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Transportation is the main carrier of population movement, so it is significant to clarify how different transportation modes influence epidemic transmission. This paper verified the relationship between different levels of facilities and epidemic transmission by use of the K-means clustering method and the Mann–Whitney U test. Next, quantile regression and negative binomial regression were adopted to evaluate the relationship between transportation modes and transmission patterns. Finally, this paper proposed a control efficiency indicator to assess the differentiated strategies. The results indicated that the epidemic appeared 2–3 days earlier in cities with strong hubs, and the diagnoses were nearly fourfold than in other cities. In addition, air and road transportation were strongly associated with transmission speed, while railway and road transportation were more correlated with severity. A prevention strategy that considered transportation facility levels resulted in a reduction of the diagnoses of about 6%, for the same cost. The results of different strategies may provide valuable insights for cities to develop more efficient control measures and an orderly restoration of public transportation during the steady phase of the epidemic.

Cell viscosity is related to some diseases, such as diabetes, atherosclerosis, and Alzheimer's disease. These diseases can cause abnormal viscosity of the cell mitochondrial matrix. 1,4-Dihydropyridine (DHP) is an important organic compound with biological activity and is widely used in drug research. However, there are few studies on its optical properties, especially in the design of viscous fluorescent probes. In this study, a fluorescent probe for viscosity detection using 1,4-dihydropyridine as the fluorophore and indole iodide salt as the recognition group was designed and synthesized. The probe has the advantages of a deep-red emission, low cytotoxicity, good biocompatibility and excellent anti-interference ability. In addition, the probe also has the ability to target mitochondria and has been successfully applied to the detection of the viscosity response of HeLa cells and living mice, and has good clinical application potential.

The spread of bacterial resistance is a rising serious threat to global public health, and has created an urgent need for the development of a new generation of antibacterial nano-agents to take the place of antibiotics. In this work, a multifunctional nanoplatform based on boron nanosheet (B NS)-coated quaternized chitosan (QCS) and the nitric oxide (NO) donor

Nivolumab, a fully human IgG4 programmed cell death-1 checkpoint inhibitor, demonstrated its benefit of prolonged survival in advanced non-small cell lung cancer (NSCLC). However, nivolumab generated unique immune-related adverse events such as thyroid dysfunctions. Herein we assessed nivolumab-induced thyroid dysfunctions in patients with previously treated advanced NSCLC in our hospital. The medical records of 11 patients with advanced NSCLC who were initiated with nivolumab treatment between June 28, 2018, and January 15, 2019, in our hospital were reviewed. Serological tests of thyroid-stimulating hormone and free tetraiodothyronine were measured at baseline and every 8 weeks. Three out of 11 patients developed new-onset hypothyroidism during the treatment, and two of three patients had transient hyperthyroidism first. Two patients were diagnosed with Grade 2 hypothyroidism and received levothyroxine therapy. The other one was Grade 1 hypothyroidism and asymptomatic. All these three patients continued nivolumab therapy. Nivolumab-induced thyroid dysfunctions in advanced NSCLC were mostly mild and controlled. Thyroid function needs to be monitored for early prediction and appropriate managements of thyroid dysfunctions.

The mechanism of regulation of PD-L1 expression by ALK translocation remains unclear. We detected PD-L1 protein expression and its regulation in lung adenocarcinoma patients with EML4-ALK fusion gene. PD-L1 and ALK expression at protein level in human lung adenocarcinoma cell lines and tumor tissue specimens was evaluated by immunohistochemistry analysis and Western blotting. The expression at DNA level and RNA level was indicated by quantitative real-time PCR analysis. The signal pathway was indicated at protein level by western blotting. The PD-L1 protein expression was higher in human lung adenocarcinoma cell lines with EML4-ALK fusion gene than that without this fusion gene. Induced expression of EML4-ALK in A549 cells significantly increased PD-L1 protein expression, whereas PD-L1 protein expression was downregulated after crizotinib and pembrolizumab successively. Significant positive correlations between PD-L1 and p-ERK, p-STAT3 or p-AKT expression were observed in ALK-translocated tumors. PD-L1 overexpression was significantly associated with shorter progressive survival and overall survival after crizotinib in ALK-translocated patients. We demonstrate that ALK translocation can upregulate PD-L1 expression by activating ERK, STAT3 and AKT pathways. ALK inhibitor combined with a PD-L1-targeted therapy may be a potential strategy in ALK-translocated lung adenocarcinoma patients.

