Displaying publications 41 - 60 of 309 in total

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  1. Multidimensional (0D-3D) nanostructures for lung cancer biomarker analysis: Comprehensive assessment on current diagnostics
    Ramanathan S, Gopinath SCB, Md Arshad MK, Poopalan P
    Biosens Bioelectron, 2019 Sep 15;141:111434.
    PMID: 31238281 DOI: 10.1016/j.bios.2019.111434
    The pragmatic outcome of a lung cancer diagnosis is closely interrelated in reducing the number of fatal death caused by the world's top cancerous disease. Regardless of the advancement made in understanding lung tumor, and its multimodal treatment, in general the percentage of survival remain low. Late diagnosis of a cancerous cell in patients is the major hurdle for the above circumstances. In the new era of a lung cancer diagnosis with low cost, portable and non-invasive clinical sampling, nanotechnology is at its inflection point where current researches focus on the implementation of biosensor conjugated nanomaterials for the generation of the ideal sensing. The present review encloses the superiority of nanomaterials from zero to three-dimensional nanostructures in its discrete and nanocomposites nanotopography on sensing lung cancer biomarkers. Recent researches conducted on definitive nanomaterials and nanocomposites at multiple dimension with distinctive physiochemical property were focused to subside the cases associated with lung cancer through the development of novel biosensors. The hurdles encountered in the recent research and future preference with prognostic clinical lung cancer diagnosis using multidimensional nanomaterials and its composites are presented.
    Matched MeSH terms: Lung Neoplasms/diagnosis*
  2. Nano-silica embedded polydimethylsiloxane on interdigitated sensor as adhesive polymer for detecting lung cancer mutation
    Abulaiti A, Salai A, Sun X, Yibulayin W, Gao Y, Gopinath SCB, et al.
    Biotechnol Appl Biochem, 2021 Feb 12.
    PMID: 33576539 DOI: 10.1002/bab.2122
    Non-small cell lung cancer (NSCLC) incited by epidermal growth factor receptor (EGFR) mutation makes up ∼85% of lung cancer diagnosed and death cases worldwide. The presented study introduced an alternative approach in detecting EGFR mutation using nano-silica integrated with polydimethylsiloxane (PDMS) polymer on interdigitated electrode (IDE) sensor. A 400 μm gap-sized aluminum IDE was modified with nano-polymer layer, which was made up of silica nanoparticles and PDMS polymer. IDE and PDMS-coated IDE (PDMS/IDE) were imaged using electron microscopes that reveals its smooth and ideal sensor morphology. The nano-silica-integrated PDMS/IDE surface was immobilized with EGFR probe and target to specify the lung cancer detection. The sensor specificity was justified through the insignificant current readouts with one-base mismatch and noncomplementary targets. The sensitivity of nano-silica-integrated PDMS/IDE was examined with mutant target spiked in human serum, where the resulting current affirms the detection of EGFR mutation. Based on the slope of the calibration curve, the sensitivity of nano-silica-integrated PDMS/IDE was 2.24E-9 A M-1 . The sensor recognizes EGFR mutation lowest at 1 aM complementary mutant target; however, the detection limit obtained based on 3σ calculation is 10 aM with regression value of 0.97.
    Matched MeSH terms: Lung Neoplasms
  3. Anaplastic lymphoma kinase (ALK) mutations in patients with adenocarcinoma of the lung
    Mohamad N, Jayalakshmi P, Rhodes A, Liam CK, Tan JL, Yousoof S, et al.
    Br J Biomed Sci, 2017 Oct;74(4):176-180.
    PMID: 28705139 DOI: 10.1080/09674845.2017.1331520
    BACKGROUND: Non-small cell lung cancer (NSCLC) is a major cause of cancer-related death. Approximately 2-16% of NSCLC patients with wild-type epidermal growth factor receptor (EGFR) harbour anaplastic lymphoma kinase (ALK) mutations. Both EGFR and ALK mutations occur most commonly in Asian patients with NSCLC. As targeted therapy is available for NSCLC patients with these mutations, it is important to establish reliable assays and testing strategies to identify those most likely to benefit from this therapy.

