1
40
4
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.bmcl.2014.07.072" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.bmcl.2014.07.072</a>
Pages
4553–4556
Issue
18
Volume
24
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Screening and identification of novel compounds with potential anti-proliferative effects on gallium-resistant lung cancer through an AXL kinase pathway.
Publisher
An entity responsible for making the resource available
Bioorganic & medicinal chemistry letters
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-09
Subject
The topic of the resource
Antineoplastic Agents/chemical synthesis/chemistry/*pharmacology; Antitumor; AXL; Cell Line; Cell Proliferation/drug effects; Cell Survival/drug effects; Dose-Response Relationship; Drug; Drug Resistance; Drug Screening Assays; Gallium; Gallium-resistance; Gallium/pharmacology; Humans; Lung cancer; Lung Neoplasms/drug therapy/*enzymology/*pathology; Molecular Structure; Naphthalenes/chemistry/*pharmacology; Neoplasm/drug effects; Proto-Oncogene Proteins/*antagonists & inhibitors/metabolism; Pyrazoles/chemistry/*pharmacology; Quinolines/chemistry/*pharmacology; Receptor Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism; Structure-Activity Relationship; Tetrazoles/chemistry/*pharmacology; Tumor; Virtual screening
Creator
An entity primarily responsible for making the resource
Oyewumi Moses O; Alazizi Adnan; Liva Sophia; Lin Li; Geldenhuys Werner J
Description
An account of the resource
The clinical application of gallium compounds as anticancer agents is hampered by development of resistance. As a potential strategy to overcome the limitation, eight series of compounds were identified through virtual screening of AXL kinase homology model. Anti-proliferative studies were carried using gallium-sensitive (S) and gallium-resistant (R) human lung adenocarcinoma (A549) cells. Compounds 5476423 and 7919469 were identified as leads. The IC50 values from treating
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.bmcl.2014.07.072" target="_blank" rel="noreferrer noopener">10.1016/j.bmcl.2014.07.072</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Alazizi Adnan
Antineoplastic Agents/chemical synthesis/chemistry/*pharmacology
Antitumor
AXL
Bioorganic & medicinal chemistry letters
Cell Line
Cell Proliferation/drug effects
Cell Survival/drug effects
Department of Pharmaceutical Sciences
Dose-Response Relationship
Drug
Drug Resistance
Drug Screening Assays
Gallium
Gallium-resistance
Gallium/pharmacology
Geldenhuys Werner J
Humans
Lin Li
Liva Sophia
Lung cancer
Lung Neoplasms/drug therapy/*enzymology/*pathology
Molecular Structure
Naphthalenes/chemistry/*pharmacology
NEOMED College of Pharmacy
Neoplasm/drug effects
Oyewumi Moses O
Proto-Oncogene Proteins/*antagonists & inhibitors/metabolism
Pyrazoles/chemistry/*pharmacology
Quinolines/chemistry/*pharmacology
Receptor Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism
Structure-Activity Relationship
Tetrazoles/chemistry/*pharmacology
Tumor
Virtual screening
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.cbi.2008.11.015" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.cbi.2008.11.015</a>
Pages
131–144
Issue
2
Volume
179
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Resveratrol-mediated chemoprevention of diethylnitrosamine-initiated hepatocarcinogenesis: inhibition of cell proliferation and induction of apoptosis.
Publisher
An entity responsible for making the resource available
Chemico-biological interactions
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
2009-05
Subject
The topic of the resource
Animal; Animals; Anticarcinogenic Agents/*antagonists & inhibitors/pharmacology; Antitumor; Apoptosis/*drug effects; Body Weight/drug effects; Cell Proliferation/drug effects; Diethylnitrosamine; Disease Models; Dose-Response Relationship; Drinking/drug effects; Drug; Drug Screening Assays; Eating/drug effects; Experimental/chemically induced/pathology/*prevention & control; Female; Immunohistochemistry; Liver Neoplasms; Organ Size/drug effects; Phenobarbital; Proto-Oncogene Proteins c-bcl-2/biosynthesis; Rats; Resveratrol; Sprague-Dawley; Stilbenes/*pharmacology
Creator
An entity primarily responsible for making the resource
Bishayee Anupam; Dhir Neetika
Description
An account of the resource
Hepatocellular carcinoma (HCC) is one of the most common cancers and lethal diseases. In view of the limited treatment and a grave prognosis of liver cancer, preventive control has been emphasized. Resveratrol, a polyphenol found in grape skins, peanuts, berries and red wine, has been shown to possess potent growth inhibitory effects against various human cancer cells. Although resveratrol has been found to exhibit chemopreventive actions in experimentally induced skin, breast, colon and esophagus rodent tumors, chemopreventive potential of this dietary constituent has not been explored well against experimental liver cancer. We evaluated the inhibitory effect of resveratrol using a two-stage model of rat hepatocarcinogenesis in Sprague-Dawley rats. Initiation was performed by a single intraperitoneal injection of diethylnitrosamine (DENA, 200 mg/kg), followed by promotion with phenobarbital (0.05%) in drinking water. The rats had free access to food supplemented with resveratrol equivalent to 50, 100 or 300 mg/kg body weight/day. Resveratrol treatment was started 4 weeks prior to the initiation and continued for 20 weeks. Resveratrol dose-dependently reduced the incidence, total number and multiplicity of visible hepatocyte nodules. Mean