Cysteine (Cys) plays important physiological roles in the human body, and abnormal Cys concentrations can cause a variety of diseases. Thus, detecting Cys with high selectivity and sensitivity in vivo is important. Near-infrared (NIR) fluorescent probes are widely employed in biological detection because of their excellent optical properties such as minimal damage to biological samples, low background interference and high signal-to-noise ratio. However, few NIR fluorescent probes that can detect Cys over homocysteine (Hcy) and glutathione (GSH) have been reported because of their similar reactivity and structure. In this work, a highly water-soluble NIR probe (CYNA) for detecting Cys whose structure is similar to that of indocyanine green and is based on cyanine skeleton was synthesized and via aromatic nucleophilic substitution–rearrangement (SNAr-rearrangement) to specific recognize the cysteine. The probe showed high selectivity toward Cys and superior biosecurity, excellent biocompatibility and prolonged dynamic imaging. It also has long fluorescence emission wavelength (820 nm), low detection limit (14 nM) and was successfully applied for visualizing Cys in living cells and mice, which has great promise for applications in noninvasive vivo biological imaging and detection.

The intelligent design of multifunctional nanoplatforms is critical for cancer therapy. Herein, NaGdF

Plants from Alisma species belong to the genus of Alisma Linn. in Alismataceae family. The tubers of A. orientale (Sam.) Juzep, also known as Ze Xie in Chinese and Takusha in Japanese, have been used in traditional medicine for a long history. Triterpenoids are the main secondary metabolites isolated from Alisma species, and reported with various bioactive properties, including anticancer, lipid-regulating, anti-inflammatory, antibacterial, antiviral and diuretic activities. In this brief review, we aimed to summarize the phytochemical and pharmacological characteristics of triterpenoids found in Alisma, and discuss their structure modification to enhance cytotoxicity as well.

HER2 mutations have emerged as oncogenic driver gene mutations in non-small cell lung cancer (NSCLC), which have not been described in detail like other driver gene mutations. Here, 295 patients with advanced lung adenocarcinoma were retrospectively screened for HER2 mutations using next-generation sequencing (NGS), and the positive cases were validated by Sanger sequencing. We identified five cases with HER2 exon 20 insertions, representing 1.7% of 295 lung adenocarcinomas. Among them, four different subtypes of HER2 exon 20 insertions were identified, including a rare subtype G778_S779insCPG never reported before with a partial response (PR) to pyrotinib and progression-free survival (PFS) of 12.8 months. Our findings reveal that HER2 exon 20 insertion mutations were detected in a small subset of lung adenocarcinomas. Given the different drug sensitivities, determining the mutation subtype by next-generation sequencing at the time of diagnosis might make sense.

Subclonal architecture and genomic evolution of small-cell lung cancer (SCLC) under treatment has not been well studied primarily due to lack of tumor specimens, particularly longitudinal samples acquired during treatment. SCLC is characterized by early hematogenous spread, which makes circulating cell-free tumor DNA (ctDNA) sequencing a promising modality for genomic profiling. Here, we perform targeted deep sequencing of 430 cancer genes on pre-treatment tumor biopsies, as well as on plasma samples collected prior to and during treatment from 22 SCLC patients. Similar subclonal architecture is observed between pre-treatment ctDNA and paired tumor DNA. Mean variant allele frequency of clonal mutations from pre-treatment ctDNA is associated with progression-free survival and overall survival. Pre- and post-treatment ctDNA mutational analysis demonstrate that mutations of DNA repair and NOTCH signaling pathways are enriched in post-treatment samples. These data suggest that ctDNA sequencing is promising to delineate genomic landscape, subclonal architecture, and genomic evolution of SCLC., Small cell lung cancer (SCLC) may evolve under treatment. But tumor tissues are often not available to study evolution of SCLC. Here, the authors utilize circulating tumor DNA to investigate the genomic evolution and subclonal architecture of SCLC during therapy.

