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/10.1016/0304-3835(83)90064-2" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/0304-3835(83)90064-2</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
169-177
Issue
2
Volume
18
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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
Human-alpha-2-macroglobulin - A Major Serum Factor Cyto-toxic For Tumor-cells
Publisher
An entity responsible for making the resource available
Cancer Letters
Date
A point or period of time associated with an event in the lifecycle of the resource
1983
1983
Subject
The topic of the resource
Oncology
Creator
An entity primarily responsible for making the resource
Koo P H
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/0304-3835(83)90064-2" target="_blank" rel="noreferrer noopener">10.1016/0304-3835(83)90064-2</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
1983
Cancer letters
Journal Article or Conference Abstract Publication
Koo P H
oncology
-
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.canlet.2018.07.042" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.canlet.2018.07.042</a>
Pages
15–20
Volume
442
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
Mechanosensitive TRPV4 channels stabilize VE-cadherin junctions to regulate tumor vascular integrity and metastasis.
Publisher
An entity responsible for making the resource available
Cancer letters
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-02
Subject
The topic of the resource
Angiogenesis; Mechanotransduction; Stiffness; TRPV4; Vascular integrity; VE-cadherin
Creator
An entity primarily responsible for making the resource
Cappelli Holly C; Kanugula Anantha K; Adapala Ravi K; Amin Vibhatsu; Sharma Priya; Midha Priya; Paruchuri Sailaja; Thodeti Charles K
Description
An account of the resource
The transient receptor potential vanilloid 4 (TRPV4) channel is a mechanosensor in endothelial cells (EC) that regulates cyclic strain-induced reorientation and flow-mediated nitric oxide production. We have recently demonstrated that TRPV4 expression is reduced in tumor EC and tumors grown in TRPV4KO mice exhibited enhanced growth and immature leaky vessels. However, the mechanism by which TRPV4 regulates tumor vascular integrity and metastasis is not known. Here, we demonstrate that VE-cadherin expression at the cell-cell contacts is significantly reduced in TRPV4-deficient tumor EC and TRPV4KO EC. In vivo angiogenesis assays with Matrigel of varying stiffness (700-900Pa) revealed a significant stiffness-dependent reduction in VE-cadherin-positive vessels in Matrigel plugs from TRPV4KO mice compared with WT mice, despite an increase in vessel growth. Further, syngeneic Lewis Lung Carcinomatumor experiments demonstrated a significant decrease in VE-cadherin positive vessels in TRPV4KO tumors compared with WT. Functionally, enhanced tumor cell metastasis to the lung was observed in TRPV4KO mice. Our findings demonstrate that TRPV4 channels regulate tumor vessel integrity by maintaining VE-cadherin expression at cell-cell contacts and identifies TRPV4 as a novel target for metastasis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.canlet.2018.07.042" target="_blank" rel="noreferrer noopener">10.1016/j.canlet.2018.07.042</a>
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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).
2019
Adapala Ravi K
Amin Vibhatsu
angiogenesis
Cancer letters
Cappelli Holly C
Department of Integrative Medical Sciences
Kanugula Anantha K
Mechanotransduction
Midha Priya
NEOMED College of Medicine
Paruchuri Sailaja
Sharma Priya
Stiffness
Thodeti Charles K
TRPV4
Vascular integrity
VE-cadherin
-
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.canlet.2016.05.014" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.canlet.2016.05.014</a>
Pages
131–141
Issue
2
Volume
378
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
Lipopolysaccharide supports maintaining the stemness of CD133(+) hepatoma cells through activation of the NF-kappaB/HIF-1alpha pathway.
