The Biology of Lung Cancer

Salehi-Rad, Ramin; Li, Rui; Paul, Manash K.; Dubinett, Steven M.; Liu, Bin

doi:10.1016/j.ccm.2019.10.003

Cited by 64 publications

(56 citation statements)

References 90 publications

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“…NSCLC is a heterogeneous disease, and recent sequencing studies have revealed the genomic landscape (Figure 1). Common genomic alterations in LUAD include KRAS, EGFR, HER2, MET, RET, ALK, and ROS1, while the important alteration in tumor suppressor includes TP53, KEAP1, LKB1, and NF1 (Figure 1) [1,14]. Interestingly the major genomic alterations in LUSC include TP53, PIK3CA, CDKN2A, NFE2L2, KEAP1, SOX2, PTEN, CDKN2A, RB1, CCND1, NOTCH1, MLL2, and HLA-A (Figure 1) [1,15] (Figure 1).…”

Section: Gene Mutation In Nsclc and Pharmacogeneticsmentioning

confidence: 99%

“…The genetic alterations data is a sum of somatic defects, homozygous deletions, focal amplifications, and major changes of gene expression. Reproduced from Salehi-Rad et al [1].…”

Section: Gene Mutation In Nsclc and Pharmacogeneticsmentioning

confidence: 99%

“…Lung cancer is the principal cause of cancer-related death worldwide and affects both smokers and non-smokers [1]. Men have the highest incidence and mortality related to lung cancer, while in women, it is third by incidence and second by mortality.…”

Section: Introductionmentioning

confidence: 99%

“…Histologically 80-85% of lung cancers are classified as non-small cell lung cancer (NSCLC), while the remaining is small cell lung cancer (SCLC). Adenocarcinoma (LUAD; ~ 65%), squamous cell carcinoma (LUSC; ~ 30%), and large cell carcinoma (LCLC) are the major subtypes of NSCLC and originates from different types of lung cells [1,3,4]. While SCLC is less frequent but more aggressive as compared to LUAD and LUSC.…”

Section: Introductionmentioning

confidence: 99%

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Updates in Pharmacogenetics of Non-Small Cell Lung Cancer

Ruwali¹,

Moharir²,

Singh³

et al. 2021

Pharmacogenetics

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Though significant clinical advances have been made, lung cancer remains the most lethal, with a low 5-year survival rate. The variability in patient response towards therapy is substantial and is associated with lung cancer’s genomic landscape. Pharmacogenetic studies have deciphered many clinically relevant associations between tumor genetic alterations and their influences on drug efficacy, toxicity sensitivity and overall outcomes of cancer treatment. Biomarkers are tools in the arsenal that can help in the prediction, prognosis, diagnosis and follow-up of cancer treatment. Bulk and single-cell next-generation sequencing of large patient cohorts have generated a better understanding of the genetic underpinnings of lung cancer, and opening up personalized therapeutic opportunities. Immunotherapy and personalized medicine are providing hope for lung cancer patients. This review highlights the genetic alterations and important lung cancer biomarkers. The pharmacogenetic associations, personalized immunotherapy and challenges associated with effective therapy are also discussed. Pharmacogenetics and pharmacogenomics can open up new vistas for optimized, personalized NSCLC treatment.

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Section: Gene Mutation In Nsclc and Pharmacogeneticsmentioning

confidence: 99%

“…The genetic alterations data is a sum of somatic defects, homozygous deletions, focal amplifications, and major changes of gene expression. Reproduced from Salehi-Rad et al [1].…”

Section: Gene Mutation In Nsclc and Pharmacogeneticsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Updates in Pharmacogenetics of Non-Small Cell Lung Cancer

Ruwali¹,

Moharir²,

Singh³

et al. 2021

Pharmacogenetics

View full text Add to dashboard Cite

show abstract

“…Lung cancer is one of the most common lung diseases and one of the most important contributors to cancer-related mortality worldwide 3,4 . Lung cancer consists mainly of either small cell lung cancer (SCLC) or non-SCLC (NSCLC) types, which make up 10-13% and 85-90% of all lung cancer cases, respectively 3,4 . Existing drugs available are still inadequate, and this has prompted a demand for upgraded therapeutic approaches.…”