M-NP@Zn-BIF (M-NP = Ag or Cu nanoparticle; Zn-BIF is a zinc-based boron imidazolate framework, Zn2(BH(2-mim)3)2(obb); 2-mim = 2-methylimidazole; obb = 4,4′-oxybis(benzoate)) composites were successfully in-situ synthesized by utilizing the reducing ability of the B H bond contained in the Zn-BIF at room temperature without any additional chemical reduction reagents. These composites (225 μg/mL) exhibited excellent catalytic activity to convert 4-nitrophenol to 4-aminophenol in 2.5 min and 6 min with a conversion rate of 99.9 %, respectively. In addition, Ag@Zn-BIF (50 μg/mL) showed highly synergistic antibacterial activity against both Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) with a bactericidal rate of approximately 99.9 %. An antibacterial mechanism was proposed for the generation of intracellular reactive oxygen species (ROS) levels. Superoxide radicals (O2–) and hydroxyl radicals ( OH) formed during the antibacterial process were shown to accelerate the death of bacteria. They also exhibited highly photocatalytic activity for Rhodamine B (RhB). When the concentration of the composites is 1000 μg/mL, the photocatalytic efficiency of Ag@Zn-BIF and Cu@Zn-BIF increased by 31.62 and 18.13 times compared with Zn-BIF, respectively. All in all, this study developed a simple and versatile integrated platform for the removal of nitrophenols, organic dyes, and the effective inactivation of bacteria in water.

The rapid development of wearable electronic devices has created a huge demand for flexible all-solid-state supercapacitors (FSSCs), and high-performance electrode materials for FSSCs are strong desired simultaneously. In this work, boron and nitrogen-doped carbon (BCN) anchored on active carbon fiber cloth (ACC) are specially designed and manufactured by immersing ACC in a mixed solution of urea, boric acid and polyethylene oxide-propylene oxide (P123) and then calcining, which can be used to assemble high-performance FSSCs as electrodes. The three-dimensional (3D) cross-linked network of BCN grown on the carbon fibers improves the transmission rate of electrons and provides abundant electrochemical reaction sites, which are conducive to the performance of supercapacitors. Thanks to this structural advantage, the ACC@BCN electrode exhibits an area specific capacitance of 1018 mF cm−2 and a volume specific capacitance of 535.8 F g−1 at a current of 1 mA cm−2. Furthermore, the symmetric FSSCs based on ACC@BCN show high energy density of 1.573 mWh cm−3 and power density of 128.7 mW cm−3, and the capacitance retention can still keep 89.5% even after 10,000 cycles. This work provides a simple and effective way for large-scale preparation of high-performance, high-stability electrode materials for wearable electronic devices.

The intelligent design of multifunctional nanoplatforms is critical for cancer therapy. Herein, NaGdF4 :Er,Yb@NaGdF4 :Nd@Cu(II) boron-imidazolate frameworks (denoted as CSNPs@Cu-BIF) nanoassemblies are designed and fabricated. Upon a single 808 nm laser irradiation, the nanoassemblies not only show the outstanding photothermal conversion capacity (η = 41.7%) but also generate cytotoxic reactive oxygen species through an in situ Fenton-like reaction and fluorescence resonance energy transfer. Importantly, the nanoassemblies simultaneously introduce remarkable antitumor efficacy via photothermal/photodynamic/chemodynamic combination therapy both in vitro and in vivo. To improve the therapeutic effect of solid tumor ablation, it is highly desirable to monitor the treatment process in real-time. Multiclinical imaging modalities of ultrasonography are employed to systematically investigate the ablation mechanism of solid tumors in vivo. Furthermore, the significant difference between the eigen temperature of CSNPs@Cu-BIF nanoassemblies obtained by the temperature-sensitive emission bands signal changes and the apparent temperature recorded by the thermal imaging camera is 14.55 K at equilibrium. This current work therefore supplies an alternative strategy in temperature feedback-controlled accurate cancer therapy.