Publisher
An entity responsible for making the resource available
Cancer letters
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-08
Subject
The topic of the resource
*Cancer stem cells; *Lipopolysaccharide; *Plasticity; *Stemness maintenance; *Tumor microenvironment; AC133 Antigen/genetics/*metabolism; alpha Subunit/genetics/*metabolism; Animals; Antineoplastic Agents – Pharmacodynamics; Antineoplastic Agents/pharmacology; Body Weights and Measures; Carcinoma; Cell Line; Cell Movement – Drug Effects; Cell Movement/drug effects; Cell Physiology; Cell Physiology – Drug Effects; Cell Proliferation/drug effects; Drug Resistance; Gene Expression Regulation; Genes; Genetic Techniques; Hepatocellular; Hepatocellular – Drug Therapy; Hepatocellular – Metabolism; Hepatocellular – Pathology; Hepatocellular/drug therapy/genetics/*metabolism/pathology; Humans; Hypoxia-Inducible Factor 1; Inbred BALB C; Lipopolysaccharides – Pharmacodynamics; Lipopolysaccharides/*pharmacology; Liver Neoplasms; Liver Neoplasms – Drug Therapy; Liver Neoplasms – Metabolism; Liver Neoplasms – Pathology; Liver Neoplasms/drug therapy/genetics/*metabolism/pathology; Male; Mice; Neoplasm; Neoplasm Invasiveness; Neoplastic; Neoplastic Stem Cells/*drug effects/metabolism/pathology; NF-kappa B – Metabolism; NF-kappa B/*metabolism; Nude; Phenotype; Proteins; Proteins – Metabolism; RNA Interference; Signal Transduction – Drug Effects; Signal Transduction/drug effects; Stem Cells – Drug Effects; Stem Cells – Metabolism; Stem Cells – Pathology; Time Factors; Transfection; Tumor Burden; Tumor Microenvironment
Creator
An entity primarily responsible for making the resource
Lai Fo-Bao; Liu Wen-Ting; Jing Ying-Ying; Yu Guo-Feng; Han Zhi-Peng; Yang Xue; Zeng Jian-Xing; Zhang Hang-Jie; Shi Rong-Yu; Li Xiao-Yong; Pan Xiao-Rong; Li Rong; Zhao Qiu-Dong; Wu Meng-Chao; Zhang Ping; Liu Jing-Feng; Wei Li-Xin
Description
An account of the resource
Due to the existence of cancer stem cells (CSCs), persistence and relapse of human hepatocellular carcinoma (HCC) are common after treatment with existing anti-cancer therapies. Emerging evidence indicates that lipopolysaccharide (LPS) plays a crucial role in aggravating HCC, but information about the effect of LPS on CSCs of HCC remains scant. Here, we report that the stemness of CD133(+) CSCs sorted from the human HCC cell line Huh7 was maintained well when cells were cultured with LPS. The reduction of CD133 expression was much lesser in cultured CSCs in the presence of LPS. In response to LPS stimulation, CSCs showed an increase in their activity of clonogenesis and tumorigenesis. LPS also supported maintaining CSC abilities of migration, invasion, and chemo-resistance. Treatment with HIF-1alpha-specific siRNA significantly reduced CD133 expression by CSCs at both mRNA and protein levels. Further, the expression of HIF-1alpha and CD133 was reduced in LPS-stimulated CSCs when the NF-kappaB inhibitor was added to the cell culture. HIF-1alpha-specific siRNA also effectively counteracted the effect of LPS on maintaining CSC abilities of migration and invasion. These data indicate that LPS, an important mediator in the liver tumor microenvironment, supports the maintenance of CSC stemness through signaling of the NF-kappaB/HIF-1alpha pathway. Our current study highlights LPS as a potential target for developing new therapeutic approaches to eliminate CSCs during the treatment of HCC.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.canlet.2016.05.014" target="_blank" rel="noreferrer noopener">10.1016/j.canlet.2016.05.014</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).
*Cancer stem cells
*Lipopolysaccharide
*Plasticity
*Stemness maintenance
*Tumor microenvironment
2016
AC133 Antigen/genetics/*metabolism
alpha Subunit/genetics/*metabolism
Animals
Antineoplastic Agents – Pharmacodynamics
Antineoplastic Agents/pharmacology
Body Weights and Measures
Cancer letters
Carcinoma
Cell Line
Cell Movement – Drug Effects
Cell Movement/drug effects
Cell Physiology
Cell Physiology – Drug Effects
Cell Proliferation/drug effects
Department of Integrative Medical Sciences
Drug Resistance
Gene Expression Regulation
Genes
Genetic Techniques
Han Zhi-Peng
Hepatocellular
Hepatocellular – Drug Therapy
Hepatocellular – Metabolism
Hepatocellular – Pathology
Hepatocellular/drug therapy/genetics/*metabolism/pathology
Humans
Hypoxia-Inducible Factor 1
Inbred BALB C
Jing Ying-Ying
Lai Fo-Bao
Li Rong
Li Xiao-Yong
Lipopolysaccharides – Pharmacodynamics
Lipopolysaccharides/*pharmacology
Liu Jing-Feng
Liu Wen-Ting
Liver Neoplasms
Liver Neoplasms – Drug Therapy
Liver Neoplasms – Metabolism
Liver Neoplasms – Pathology
Liver Neoplasms/drug therapy/genetics/*metabolism/pathology
Male
Mice
NEOMED College of Medicine
Neoplasm
Neoplasm Invasiveness
Neoplastic
Neoplastic Stem Cells/*drug effects/metabolism/pathology
NF-kappa B – Metabolism
NF-kappa B/*metabolism
Nude
Pan Xiao-Rong
Phenotype
Proteins
Proteins – Metabolism
RNA Interference
Shi Rong-Yu
Signal Transduction – Drug Effects
Signal Transduction/drug effects
Stem Cells – Drug Effects
Stem Cells – Metabolism
Stem Cells – Pathology
Time Factors
Transfection
Tumor Burden
Tumor Microenvironment
Wei Li-Xin
Wu Meng-Chao
Yang Xue
Yu Guo-Feng
Zeng Jian-Xing
Zhang Hang-Jie
Zhang Ping
Zhao Qiu-Dong
-
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.canlet.2010.01.030" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.canlet.2010.01.030</a>
Pages
1–12
Issue
1
Volume
294
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
Vanadium in the detection, prevention and treatment of cancer: the in vivo evidence.