    MATERIALS AND METHODS: Patients diagnosed with adenocarcinoma of the lung between 2010 and 2014 were tested for EGFR mutations. Of these, 92 cases were identified as EGFR wild type and suitable candidates for ALK testing utilising immunohistochemistry and the rabbit monoclonal antibody D5F3. The reliability of the IHC was confirmed by validating the results against those achieved by fluorescence in situ hybridisation (FISH) to detect ALK gene rearrangements.

    RESULTS: Twelve (13%) cases were positive for ALK expression using immunohistochemistry. Of the 18 evaluable cases tested by FISH, there was 100% agreement with respect to ALK rearrangement/ALK expression between the assays, with 11 cases ALK negative and 7 cases ALK positive by both assays. ALK tumour expression was significantly more common in female compared to male patients (29.6% vs. 6.2%, P 

    Matched MeSH terms: Lung Neoplasms
  4. Fulltext Bilateral spontaneous persistent open pneumothorax with chylothorax
    Khajotia R, Raman S
    Can Fam Physician, 2012 Jul;58(7):757-60.
    PMID: 22859639
    Matched MeSH terms: Lung Neoplasms/complications; Lung Neoplasms/diagnosis*
  5. Fulltext Pathological transition as the arising mechanism for drug resistance in lung cancer
    Chen Y, Tang WY, Tong X, Ji H
    Cancer Commun (Lond), 2019 10 01;39(1):53.
    PMID: 31570104 DOI: 10.1186/s40880-019-0402-8
    Despite the tremendous efforts for improving therapeutics of lung cancer patients, its prognosis remains disappointing. This can be largely attributed to the lack of comprehensive understanding of drug resistance leading to insufficient development of effective therapeutics in clinic. Based on the current progresses of lung cancer research, we classify drug resistance mechanisms into three different levels: molecular, cellular and pathological level. All these three levels have significantly contributed to the acquisition and evolution of drug resistance in clinic. Our understanding on drug resistance mechanisms has begun to change the way of clinical practice and improve patient prognosis. In this review, we focus on discussing the pathological changes linking to drug resistance as this has been largely overlooked in the past decades.
    Matched MeSH terms: Lung Neoplasms/drug therapy*; Lung Neoplasms/pathology*
  6. Fulltext NF-κB-Dependent Lymphoid Enhancer Co-option Promotes Renal Carcinoma Metastasis
    Rodrigues P, Patel SA, Harewood L, Olan I, Vojtasova E, Syafruddin SE, et al.
    Cancer Discov, 2018 Jul;8(7):850-865.
    PMID: 29875134 DOI: 10.1158/2159-8290.CD-17-1211
    Metastases, the spread of cancer cells to distant organs, cause the majority of cancer-related deaths. Few metastasis-specific driver mutations have been identified, suggesting aberrant gene regulation as a source of metastatic traits. However, how metastatic gene expression programs arise is poorly understood. Here, using human-derived metastasis models of renal cancer, we identify transcriptional enhancers that promote metastatic carcinoma progression. Specific enhancers and enhancer clusters are activated in metastatic cancer cell populations, and the associated gene expression patterns are predictive of poor patient outcome in clinical samples. We find that the renal cancer metastasis-associated enhancer complement consists of multiple coactivated tissue-specific enhancer modules. Specifically, we identify and functionally characterize a coregulatory enhancer cluster, activated by the renal cancer driver HIF2A and an NF-κB-driven lymphoid element, as a mediator of metastasis in vivo We conclude that oncogenic pathways can acquire metastatic phenotypes through cross-lineage co-option of physiologic epigenetic enhancer states.Significance: Renal cancer is associated with significant mortality due to metastasis. We show that in metastatic renal cancer, functionally important metastasis genes are activated via co-option of gene regulatory enhancer modules from distant developmental lineages, thus providing clues to the origins of metastatic cancer. Cancer Discov; 8(7); 850-65. ©2018 AACR.This article is highlighted in the In This Issue feature, p. 781.
