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Article ; Online ; Conference proceedings: High-Content Analysis--CHI's Seventh Annual Conference--Developments in HCA and Pathway Analysis.

Robertson, Fredika M

IDrugs : the investigational drugs journal

2010 Volume 13, Issue 3, Page(s) 149–152

Abstract: CHI's Seventh Annual Conference on High-Content Analysis (HCA), held in San Francisco, incorporated topics covering new developments in the field of HCA, including hardware and software updates, new biological models for HCA and pathway analysis. This ... ...

Abstract	CHI's Seventh Annual Conference on High-Content Analysis (HCA), held in San Francisco, incorporated topics covering new developments in the field of HCA, including hardware and software updates, new biological models for HCA and pathway analysis. This conference report highlights selected presentations on the use of HCA for the characterization of stem cells, cell-colony analysis, the validation of disease models and the identification of antiparasitic compounds.
MeSH term(s)	Animals ; Animals, Genetically Modified ; Antiparasitic Agents/pharmacology ; Caenorhabditis elegans/enzymology ; Caenorhabditis elegans/genetics ; Drug Discovery/trends ; Embryonic Stem Cells/metabolism ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Gene Regulatory Networks/drug effects ; High-Throughput Screening Assays/trends ; Humans ; Models, Biological ; Neoplastic Stem Cells/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Systems Biology/trends ; Ubiquitin-Protein Ligases/metabolism ; Zebrafish/genetics ; Zebrafish/metabolism ; alpha 1-Antitrypsin Deficiency/enzymology ; alpha 1-Antitrypsin Deficiency/genetics
Chemical Substances	Antiparasitic Agents ; Fibroblast Growth Factors (62031-54-3) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2010-03
Publishing country	England
Document type	Congresses
ZDB-ID	2086568-5
ISSN	2040-3410 ; 1369-7056
ISSN (online)	2040-3410
ISSN	1369-7056
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online ; Conference proceedings: A global approach to inflammatory breast cancer.

Robertson, Fredika M / Cristofanilli, Massimo

Future oncology (London, England)

2011 Volume 7, Issue 1, Page(s) 25–30

Abstract: Inflammatory breast cancer (IBC) is the most aggressive and deadly form of breast cancer. In spite of the comprehensive multidisciplinary approach to the management of this disease, the prognosis remains dismal. Moreover, there have been no major ... ...

Abstract	Inflammatory breast cancer (IBC) is the most aggressive and deadly form of breast cancer. In spite of the comprehensive multidisciplinary approach to the management of this disease, the prognosis remains dismal. Moreover, there have been no major advancements in understanding the etiology and biology of IBC and no significant improvements in the diagnosis of the disease. The International Inflammatory Breast Cancer Conference was established in 2008 with the intention of creating a forum for the discussion, collaboration and development of proposals and working hypotheses. Furthermore, the conference represented an opportunity to raise awareness regarding IBC. The second international conference reported on several new exciting projects based on work from investigators and research teams devoted to making a difference in the fight against this disease.
MeSH term(s)	Animals ; Disease Models, Animal ; Female ; Humans ; Inflammatory Breast Neoplasms/genetics ; Inflammatory Breast Neoplasms/mortality ; Inflammatory Breast Neoplasms/therapy
Language	English
Publishing date	2011-01
Publishing country	England
Document type	Congresses
ZDB-ID	2184533-5
ISSN	1744-8301 ; 1479-6694
ISSN (online)	1744-8301
ISSN	1479-6694
DOI	10.2217/fon.10.177
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Targeting SH2 domains in breast cancer.

Morlacchi, Pietro / Robertson, Fredika M / Klostergaard, Jim / McMurray, John S

Future medicinal chemistry

2014 Volume 6, Issue 17, Page(s) 1909–1926

Abstract: Breast cancer is among the most commonly diagnosed cancer types in women worldwide and is the second leading cause of cancer-related disease in the USA. SH2 domains recruit signaling proteins to phosphotyrosine residues on aberrantly activated growth ... ...