Publisher
An entity responsible for making the resource available
Cancer letters
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-08
Subject
The topic of the resource
10-Dimethyl-1; 2-benzanthracene; 9; Animal; Animals; Biological; Breast Neoplasms – Chemically Induced; Breast Neoplasms – Diagnosis; Breast Neoplasms – Drug Therapy; Cell Division – Drug Effects; Cell Division/drug effects; Disease Models; Experimental/chemically induced/diagnosis/drug therapy; Experimental/drug therapy/pathology; Female; Glioblastoma/drug therapy; Glioma – Drug Therapy; Heterologous; Humans; Hydrocarbons; Male; Mammary Neoplasms; Metals; Metals – Diagnostic Use; Metals – Therapeutic Use; Models; Neoplasm Staging; Neoplasm Transplantation; Neoplasms; Neoplasms – Diagnosis; Neoplasms – Drug Therapy; Neoplasms – Pathology; Neoplasms – Prevention and Control; Neoplasms/*diagnosis/drug therapy/prevention & control; Organometallic Compounds – Therapeutic Use; Organometallic Compounds/therapeutic use; Rats; Trace Elements – Diagnostic Use; Trace Elements – Therapeutic Use; Trace Elements/therapeutic use; Transplantation; Vanadium Compounds; Vanadium Compounds – Therapeutic Use; Vanadium Compounds/therapeutic use/toxicity; Vanadium/*therapeutic use/toxicity; Xenografts
Creator
An entity primarily responsible for making the resource
Bishayee Anupam; Waghray Abhijeet; Patel Mehool A; Chatterjee Malay
Description
An account of the resource
Vanadium, a dietary micronutrient, is yet to be established as an essential part of the human diet. Over the past century, several biological effects of vanadium, such as insulin-mimetic action as well as amelioration of hyperlipidemia and hypertension, have been discovered. This transition element is known to influence a battery of enzymatic systems, namely phosphatases, ATPases, peroxidases, ribonucleases, protein kinases and oxidoreductases. Multiple biochemical and molecular actions of vanadium have been implicated in its inhibitory effects on various tumor cells of human origin. Successful in vitro studies over the past few decades have advanced the anticancer research on vanadium into the preclinical stage. Vanadium in several animal cancer models provides protection against all stages of carcinogenesis–initiation, promotion, and progression. This review focuses on the current advances in cancer prevention and treatment as well as early detection by vanadium compounds in preclinical animal models while pointing to possible mechanisms of such diverse beneficial effects. Clinical pharmacokinetic and potential toxicity studies on vanadium are also highlighted in this review. Supporting and challenging evidence as well as future directions of vanadium research exploring the possibility of using this dietary agent for detection, prevention and treatment of human cancers are critically discussed.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.canlet.2010.01.030" target="_blank" rel="noreferrer noopener">10.1016/j.canlet.2010.01.030</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).
10-Dimethyl-1
2-benzanthracene
2010
9
Animal
Animals
Biological
Bishayee Anupam
Breast Neoplasms – Chemically Induced
Breast Neoplasms – Diagnosis
Breast Neoplasms – Drug Therapy
Cancer letters
Cell Division – Drug Effects
Cell Division/drug effects
Chatterjee Malay
Disease Models
Experimental/chemically induced/diagnosis/drug therapy
Experimental/drug therapy/pathology
Female
Glioblastoma/drug therapy
Glioma – Drug Therapy
Heterologous
Humans
Hydrocarbons
Male
Mammary Neoplasms
Metals
Metals – Diagnostic Use
Metals – Therapeutic Use
Models
Neoplasm Staging
Neoplasm Transplantation
Neoplasms
Neoplasms – Diagnosis
Neoplasms – Drug Therapy
Neoplasms – Pathology
Neoplasms – Prevention and Control
Neoplasms/*diagnosis/drug therapy/prevention & control
Organometallic Compounds – Therapeutic Use
Organometallic Compounds/therapeutic use
Patel Mehool A
Rats
Trace Elements – Diagnostic Use
Trace Elements – Therapeutic Use
Trace Elements/therapeutic use
Transplantation
Vanadium Compounds
Vanadium Compounds – Therapeutic Use
Vanadium Compounds/therapeutic use/toxicity
Vanadium/*therapeutic use/toxicity
Waghray Abhijeet
Xenografts