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Purpose: Chemoresistance in small-cell lung cancer (SCLC) is reportedly attributed to the existence of resistant cancer stem cells (CSC). Studies involving CSC-specific markers and related mechanisms in SCLC remain limited. This study explored the role of the voltage-dependent calcium channel α2δ1 subunit as a CSC marker in chemoresistance of SCLC, and explored the potential mechanisms of α2δ1-mediated chemoresistance and strategies of overcoming the resistance.Experimental Design: α2δ1-positive cells were identified and isolated from SCLC cell lines and patient-derived xenograft (PDX) models, and CSC-like properties were subsequently verified. Transcriptome sequencing and Western blotting were carried out to identify pathways involved in α2δ1-mediated chemoresistance in SCLC. In addition, possible interventions to overcome α2δ1-mediated chemoresistance were examined.Results: Different proportions of α2δ1+ cells were identified in SCLC cell lines and PDX models. α2δ1+ cells exhibited CSC-like properties (self-renewal, tumorigenic, differentiation potential, and high expression of genes related to CSCs and drug resistance). Chemotherapy induced the enrichment of α2δ1+ cells instead of CD133+ cells in PDXs, and an increased proportion of α2δ1+ cells corresponded to increased chemoresistance. Activation and overexpression of ERK in the α2δ1-positive H1048 cell line was identified at the protein level. mAb 1B50-1 was observed to improve the efficacy of chemotherapy and delay relapse as maintenance therapy in PDX models.Conclusions: SCLC cells expressing α2δ1 demonstrated CSC-like properties, and may contribute to chemoresistance. ERK may play a key role in α2δ1-mediated chemoresistance. mAb 1B50-1 may serve as a potential anti-SCLC drug. Clin Cancer Res; 24(9); 2148–58. ©2018 AACR.

Supplemental Experimental Procedures The establishment of PDX models. Table S1. PDXs and corresponding clinical data Table S2: Antibody for Flow Cytometry. Table S3: qRT-PCR primer sequences. Table S4: Antibodies used in Western blots. Supplemental Experimental data Figure S1: Stem cell properties of α2Î'1+ H69 cells. Figure S2: The proportion of É'2Î'1+ and CD133+ cells in parental and 2nd generation PDXs Figure S3: Treatment curves of five PDX models Figure S4:Stem cell properties of α2Î'1+ Bclu80 cells. Figure S5: Differential genes and pathway enrichment in É'2Î'1 positive H1048 cells by RNA-Sequencing and analysis of protein interaction network. Table S5: Comparison of tumorigenic sufficiency for É'2Î'1/CD133 FACS-sorted H1048 cells in vivo. Table S6: Comparison of tumorigenic sufficiency for É'2Î'1 FACS-sorted H1048, H69 cells and Bclu80 PDX models in vivo. Table S7: Serial transplantation assay was performed into mice for validating self-renewal in vivo. Table S8: HE staining and immunochemistry results of SCLC patients and corresponding PDX models. Table S9. The differential expression genes of É'2Î'1+ and É'2Î'1- H1048 cells using RNA-Sequencing. Supplemental References

Purpose:Genomic analyses of small-cell lung cancer (SCLC) are limited by the availability of tumor specimens. This study aimed to investigate the suitability of single-cell sequencing of circulating tumor cells (CTC) as a method of inferring the evolution and progression of SCLCs.Experimental Design:Between July 1, 2011, and July 28, 2014, 48 consecutively diagnosed patients with SCLC were recruited for this study. CTCs were captured from each patient with CellSearch system. Somatic mutations and copy number alterations (CNA) were monitored by single-cell sequencing of CTCs during chemotherapy.Results:Single-cell sequencing of CTCs can provide a mutational atlas for SCLC. A 10-CNA score based on single CTCs was established as a classifier for outcomes of initial chemotherapy in patients with SCLC. The survival analyses demonstrated that patients with low CNA scores (P = 0.0042; and OS: 223.5 days vs. 424 days, P = 0.0006). The positive predictive value and negative predictive value of the CNA score for clinical subtype (refractory vs. sensitive) were 80.0% and 93.7%, respectively. By tracing allele-specific CNAs in CTCs isolated at different time points during chemotherapy, we showed that CNA heterogeneity might result from allelic losses of initially consistent CNAs.Conclusions:Single CTC-based sequencing can be utilized to depict the genomic profiles and evolutionary history of SCLC, thus offering the potential for clinical stratification of patients with SCLC.