    Matched MeSH terms: Lung Neoplasms/secondary
  7. Fulltext Gender-Specific Molecular and Clinical Features Underlie Malignant Pleural Mesothelioma
    De Rienzo A, Archer MA, Yeap BY, Dao N, Sciaranghella D, Sideris AC, et al.
    Cancer Res, 2016 Jan 15;76(2):319-28.
    PMID: 26554828 DOI: 10.1158/0008-5472.CAN-15-0751
    Malignant pleural mesothelioma (MPM) is an aggressive cancer that occurs more frequently in men, but is associated with longer survival in women. Insight into the survival advantage of female patients may advance the molecular understanding of MPM and identify therapeutic interventions that will improve the prognosis for all MPM patients. In this study, we performed whole-genome sequencing of tumor specimens from 10 MPM patients and matched control samples to identify potential driver mutations underlying MPM. We identified molecular differences associated with gender and histology. Specifically, single-nucleotide variants of BAP1 were observed in 21% of cases, with lower mutation rates observed in sarcomatoid MPM (P < 0.001). Chromosome 22q loss was more frequently associated with the epithelioid than that nonepitheliod histology (P = 0.037), whereas CDKN2A deletions occurred more frequently in nonepithelioid subtypes among men (P = 0.021) and were correlated with shorter overall survival for the entire cohort (P = 0.002) and for men (P = 0.012). Furthermore, women were more likely to harbor TP53 mutations (P = 0.004). Novel mutations were found in genes associated with the integrin-linked kinase pathway, including MYH9 and RHOA. Moreover, expression levels of BAP1, MYH9, and RHOA were significantly higher in nonepithelioid tumors, and were associated with significant reduction in survival of the entire cohort and across gender subgroups. Collectively, our findings indicate that diverse mechanisms highly related to gender and histology appear to drive MPM.
    Matched MeSH terms: Lung Neoplasms/genetics*; Lung Neoplasms/pathology
  8. NOTCH1 Signaling Regulates Self-renewal and Platinum Chemoresistance of Cancer Stem-like Cells in Human Non-small Cell Lung Cancer
    Zhang Y, Xu W, Guo H, Zhang Y, He Y, Lee SH, et al.
    Cancer Res, 2017 Apr 17.
    PMID: 28416482 DOI: 10.1158/0008-5472.CAN-16-1633
    Cancer stem-like cells (CSC) are thought to drive tumor initiation, metastasis, relapse and therapeutic resistance, but their specific pathogenic characters in many cancers including non-small cell lung cancer (NSCLC) have yet to be well defined. Here we develop findings that the growth factor HGF promotes CSC sphere formation in NSCLC cell populations. In patient-derived sphere-forming assays (PD-SFA) with HGF, CD49f and CD104 were defined as novel markers of lung CSC (LCSC). In particular, we isolated a subpopulation of CD166(+)CD49f(hi)CD104(-)Lin(-) LCSC present in all human specimens of NSCLC examined, regardless of their histological subtypes or genetic driver mutations. This specific cell population was tumorigenic and capable of self-renewal, giving rise to tumor spheres in vitro and orthotopic lung tumors in immune-compromised mice. Mechanistic investigations established that NOTCH1 was preferentially expressed in this cell subpopulation and required for self-renewal via the transcription factor HES1. Through a distinct HES1-independent pathway, NOTCH1 also protected LCSCs from cisplatin-induced cell death. Notably, treatment with a γ-secretase inhibitor that blunts NOTCH1 function ablated self-renewing LCSC activity and restored platinum sensitivity in vitro and in vivo Overall, our results define the pathogenic characters of a cancer stem-like subpopulation in lung cancer, the targeting of which may relieve platinum resistance in this disease.
    Matched MeSH terms: Lung Neoplasms
  9. Fulltext Results from the European Prospective Investigation into Cancer and Nutrition Link Vitamin B6 Catabolism and Lung Cancer Risk
    Zuo H, Ueland PM, Midttun Ø, Vollset SE, Tell GS, Theofylaktopoulou D, et al.