Abstract	Breast cancer is among the most commonly diagnosed cancer types in women worldwide and is the second leading cause of cancer-related disease in the USA. SH2 domains recruit signaling proteins to phosphotyrosine residues on aberrantly activated growth factor and cytokine receptors and contribute to cancer cell cycling, metastasis, angiogenesis and so on. Herein we review phosphopeptide mimetic and small-molecule approaches targeting the SH2 domains of Grb2, Grb7 and STAT3 that inhibit their targets and reduce proliferation in in vitro breast cancer models. Only STAT3 inhibitors have been evaluated in in vivo models and have led to tumor reduction. Taken together, these studies suggest that targeting SH2 domains is an important approach to the treatment of breast cancer.
MeSH term(s)	Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Female ; GRB2 Adaptor Protein/antagonists & inhibitors ; GRB2 Adaptor Protein/metabolism ; GRB7 Adaptor Protein/antagonists & inhibitors ; GRB7 Adaptor Protein/metabolism ; Humans ; Phosphopeptides/chemistry ; Phosphopeptides/metabolism ; Phosphopeptides/therapeutic use ; Protein Binding ; STAT3 Transcription Factor/antagonists & inhibitors ; STAT3 Transcription Factor/metabolism ; Small Molecule Libraries/chemistry ; Small Molecule Libraries/metabolism ; Small Molecule Libraries/therapeutic use ; src Homology Domains
Chemical Substances	GRB2 Adaptor Protein ; Phosphopeptides ; STAT3 Transcription Factor ; Small Molecule Libraries ; GRB7 Adaptor Protein (149058-53-7)
Language	English
Publishing date	2014
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	1756-8927
ISSN (online)	1756-8927
DOI	10.4155/fmc.14.120
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Article: The consequences of selective inhibition of signal transducer and activator of transcription 3 (STAT3) tyrosine705 phosphorylation by phosphopeptide mimetic prodrugs targeting the Src homology 2 (SH2) domain.

McMurray, John S / Mandal, Pijus K / Liao, Warren S / Klostergaard, Jim / Robertson, Fredika M

JAK-STAT

2013 Volume 1, Issue 4, Page(s) 263–347

Abstract: Herein we review our progress on the development of phosphopeptide-based prodrugs targeting the SH2 domain of STAT3 to prevent recruitment to cytokine and growth factor receptors, activation, nuclear translocation and transcription of genes involved in ... ...

Abstract	Herein we review our progress on the development of phosphopeptide-based prodrugs targeting the SH2 domain of STAT3 to prevent recruitment to cytokine and growth factor receptors, activation, nuclear translocation and transcription of genes involved in cancer. We developed high affinity phosphopeptides (K I = 46-200 nM). Corresponding prodrugs inhibited constitutive and IL-6 induced Tyr705 phosphorylation at 0.5-1 μM in a variety of human cancer cell lines. They were not cytotoxic at 5 μM in vitro but they inhibited tumor growth in a human xenograft breast cancer model in mice, accompanied by reduced VEGF expression and angiogenesis.
Language	English
Publishing date	2013-08-24
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2682221-0
ISSN	2162-3996 ; 2162-3988
ISSN (online)	2162-3996
ISSN	2162-3988
DOI	10.4161/jkst.22682
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Article: Cyclooxygenase-2 directly regulates gene expression of P450 Cyp19 aromatase promoter regions pII, pI.3 and pI.7 and estradiol production in human breast tumor cells.

Prosperi, Jenifer R / Robertson, Fredika M

Prostaglandins & other lipid mediators

2006 Volume 81, Issue 1-2, Page(s) 55–70

Abstract: The present studies evaluated the direct effects of the presence of human cyclooxygenase-2 (Cox-2) on gene expression of specific promoter regions of the P450 Cyp19 enzyme aromatase enzyme and its product, estradiol, in Cox-2 null estrogen-dependent MCF- ... ...