Background The aim of this study was to estimate the efficacy and safety of bevacizumab combined with epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs) in advanced non‐small cell lung cancer (NSCLC) patients. Methods We searched randomized controlled trials (RCTs) on bevacizumab combined with EGFR TKIs in the NSCLC Cochrane Library, Web of Science, PubMed and Embase. The data were extracted and assessed according to the Cochrane Handbook. We calculated the hazard ratio (HR), risk ratio (RR), and confidence interval (CI), and accomplished this meta‐analysis with Stata 14 software. Results Of 1301 articles scanned, five articles were involved in this meta‐analysis. We determined that compared with using EGFR TKIs alone, combination treatment significantly prolongs progression‐free survival (PFS) (HR = 0.61, 95% CI = 0.52–0.70; p

Background The aim of this network meta‐analysis (NMA) was to evaluate the efficacy and safety of PD‐1/PD‐L1 inhibitors, alone or in combination with chemotherapy, as first‐line treatment for wild‐type advanced non‐small cell lung cancer. Methods We systematically searched databases, Clinical Trial.gov and included randomized clinical trials focusing on advanced NSCLC using PD‐1/PD‐L1 inhibitors as first‐line treatment. Hazard ratio for overall survival and progression‐free survival, odds ratio for any‐cause high‐adverse events (grade 3 or higher) were documented according to Bayesian NMA. Subgroup analysis was performed according to PD‐L1 level and histology. Results Thirteen trials including 9154 patients were included. In the PD‐L1 nonselective cohort, chemotherapy in combination with pembrolizumab and atezolizumab, respectively, were significantly better than any other treatment strategies in both OS benefit (HR = 0.63; HR = 0.85) and PFS benefit (HR = 0.52; HR = 0.63). In subgroup analysis, pembrolizumab appeared to provide the best OS benefit (HR = 0.67) as well as the best PFS benefit (HR = 0.67) in the PD‐L1 ≥ 50% cohort. In contrast, pembrolizumab combined with chemotherapy exhibited the best OS benefit in the PD‐L1

Many experimentally-accessible, finite-sized interacting quantum systems are most appropriately described by the canonical ensemble of statistical mechanics. Conventional numerical simulation methods either approximate them as being coupled to a particle bath, or use projective algorithms which may suffer from non-optimal scaling with system size or large algorithmic prefactors. In this paper, we introduce a highly stable, recursive Auxiliary Field Quantum Monte Carlo approach that can directly simulate systems in the canonical ensemble. We apply the method to the fermion Hubbard model in one and two spatial dimensions in a regime known to exhibit a significant "sign" problem and find improved performance over existing approaches including rapid convergence to ground state expectation values. The effects of excitations above the ground state are quantified using an estimator-agnostic approach including studying the temperature dependence of the purity and overlap fidelity of the canonical and grand canonical density matrices. As an important application, we show that thermometry approaches often exploited in ultra-cold atoms that employ an analysis of the velocity distribution in the grand canonical ensemble may be subject to errors leading to an under-estimation of extracted temperatures with respect to the Fermi temperature., 14 pages, 7 figures, and Supplemental Information with key derivations. For associated data and code repository see: https://github.com/DelMaestroGroup/papers-code-CanEnsAFQMC

