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"Get a quick, expert overview of the many key facets of lung cancer evaluation and management with this concise, practical resource. This easy-to-read reference presents a summary of today's best evidence-based approaches to diagnosis and management in this critical area."--
Lungs --- Cancer. --- Lung cancer
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Lungs --- Cancer. --- Lung cancer --- Diseases, Obstructive.
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Approximately 40% of lung cancer patients will develop central nervous system (CNS) metastases during the course of their disease. Most of these are brain metastases, but up to 10% will develop leptomeningeal metastases. Known risk factors for CNS metastases development are small cell lung cancer (SCLC), adenocarcinoma histology, epidermal growth factor receptor (EGFR) mutant or anaplastic lymphoma kinase (ALK) rearranged lung cancer, advanced nodal status, tumor stage and younger age. CNS metastases can have a negative impact on quality of life (QoL) and overall survival (OS). The proportion of lung cancer patients diagnosed with CNS metastases has increased over the years due to increased use of brain imaging as part of initial cancer staging, advances in imaging techniques and better systemic disease control. Post contrast gadolinium enhanced magnetic resonance imaging (gd-MRI) is preferred, however when this is contra-indicated a contrast enhanced computed tomography (CE-CT) is mentioned as an alternative option. When CNS metastases are diagnosed, local treatment options consist of radiotherapy (stereotactic or whole brain) and surgery. Local treatment can be complicated by symptomatic radiation necrosis for which no high level evidence based treatment exists. Moreover, differential diagnosis with metastasis progression is difficult. Systemic treatment options have expanded over the last years. Until recently, chemotherapy was the only treatment option with a poor penetration in the CNS. Angiogenesis inhibitors are promising in the treatment of primary CNS tumors as well as radiation necrosis but clinical trials of anti-angiogenic agents in NSCLC have largely excluded patients with CNS metastases. Furthermore, research has also focused on methods to prevent development of CNS disease, for example with prophylactic cranial irradiation. Recently, checkpoint inhibitors have become available for NSCLC patients, and tyrosine kinase inhibitors (TKIs) have improved prognosis significantly in those with a druggable driver mutation. Newer TKIs are often designed to have better CNS penetration compared to first-generation TKIs. Despite advances in treatment options CNS metastases remain a problem in lung cancer and cause morbidity and mortality. This Research Topic provides an extensive resource of articles describing advances in CNS metastases management in lung cancer patients, from prevention to diagnosis and treatment.
lung cancer --- driver mutations --- treatment --- brain metastases --- leptomeningeal metastases --- cranial radiation --- prediction --- diagnosis
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Approximately 40% of lung cancer patients will develop central nervous system (CNS) metastases during the course of their disease. Most of these are brain metastases, but up to 10% will develop leptomeningeal metastases. Known risk factors for CNS metastases development are small cell lung cancer (SCLC), adenocarcinoma histology, epidermal growth factor receptor (EGFR) mutant or anaplastic lymphoma kinase (ALK) rearranged lung cancer, advanced nodal status, tumor stage and younger age. CNS metastases can have a negative impact on quality of life (QoL) and overall survival (OS). The proportion of lung cancer patients diagnosed with CNS metastases has increased over the years due to increased use of brain imaging as part of initial cancer staging, advances in imaging techniques and better systemic disease control. Post contrast gadolinium enhanced magnetic resonance imaging (gd-MRI) is preferred, however when this is contra-indicated a contrast enhanced computed tomography (CE-CT) is mentioned as an alternative option. When CNS metastases are diagnosed, local treatment options consist of radiotherapy (stereotactic or whole brain) and surgery. Local treatment can be complicated by symptomatic radiation necrosis for which no high level evidence based treatment exists. Moreover, differential diagnosis with metastasis progression is difficult. Systemic treatment options have expanded over the last years. Until recently, chemotherapy was the only treatment option with a poor penetration in the CNS. Angiogenesis inhibitors are promising in the treatment of primary CNS tumors as well as radiation necrosis but clinical trials of anti-angiogenic agents in NSCLC have largely excluded patients with CNS metastases. Furthermore, research has also focused on methods to prevent development of CNS disease, for example with prophylactic cranial irradiation. Recently, checkpoint inhibitors have become available for NSCLC patients, and tyrosine kinase inhibitors (TKIs) have improved prognosis significantly in those with a druggable driver mutation. Newer TKIs are often designed to have better CNS penetration compared to first-generation TKIs. Despite advances in treatment options CNS metastases remain a problem in lung cancer and cause morbidity and mortality. This Research Topic provides an extensive resource of articles describing advances in CNS metastases management in lung cancer patients, from prevention to diagnosis and treatment.
