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  1. Article ; Online: Stearoyl-CoA desaturase 5 (SCD5), a Δ-9 fatty acyl desaturase in search of a function.

    Igal, R Ariel / Sinner, Débora I

    Biochimica et biophysica acta. Molecular and cell biology of lipids

    2020  Volume 1866, Issue 1, Page(s) 158840

    Abstract: A large body of research has demonstrated that human stearoyl-CoA desaturase 1 (SCD1), a universally expressed fatty acid Δ9-desaturase that converts saturated fatty acids (SFA) into monounsaturated fatty acids (MUFA), is a central regulator of metabolic ...

    Abstract A large body of research has demonstrated that human stearoyl-CoA desaturase 1 (SCD1), a universally expressed fatty acid Δ9-desaturase that converts saturated fatty acids (SFA) into monounsaturated fatty acids (MUFA), is a central regulator of metabolic and signaling pathways involved in cell proliferation, differentiation, and survival. Unlike SCD1, stearoyl-CoA desaturase 5 (SCD5), a second SCD isoform found in a variety of vertebrates, including humans, has received considerably less attention but new information on the catalytic properties, regulation and biological functions of this enzyme has begun to emerge. This review will examine the new evidence that supports key metabolic and biological roles for SCD5, as well as the potential implication of this desaturase in the mechanisms of human diseases.
    MeSH term(s) Amino Acid Sequence ; Animals ; Cell Survival ; Cleft Palate/enzymology ; Cleft Palate/genetics ; Cleft Palate/pathology ; Fatty Acids/metabolism ; Fatty Acids, Monounsaturated/metabolism ; Gene Expression Regulation ; Humans ; Lipid Metabolism/genetics ; Neoplasms/enzymology ; Neoplasms/genetics ; Neoplasms/pathology ; Neurodegenerative Diseases/enzymology ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/pathology ; Sequence Alignment ; Sequence Homology, Amino Acid ; Signal Transduction ; Stearoyl-CoA Desaturase/genetics ; Stearoyl-CoA Desaturase/metabolism
    Chemical Substances Fatty Acids ; Fatty Acids, Monounsaturated ; SCD1 protein, human (EC 1.14.19.1) ; SCD5 protein, human (EC 1.14.19.1) ; Stearoyl-CoA Desaturase (EC 1.14.19.1)
    Language English
    Publishing date 2020-10-10
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 60-7
    ISSN 1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbalip.2020.158840
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  2. Article: Stearoyl CoA desaturase-1: New insights into a central regulator of cancer metabolism.

    Igal, R Ariel

    Biochimica et biophysica acta

    2016  Volume 1861, Issue 12 Pt A, Page(s) 1865–1880

    Abstract: The processes of cell proliferation, cell death and differentiation involve an intricate array of biochemical and morphological changes that require a finely tuned modulation of metabolic pathways, chiefly among them is fatty acid metabolism. The ... ...

    Abstract The processes of cell proliferation, cell death and differentiation involve an intricate array of biochemical and morphological changes that require a finely tuned modulation of metabolic pathways, chiefly among them is fatty acid metabolism. The critical participation of stearoyl CoA desaturase-1 (SCD1), the fatty acyl Δ9-desaturing enzyme that converts saturated fatty acids (SFA) into monounsaturated fatty acids (MUFA), in the mechanisms of replication and survival of mammalian cells, as well as their implication in the biological alterations of cancer have been actively investigated in recent years. This review examines the growing body of evidence that argues for a role of SCD1 as a central regulator of the complex synchronization of metabolic and signaling events that control cellular metabolism, cell cycle progression, survival, differentiation and transformation to cancer.
    MeSH term(s) Animals ; Cell Cycle/physiology ; Cell Differentiation/physiology ; Cell Proliferation/physiology ; Cell Transformation, Neoplastic/metabolism ; Humans ; Metabolic Networks and Pathways/physiology ; Neoplasms/metabolism ; Stearoyl-CoA Desaturase/metabolism
    Chemical Substances Stearoyl-CoA Desaturase (EC 1.14.19.1)
    Language English
    Publishing date 2016
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbalip.2016.09.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Stearoyl-CoA desaturase 5 (SCD5), a Δ-9 fatty acyl desaturase in search of a function