The mechanism of chemo-resistance in small cell lung cancer (SCLC) is unclear. This study aims to explore the resistance-related genomic profiles of residual tumors after neo-adjuvant chemotherapy (NAC) in SCLC through the whole-exome sequencing (WES).A total of 416 limited diseases (LD) SCLC patients underwent surgery were retrospectively analyzed, of which 40 patients received NAC. Then we selected 29 patients undergoing NAC (n = 19) and chemotherapy naïve (CTN, n = 10) to perform WES sequence with formalin-fixed paraffin-embedded samples including tumor and paired para-tumor.In total, single nucleotide variation and mutation rate were similar between NAC and CTN groups. The mutation signatures were significantly discrepant between NAC and CTN groups, as well as among patients with partial response (PR), stable disease (SD), and progressive disease. There were more copy number variation deletions in NAC group compared with CTN group. The inactivation of TP53 and RB1 were the most significantly events in both NAC and CTN groups. RB1 nonsense mutations were recurrent in NAC group (9/19 vs. 0/9, 47.4% vs. 0%) with favorable survival, while the frame-shift deletions were frequent in CTN group (3/9 vs. 3/19, 33.3% vs.15.8%). Integrated function enrichment revealed that the frequently mutant genes were involved in cell cycle, metabolic reprogramming, and oncogenic signaling pathways in NAC group, such as BTG2 pathway, glycolysis in senescence and P53 pathway. A total of 27 genes presented frequently mutant in NAC group and might played a positive role in drug resistance. Multiple genes including BRINP3, MYH6, ST18, and PCHD15, which were associated with prognosis, occurred mutant frequently in PR and SD groups.Residual tumors after neo-adjuvant therapy exhibited different mutation signature spectrum. Multiple genes including RB1 nonsense mutations, BRINP3, MYH6, ST18, and PCHD15 were with frequent mutation in residual tumors, which might participate chemo-resistance and influenced the prognosis in patients with limited disease SCLC.

This study aimed to investigate the performance of least-squares support vector machines to predict carcass characteristics in Tan sheep using noninvasive in vivo measurements. A total of 80 six-month-old Tan sheep (37 rams and 43 ewes) were examined. Back fat thickness and eye muscle area between the 12th and 13th ribs were measured using real-time ultrasound in live Tan sheep. All carcasses were dissected to hind leg, longissimus dorsi muscle, lean meat, fat, and bone to determine carcass composition. Multiple linear regression (MLR), partial least squares regression (PLSR), and least-squares support vector machines (LSSVM) were applied to correlate the live Tan sheep characteristics with carcass composition. The results showed that the LSSVM model had a better efficacy for estimating carcass weight, longissimus dorsi muscle weight, lean meat weight, fat weight, lean meat, and fat percentage in live lambs (R = 0.94, RMSE = 0.62; R = 0.73, RMSE = 0.02; R = 0.86, RMSE = 0.47; R = 0.78, RMSE = 0.63; R = 0.73, RMSE = 0.02; R = 0.65, RMSE = 0.03, respectively). LSSVM algorithm was a potential alternative to the conventional MLR method. The results demonstrated that LSSVM model might have great potential to be applied to the evaluation of sheep with superior carcass traits by combining with real-time ultrasound technology.