Abstract	The present studies evaluated the direct effects of the presence of human cyclooxygenase-2 (Cox-2) on gene expression of specific promoter regions of the P450 Cyp19 enzyme aromatase enzyme and its product, estradiol, in Cox-2 null estrogen-dependent MCF-7 breast tumor cells and in a stable clone of MCF-7 cells containing transfected Cox-2 cDNA, designated as MCF-7/Cox-2 Clone 10. Clone 10 human breast tumor cells have significantly increased gene expression of total mRNA of the P450 Cyp19 enzyme aromatase, with high levels of gene expression of specific aromatase promoter (p) regions pII, pI.3, and p1.7, with no significant change in mRNA levels of p1.4. Clone 10 human breast tumor cells produced significantly increased amounts of both prostaglandin E2 (PGE2) derived from Cox-2 enzyme activity and estradiol derived from aromatase enzyme activity (p<0.01), compared to MCF-7/vector control cells. The greatest inhibition of PGE2 or estradiol production was observed by the combination of the selective Cox-2 inhibitor celecoxib (25 microM) and the aromatase inhibitor, formestane (10nM) (p<0.01). The greatest anti-proliferative effect in Cox-2 null MCF-7/vector control cells was observed with the combination of 25 microM celecoxib and 10nM formestane but not with 10 microM celecoxib, suggesting that there are Cox-2-independent mechanisms involved in the anti-proliferative effect of this agent at doses greater than 10 microM. Celecoxib (25 microM) also significantly inhibited proliferation of MCF-7/Cox-2 Clone 10 human breast tumor cells, with no further anti-proliferative activity with the addition of 10 nM formestane observed at either 24 or 48 h of treatment. These studies demonstrate that Cox-2 directly regulates gene expression of specific aromatase promoter regions and regulates aromatase enzyme activity. Agents that inhibit Cox-2 or block the biological effects of PGE2 may be useful in significantly limiting aromatase activity and proliferation of human breast tumor cells regardless of the presence of Cox-2. In addition, the unique human breast tumor cell model used in these studies may be a useful tool in identifying the spectrum of activities of agents that block the biological effects of PGE2 and estradiol.
MeSH term(s)	Androstenedione/analogs & derivatives ; Androstenedione/metabolism ; Aromatase/genetics ; Aromatase/metabolism ; Aromatase Inhibitors/metabolism ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Celecoxib ; Cell Line, Tumor ; Cell Proliferation ; Cyclooxygenase 2/metabolism ; Cyclooxygenase Inhibitors/metabolism ; Estradiol/metabolism ; Female ; Gene Expression Regulation, Enzymologic ; Humans ; Promoter Regions, Genetic ; Pyrazoles/metabolism ; Sulfonamides/metabolism
Chemical Substances	Aromatase Inhibitors ; Cyclooxygenase Inhibitors ; Pyrazoles ; Sulfonamides ; Androstenedione (409J2J96VR) ; Estradiol (4TI98Z838E) ; Aromatase (EC 1.14.14.1) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Celecoxib (JCX84Q7J1L) ; formestane (PUB9T8T355)
Language	English
Publishing date	2006-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	1426962-4
ISSN	2212-196X ; 1098-8823 ; 0090-6980
ISSN (online)	2212-196X
ISSN	1098-8823 ; 0090-6980
DOI	10.1016/j.prostaglandins.2006.07.003
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Article: Vascular endothelial growth factor as a survival factor in tumor-associated angiogenesis.

Affara, Nesrine I / Robertson, Fredika M

In vivo (Athens, Greece)

2004 Volume 18, Issue 5, Page(s) 525–542

Abstract: This review focuses on vascular endothelial growth factors (VEGF), a group of structurally-related proteins that serve as key growth factors for tumor-associated angiogenesis. Pathways induced by VEGF proteins that regulate biological functions of key ... ...

Abstract	This review focuses on vascular endothelial growth factors (VEGF), a group of structurally-related proteins that serve as key growth factors for tumor-associated angiogenesis. Pathways induced by VEGF proteins that regulate biological functions of key cell types involved in tumor angiogenesis, including vascular endothelial cells, pericytes and tumor cells, are discussed. Strategies that are currently being developed and tested based on the emerging definitions of the roles of the multiple cell types involved in tumor vessel development, their selective production of VEGF-related proteins and other pro-angiogenic growth factors, their expression of associated receptors as well as identification of signal transduction pathways involved in VEGF-induced tumor survival and tumor-associated angiogenesis will be reviewed.
MeSH term(s)	Disease Progression ; Humans ; Neoplasms/blood supply ; Neoplasms/pathology ; Neoplasms/physiopathology ; Neovascularization, Pathologic ; Signal Transduction ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	Vascular Endothelial Growth Factor A
Language	English
Publishing date	2004-09
Publishing country	Greece
Document type	Journal Article ; Review
ZDB-ID	807031-3
ISSN	1791-7549 ; 0258-851X
ISSN (online)	1791-7549
ISSN	0258-851X
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 2288: Show issues

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Article ; Online: The paradox of E-cadherin: role in response to hypoxia in the tumor microenvironment and regulation of energy metabolism.

Chu, Khoi / Boley, Kimberley M / Moraes, Ricardo / Barsky, Sanford H / Robertson, Fredika M

Oncotarget

2013 Volume 4, Issue 3, Page(s) 446–462

Abstract: E-Cadherin is a cell:cell adhesion molecule critical for appropriate embryonic and mammary development. In cancer, E-Cadherin has been primarily viewed as being lost during the process of epithelial-mesenchymal transition (EMT), which occurs with a ... ...