Background To explore the efficacy and safety of crizotinib versus platinum-based double agent chemotherapy as the first-line treatment in patients with advanced anaplastic lymphoma kinase (ALK)-positive lung adenocarcinoma. Method We retrospectively analyzed data from 19 patients with advanced ALK-positive lung adenocarcinoma who had received no previous systemic treatment for advanced disease. Seven patients received oral crizotinib at a dose of 250 mg twice daily; 12 patients were administered standard chemotherapy (pemetrexed, paclitaxel, vinorelbine or gemcitabine plus either cisplatin or carboplatin) every three weeks for up to six cycles. The primary endpoint was overall response rate (ORR), disease control rate (DCR), and safety. Results The ORR was significantly higher with crizotinib than with chemotherapy (83.3% in the crizotinib vs. 25.0% in the chemotherapy group, P < 0.05); the DCRs were 100% and 75%, respectively (P < 0.05). The common adverse events associated with crizotinib were visual abnormality and diarrhea, whereas those associated with chemotherapy were neutropenia and nausea. In the crizotinib group, liver aminotransferase elevation (adverse events grade 3 or 4) occurred in one patient (14.3%). In the chemotherapy group, the same grade neutropenia adverse event occurred in two patients (16.6%). The incidence of treatment-related grade 3 or 4 adverse events was similar in both groups. Compared with chemotherapy, crizotinib was associated with a greater reduction in lung cancer symptoms and a greater improvement in quality of life. Conclusion As a first-line treatment, crizotinib was superior to platinum-based double chemotherapy in patients with previously untreated advanced ALK-positive lung adenocarcinoma. Therefore, crizotinib is an optimal therapy as a first-line treatment in these patients.

Background Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) effectively treat advanced non-small cell lung cancer with EGFR-mutation. However, most patients develop acquired resistance without effective therapy subsequent to EGFR-TKI failure. We evaluated the efficacy of subsequent treatment strategies for EGFR-TKI resistance. Methods We retrospectively analyzed 240 patients with advanced lung adenocarcinoma with EGFR-TKI failure and following subsequent treatment. According to the first subsequent strategies after EGFR-TKI failure, patients were divided into groups of EGFR-TKI continuation (21 cases), EGFR-TKI continuation with chemotherapy (23 cases), chemotherapy alone (143 cases), and best supportive care (BSC) (53 cases). Results Except for 53 cases of BSC, the disease control rates (DCR) of the remaining 187 patients in the EGFR-TKI continuation, EGFR-TKI continuation with chemotherapy, and chemotherapy alone groups were 66.7%, 73.9%, and 44.8%, respectively. The median post-progression progression-free survival (PFS) for the three groups was 3.0, 3.3, and 2.0 months, respectively. The DCR for the EGFR-TKI continuation with chemotherapy group was significantly higher than the chemotherapy alone group (P = 0.006). The post-progression PFS of the EGFR-TKI continuation with chemotherapy group was significantly longer than the chemotherapy alone group (P = 0.037). The median overall survival in the EGFR-TKI continuation, EGFR-TKI continuation with chemotherapy, chemotherapy alone, and BSC groups were 6.9, 11.6, 8.8, and 0.9 months, respectively. Compared to the BSC group, all groups achieved a survival benefit (P

Background To evaluate the efficacy and safety of Icotinib – an orally administered, highly potent selective inhibitor of epidermal growth factor receptor (EGFR) and its active mutations, in the treatment of patients with advanced non-small cell lung cancer (NSCLC). Methods A total of 101 patients with stage IIIb/IV NSCLC were treated with 125 mg Icotinib three times a day until disease progression or intolerable toxicity. Response rate was evaluated using response evaluation criteria in solid tumors and progression-free survival (PFS) was collected. Results The overall response rate (ORR) and disease control rate (DCR) were 37.6% (38/101) and 79.2% (80/101), respectively. The median PFS was 6.5 months. Multivariate analysis showed that female gender (P = 0.048, 95% confidence interval [CI] 1.010–6.016) and occurrence of rash (P = 0.002, 95% CI 1.667–9.809) were the independent predictive factors for ORR, while a performance status (PS) score of 0–1 (P = 0.001, 95% CI 0.024–0.402) and rash (P = 0.042, 95% CI 1.089–76.557) were the independent predictive factors for DCR. In addition, PS scores of 0–1 (P < 0.001, 95% CI 0.135–0.509), and non-smoking (P = 0.017, 95% CI 0.342–0.900) were found to be independent influencing factors for PFS. Moreover, patients with EGFR mutations had better PFS than patients with wild type EGFR, while patients with EGFR exon 19 deletion had better survival than those with EGFR exon 21 mutation. The most common adverse effects of Icotinib were rash (35.6%) and diarrhea (17.8%), which was tolerable. Conclusion Treatment of stage IIIb/IV NSCLC patients with Icotinib was effective and tolerable, specifically in patients with EGFR mutation.