Breast cancer (BCa) is the most common malignancy threatening the health of women worldwide, and the incidence rate has significantly increased in the last 10 years. Mammalian STE20‑like protein kinase 1 (MST1) is involved in the development of various types of malignant tumor. The present study aimed to investigate the role of MST1 in BCa and its potential involvement in the poor prognosis of patients with BCa. Reverse transcription‑quantitative PCR and immunohistochemistry were used to analyze the expression levels of MST1 in BCa, and the clinicopathological characteristics and prognosis of patients with BCa were further analyzed by statistical analysis. MST1 was overexpressed in BCa cell lines (MCF‑7, MDA‑MB‑231 and SKBR3). Cell Counting Kit‑8, 5‑ethynyl‑2'‑deoxyuridine and flow cytometry assays were used to analyze cell proliferation and apoptosis, respectively, and a wound healing assay was used to analyze cell migration. The results of the present study revealed that the downregulated expression levels of MST1 in BCa were closely associated with the poor prognosis of patients, and MST1 may be an independent risk factor for BCa. The overexpression of MST1 significantly inhibited the proliferation and migration, and promoted the apoptosis of BCa cells. In addition, the overexpression of MST1 significantly activated the Hippo signaling pathway. Treatment with XMU‑MP‑1 downregulated the expression levels of MST1 and partially reversed the inhibitory effects of MST1 on proliferation, migration and apoptosis‑related proteins, and inhibited the Hippo signaling pathway. In conclusion, the results of the present study suggested that MST1 expression levels may be downregulated in BCa and closely associated with tumor size and clinical stage, as well as the poor prognosis of affected patients. Furthermore, MST1 may inhibit the progression of BCa by targeting the Hippo signaling pathway.

An exciting development in the field of correlated systems is the possibility of realizing two-dimensional (2D) phases of quantum matter. For a systems of bosons, an example of strong correlations manifesting themselves in a 2D environment is provided by helium adsorbed on graphene. We construct the effective Bose-Hubbard model for this system which involves hard-core bosons $(U\approx\infty)$, repulsive nearest-neighbor $(V>0)$ and small attractive $(V', 22 pages, 18 figures. Reorganized text and extended an appendix. For associated data and code repository see: https://github.com/DelMaestroGroup/papers-code-BoseHubbardModelHeAdsorptionGraphene

Patient mortality rates have remained stubbornly high for the past decades in small cell lung cancer (SCLC) because of having no standard targeted therapies with confirmed advantages at present. Poly [ADP-ribose] polymerase (PARP) inhibitors have shown promise in preclinical models but have had unsatisfactory clinical results in SCLC. By RNA-seq and isobaric tags for relative and absolute quantification (ITRAQ), we revealed that PARP1 inhibition led to the relocalization of forkhead box-O3a (FOXO3a) from nuclear to cytoplasm. By performing co-Immunoprecipitation (co-IP) and CRISPR-Cas9-mediated knockout plasmid we showed that FOXO3a was subject to exportin 1 (XPO1)-dependent nuclear export. We demonstrated the effects of the PARP inhibitor BMN673 on apoptosis and DNA damage were markedly enhanced by simultaneous inhibition of XPO1 in vitro. The combination of BMN673 and the XPO1 inhibitor selinexor inhibited primary SCLC cell proliferation in mini-patient-derived xenotransplants (miniPDXs) and markedly inhibited tumor growth without significant toxicity in xenograft models. The efficacy was enhanced for more than 2.5 times, compared to the single agent. Based on these findings, we further designed a novel dual PARP-XPO1 inhibitor and showed its effectiveness in SCLC. In this work, we illustrated that combining a PARP inhibitor with an XPO1 inhibitor is associated with significantly improved efficacy and tolerability. Dual PARP-XPO1 inhibition restored the FOXO3a balance and activity in SCLC. Collectively, targeting PARP1 and XPO1 opens new avenues for therapeutic intervention against SCLC, warranting further investigation in potential clinical trials.

BACKGROUND: Lung cancer is the most malignant tumor with the highest morbidity and mortality. This study aimed to investigate the role of the expression and the significance of the p42.3 gene in non-small cell lung cancer (NSCLC). METHODS: Lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) were analyzed based on the biological information data of The Cancer Genome Atlas (TCGA). Furthermore, 142 postoperative tumor tissue and normal tissue samples (70 cases of LUAD and 72 cases of LUSC) from NSCLC patients admitted to our hospital from 2005 to 2009 were retrospectively collected. Paraffin-embedded tissues were used to make the tissue microarrays (TMA), and the expression of the p42.3 protein was detected by immunohistochemical staining. RESULTS: The expression of p42.3 in both LUAD and LUSC was significantly upregulated (P

In this paper, we consider a non-uniform flexible structure with time delay under Cattaneo's law of heat condition. We prove that the system is well-posed, and the system is exponential dec...