Abstract	E-Cadherin is a cell:cell adhesion molecule critical for appropriate embryonic and mammary development. In cancer, E-Cadherin has been primarily viewed as being lost during the process of epithelial-mesenchymal transition (EMT), which occurs with a switch from E-Cadherin expression to a gain of N-Cadherin and other mesenchymal markers. EMT has been shown to play a role in the metastatic process while the reverse process, mesenchymal-epithelial transition (MET), is important for metastatic colonization. Here we report an unexpected role of E-Cadherin in regulating tumorigenicity and hypoxia responses of breast tumors in vivo. Reduced expression of E-Cadherin led to a dramatic reduction of the in vivo growth capability of SUM149, Mary-X and 4T1 tumor cells. Furthermore, over-expression of ZEB1, a known transcriptional repressor of E-Cadherin, led to reduced in vivo growth of SUM149 tumors. Gene set enrichment analysis identified the loss of hypoxia response genes as a major mechanism in mediating the lack of in vivo growth of SUM149 cells that lacked E-Cadherin or over-expressed ZEB1. The in vivo growth defect of SUM149 E-Cadherin knockdown tumors was rescued by the hypoxia-inducible 1α transcription factor (HIF-1α). Given the importance of HIF-1α in cellular metabolism, we observed reduced glycolytic capacity in SUM149 and 4T1 cells that had E-Cadherin knocked down. Our observations shed light on the complex functions of E-Cadherin in retention of an epithelial phenotype and as a mediator of survival of aggressive breast cancer under hypoxic conditions in vivo. Furthermore, we find that patients with basal subtype breast cancer and high E-Cadherin expression in their tumors had a poor clinical outcome. Our data suggests a novel function for E-Cadherin as a bona fide signaling molecule required for the in vivo growth of aggressive breast cancer tumor cells, that retain E-Cadherin expression, in mediating their metabolic function.
MeSH term(s)	Animals ; Blotting, Western ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cadherins/genetics ; Cadherins/metabolism ; Cell Line, Tumor ; Energy Metabolism/genetics ; Epithelial-Mesenchymal Transition/genetics ; Female ; Gene Expression Profiling ; Glycolysis/genetics ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Hypoxia ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; MCF-7 Cells ; Metabolomics ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Oligonucleotide Array Sequence Analysis ; Prognosis ; RNA Interference ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Tumor Burden/genetics ; Tumor Microenvironment/genetics ; Xenograft Model Antitumor Assays/methods ; Zinc Finger E-box-Binding Homeobox 1
Chemical Substances	Cadherins ; HIF1A protein, human ; Homeodomain Proteins ; Hypoxia-Inducible Factor 1, alpha Subunit ; Transcription Factors ; ZEB1 protein, human ; Zinc Finger E-box-Binding Homeobox 1
Language	English
Publishing date	2013-03-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.872
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Efficient synthesis of apricoxib, CS-706, a selective cyclooxygenase-2 inhibitor, and evaluation of inhibition of prostaglandin E2 production in inflammatory breast cancer cells.

Mandal, Pijus K / Freiter, Eric M / Bagsby, Allison L / Robertson, Fredika M / McMurray, John S

Bioorganic & medicinal chemistry letters

2011 Volume 21, Issue 20, Page(s) 6071–6073

Abstract: An efficient synthesis of apricoxib (CS-706), a selective cyclooxygenase inhibitor, was developed using copper catalyzed homoallylic ketone formation from methyl 4-ethoxybenzoate followed by ozonolysis to an aldehyde, and condensation with sulfanilamide. ...

Abstract	An efficient synthesis of apricoxib (CS-706), a selective cyclooxygenase inhibitor, was developed using copper catalyzed homoallylic ketone formation from methyl 4-ethoxybenzoate followed by ozonolysis to an aldehyde, and condensation with sulfanilamide. This method provided multi-gram access of aprocoxib in good yield. Apricoxib exhibited potency equal to celecoxib at inhibition of prostaglandin E2 synthesis in two inflammatory breast cancer cell lines.
MeSH term(s)	Cell Line, Tumor ; Cyclooxygenase 2 Inhibitors/chemical synthesis ; Cyclooxygenase 2 Inhibitors/pharmacology ; Dinoprostone/antagonists & inhibitors ; Female ; Humans ; Inflammatory Breast Neoplasms/drug therapy ; Pyrroles/chemical synthesis ; Pyrroles/pharmacology ; Sulfonamides/chemical synthesis ; Sulfonamides/pharmacology
Chemical Substances	Cyclooxygenase 2 Inhibitors ; Pyrroles ; Sulfonamides ; apricoxib (5X5HB3VZ3Z) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2011-08-19
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1063195-1
ISSN	1464-3405 ; 0960-894X
ISSN (online)	1464-3405
ISSN	0960-894X
DOI	10.1016/j.bmcl.2011.08.050
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Zs.A 3203: Show issues

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Article ; Online: Toxicological and pathophysiological roles of reactive oxygen and nitrogen species.