    Igal, R. Ariel / Sinner, Débora I

    Biochimica et biophysica acta. 2021 Jan., v. 1866, no. 1

    2021  

    Abstract: A large body of research has demonstrated that human stearoyl-CoA desaturase 1 (SCD1), a universally expressed fatty acid Δ9-desaturase that converts saturated fatty acids (SFA) into monounsaturated fatty acids (MUFA), is a central regulator of metabolic ...

    Abstract A large body of research has demonstrated that human stearoyl-CoA desaturase 1 (SCD1), a universally expressed fatty acid Δ9-desaturase that converts saturated fatty acids (SFA) into monounsaturated fatty acids (MUFA), is a central regulator of metabolic and signaling pathways involved in cell proliferation, differentiation, and survival. Unlike SCD1, stearoyl-CoA desaturase 5 (SCD5), a second SCD isoform found in a variety of vertebrates, including humans, has received considerably less attention but new information on the catalytic properties, regulation and biological functions of this enzyme has begun to emerge. This review will examine the new evidence that supports key metabolic and biological roles for SCD5, as well as the potential implication of this desaturase in the mechanisms of human diseases.
    Keywords cell proliferation ; humans ; stearoyl-CoA desaturase
    Language English
    Dates of publication 2021-01
    Publishing place Elsevier B.V.
    Document type Article
    Note NAL-AP-2-clean
    ISSN 1388-1981
    DOI 10.1016/j.bbalip.2020.158840
    Database NAL-Catalogue (AGRICOLA)

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  4. Article: Stearoyl CoA desaturase-1: New insights into a central regulator of cancer metabolism

    Igal, R. Ariel

    Biochimica et biophysica acta. 2016 Dec., v. 1861, no. 12

    2016  

    Abstract: The processes of cell proliferation, cell death and differentiation involve an intricate array of biochemical and morphological changes that require a finely tuned modulation of metabolic pathways, chiefly among them is fatty acid metabolism. The ... ...

    Abstract The processes of cell proliferation, cell death and differentiation involve an intricate array of biochemical and morphological changes that require a finely tuned modulation of metabolic pathways, chiefly among them is fatty acid metabolism. The critical participation of stearoyl CoA desaturase-1 (SCD1), the fatty acyl Δ9-desaturing enzyme that converts saturated fatty acids (SFA) into monounsaturated fatty acids (MUFA), in the mechanisms of replication and survival of mammalian cells, as well as their implication in the biological alterations of cancer have been actively investigated in recent years. This review examines the growing body of evidence that argues for a role of SCD1 as a central regulator of the complex synchronization of metabolic and signaling events that control cellular metabolism, cell cycle progression, survival, differentiation and transformation to cancer.
    Keywords biochemical pathways ; cell cycle ; cell death ; cell proliferation ; fatty acid metabolism ; mammals ; monounsaturated fatty acids ; neoplasms ; saturated fatty acids
    Language English
    Dates of publication 2016-12
    Size p. 1865-1880.
    Publishing place Elsevier B.V.
    Document type Article
    ISSN 1388-1981
    DOI 10.1016/j.bbalip.2016.09.009
    Database NAL-Catalogue (AGRICOLA)

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  5. Article: Roles of StearoylCoA Desaturase-1 in the Regulation of Cancer Cell Growth, Survival and Tumorigenesis.

    Igal, R Ariel

    Cancers

    2011  Volume 3, Issue 2, Page(s) 2462–2477

    Abstract: The development and maintenance of defining features of cancer, such as unremitting cell proliferation, evasion of programmed cell death, and the capacity for colonizing local tissues and distant organs, demand a massive production of structural, ... ...