lung cancer --- driver mutations --- treatment --- brain metastases --- leptomeningeal metastases --- cranial radiation --- prediction --- diagnosis
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Approximately 40% of lung cancer patients will develop central nervous system (CNS) metastases during the course of their disease. Most of these are brain metastases, but up to 10% will develop leptomeningeal metastases. Known risk factors for CNS metastases development are small cell lung cancer (SCLC), adenocarcinoma histology, epidermal growth factor receptor (EGFR) mutant or anaplastic lymphoma kinase (ALK) rearranged lung cancer, advanced nodal status, tumor stage and younger age. CNS metastases can have a negative impact on quality of life (QoL) and overall survival (OS). The proportion of lung cancer patients diagnosed with CNS metastases has increased over the years due to increased use of brain imaging as part of initial cancer staging, advances in imaging techniques and better systemic disease control. Post contrast gadolinium enhanced magnetic resonance imaging (gd-MRI) is preferred, however when this is contra-indicated a contrast enhanced computed tomography (CE-CT) is mentioned as an alternative option. When CNS metastases are diagnosed, local treatment options consist of radiotherapy (stereotactic or whole brain) and surgery. Local treatment can be complicated by symptomatic radiation necrosis for which no high level evidence based treatment exists. Moreover, differential diagnosis with metastasis progression is difficult. Systemic treatment options have expanded over the last years. Until recently, chemotherapy was the only treatment option with a poor penetration in the CNS. Angiogenesis inhibitors are promising in the treatment of primary CNS tumors as well as radiation necrosis but clinical trials of anti-angiogenic agents in NSCLC have largely excluded patients with CNS metastases. Furthermore, research has also focused on methods to prevent development of CNS disease, for example with prophylactic cranial irradiation. Recently, checkpoint inhibitors have become available for NSCLC patients, and tyrosine kinase inhibitors (TKIs) have improved prognosis significantly in those with a druggable driver mutation. Newer TKIs are often designed to have better CNS penetration compared to first-generation TKIs. Despite advances in treatment options CNS metastases remain a problem in lung cancer and cause morbidity and mortality. This Research Topic provides an extensive resource of articles describing advances in CNS metastases management in lung cancer patients, from prevention to diagnosis and treatment.
lung cancer --- driver mutations --- treatment --- brain metastases --- leptomeningeal metastases --- cranial radiation --- prediction --- diagnosis
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Tissue fibrosis may occur for unknown causes or be the consequence of many pathological conditions including chronic inflammatory or infectious diseases, autoimmune disorders, graft rejection, or malignancy. On the other hand, malignant tumors have been identified in fibrotic tissues decades ago, and now accumulating evidence suggests that fibrotic lesions enhance the risk of cancer in several organs such as liver, lungs, and breast. Disruption of an organ parenchymal cells and of its normal structural scaffold during tissue fibrogenesis appears to induce loss of cell polarity, promoting uncontrolled cell proliferation that may eventually lead to cancer development. Many cellular and molecular abnormalities including aberrant expression of microRNAs, genetic and epigenetic alterations, evasion or delayed apoptosis, unregulated intracellular signal pathways, and dysregulation or defective intercellular communications have been proposed to explain this link between fibrogenesis and carcinogenesis. However, the precise mechanisms of this fibrosis-to-cancer transition remain unclear. This book presents a collection of reviews and original articles summarizing recent advances in understanding the molecular mechanisms of cancer development in fibrotic organs.