Purpose: Chemoresistance in small-cell lung cancer (SCLC) is reportedly attributed to the existence of resistant cancer stem cells (CSC). Studies involving CSC-specific markers and related mechanisms in SCLC remain limited. This study explored the role of the voltage-dependent calcium channel α2δ1 subunit as a CSC marker in chemoresistance of SCLC, and explored the potential mechanisms of α2δ1-mediated chemoresistance and strategies of overcoming the resistance. Experimental Design: α2δ1-positive cells were identified and isolated from SCLC cell lines and patient-derived xenograft (PDX) models, and CSC-like properties were subsequently verified. Transcriptome sequencing and Western blotting were carried out to identify pathways involved in α2δ1-mediated chemoresistance in SCLC. In addition, possible interventions to overcome α2δ1-mediated chemoresistance were examined. Results: Different proportions of α2δ1+ cells were identified in SCLC cell lines and PDX models. α2δ1+ cells exhibited CSC-like properties (self-renewal, tumorigenic, differentiation potential, and high expression of genes related to CSCs and drug resistance). Chemotherapy induced the enrichment of α2δ1+ cells instead of CD133+ cells in PDXs, and an increased proportion of α2δ1+ cells corresponded to increased chemoresistance. Activation and overexpression of ERK in the α2δ1-positive H1048 cell line was identified at the protein level. mAb 1B50-1 was observed to improve the efficacy of chemotherapy and delay relapse as maintenance therapy in PDX models. Conclusions: SCLC cells expressing α2δ1 demonstrated CSC-like properties, and may contribute to chemoresistance. ERK may play a key role in α2δ1-mediated chemoresistance. mAb 1B50-1 may serve as a potential anti-SCLC drug. Clin Cancer Res; 24(9); 2148–58. ©2018 AACR.

Background The Th1 cell-specific transcription factor TBX21 functions as a regulator of expression of a Th1 cytokine, interferon gamma (IFN-γ). However, the specific function of TBX21 correlated with cancer stemness remains unclear. Methods Using univariate and multivariate survival analysis, TBX21was identified as an independent predictive factor and was associated with poor prognosis in 1389 patients with lung adenocarcinoma (LUAD). Its mechanism in the prognosis was explored by functional enrichment analysis and validated in bioexperiments. Results In the training and test sets, TBX21 could classify 1389 LUAD patients into high and low-risk groups with significantly different prognosis (P < 0.01). Its prognostic power was independent of other clinical factors including stage, age, gender and smoking status. Functional studies indicated that downregulating TBX21 in lung cancer cells decreased the fraction of cancer stem cells and their sphere and tumor initiation frequency. Furthermore, the study showed that TBX21 activation transduced a TBX21–IL-4 signaling cascade to promote tumor initiation, tumor growth and expression of stemness markers. Conclusions These data demonstrated a key role of TBX21 in the maintenance of cancer stemness and that the TBX21–IL-4 pathway is a crucial factor contributing to lung carcinogenesis. Graphical abstract TBX21 prognostic model correlated with cancer stemness via TBX21-IL-4 pathway in LUAD patients Electronic supplementary material The online version of this article (10.1186/s13287-018-0820-6) contains supplementary material, which is available to authorized users.

In this short note, we revisit the blow-up of solution for the initial boundary value problem of semilinear pseudo-parabolic equations with low/critical initial energy stated in Xu and Su (2013) [4] , and amend the proofs of the original paper.