Subclonal architecture and genomic evolution of small-cell lung cancer (SCLC) under treatment has not been well studied primarily due to lack of tumor specimens, particularly longitudinal samples acquired during treatment. SCLC is characterized by early hematogenous spread, which makes circulating cell-free tumor DNA (ctDNA) sequencing a promising modality for genomic profiling. Here, we perform targeted deep sequencing of 430 cancer genes on pre-treatment tumor biopsies, as well as on plasma samples collected prior to and during treatment from 22 SCLC patients. Similar subclonal architecture is observed between pre-treatment ctDNA and paired tumor DNA. Mean variant allele frequency of clonal mutations from pre-treatment ctDNA is associated with progression-free survival and overall survival. Pre- and post-treatment ctDNA mutational analysis demonstrate that mutations of DNA repair and NOTCH signaling pathways are enriched in post-treatment samples. These data suggest that ctDNA sequencing is promising to delineate genomic landscape, subclonal architecture, and genomic evolution of SCLC.

Status of epidermal growth factor receptor (EGFR) gene is a predictor of response to EGFR tyrosine kinase inhibitor (TKI). However, little is know about the relationship between EGFR status and response to chemotherapy. We evaluated the prediction value of EGFR mutation status on response to first-line chemotherapy in patients with advanced non-small-cell lung cancer (NSCLC).The data of 181 patients with stage IIIb/IV NSCLC who diagnosed by histopathology from January 10, 2006 to December 20, 2013 in Beijing Chest Hospital, Capital Medical University were collected. The relationships between EGFR gene status, clinical characteristics and response and progression-free survival (PFS) were analyzed.All of the 181 patients' EGFR statuses were determined. 75 (41.4%) patients harbored EGFR-activating mutations and 106 (58.6%) patients were EGFR wild-type. All patients received first-line chemotherapy. The objective response rate (ORR) was 26.0% and disease control rate (DCR) was 70.2%. Patients with EGFR-activating mutations had a higher DCR than patients with EGFR wild-type (84.0% vs 60.4%, P=0.001) did. Subgroup analysis showed that the ORR and DCR in patients with EGFR exon 19 deletions were remarkably higher than those with EGFR wild-type (P = 0.049, 0.002, respectively). The DCR in patients with EGFR exon 21 L858R mutation was significantly higher than that in patients with EGFR wild-type (P=0.010). 168 patients were available for response evaluation in all of 181 patients and median PFS was 4.3 mo. The PFS of patients with adenocarcinoma was significantly higher than that patients with squamous cell carcinoma (4.7 mo vs 3.0 mo, P=0.036). The PFS in patients harbored EGFR-activating mutations was significantly higher than that in the patients with EGFR wild-type (6.3 mo vs 3.0 mo, P=0.002). The PFS of patients with a performance status (PS) of 0-1 was significantly higher than that in patients with a PS of 2 (4.4 months vs. 0.7 months, P= 0.016). Cox multivariate analysis indicates the EGFR-activating mutation is an independent factor affecting PFS (HR=0.654, 95%CI: 0.470-0.909, P=0.012).EGFR-activating mutation is a predictor for PFS of first-line chemotherapy in advanced NSCLC patients. .背景与目的 表皮生长因子受体（epidermal growth factor receptor, EGFR）基因状态是表皮生长因子受体酪氨酸激酶抑制剂（epidermal growth factor receptor tyrosine kinase inhibitor, EGFR-TKI）疗效的预测因素，但其对化疗疗效的预测作用尚不明确。本研究旨在探讨对晚期非小细胞肺癌（non-small cell lung cancer, NSCLC）患者一线化疗疗效的预测意义。方法 收集首都医科大学附属北京胸科医院自2006年1月10日-2013年12月20日经组织病理学证实的181例IIIb期/IV期的NSCLC患者。分析EGFR基因状态、临床特征与化疗疗效及无疾病进展生存期（progression-free survival, PFS）之间的关系。结果 181例患者均进行了EGFR基因检测，EGFR突变患者75例（41.4%），野生型为106例（58.6%）。全部患者均接受一线化疗，客观缓解率（objective response rate, ORR）为26.0%，疾病控制率（disease control rate, DCR）为70.2%。EGFR突变患者的DCR显著高于EGFR野生型患者高（84.0% vs 60.4%, P=0.001）。亚组分析显示，19外显子缺失突变患者化疗的ORR、DCR均高于EGFR野生型患者（P值分别为0.049，0.002）。21外显子L858R突变患者的DCR高于EGFR野生型患者（P=0.010）。全部患者中，168例患者可评价PFS，中位PFS为4.3个月，其中腺癌患者PFS较鳞癌患者延长（4.7个月 vs 3.0个月，P=0.036）；突变患者PFS长于野生型患者（6.3个月 vs 3.0个月，P=0.002）；体力状况评分（performance status, PS）0-1分组患者PFS较评分为2分延长（4.4个月 vs 0.7个月，P=0.016）。Cox多因素分析显示，EGFR突变是影响PFS的独立因素（HR=0.654, 95%CI: 0.470-0.909, P=0.012）。结论 EGFR突变是晚期NSCLC患者一线化疗PFS的预测因素。.

