PI3K/Akt/mTOR Pathways Inhibitors with Potential Prospects in Non-Small-Cell Lung Cancer.

Alharbi, KS; Shaikh, MAJ; Almalki, WH; Kazmi, I; Al-Abbasi, FA; Alzarea, SI; Imam, SS; Alshehri, S; Ghoneim, MM; Singh, SK; Chellappan, DK; Oliver, BG; Dua, K; Gupta, G

PI3K/Akt/mTOR Pathways Inhibitors with Potential Prospects in Non-Small-Cell Lung Cancer.

Alharbi, KS Shaikh, MAJ Almalki, WH Kazmi, I Al-Abbasi, FA Alzarea, SI Imam, SS Alshehri, S Ghoneim, MM Singh, SK Chellappan, DK Oliver, BG Dua, K

Gupta, G

Permalink

Publisher:: Begell House
Publication Type:: Journal Article
Citation:: J Environ Pathol Toxicol Oncol, 2022, 41, (4), pp. 85-102
Issue Date:: 2022

Closed Access

	Filename	Description	Size
	19911770_9563307540005671.pdf		6.98 MB	Adobe PDF	View/Open

Copyright Clearance Process

Recently Added
In Progress
Closed Access

This item is closed access and not available.

Full metadata record

Field	Value	Language
dc.contributor.author	Alharbi, KS
dc.contributor.author	Shaikh, MAJ
dc.contributor.author	Almalki, WH
dc.contributor.author	Kazmi, I
dc.contributor.author	Al-Abbasi, FA
dc.contributor.author	Alzarea, SI
dc.contributor.author	Imam, SS
dc.contributor.author	Alshehri, S
dc.contributor.author	Ghoneim, MM
dc.contributor.author	Singh, SK
dc.contributor.author	Chellappan, DK
dc.contributor.author	Oliver, BG
dc.contributor.author	Dua, K https://orcid.org/0000-0002-7507-1159
dc.contributor.author	Gupta, G
dc.date.accessioned	2022-11-25T00:44:47Z
dc.date.available	2022-11-25T00:44:47Z
dc.date.issued	2022
dc.identifier.citation	J Environ Pathol Toxicol Oncol, 2022, 41, (4), pp. 85-102
dc.identifier.issn	0731-8898
dc.identifier.issn	2162-6537
dc.identifier.uri	http://hdl.handle.net/10453/163736
dc.description.abstract	Lung cancer is the leading cause of cancer-related mortality across the globe. The most prevalent pathological form of lung cancer is non-small-cell lung cancer (NSCLC). Elevated stimulation of the PI3K/Akt/mTOR pathway causes a slew of cancer-related symptoms, making it a promising target for new anticancer drugs. The PI3K/Akt/mTOR path is involved extensively in carcinogenesis and disease advancement in NSCLC. Several new inhibitors targeting this pathway have been discovered in preclinical investigations and clinical trials. The etiology and epidemiology of NSCLC and biology of the PI3K/Akt/mTOR cascade and its role in NSCLC pathogenesis have all been discussed in this article. In this article, we've reviewed PI3K/Akt/mTOR cascade inhibitors that have been proven in vitro and in preclinical trials to be effective in NSCLC. Drugs targeting the PI3K/Akt/mTOR path in the treatment of NSCLC were also addressed. A better knowledge of the underlying molecular biology, including epigenetic changes, is also critical to detecting relevant biomarkers and guiding combination methods. Additionally, improved clinical trial designs will increase the capacity to test novel drugs and combinations for accounting for genomic variation and eventually improve patient outcomes.
dc.format	Print
dc.language	eng
dc.publisher	Begell House
dc.relation.ispartof	J Environ Pathol Toxicol Oncol
dc.relation.isbasedon	10.1615/JEnvironPatholToxicolOncol.2022042281
dc.rights	info:eu-repo/semantics/closedAccess
dc.subject.classification	Oncology & Carcinogenesis
dc.subject.mesh	Humans
dc.subject.mesh	Carcinoma, Non-Small-Cell Lung
dc.subject.mesh	Proto-Oncogene Proteins c-akt
dc.subject.mesh	Phosphatidylinositol 3-Kinases
dc.subject.mesh	Lung Neoplasms
dc.subject.mesh	Phosphoinositide-3 Kinase Inhibitors
dc.subject.mesh	MTOR Inhibitors
dc.subject.mesh	TOR Serine-Threonine Kinases
dc.subject.mesh	Humans
dc.subject.mesh	Carcinoma, Non-Small-Cell Lung
dc.subject.mesh	Lung Neoplasms
dc.subject.mesh	Proto-Oncogene Proteins c-akt
dc.subject.mesh	Phosphatidylinositol 3-Kinases
dc.subject.mesh	TOR Serine-Threonine Kinases
dc.subject.mesh	Phosphoinositide-3 Kinase Inhibitors
dc.subject.mesh	MTOR Inhibitors
dc.title	PI3K/Akt/mTOR Pathways Inhibitors with Potential Prospects in Non-Small-Cell Lung Cancer.
dc.type	Journal Article
utslib.citation.volume	41
utslib.location.activity	United States
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Health
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney/Faculty of Health/Public Health
pubs.organisational-group	/University of Technology Sydney/Faculty of Health/Graduate School of Health
pubs.organisational-group	/University of Technology Sydney/Faculty of Health/Graduate School of Health/GSH.Pharmacy
pubs.organisational-group	/University of Technology Sydney/Centre for Health Technologies (CHT)
utslib.copyright.status	closed_access	*
dc.date.updated	2022-11-25T00:44:45Z
pubs.issue	4
pubs.publication-status	Published
pubs.volume	41
utslib.citation.issue	4

Abstract:

Lung cancer is the leading cause of cancer-related mortality across the globe. The most prevalent pathological form of lung cancer is non-small-cell lung cancer (NSCLC). Elevated stimulation of the PI3K/Akt/mTOR pathway causes a slew of cancer-related symptoms, making it a promising target for new anticancer drugs. The PI3K/Akt/mTOR path is involved extensively in carcinogenesis and disease advancement in NSCLC. Several new inhibitors targeting this pathway have been discovered in preclinical investigations and clinical trials. The etiology and epidemiology of NSCLC and biology of the PI3K/Akt/mTOR cascade and its role in NSCLC pathogenesis have all been discussed in this article. In this article, we've reviewed PI3K/Akt/mTOR cascade inhibitors that have been proven in vitro and in preclinical trials to be effective in NSCLC. Drugs targeting the PI3K/Akt/mTOR path in the treatment of NSCLC were also addressed. A better knowledge of the underlying molecular biology, including epigenetic changes, is also critical to detecting relevant biomarkers and guiding combination methods. Additionally, improved clinical trial designs will increase the capacity to test novel drugs and combinations for accounting for genomic variation and eventually improve patient outcomes.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/163736