bleomycin --- n/a --- regeneration --- antitumor efficacy --- lung cancer --- SOX2 --- leiomyosarcoma --- lung cancer (LC) --- nanoparticles --- cytokines --- hepatocellular carcinoma --- metabolic reprogramming --- hepatic stellate cells --- angiogenesis --- transforming growth factor-? --- anaplastic lymphoma kinase --- idiopathic pulmonary fibrosis --- growth factor --- pathogenesis --- cancer-associated fibroblasts --- fibrosis --- lipopolysaccharide --- DHA --- lncRNA --- SREBP-1 --- YAP --- protein S --- non-small cell lung cancer (NSCLC) --- omega-3 fatty acid --- inflammation --- metastasis --- clinical symptoms --- miRNA --- smooth muscle tumor of uncertain malignant potential --- Wnt --- interstitial fluid pressure --- heterogeneity --- hepatocytes --- myometrium --- tumor necrosis factor ? --- tumor --- tumor microenvironment --- extracellular matrix --- TAZ --- carcinogenesis --- cystic formation --- pulmonary fibrosis --- HBV --- cytokine --- genetic instability --- diagnosis --- EMT --- crizotinib --- Hippo pathway --- GPR120 --- marker --- HCV --- non-alcoholic steatohepatitis --- pathology --- common pathways --- apoptosis --- type I collagen --- GPR40 --- acute lung injury --- uterine fibroid --- renal injury --- pathophysiology --- reactive oxygen species --- immunohistochemistry --- SMAD --- butylidenephthalide --- leiomyoma --- cirrhosis --- Erk1/2 --- targeted therapy --- TGF-? --- mechanotransduction --- therapy --- breast cancer --- hepatocellular carcinoma (HCC) --- hepatic stellate cells (HSCs) --- idiopathic pulmonary fibrosis (IPF) --- cancer-associated fibroblasts (CAFs) --- cancer --- signal pathway --- tumor stiffness
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This Special Issue of Cancers (Basel) is mainly dedicated to selecting papers from the talks given during the first Joint Meeting on Lung Cancer (JMLC) between the MD Anderson Cancer Center (Houston, Texas USA) and the Hospital University Federation (HUF) OncoAge (University Côte d’Azur, Nice, France) (Nice, September 2018). The central theme of JMLC is to discuss new advances and exchange ideas regarding lung cancer. Notably, the talks covered different topics on new therapeutic strategies (targeted therapy and immuno-oncology), molecular and cellular biology, biomarkers, and the epidemiology of lung cancer. Special attention was also given to lung cancer in elderly patients. The articles published in this Special Issue covered subjects such as the assessment of new biomarkers and new approaches for the early detection of lung cancer, epidemiological data, and emphasized a place for the newly characterized cellular pathways in lung cancer, which opens room for therapeutic perspectives for lung cancer patients.
microRNAs --- multiplexed --- screening --- education --- non-smoker --- image analysis --- artificial intelligence --- research --- lung cancer --- spatial analysis --- optimization --- fluorescence --- geriatric assessment --- geriatric interventions --- TNBC --- liquid biopsy --- non-small cell lung cancer --- integrated approaches --- well-being --- hormone-like action --- EGFR mutations --- reversal of EMT --- tumor plasticity --- immune profiling --- macrophage --- multiplexed methodologies --- targeted treatment --- techniques --- immune-oncology --- bioinformatics --- MALAT1 --- long non-coding RNAs --- CD8 T Cells --- personal medicine --- EGFR TKIs --- lncRNA --- hormones --- elderly --- interleukin-1? and immunometabolism --- chromogenic --- xenograft --- metastasis --- PD-1/PD-L1 checkpoint blockade --- immunotherapy --- molecular --- cancer tissues --- digital --- NSCLC --- immune blockade --- lung adenocarcinoma --- circulating tumor cells --- brightfield --- non-coding RNAs --- older adults --- cancer --- tumor microenvironment --- aging --- rational therapy
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The metabolomics approach, defined as the study of all endogenously-produced low-molecular-weight compounds, appeared as a promising strategy to define new cancer biomarkers. Information obtained from metabolomic data can help to highlight disrupted cellular pathways and, consequently, contribute to the development of new-targeted therapies and the optimization of therapeutics. Therefore, metabolomic research may be more clinically translatable than other omics approaches, since metabolites are closely related to the phenotype and the metabolome is sensitive to many factors. Metabolomics seems promising to identify key metabolic pathways characterizing features of pathological and physiological states. Thus, knowing that tumor metabolism markedly differs from the metabolism of normal cells, the use of metabolomics is ideally suited for biomarker research. Some works have already focused on the application of metabolomic approaches to different cancers, namely lung, breast and liver, using urine, exhaled breath and blood. In this Special Issue we contribute to a more complete understanding of cancer disease using metabolomics approaches.