OBJECTIVES: MicroRNAs (miRNAs) play a key role in governing posttranscriptional regulation through binding to the mRNAs of target genes. This study is to assess miRNAs expression profiles for identifying brain metastasis-related miRNAs to develop the predictive model by microarray in tumor tissues. METHODS: For this study, we screened the significant brain metastasis-related miRNAs from 77 lung adenocarcinoma (LUAD) patients with brain metastasis (BM+) or non-brain metastasis (BM−). A predictive model was developed from the training set (n=42) using a random Forest supervised classification algorithm and a Class Centered Method, and then validated in a test set (n=35) and further analysis in GSE62182 (n=73). The independence of this signature in BM prediction was measured by multivariate logistic regression analysis. RESULTS: From the training set, the predictive model (including hsa-miR-210, hsa-miR-214 and hsa-miR-15a) stratified the patients into two groups with significantly different BM subtypes (90.4% of accuracy). The similar predictive power (91.4% of accuracy) was obtained in the test cohort. As an independent predictive factor, it was closely associated with BM and had high sensitivity and specificity in predicting BM in clinical practice. Moreover, functional enrichment analysis demonstrated that this signature involved in the signaling pathways positively correlated with cancer metastasis. CONCLUSION: These results suggested that the three-miRNA signature could develop a new random Forest model to predict the BM of LUAD patients. These findings emphasized the importance of miRNAs in diagnosing BM, and provided evidence for selecting treatment decisions and designing clinical trials.

Background: Immunotherapy can induce a long response in part patients of lung squamous cell carcinoma (LUSC). And accurate biomarkers are needed for suitable populations. As important tumor suppressor, tumor protein p53 (TP53) and low density lipoprotein receptor-related protein 1B (LRP1B) genes may be associated with immunogenicity. However, the interaction of TP53 and LRP1B and its potential association with response to immunotherapy are not fully understood in LUSC. Methods: Three cohorts were divided into four groups, respectively (A: TP53mut and LRP1Bmut, B: TP53mut and LRP1Bwild, C: TP53wild and LRP1Bmut, D: TP53wild and LRP1Bwild). 525 LUSCs form Geneplus database which performed next-generation sequencing were assessed the differences of genomic landscape, tumor mutation burden (TMB), and PD-L1 expression in four groups (cohort 1). TCGA-LUSC RNA data (n=466) from cBioPortal were used to evaluate immune cell infiltration thought single sample gene set enrichment analysis (cohort 2). The LUSCs (n=125) which received immunotherapy of POPLAR and OAK cohort were used to evaluate the efficacy of immunotherapy in four groups (cohort 3). Results: The proportion of patients in A, B, C and D groups of cohort 1 was 26%, 59%, 2%, 13%, respectively, suggesting that most patients with LRP1B mutation also carry TP53 mutation (98.6%) in LUSC. This similar ratio is 88.2% in cohort 2 and 74.3% in cohort 3. For group A, the most common mutated gene except TP53 and LRP1B was CDKN2A (31%). Group B was MLL2(28%). Group C was CDKN2A (33%). Group D was FAT1 (13%). The median TMB was 14.4 mutations/Mb (2.9-80.0) in group A, 9.8 (0.96-95.0) in group B, 11.5 (2-25) in group C, 3.8 (0.96-18.2) in group D. TP53 and LRP1B co-mutation had a highest TMB compared with the other three groups in all cohorts, while TP53wild and LRP1Bwild completely opposite. In cohort 1, PD-L1 expression had no significant difference in four groups. In cohort 3, progression-free survival (PFS) was longer in group D compared with the other three groups (p = 0.047, A: 1.5m, B: 1.6m, C: 2.1m, D: 4.2m). The same trend on overall survival (OS) were found but it was not significant. Group D also had a higher disease control rate (A: 50%, B: 46%, C: 44%, D: 69%). We than divide into two groups (D vs Other) to compare PFS and OS. It showed that group D had a prolonged PFS (p = 0.02) and OS (p = 0.03). Multivariate cox regression analysis showed that the results were independent of TMB, gender and age. Analysis of immune cell infiltration in cohort 2 showed that the better outcomes of group D might associated with elevated infiltrations of activated dendritic cell and activated CD8 T cell. Conclusion: TP53mut and LRP1Bmut, which accounted for a high proportion of LUSC, was associated with high TMB. And TP53wild and LRP1Bwild has better anti-PD-L1 outcome in LUSC. This might be related with a stronger activated dendritic cell and activated CD8 T cell infiltration despite lower TMB. Citation Format: Jiangyong Yu, Zhipeng Zhou, Ping Zhang, Pansong Li, Xu Li, Min Tang, Nannan Fan, Xiaonan Wu, Xin Nie, Xiaoyan Chen, Di Ma, Xi Chen, Yanfang Guan, Xuefeng Xia, Ling Yang, Xin Yi, Lin Li. Association of TP53 and LRP1B co-mutation status with response to immunotherapy in lung squamous cell carcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2492.