    Cancer Res, 2018 Jan 01;78(1):302-308.
    PMID: 29070616 DOI: 10.1158/0008-5472.CAN-17-1923
    Circulating pyridoxal-5'-phosphate (PLP) has been linked to lung cancer risk. The PAr index, defined as the ratio 4-pyridoxic acid/(pyridoxal + PLP), reflects increased vitamin B6 catabolism during inflammation. PAr has been defined as a marker of lung cancer risk in a prospective cohort study, but analysis of a larger numbers of cases are needed to deepen the significance of this study. Here, we conducted a nested case-control study within the European Prospective Investigation into Cancer and Nutrition (EPIC, n = 521,330), which included 892 incident lung cancer cases and 1,748 controls matched by center, gender, date of blood collection, and date of birth. The association of PAr with risk of lung cancer was evaluated by using conditional logistic regression. Study participants with elevated PAr experienced higher risk of lung cancer in a dose-response fashion, with a doubling in PAr levels associated with 52% higher odds of lung cancer after adjustment for tobacco smoking, serum cotinine levels, educational attainment, and BMI [OR, 1.52; 95% confidence interval (CI) 1.27-1.81; P < 0.001]. Additional adjustment for intake of vegetables and fruits and physical activity did not materially affect risk association. The association of PAr with lung cancer risk was similar in both genders but slightly stronger in former smokers and in participants diagnosed with squamous cell carcinoma. This study provides robust evidence that increased vitamin B6 catabolism is independently associated with a higher risk of future lung cancer.Significance: This large cohort study firmly establishes an association between an index of vitamin B6 levels with lung cancer risk. Cancer Res; 78(1); 302-8. ©2017 AACR.
    Matched MeSH terms: Lung Neoplasms/etiology*
  10. Role of UGT1A1*6, UGT1A1*28 and ABCG2 c.421C>A polymorphisms in irinotecan-induced neutropenia in Asian cancer patients
    Jada SR, Lim R, Wong CI, Shu X, Lee SC, Zhou Q, et al.
    Cancer Sci, 2007 Sep;98(9):1461-7.
    PMID: 17627617
    The objectives of the present study were (i) to study the pharmacogenetics of UGT1A1*6, UGT1A1*28 and ABCG2 c.421C>A in three distinct healthy Asian populations (Chinese, Malays and Indians), and (ii) to investigate the polygenic influence of these polymorphic variants in irinotecan-induced neutropenia in Asian cancer patients. Pharmacokinetic and pharmacogenetic analyses were done after administration of irinotecan as a 90-min intravenous infusion of 375 mg/m(2) once every 3 weeks (n = 45). Genotypic-phenotypic correlates showed a non-significant influence of UGT1A1*28 and ABCG2 c.421C>A polymorphisms on the pharmacokinetics of SN-38 (P > 0.05), as well as severity of neutropenia (P > 0.05). Significantly higher exposure levels to SN-38 (P = 0.018), lower relative extent of glucuronidation (REG; P = 0.006) and higher biliary index (BI; P = 0.003) were found in cancer patients homozygous for the UGT1A1*6 allele compared with patients harboring the reference genotype. The mean absolute neutrophil count (ANC) was 85% lower and the prevalence of grade 4 neutropenia (ANC < or = 500/microL) was 27% in patients homozygous for UGT1A1*6 compared with the reference group. Furthermore, the presence of the UGT1A1*6 allele was associated with an approximately 3-fold increased risk of developing severe grade 4 neutropenia compared with patients harboring the reference genotype. These exploratory findings suggest that homozygosity for UGT1A1*6 allele may be associated with altered SN-38 disposition and may increase the risk of severe neutropenia in Asian cancer patients, particularly in the Chinese cancer patients who comprised 80% (n = 36) of the patient population in the present study.