Roberts, Ruth A / Smith, Robert A / Safe, Stephen / Szabo, Csaba / Tjalkens, Ronald B / Robertson, Fredika M

Toxicology

2010 Volume 276, Issue 2, Page(s) 85–94

Abstract: Oxidative and Nitrative Stress in Toxicology and Disease' was the subject of a symposium held at the EUROTOX meeting in Dresden 15th September 2009. Reactive oxygen (ROS) and reactive nitrogen species (RNS) produced during tissue pathogenesis and in ... ...

Abstract	'Oxidative and Nitrative Stress in Toxicology and Disease' was the subject of a symposium held at the EUROTOX meeting in Dresden 15th September 2009. Reactive oxygen (ROS) and reactive nitrogen species (RNS) produced during tissue pathogenesis and in response to viral or chemical toxicants, induce a complex series of downstream adaptive and reparative events driven by the associated oxidative and nitrative stress. As highlighted by all the speakers, ROS and RNS can promote diverse biological responses associated with a spectrum of disorders including neurodegenerative/neuropsychiatric and cardiovascular diseases. Similar pathways are implicated during the process of liver and skin carcinogenesis. Mechanistically, reactive oxygen and nitrogen species drive sustained cell proliferation, cell death including both apoptosis and necrosis, formation of nuclear and mitochondrial DNA mutations, and in some cases stimulation of a pro-angiogenic environment. Here we illustrate the pivotal role played by oxidative and nitrative stress in cell death, inflammation and pain and its consequences for toxicology and disease pathogenesis. Examples are presented from five different perspectives ranging from in vitro model systems through to in vivo animal model systems and clinical outcomes.
MeSH term(s)	Animals ; Cell Death/physiology ; Humans ; Inflammation/physiopathology ; Neoplasms/physiopathology ; Oxidative Stress ; Pain/physiopathology ; Reactive Nitrogen Species/metabolism ; Reactive Nitrogen Species/toxicity ; Reactive Oxygen Species/metabolism ; Reactive Oxygen Species/toxicity
Chemical Substances	Reactive Nitrogen Species ; Reactive Oxygen Species
Language	English
Publishing date	2010-07-17
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	184557-3
ISSN	1879-3185 ; 0300-483X
ISSN (online)	1879-3185
ISSN	0300-483X
DOI	10.1016/j.tox.2010.07.009
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Zs.A 888: Show issues

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Article: Efficient synthesis of apricoxib, CS-706, a selective cyclooxygenase-2 inhibitor, and evaluation of inhibition of prostaglandin E2 production in inflammatory breast cancer cells

Mandal, Pijus K / Freiter, Eric M / Bagsby, Allison L / Robertson, Fredika M / McMurray, John S

Bioorganic & medicinal chemistry letters. 2011 Oct. 15, v. 21, no. 20

2011

Abstract	An efficient synthesis of apricoxib (CS-706), a selective cyclooxygenase inhibitor, was developed using copper catalyzed homoallylic ketone formation from methyl 4-ethoxybenzoate followed by ozonolysis to an aldehyde, and condensation with sulfanilamide. This method provided multi-gram access of aprocoxib in good yield. Apricoxib exhibited potency equal to celecoxib at inhibition of prostaglandin E2 synthesis in two inflammatory breast cancer cell lines.
Keywords	copper ; ozonolysis ; prostaglandin synthase ; prostaglandins ; sulfanilamide ; breast neoplasms
Language	English
Dates of publication	2011-1015
Size	p. 6071-6073.
Publishing place	Elsevier Ltd
Document type	Article
Note	2019-12-06
ZDB-ID	1063195-1
ISSN	1464-3405 ; 0960-894X
ISSN (online)	1464-3405
ISSN	0960-894X
DOI	10.1016/j.bmcl.2011.08.050
Database	NAL-Catalogue (AGRICOLA)

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