2018
DOI: 10.22159/ajpcr.2018.v11i8.26271
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A Review: Status of Genetic Modulated Nonsmall Cell Lung Cancer Targets and Treatment (Current Updates in Drugs for Non-Small Cell Lung Cancer Treatment)

Abstract: Genetic modifications or mutations has been a bottleneck for the treatment of cancer; it is widely known to play a vital role in the progression of metastatic level/stage within the nonsmall cell lung cancer (NSCLC). The NSCLC of cancer is responsible for lung cancer lawsuits. In the various genetic mutations related study has been concluded with the various genes findings, which are named as the epidermal growth factor receptor, anaplastic lymphoma kinase, Kristen rat sarcoma virus, ROS proto-oncogene 1, huma… Show more

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Cited by 3 publications
(2 citation statements)
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References 59 publications
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“…It is one of tumour survival kinase which is commonly overexpressed in tumour for apoptosis escape and metastasis. 15,16 Moreover, after activation, AKT will also be translocated into nucleus and regulate the gene responsible for cellular proliferation. 17 Furthermore, AFB1 is estimated to have the ability to interact with one of seven predicted proteins within HCC mechanism.…”
Section: Discussionmentioning
confidence: 99%
“…It is one of tumour survival kinase which is commonly overexpressed in tumour for apoptosis escape and metastasis. 15,16 Moreover, after activation, AKT will also be translocated into nucleus and regulate the gene responsible for cellular proliferation. 17 Furthermore, AFB1 is estimated to have the ability to interact with one of seven predicted proteins within HCC mechanism.…”
Section: Discussionmentioning
confidence: 99%
“…Osimertinib Mesylate (OM) is the third-generation of kinase inhibitor and is used for the first-line treatment of patients with metastatic Non-Small Cell Lung Carcinoma (NSCLC) whose tumors have epidermal growth factor receptor (EGFR) exon 19 deletions or exon 21 L858R mutations and the treatment of patients with metastatic EGFR T790M mutation-positive NSCLC, whose disease has progressed on or after EGFR Tyrosine Kinase Inhibitor (TKI) therapy [1,2]. The mechanism action of OM binds irreversibly to certain mutant forms of EGFR (T790M, L858R, and exon 19 deletions) at approximately 9-fold lower concentrations than wildtype [3].…”
Section: Introductionmentioning
confidence: 99%