    Matched MeSH terms: Lung Neoplasms/drug therapy; Lung Neoplasms/genetics
  11. Fulltext Targeting of CD133+ Cancer Stem Cells by Mesenchymal Stem Cell Expressing TRAIL Reveals a Prospective Role of Apoptotic Gene Regulation in Non-Small Cell Lung Cancer
    Fakiruddin KS, Lim MN, Nordin N, Rosli R, Zakaria Z, Abdullah S
    Cancers (Basel), 2019 08 28;11(9).
    PMID: 31466290 DOI: 10.3390/cancers11091261
    Mesenchymal stem cells (MSCs) are emerging as vehicles for anti-tumor cytotherapy; however, investigation on its efficacy to target a specific cancer stem cell (CSC) population in non-small cell lung cancer (NSCLC) is lacking. Using assays to evaluate cell proliferation, apoptosis, and gene expression, we investigated the efficacy of MSCs expressing tumour necrosis factor (TNF)-related apoptosis inducing ligand (MSC-TRAIL) to target and destroy CD133+ (prominin-1 positive) NSCLC-derived CSCs. Characterization of TRAIL death receptor 5 (DR5) revealed that it was highly expressed in the CD133+ CSCs of both H460 and H2170 cell lines. The human MSC-TRAIL generated in the study maintained its multipotent characteristics, and caused significant tumor cell inhibition in NSCLC-derived CSCs in a co-culture. The MSC-TRAIL induced an increase in annexin V expression, an indicator of apoptosis in H460 and H2170 derived CD133+ CSCs. Through investigation of mitochondria membrane potential, we found that MSC-TRAIL was capable of inducing intrinsic apoptosis to the CSCs. Using pathway-specific gene expression profiling, we uncovered candidate genes such as NFKB1, BAG3, MCL1, GADD45A, and HRK in CD133+ CSCs, which, if targeted, might increase the sensitivity of NSCLC to MSC-TRAIL-mediated inhibition. As such, our findings add credibility to the utilization of MSC-TRAIL for the treatment of NSCLC through targeting of CD133+ CSCs.
    Matched MeSH terms: Lung Neoplasms
  12. Fulltext Efficacy of Afatinib in the Treatment of Patients with Non-Small Cell Lung Cancer and Head and Neck Squamous Cell Carcinoma: A Systematic Review and Meta-Analysis
    Maarof NNN, Alsalahi A, Abdulmalek E, Fakurazi S, Tejo BA, Abdul Rahman MB
    Cancers (Basel), 2021 Feb 08;13(4).
    PMID: 33567737 DOI: 10.3390/cancers13040688
    Several randomized controlled trials (RCTs) evaluated the afatinib efficacy in patients with advanced non-small cell lung cancer (NSCLC) and recurrent/metastatic head and neck squamous cell carcinoma (R/M HNSCC). This review systemically outlined and meta-analyzed the afatinib efficacy in NSCLC and R/M HNSCC in terms of overall survival (OS) and progression-free survival (PFS) endpoints. Records were retrieved from PubMed, Web of Science, and ScienceDirect from 2011 to 2020. Eight afatinib RCTs were included and assessed for the risk of bias. In meta-analysis, overall pooled effect size (ES) of OS in afatinib group (AG) significantly improved in all RCTs and NSCLC-RCTs [hazard ratios (HRs): 0.89 (95% CI: 0.81-0.98, p = 0.02); I2 = 0%, p = 0.71/ 0.86 (95% CI: 0.76-0.97; p = 0.02); I2 = 0%, p = 0.50, respectively]. ES of PFS in AG significantly improved in all RCTs, NSCLC-RCTs, and HNSCC-RCTs [HRs: 0.75 (95% CI: 0.68-0.83; p < 0.00001); I2 = 26%, p = 0.24; 0.75 (95% CI: 0.66-0.84; p < 0.00001); I2 = 47%, p = 0.15/0.76 (95% CI: 0.65-88; p = 0.0004); I2 = 34%, p = 0.0004, respectively]. From a clinical viewpoint of severity, interstitial lung disease, dyspnea, pneumonia, acute renal failure, and renal injury were rarely incident adverse events in the afatinib group. In conclusion, first- and second-line afatinib monotherapy improved the survival of patients with NSCLC, while second-line afatinib monotherapy could be promising for R/M HNSCC. The prospective protocol is in PROSPERO (ID = CRD42020204547).