Purpose: Genomic analyses of small-cell lung cancer (SCLC) are limited by the availability of tumor specimens. This study aimed to investigate the suitability of single-cell sequencing of circulating tumor cells (CTC) as a method of inferring the evolution and progression of SCLCs. Experimental Design: Between July 1, 2011, and July 28, 2014, 48 consecutively diagnosed patients with SCLC were recruited for this study. CTCs were captured from each patient with CellSearch system. Somatic mutations and copy number alterations (CNA) were monitored by single-cell sequencing of CTCs during chemotherapy. Results: Single-cell sequencing of CTCs can provide a mutational atlas for SCLC. A 10-CNA score based on single CTCs was established as a classifier for outcomes of initial chemotherapy in patients with SCLC. The survival analyses demonstrated that patients with low CNA scores ( Conclusions: Single CTC-based sequencing can be utilized to depict the genomic profiles and evolutionary history of SCLC, thus offering the potential for clinical stratification of patients with SCLC.

Background Lung cancer is the most malignant tumor with the highest morbidity and mortality. This study aimed to investigate the role of the expression and the significance of the p42.3 gene in non-small cell lung cancer (NSCLC). Methods Lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) were analyzed based on the biological information data of The Cancer Genome Atlas (TCGA). Furthermore, 142 postoperative tumor tissue and normal tissue samples (70 cases of LUAD and 72 cases of LUSC) from NSCLC patients admitted to our hospital from 2005 to 2009 were retrospectively collected. Paraffin-embedded tissues were used to make the tissue microarrays (TMA), and the expression of the p42.3 protein was detected by immunohistochemical staining. Results The expression of p42.3 in both LUAD and LUSC was significantly upregulated (P

In this paper, we study the fractional pseudo-parabolic equations \begin{document}$ u_{t} + \left(-\Delta\right)^{s} u + \left(-\Delta\right)^{s} u_{t} = u\log \left| u \right| $\end{document}. Firstly, we recall the relationship between the fractional Laplace operator \begin{document}$ \left(-\Delta\right)^{s} $\end{document} and the fractional Sobolev space \begin{document}$ H^{s} $\end{document} and discuss the invariant sets and the vacuum isolating behavior of solutions with the help of a family of potential wells. Then, we derive a threshold result of existence of weak solution: for the low initial energy case (i.e., \begin{document}$ J(u_{0}) < d $\end{document}), the solution is global in time with \begin{document}$ I(u_{0}) >0 $\end{document} or \begin{document}$ \Vert u_{0}\Vert_{{X_{0}(\Omega)}} = 0 $\end{document} and blows up at \begin{document}$ +\infty $\end{document} with \begin{document}$ I(u_{0}) < 0 $\end{document}; for the critical initial energy case (i.e., \begin{document}$ J(u_{0}) = d $\end{document}), the solution is global in time with \begin{document}$ I(u_{0}) \geq0 $\end{document} and blows up at \begin{document}$ +\infty $\end{document} with \begin{document}$ I(u_{0}) < 0 $\end{document}. The decay estimate of the energy functional for the global solution is also given.