nodular volume and nodular volume as percentage of liver volume were also inhibited upon resveratrol treatment. Histopathological examination of liver tissue confirmed the protective effect of resveratrol. Immunohistochemical detection of cell proliferation and assay of apoptosis indicated a decrease in cell proliferation and increase of apoptotic cells in the livers of resveratrol-supplemented rats. Resveratrol also induced the expression of pro-apoptotic protein Bax, reduced anti-apoptotic Bcl-2 expression, with a concurrent increase in Bax/Bcl-2 ratio with respect to DENA control. The present study provides evidence, for the first time, that resveratrol exerts a significant chemopreventive effect on DENA-initiated hepatocarcinogenesis through inhibition of cell proliferation and induction of apoptosis. Resveratrol-induced apoptogenic signal during rat liver carcinogenesis may be mediated through the downregulation of Bcl-2 and upregulation of Bax expression. Due to a favorable toxicity profile, resveratrol can potentially be developed as a chemopreventive drug against human HCC.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.cbi.2008.11.015" target="_blank" rel="noreferrer noopener">10.1016/j.cbi.2008.11.015</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2009
Animal
Animals
Anticarcinogenic Agents/*antagonists & inhibitors/pharmacology
Antitumor
Apoptosis/*drug effects
Bishayee Anupam
Body Weight/drug effects
Cell Proliferation/drug effects
Chemico-biological interactions
Dhir Neetika
Diethylnitrosamine
Disease Models
Dose-Response Relationship
Drinking/drug effects
Drug
Drug Screening Assays
Eating/drug effects
Experimental/chemically induced/pathology/*prevention & control
Female
Immunohistochemistry
Liver Neoplasms
Organ Size/drug effects
Phenobarbital
Proto-Oncogene Proteins c-bcl-2/biosynthesis
Rats
Resveratrol
Sprague-Dawley
Stilbenes/*pharmacology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.heares.2015.07.002" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.heares.2015.07.002</a>
Pages
59–66
Volume
328
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Canertinib induces ototoxicity in three preclinical models.
Publisher
An entity responsible for making the resource available
Hearing research
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-10
Subject
The topic of the resource
Animals; Antineoplastic Agents/*adverse effects/pharmacology; Antitumor; Auditory; Canertinib; Carcinoma; Drug Screening Assays; Ear; Electrophysiology; ERBB; ErbB Receptors/*antagonists & inhibitors; Female; Hair Cells; Hearing Loss/*chemically induced; Hearing/*drug effects; Inbred C57BL; Inbred CBA; Lung Neoplasms/drug therapy; Male; Mice; Morpholines/*adverse effects/pharmacology; Neuregulin-1/metabolism; Non-small cell lung cancer; Non-Small-Cell Lung/drug therapy; NRG1; Ototoxicity; Outer hair cell; Outer/*drug effects; Signal Transduction/drug effects; Zebrafish
Creator
An entity primarily responsible for making the resource
Tang Jian; Qian Yi; Li Hui; Kopecky Benjamin J; Ding Dalian; Ou Henry C; DeCook Rhonda; Chen Xiaojie; Sun Zhenyu; Kobel Megan; Bao Jianxin
Description
An account of the resource
Neuregulin-1 (NRG1) ligand and its epidermal growth factor receptor (EGFR)/ERBB family regulate normal cellular proliferation and differentiation in many tissues including the cochlea. Aberrant NRG1 and ERBB signaling cause significant hearing impairment in mice. Dysregulation of the same signaling pathway in humans is involved in certain types of cancers such as breast cancer or non-small cell lung cancer (NSCLC). A new irreversible pan-ERBB inhibitor, canertinib, has been tested in clinical trials for the treatment of refractory NSCLC. Its possible ototoxicity was unknown. In this study, a significant dose-dependent canertinib ototoxicity was observed in a zebrafish model. Canertinib ototoxicity was further confirmed in two mouse models with different genetic backgrounds. The data strongly suggested an evolutionally preserved ERBB molecular mechanism underlying canertinib ototoxicity. Thus, these results imply that clinical monitoring of hearing loss should be considered for clinical testing of canertinib or other pan-ERBB inhibitors.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.heares.2015.07.002" target="_blank" rel="noreferrer noopener">10.1016/j.heares.2015.07.002</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2015
Animals
Antineoplastic Agents/*adverse effects/pharmacology
Antitumor
Auditory
Bao Jianxin
Canertinib
Carcinoma
Chen Xiaojie
DeCook Rhonda
Department of Anatomy & Neurobiology
Ding Dalian
Drug Screening Assays
Ear
Electrophysiology
ERBB
ErbB Receptors/*antagonists & inhibitors
Female
Hair Cells
Hearing Loss/*chemically induced
Hearing research
Hearing/*drug effects
Inbred C57BL
Inbred CBA
Kobel Megan
Kopecky Benjamin J
Li Hui
Lung Neoplasms/drug therapy
Male
Mice
Morpholines/*adverse effects/pharmacology
NEOMED College of Medicine
Neuregulin-1/metabolism
Non-small cell lung cancer
Non-Small-Cell Lung/drug therapy
NRG1
Ototoxicity
Ou Henry C
Outer hair cell
Outer/*drug effects
Qian Yi
Signal Transduction/drug effects
Sun Zhenyu
Tang Jian
Zebrafish
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1158/1940-6207.CAPR-09-0171" target="_blank" rel="noreferrer noopener">http://doi.org/10.1158/1940-6207.CAPR-09-0171</a>
Pages
753–763
Issue
6
Volume
3
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Resveratrol suppresses oxidative stress and inflammatory response in diethylnitrosamine-initiated rat hepatocarcinogenesis.