    Matched MeSH terms: Lung Neoplasms
  13. Fulltext The Role of MicroRNAs in Lung Cancer Metabolism
    Azizi MIHN, Othman I, Naidu R
    Cancers (Basel), 2021 Apr 05;13(7).
    PMID: 33916349 DOI: 10.3390/cancers13071716
    MicroRNAs (miRNAs) are short-strand non-coding RNAs that are responsible for post-transcriptional regulation of many biological processes. Their differential expression is important in supporting tumorigenesis by causing dysregulation in normal biological functions including cell proliferation, apoptosis, metastasis and invasion and cellular metabolism. Cellular metabolic processes are a tightly regulated mechanism. However, cancer cells have adapted features to circumvent these regulations, recognizing metabolic reprogramming as an important hallmark of cancer. The miRNA expression profile may differ between localized lung cancers, advanced lung cancers and solid tumors, which lead to a varying extent of metabolic deregulation. Emerging evidence has shown the relationship between the differential expression of miRNAs with lung cancer metabolic reprogramming in perpetuating tumorigenesis. This review provides an insight into the role of different miRNAs in lung cancer metabolic reprogramming by targeting key enzymes, transporter proteins or regulatory components alongside metabolic signaling pathways. These discussions would allow a deeper understanding of the importance of miRNAs in tumor progression therefore providing new avenues for diagnostic, therapeutic and disease management applications.
    Matched MeSH terms: Lung Neoplasms
  14. Erlotinib-loaded carboxymethyl temarind gum semi-interpenetrating nanocomposites
    Bera H, Abbasi YF, Lee Ping L, Marbaniang D, Mazumder B, Kumar P, et al.
    Carbohydr Polym, 2020 Feb 15;230:115664.
    PMID: 31887927 DOI: 10.1016/j.carbpol.2019.115664
    Erlotinib-loaded carboxymethyl temarind gum-g-poly(N-isopropylacrylamide)-montmorillonite based semi-IPN nanocomposites were synthesized and characterized for their in vitro performances for lung cancer therapy. The placebo matrices exhibited outstanding biodegradability and pH-dependent swelling profiles. The molar mass (M¯ c) between the crosslinks of these composites was declined with temperature. The solid state characterization confirmed the semi-IPN architecture of these scaffolds. The corresponding drug-loaded formulations displayed excellent drug-trapping capacity (DEE, 86-97 %) with acceptable zeta potential (-16 to -13 mV) and diameter (967-646 nm). These formulations conferred sustained drug elution profiles (Q8h, 77-99 %) with an initial burst release. The drug release profile of the optimized formulation (F-3) was best fitted in the first order kinetic model with Fickian diffusion driven mechanism. The mucin adsorption to F-3 followed Langmuir isotherms. The results of MTT assay, AO/EB staining and confocal analyses revealed that the ERL-loaded formulation suppressed A549 cell proliferation and induced apoptosis more effectively than pristine drug.
    Matched MeSH terms: Lung Neoplasms/drug therapy
  15. Fulltext A review on chitosan and its development as pulmonary particulate anti-infective and anti-cancer drug carriers
    Rasul RM, Tamilarasi Muniandy M, Zakaria Z, Shah K, Chee CF, Dabbagh A, et al.
    Carbohydr Polym, 2020 Dec 15;250:116800.