    Abstract The development and maintenance of defining features of cancer, such as unremitting cell proliferation, evasion of programmed cell death, and the capacity for colonizing local tissues and distant organs, demand a massive production of structural, signaling and energy-storing lipid biomolecules of appropriate fatty acid composition. Due to constitutive activation of fatty acid biosynthesis, cancer cell lipids are enriched with saturated (SFA) and, in particular, monounsaturated fatty acids (MUFA), which are generated by StearoylCoA desaturase-1, the main enzyme that transforms SFA into MUFA. An increasing number of experimental and epidemiological studies suggest that high levels of SCD1 activity is a major factor in establishing the biochemical and metabolic perturbations that favors the oncogenic process. This review examines evidence that suggests the critical implication of SCD1 in the modulation of multiple biological mechanisms, specifically lipid biosynthesis and proliferation and survival signaling pathways that contribute to the development and progression of cancer.
    Language English
    Publishing date 2011-05-20
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers3022462
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Stearoyl-CoA desaturase-1: a novel key player in the mechanisms of cell proliferation, programmed cell death and transformation to cancer.

    Igal, R Ariel

    Carcinogenesis

    2010  Volume 31, Issue 9, Page(s) 1509–1515

    Abstract: As part of a shift toward macromolecule production to support continuous cell proliferation, cancer cells coordinate the activation of lipid biosynthesis and the signaling networks that stimulate this process. A ubiquitous metabolic event in cancer is ... ...

    Abstract As part of a shift toward macromolecule production to support continuous cell proliferation, cancer cells coordinate the activation of lipid biosynthesis and the signaling networks that stimulate this process. A ubiquitous metabolic event in cancer is the constitutive activation of the fatty acid biosynthetic pathway, which produces saturated fatty acids (SFAs) and monounsaturated fatty acids (MUFAs) to sustain the increasing demand of new membrane phospholipids with appropriate acyl composition. In cancer cells, the tandem activation of the fatty acid biosynthetic enzymes adenosine triphosphate citrate lyase, acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) leads to increased synthesis of SFA and their further conversion into MUFA by stearoyl-CoA desaturase (SCD) 1. The roles of adenosine triphosphate citrate lyase, ACC and FAS in the pathogenesis of cancer have been a subject of extensive investigation. However, despite early experimental and epidemiological observations reporting elevated levels of MUFA in cancer cells and tissues, the involvement of SCD1 in the mechanisms of carcinogenesis remains surprisingly understudied. Over the past few years, a more detailed picture of the functional relevance of SCD1 in cell proliferation, survival and transformation to cancer has begun to emerge. The present review addresses the mounting evidence that argues for a key role of SCD1 in the coordination of the intertwined pathways of lipid biosynthesis, energy sensing and the transduction signals that influence mitogenesis and tumorigenesis, as well as the potential value of this enzyme as a target for novel pharmacological approaches in cancer interventions.
    MeSH term(s) Animals ; Apoptosis ; Cell Proliferation ; Cell Transformation, Neoplastic ; Humans ; Neoplasms/enzymology ; Neoplasms/pathology ; Stearoyl-CoA Desaturase/physiology
    Chemical Substances Stearoyl-CoA Desaturase (EC 1.14.19.1)
    Language English
    Publishing date 2010-09
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 603134-1
    ISSN 1460-2180 ; 0143-3334
    ISSN (online) 1460-2180
    ISSN 0143-3334
    DOI 10.1093/carcin/bgq131
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    Zs.A 1558: Show issues Location:
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  7. Article ; Online: Roles of StearoylCoA Desaturase-1 in the Regulation of Cancer Cell Growth, Survival and Tumorigenesis

    R. Ariel Igal

    Cancers, Vol 3, Iss 2, Pp 2462-

    2011  Volume 2477

    Abstract: The development and maintenance of defining features of cancer, such as unremitting cell proliferation, evasion of programmed cell death, and the capacity for colonizing local tissues and distant organs, demand a massive production of structural, ... ...