Publisher
An entity responsible for making the resource available
Cancer prevention research (Philadelphia, Pa.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-06
Subject
The topic of the resource
Animals; Antioxidants/*pharmacology/therapeutic use; Antitumor; Carcinogens/toxicity; Chemical and Drug Induced Liver Injury/*etiology/metabolism/pathology; Diethylnitrosamine/toxicity; Dose-Response Relationship; Drug; Drug Screening Assays; Enzyme Induction/drug effects; Experimental/chemically induced/metabolism/pathology/*prevention & control; Female; Hyperplasia; Inflammation/*prevention & control; Lipid Peroxidation/drug effects; Liver Neoplasms; Liver/drug effects/metabolism/pathology; Messenger/biosynthesis/genetics; NF-E2-Related Factor 2/biosynthesis/genetics; Nitric Oxide Synthase Type II/biosynthesis/genetics; Oxidative Stress/*drug effects; Phenobarbital/toxicity; Precancerous Conditions/*chemically induced/metabolism/pathology; Rats; Resveratrol; RNA; Sprague-Dawley; Stilbenes/*pharmacology/therapeutic use; Tyrosine/analogs & derivatives/analysis
Creator
An entity primarily responsible for making the resource
Bishayee Anupam; Barnes Kendra F; Bhatia Deepak; Darvesh Altaf S; Carroll Richard T
Description
An account of the resource
Hepatocellular carcinoma (HCC), one of the most frequent and deadliest cancers, has been increasing considerably in the United States. In the absence of a proven effective therapy for HCC, novel chemopreventive strategies are urgently needed to lower the current morbidity and mortality of HCC. Recently, we have reported that resveratrol, a compound present in grapes and red wine, significantly prevents diethylnitrosamine (DENA)-induced liver tumorigenesis in rats, although the mechanism of action is not completely understood. In the present study, we have examined the underlying mechanisms of resveratrol chemoprevention of hepatocarcinogenesis by investigating the effects of resveratrol on oxidative damage and inflammatory markers during DENA-initiated rat liver carcinogenesis. There was a significant increase in hepatic lipid peroxidation and protein oxidation in carcinogen control animals compared with their normal counterparts at the end of the study (20 weeks). Elevated expressions of inducible nitric oxide synthase and 3-nitrotyrosine were noticed in the livers of the same animals. Dietary resveratrol (50-300 mg/kg) administered throughout the study reversed all the aforementioned markers in a dose-responsive fashion in rats challenged with DENA. Resveratrol also elevated the protein and mRNA expression of hepatic nuclear factor E2-related factor 2 (Nrf2). Results of the present investigation provide evidence that attenuation of oxidative stress and suppression of inflammatory response mediated by Nrf2 could be implicated, at least in part, in the chemopreventive effects of this dietary agent against chemically induced hepatic tumorigenesis in rats. The outcome of this study may benefit the development of resveratrol in the prevention and intervention of human HCC.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1158/1940-6207.CAPR-09-0171" target="_blank" rel="noreferrer noopener">10.1158/1940-6207.CAPR-09-0171</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2010
Animals
Antioxidants/*pharmacology/therapeutic use
Antitumor
Barnes Kendra F
Bhatia Deepak
Bishayee Anupam
Cancer prevention research (Philadelphia, Pa.)
Carcinogens/toxicity
Carroll Richard T
Chemical and Drug Induced Liver Injury/*etiology/metabolism/pathology
Darvesh Altaf S
Department of Pharmaceutical Sciences
Diethylnitrosamine/toxicity
Dose-Response Relationship
Drug
Drug Screening Assays
Enzyme Induction/drug effects
Experimental/chemically induced/metabolism/pathology/*prevention & control
Female
Hyperplasia
Inflammation/*prevention & control
Lipid Peroxidation/drug effects
Liver Neoplasms
Liver/drug effects/metabolism/pathology
Messenger/biosynthesis/genetics
NEOMED College of Pharmacy
NF-E2-Related Factor 2/biosynthesis/genetics
Nitric Oxide Synthase Type II/biosynthesis/genetics
Oxidative Stress/*drug effects
Phenobarbital/toxicity
Precancerous Conditions/*chemically induced/metabolism/pathology
Rats
Resveratrol
RNA
Sprague-Dawley
Stilbenes/*pharmacology/therapeutic use
Tyrosine/analogs & derivatives/analysis