    PMID: 33049807 DOI: 10.1016/j.carbpol.2020.116800
    Chitosan, as a biodegradable and biocompatible polymer, is characterized by anti-microbial and anti-cancer properties. It lately has received a widespread interest for use as the pulmonary particulate backbone materials of drug carrier for the treatment of infectious disease and cancer. The success of chitosan as pulmonary particulate drug carrier is a critical interplay of their mucoadhesive, permeation enhancement and site/cell-specific attributes. In the case of nanocarriers, various microencapsulation and micro-nano blending systems have been devised to equip them with an appropriate aerodynamic character to enable efficient pulmonary aerosolization and inhalation. The late COVID-19 infection is met with acute respiratory distress syndrome and cancer. Chitosan and its derivatives are found useful in combating HCoV and cancer as a function of their molecular weight, substituent type and its degree of substitution. The interest in chitosan is expected to rise in the next decade from the perspectives of drug delivery in combination with its therapeutic performance.
    Matched MeSH terms: Lung Neoplasms/pathology
  16. Fulltext Fine mapping of chromosome 5p15.33 based on a targeted deep sequencing and high density genotyping identifies novel lung cancer susceptibility loci
    Kachuri L, Amos CI, McKay JD, Johansson M, Vineis P, Bueno-de-Mesquita HB, et al.
    Carcinogenesis, 2016 Jan;37(1):96-105.
    PMID: 26590902 DOI: 10.1093/carcin/bgv165
    Chromosome 5p15.33 has been identified as a lung cancer susceptibility locus, however the underlying causal mechanisms were not fully elucidated. Previous fine-mapping studies of this locus have relied on imputation or investigated a small number of known, common variants. This study represents a significant advance over previous research by investigating a large number of novel, rare variants, as well as their underlying mechanisms through telomere length. Variants for this fine-mapping study were identified through a targeted deep sequencing (average depth of coverage greater than 4000×) of 576 individuals. Subsequently, 4652 SNPs, including 1108 novel SNPs, were genotyped in 5164 cases and 5716 controls of European ancestry. After adjusting for known risk loci, rs2736100 and rs401681, we identified a new, independent lung cancer susceptibility variant in LPCAT1: rs139852726 (OR = 0.46, P = 4.73×10(-9)), and three new adenocarcinoma risk variants in TERT: rs61748181 (OR = 0.53, P = 2.64×10(-6)), rs112290073 (OR = 1.85, P = 1.27×10(-5)), rs138895564 (OR = 2.16, P = 2.06×10(-5); among young cases, OR = 3.77, P = 8.41×10(-4)). In addition, we found that rs139852726 (P = 1.44×10(-3)) was associated with telomere length in a sample of 922 healthy individuals. The gene-based SKAT-O analysis implicated TERT as the most relevant gene in the 5p15.33 region for adenocarcinoma (P = 7.84×10(-7)) and lung cancer (P = 2.37×10(-5)) risk. In this largest fine-mapping study to investigate a large number of rare and novel variants within 5p15.33, we identified novel lung and adenocarcinoma susceptibility loci with large effects and provided support for the role of telomere length as the potential underlying mechanism.
    Matched MeSH terms: Lung Neoplasms/genetics*
  17. Primitive neuroectodermal tumor of the lung with pericardial extension: a case report
    Shah Mohd Shah A, Mohamed Z, Abdullah A, Abdul Malek PM, Saidin N, Maskon O
    Cardiovasc. Pathol., 2007 Nov-Dec;16(6):351-3.
    PMID: 18005874
    A 16-year-old student presented with a 4-week history of progressive shortness of breath, loss of appetite, and occasional blood-tinged sputum. The chest X-ray revealed massive right-sided pleural effusion with cardiomegaly. An echocardiogram revealed a large pericardial mass with massive pericardial effusion. Subsequent computed tomography of the thorax revealed a large heterogeneous mass in the right lung with extension into the pericardium. Lung biopsy revealed primitive neuroectodermal tumor (PNET) with small round blue cells, Homer-Wright rosettes, and CD99 positivity. We discuss pericardial metastases of PNET and its implication in this patient.
    Matched MeSH terms: Lung Neoplasms/drug therapy; Lung Neoplasms/immunology; Lung Neoplasms/pathology*
  18. Fulltext Upper Gastrointestinal Bleed due to Duodenal Metastases of Lung Adenocarcinoma: Report of Two Cases and Review of Literature
    Kosasih S, Muhammad Nawawi KN, Wong Z, Chia Hsin DC, Ban AY, Raja Ali RA
    Case Rep Med, 2019;2019:3437056.