Background Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) effectively treat advanced non-small cell lung cancer with EGFR-mutation. However, most patients develop acquired resistance without effective therapy subsequent to EGFR-TKI failure. We evaluated the efficacy of subsequent treatment strategies for EGFR-TKI resistance. Methods We retrospectively analyzed 240 patients with advanced lung adenocarcinoma with EGFR-TKI failure and following subsequent treatment. According to the first subsequent strategies after EGFR-TKI failure, patients were divided into groups of EGFR-TKI continuation (21 cases), EGFR-TKI continuation with chemotherapy (23 cases), chemotherapy alone (143 cases), and best supportive care (BSC) (53 cases). Results Except for 53 cases of BSC, the disease control rates (DCR) of the remaining 187 patients in the EGFR-TKI continuation, EGFR-TKI continuation with chemotherapy, and chemotherapy alone groups were 66.7%, 73.9%, and 44.8%, respectively. The median post-progression progression-free survival (PFS) for the three groups was 3.0, 3.3, and 2.0 months, respectively. The DCR for the EGFR-TKI continuation with chemotherapy group was significantly higher than the chemotherapy alone group (P = 0.006). The post-progression PFS of the EGFR-TKI continuation with chemotherapy group was significantly longer than the chemotherapy alone group (P = 0.037). The median overall survival in the EGFR-TKI continuation, EGFR-TKI continuation with chemotherapy, chemotherapy alone, and BSC groups were 6.9, 11.6, 8.8, and 0.9 months, respectively. Compared to the BSC group, all groups achieved a survival benefit (P

Xiaojuan Qiao,1–3,* XiaoranZhai,1,2,* JinghuiWang,4 XiaotingZhao,1,2 XinjieYang,4 Jialin Lv,4 LiMa,1,2 Lina Zhang,1,2 YueWang,1,2 Shucai Zhang,4 Wentao Yue1,21Department of Cellular and Molecular Biology, Beijing Chest Hospital, Capital Medical University, 2Department of Cellular and Molecular Biology, Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing, 3Health Care Ward, The First Hospital Affiliated to Inner Mongolia Medical University, Hohhot, 4Department of Medical Oncology, Beijing Chest Hospital, Capital Medical University, Beijing, People’s Republic of China*These authors contributed equally tothis workBackground: Matrix metalloproteinase 9 (MMP-9) plays an important role in tumor invasion and metastasis, including lung cancer. However, whether variations in serum MMP-9 levels can serve as a biomarker for monitoring chemotherapy curative effect remains unclear. This study was designed to investigate the association between variations in serum MMP-9 levelsand chemotherapy curative effect in patients with lung cancer.Patients and methods: A total of 82 patients with advanced lung cancer were included. All newly diagnosed patients were treated with platinum-based doublet chemotherapy. Serial measurements of serum MMP-9 levels were performed by enzyme-linked immunosorbent assay. Inthis manner, we chose four time points to examine the association, including before chemotherapy, and 3weeks after the beginning of the first, second, and fourth cycles of chemotherapy.Results: Compared with the serum level of MMP-9 before progressive disease, patients with progressive disease had elevated serum levels of MMP-9. Compared with the previous time point of collecting specimens, the serum levels of MMP-9 in the patients with a complete response/partial response/stable disease decreased or were maintained stable. The differences of variation in serum MMP-9 levels in patients with different chemotherapy curative effects were all statistically significant after one cycle, two cycles, and four cycles (after one cycle: P