Section: Introductionmentioning

confidence: 99%

Tempol Differently Affects Cellular Redox Status and Antioxidant Enzymes in Various Lung-related Cells

park

2021

Preprint

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Tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl) is a potential redox agent in cells. The present study investigated changes in cellular redox status [reactive oxygen species (ROS) and glutathione (GSH) levels] and in antioxidant enzymes, in Tempol-treated Calu-6 and A549 lung cancer cells, normal lung WI-38 VA-13 cells, and primary pulmonary fibroblasts. Results demonstrated that Tempol (0.5 ~ 4 mM) either increased or decreased general ROS levels in lung cancer and normal cells at 48 h and specifically increased O2•− levels in these cells. In addition, Tempol differentially altered the expression and activity of superoxide dismutase, catalase, and thioredoxin reductase1 (TrxR1) in A549, Calu-6, and WI-38 VA-13 cells. In particular, Tempol increased TrxR1 protein levels in these cells. Tempol at 1 mM inhibited the growth of lung cancer and normal cells by about 50% at 48 h but also significantly induced cell death, as evidenced by annexin V-positive cells. Furthermore, down-regulation of TrxR1 by siRNA somewhat affected the levels of cell growth inhibition and death as well as ROS in Tempol-treated cells. In addition, Tempol increased the numbers of GSH-depleted cells in both cancer cells and normal cells at 48h. In conclusion, Tempol differentially increased or decreased levels of ROS and various antioxidant enzymes in lung cancer and normal cells, and induced growth inhibition and death in all lung cells along with an increase in O2•− levels and GSH depletion.

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Design, Synthesis, and Biological Evaluation of Novel Quercetin Derivatives as PPAR‐γ Partial Agonists by Modulating Epithelial–Mesenchymal Transition in Lung Cancer Metastasis

et al. 2023

Self Cite

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Epithelial‐to‐mesenchymal transition (EMT) is responsible for driving metastasis of multiple cancer types including lung cancer. Peroxisome proliferator‐activated receptor (PPAR)‐γ, a ligand‐activated transcription factor, controls expression of variety of genes involved in EMT. Although several synthetic compounds act as potent full agonists for PPAR‐γ, their long term application is restricted due to serious adverse effects. Therefore, partial agonists involving reduced and balanced PPAR‐γ activity are more effective and valued. A previous study discerned the efficacy of quercetin and its derivatives to attain favorable stabilization with PPAR‐γ. Here this work is extended by synthesizing five novel quercetin derivatives (QDs) namely thiosemicarbazone (QUETSC)) and hydrazones (quercetin isonicotinic acid hydrazone (QUEINH), quercetin nicotinic acid hydrazone (QUENH), quercetin 2‐furoic hydrazone (QUE2FH), and quercetin salicyl hydrazone (QUESH)) and their effects are analyzed in modulating EMT in lung cancer cell lines via PPAR‐γ partial activation. QDs‐treated A549 cells diminish cell proliferation strongly at nanomolar concentration compared to NCI‐H460 cells. Of the five screened derivatives, QUETSC, QUE2FH, and QUESH exhibit the property of partial activation as compared to the overexpressive level of rosiglitazone. Consistently, these QDs also suppress EMT process by markedly downregulating the levels of mesenchymal markers (Snail, Slug, and zinc finger E‐box binding homeobox 1) and concomitant upregulation of epithelial marker (E‐cadherin).

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The Biology of Lung Cancer

Cited by 64 publications

References 90 publications

Updates in Pharmacogenetics of Non-Small Cell Lung Cancer

Updates in Pharmacogenetics of Non-Small Cell Lung Cancer

Tempol Differently Affects Cellular Redox Status and Antioxidant Enzymes in Various Lung-related Cells

Design, Synthesis, and Biological Evaluation of Novel Quercetin Derivatives as PPAR‐γ Partial Agonists by Modulating Epithelial–Mesenchymal Transition in Lung Cancer Metastasis

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