    PMID: 31772583 DOI: 10.1155/2019/3437056
    Upper gastrointestinal bleeding as a result of gastrointestinal metastases from lung cancer is extremely rare. We report two cases of patients with duodenal metastases from lung adenocarcinoma presented with recurrent melena. Histopathological examination and immunohistochemical staining of the duodenal biopsies supported the diagnosis of metastatic lung adenocarcinoma.
    Matched MeSH terms: Lung Neoplasms
  19. Fulltext Cephalomannine inhibits hypoxia-induced cellular function via the suppression of APEX1/HIF-1α interaction in lung cancer
    Ullah A, Leong SW, Wang J, Wu Q, Ghauri MA, Sarwar A, et al.
    Cell Death Dis, 2021 05 14;12(5):490.
    PMID: 33990544 DOI: 10.1038/s41419-021-03771-z
    Lung cancer (LC) is one of the leading causes of cancer-related death. As one of the key features of tumor microenvironment, hypoxia conditions are associated with poor prognosis in LC patients. Upregulation of hypoxic-induced factor-1α (HIF-1α) leads to the activation of various factors that contribute to the increased drug resistance, proliferation, and migration of tumor cells. Apurinic/apyrimidinic endonuclease-1 (APEX1) is a multi-functional protein that regulates several transcription factors, including HIF-1α, that contribute to tumor growth, oxidative stress responses, and DNA damage. In this study, we explored the mechanisms underlying cell responses to hypoxia and modulation of APEX1, which regulate HIF-1α and downstream pathways. We found that hypoxia-induced APEX1/HIF-1α pathways regulate several key cellular functions, including reactive oxygen species (ROS) production, carbonic anhydrase 9 (CA9)-mediated intracellular pH, migration, and angiogenesis. Cephalomannine (CPM), a natural compound, exerted inhibitory effects in hypoxic LC cells via the inhibition of APEX1/HIF-1α interaction in vitro and in vivo. CPM can significantly inhibit cell viability, ROS production, intracellular pH, and migration in hypoxic LC cells as well as angiogenesis of HUVECs under hypoxia through the inhibition of APEX1/HIF-1α interaction. Taken together, CPM could be considered as a promising compound for LC treatment.
    Matched MeSH terms: Lung Neoplasms/genetics*; Lung Neoplasms/pathology
  20. Emerging trends in the novel drug delivery approaches for the treatment of lung cancer
    Sharma P, Mehta M, Dhanjal DS, Kaur S, Gupta G, Singh H, et al.
    Chem Biol Interact, 2019 Aug 25;309:108720.
    PMID: 31226287 DOI: 10.1016/j.cbi.2019.06.033
    Cancer is one of the major diseases that cause a high number of deaths globally. Of the major types of cancers, lung cancer is known to be the most chronic form of cancer in the world. The conventional management of lung cancer includes different medical interventions like chemotherapy, surgical removal, and radiation therapy. However, this type of approach lacks specificity and also harms the adjacent normal cells. Lately, nanotechnology has emerged as a promising intervention in the management and treatment of lung cancers. Nanotechnology has revolutionized the existing modalities and focuses primarily on reducing toxicity and improving the bioavailability of anticancer drugs to the target tumor cells. Nanocarrier systems are being currently used extensively to exploit and to overcome the obstructions induced by cancers in the lungs. The nano-carrier-loaded therapeutic drug delivery methods have shown promising potential in treating lung cancer as its target is to control the growth of tumor cells. In this review, various modes of nano drug delivery options like liposomes, dendrimers, quantum dots, carbon nanotubes and metallic nanoparticles have been discussed. Nano-carrier drug delivery systems emerge as a promising approach and thus is expected to provide newer and advanced avenues in cancer therapeutics.
    Matched MeSH terms: Lung Neoplasms/drug therapy*; Lung Neoplasms/pathology
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