cell transporters --- pharmacodynamics --- cell growth --- in vitro study --- metabolomic signatures --- endometabolome --- lung cancer --- metabolomics --- chemometric methods --- bladder cancer --- mTOR --- metabolite profiling --- metabolic pathways --- hepatocellular carcinoma --- glutamate --- senescence MCF7 --- breath analysis --- bio actives --- biomarker --- gas chromatography–mass spectrometry (GC–MS) --- GC-MS --- lung --- omics --- nutraceuticals --- glutaminase --- metabolism --- acylcarnitines --- Erwinaze --- Kidrolase --- glutathione --- targeted metabolomics --- apoptosis --- SLC1A5 --- essential amino acids --- cancer progression --- ASCT2 --- HR MAS --- alanine --- analytical platforms --- volatile organic compound --- glutaminolysis --- isotope tracing analysis --- asparaginase --- vitamin E --- breast cancer --- prognosis --- early diagnosis --- tocotrienols --- NMR --- prostate cancer --- in vitro --- cancer --- MDA-MB-231
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This Special Issue Book, “Marine Bioactive Peptides: Structure, Function, andTherapeutic Potential"" includes up-to-date information regarding bioactivepeptides isolated from marine organisms. Marine peptides have been found invarious phyla, and their numbers have grown in recent years. These peptidesare diverse in structure and possess broad-spectrum activities that have greatpotential for medical applications. Various marine peptides are evolutionaryancient molecular factors of innate immunity that play a key role in host defense.A plethora of biological activities, including antibacterial, antifungal, antiviral,anticancer, anticoagulant, endotoxin-binding, immune-modulating, etc., makemarine peptides an attractive molecular basis for drug design. This Special IssueBook presents new results in the isolation, structural elucidation, functionalcharacterization, and therapeutic potential evaluation of peptides found inmarine organisms. Chemical synthesis and biotechnological production of marinepeptides and their mimetics is also a focus of this Special Issue Book.
cone snail --- tilapia --- n/a --- animal models --- BRICHOS domain --- recombinant peptide --- calcium absorption --- plastein reaction --- antioxidant activity --- endothelial dysfunction --- C3a --- lung cancer --- invertebrate immunity --- identification --- zinc bioavailability --- NA-inhibitory peptide --- nuclear magnetic resonance (NMR) --- review --- ACE-inhibitory activity --- intestinal absorption --- hairtail (Trichiurus japonicas) --- DU-145 cells --- peptide --- crustacean --- venom duct --- Kalloconus --- drug design --- molecular symmetry --- arenicin --- ?-helix --- APETx2 --- conotoxins --- functional diversity --- docking --- conotoxin --- neuraminidase --- angiotensin II --- polychaeta --- influenza virus --- phylogeny --- gene expression --- host defense peptide --- Perinereis aibuhitensis --- anti-diabetic activity --- conopeptides --- SHRs --- Chlorella pyrenoidosa protein hydrolysate (CPPH) --- metastasis --- Caco-2 cell monolayer --- Nrf2 --- caco-2 cells --- HUVEC --- PYP15 --- sea cucumber --- decapeptide --- cytotoxic --- arenicin-1 --- marine peptides --- cell proliferation --- Conus --- Conus ateralbus --- self-production of hydrogen peroxide --- antimicrobial activity --- molecular dynamics --- machine learning --- tachyplesins --- ion channels --- gut microbiota --- Anthopleura anjunae oligopeptide --- signaling pathways --- half-fin anchovy hydrolysates --- NF-?B --- Chlorella pyrenoidosa protein hydrolysate-calcium chelate (CPPH-Ca) --- antihypertensive effect --- QAGLSPVR --- antimicrobial peptides --- vasculogenic mimicry --- antibacterial --- ?-hairpin --- innate immunity --- transcriptome sequencing --- HIF-1? --- Gracilariopsis lemaneiformis --- function --- ACE-inhibitory peptide --- complement --- peptide-zinc complex --- structure-activity relationship --- multi-functional peptides --- cod skin --- adsorption --- Maillard reaction products --- molecular docking --- antibacterial peptide --- PI3K/AKT/mTOR signaling pathway --- Arenicola marina --- structure–activity relationship --- antimicrobial peptide --- Rana-box --- acid-sensing ion channel --- Neptunea arthritica cumingii --- apoptosis --- membrane damage --- proteolytic system --- toxin --- polyphemusins --- computational studies --- muscle --- oyster zinc-binding peptide --- abalone --- pain relief --- transport routes --- cytotoxicity --- dexamethasone --- cell death --- host?microbe relationship --- anti-LPS factor --- MMPs --- protein synthesis --- structure --- Pyropia yezoensis peptide --- cone snails --- chemical synthesis --- prostate cancer --- Ugr 9-1 --- myotube atrophy
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