)group,and control group(n=6 in each group).The largest d...

An inhibitor of HIF-α subunit expression suppresses hypoxiainduced dedifferentiation of human NSCLC into cancer stem cell-like cells

AIM:To investigate whether hypoxia induces dedifferentiation of non-small cell lung cancer(NSCLC) cells and whether a hypoxia-inducible factor(HIF) inhibitor is able to suppress the process.METHODS:Human lung adenocarcinoma A549 cells and squamous carcinoma QG56 cells were cultured under normoxic(21%O_2) or hypoxic(4%or 1%O_2) conditions.The expression of the following genes were examined by reverse transcription-polymerase chain reaction,Western blotting and/or immunofluorescence:HIF-1α and HIF-2αsubunits;differentiation marker genes,namely surfactant protein C(SP-C)(type Ⅱ alveolar cell marker),CC10(type I alveolar cell marker) and aquaporin 5(AQP5)(Clara cell marker);and stem cell-associated genes,namely CD133,0CT4,and Musashi-1(MSI1).The tumor sphere-forming ability of the cells was evaluated by culturing them in serum-free growth factor-rich medium containing epidermal growth factor(EGF) and fibroblast growth factor(FGF).CD133 expression in hypoxic regions in A549 tumors was examined by double-immunostaining of tissue cryosections with an anti-2-nitroimidazole EF5 antibody and an anti-CD133 antibody.The metastatic ability of A549 cells was examined macroscopically and histologically after injecting them into the tail vein of immunocompromised mice.RESULTS:A549 cells primarily expressed SP-C,and QG56 cells expressed CC10 and AQP5.Exposure of A549 cells to hypoxia resulted in a marked downregulation of SP-C and upregulation of CD133,OCT4,and MSI1 in a time-dependent manner.Moreover,hypoxia mimetics,namely desferrioxamine and cobalt chloride,elicited similar effects.Ectopic expression of the constitutively active HIF-la subunit also caused the downregulation of SP-C and upregulation of CD133 and MSI1 but not OCT4,which is a direct target of HIF-2.Hypoxia enhanced the sphere-forming activity of A549 cells in serum-free medium containing EGF and FGF.Similarly,hypoxia downregulated the expression of CC10 and AQP5 genes and upregulated CD133,OCT4,and MSI1 genes in QG56 cells.TX-402(3-amino-2-quinoxalinecarbonitrile 1,4-dioxide),which is a small molecule inhibitor of the expression of HIF-1α and HIF-2αsubunits under hypoxic conditions,inhibited the upregulation of SP-C'and hypoxia-induced down-regulation of CD133,OCT4,and MSI1.Notably,TX-402 significantly suppressed the hypoxia-enhanced lung-colonizing ability of A549 cells.CONCLUSION:Hypoxia induces the de-differentiation of NSCLC cells into cancer stem cell-like cells,and HIF inhibitors are promising agents to prevent this process.

Synchronous lung and breast cancer

Synchronous tumors are an uncommon finding. We present a case of metastatic carcinoma of right breast and a left lung adenocarcinoma in a patient with previous history of left breast cancer diagnosed twelve years ago. She was then treated with chemotherapy, radiotherapy and hormone therapy. Initially, the greatest diagnostic challenge was which of them had spread or if both had. Or even if, any of these lesions resulted from the primary left breast cancer. So, specimens of different metastatic lesions were crucial to answer this query and to decide the best therapeutic approach. Sequencing the treatment options in managing two synchronous secondary malignancies, where one of them is metastatic and the other one is potentially curable, was a demanding clinical decision.

血清癌胚抗原、细胞角蛋白片段19、鳞状细胞癌抗原、血清铁蛋白、C反应蛋白对非小细胞肺癌的诊断效能

目的观察血清癌胚抗原(CEA)、细胞角蛋白片段19(CYFRA21-1)、鳞状细胞癌抗原(SCC)、血清铁蛋白(SF)、C反应蛋白(CRP)对非小细胞肺癌(NSCLC)的诊断效能,为NSCLC的早期诊断提供参考。方法经病理证实的NSCLC患者316例,记为NSCLC组;同期住院的其他肺病患者316例作为对照组。患者入院后采集肘部静脉血,采用免疫比浊法检测血清CRP,采用化学发光法检测血清CEA、CYFRA21-1、SCC、SF,比较两组患者血清CEA、CYFRA21-1、SCC、SF、CRP水平,采用多因素logistic回归分析法分析NSCLC发病的影响因素。绘制受试者工作特征曲线,评价血清CEA、CYFRA21-1、SCC、SF、CRP单项检测或多项指标联合检测对NSCLC的诊断效能。结果NSCLC组患者血清CEA、CYFRA21-1、SCC、SF、CRP水平均高于对照组(P均<0.05),血清CRP、CEA、CYFRA21-1、SCC、SF水平是NSCLC发病的影响因素(P均<0.05)。血清CRP、CEA、CYFRA21-1、SCC、SF单项检测诊断NSCLC的AUC分别为73.4%、72.1%、70.1%、64.9%、70.0%。CRP+CEA、CRP+SCC、CRP+SF、CEA+CYFRA21-1、CYFRA21-1+SCC、CYFRA21-1+SF两项指标联合检测诊断NSCLC的AUC分别为79.1%、73.7%、77.3%、76.4%、71.2%、76.6%。CRP+CEA+CYFRA21-1、CRP+CEA+SCC、CRP+CEA+SF、CRP+CYFRA21-1+SCC、CRP+CYFRA21-1+SF、CRP+SCC+SF、CEA+CYFRA21-1+SCC、CEA+CYFRA21-1+SF、CYFRA21-1+SCC+SF三项指标联合检测诊断NSCLC的AUC分别为80.7%、80.4%、81.3%、77.2%、79.9%、79.8%、77.3%、81.3%、78.4%。CEA+CYFRA21-1+SCC+CRP、CEA+CYFRA21-1+SCC+SF四项指标联合检测诊断NSCLC的AUC分别为81.2%、82.3%。五项指标联合检测诊断NSCLC的AUC为84%。结论NSCLC患者血清CEA、CYFRA21-1、SCC、SF、CRP水平升高,是NSCLC发病的影响因素。检测血清CEA、CYFRA21-1、SCC、SF、CRP有助于NSCLC的诊断,且多项指标联合检测的诊断效能优于单项检测。

养心草提取物抗肺癌活性部位筛选

目的筛选养心草抗肺癌活性部位。方法运用系统溶剂法制备养心草各提取部位;体外培养肝癌A549细胞,采用MTT法检测细胞株半数抑制浓度(IC50),以IC50作为评价指标,初步筛选出养心草抗肿瘤的有效部位。同时,建立肺癌LLC细胞移植瘤小鼠模型,通过观察肿瘤体积、小鼠体质量、脏器指数及瘤体质量的变化,对养心草的抗肿瘤效果进行评价养心草石油醚部位及乙酸乙酯部位的体内抗肺癌作用。结果MTT实验结果表明养心草不同提取部位中石油醚部位和乙酸乙酯部位对肺癌A549细胞的增殖显示较强的抑制作用;体内小鼠肺癌LLC细胞移植瘤实验表明石油醚部位和乙酸乙酯部位可明显抑制小鼠肿瘤的生长(P<0.05),且具有剂量依赖性,并对鼠体质量及脏器指数未产生显著影响(P>0.05)。结论养心草的石油醚部位和乙酸乙酯部位是其抗肺癌的有效部位。