    Abstract The development and maintenance of defining features of cancer, such as unremitting cell proliferation, evasion of programmed cell death, and the capacity for colonizing local tissues and distant organs, demand a massive production of structural, signaling and energy-storing lipid biomolecules of appropriate fatty acid composition. Due to constitutive activation of fatty acid biosynthesis, cancer cell lipids are enriched with saturated (SFA) and, in particular, monounsaturated fatty acids (MUFA), which are generated by StearoylCoA desaturase-1, the main enzyme that transforms SFA into MUFA. An increasing number of experimental and epidemiological studies suggest that high levels of SCD1 activity is a major factor in establishing the biochemical and metabolic perturbations that favors the oncogenic process. This review examines evidence that suggests the critical implication of SCD1 in the modulation of multiple biological mechanisms, specifically lipid biosynthesis and proliferation and survival signaling pathways that contribute to the development and progression of cancer.
    Keywords fatty acid synthesis and desaturation ; cancer ; cell cycle ; apoptosis ; lipogenesis ; Akt signaling ; AMPK ; cancer therapeutics ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Oncology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Subject code 571
    Language English
    Publishing date 2011-05-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Genistein downregulates de novo lipid synthesis and impairs cell proliferation in human lung cancer cells.

    Hess, Daniel / Igal, R Ariel

    Experimental biology and medicine (Maywood, N.J.)

    2011  Volume 236, Issue 6, Page(s) 707–713

    Abstract: Cancer cells require high levels of lipid synthesis to produce structural, signaling and energetic lipids to support continuous replication. We and others have reported that constitutively increased lipogenesis, mainly by the tandem activation of acetyl- ... ...

    Abstract Cancer cells require high levels of lipid synthesis to produce structural, signaling and energetic lipids to support continuous replication. We and others have reported that constitutively increased lipogenesis, mainly by the tandem activation of acetyl-CoA carboxylase, fatty acid synthase and stearoyl-CoA desaturase-1 (SCD1), is critical to sustain the biological features of cancer cells, making this metabolic pathway a potential anticancer target for nutritional and pharmacological interventions. Isoflavones are biologically potent botanical compounds that possess clear antilipogenic and anticancer properties; however, the regulatory effects of these nutraceutical agents on lipid biosynthesis in cancer cells are still not well understood. Here we show that genistein, an isoflavone abundant in soybeans, decreased the levels of SCD1 protein in H460 human lung adenocarcinoma cells, consequently reducing the rate of biosynthesis of oleic acid as well as its presence in cancer cell lipids. Moreover, genistein promoted a marked reduction in de novo synthesis of major phospholipids, triacylglycerol and cholesterolesters. Finally, cancer cells treated with genistein displayed a dramatic reduction in cell proliferation as a result of a blockade in cell cycle progression through G(2)/M phases. As a whole, our data suggest that, by globally downregulating lipid biosynthesis, genistein suppresses cancer cell growth, emphasizing the relevance of this botanical compound as a potential therapeutic agent against lung cancer, a disease for which therapeutic choices remain limited.
    MeSH term(s) Cell Line, Tumor ; Cell Proliferation/drug effects ; Cytostatic Agents/pharmacology ; Down-Regulation ; Genistein/pharmacology ; Humans ; Lipids/biosynthesis ; Lung Neoplasms
    Chemical Substances Cytostatic Agents ; Lipids ; Genistein (DH2M523P0H)
    Language English
    Publishing date 2011-06-01
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 4015-0
    ISSN 1535-3699 ; 1525-1373 ; 0037-9727
    ISSN (online) 1535-3699 ; 1525-1373
    ISSN 0037-9727
    DOI 10.1258/ebm.2011.010265
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    Ua VI Zs.111: Show issues Location:
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  9. Article: Inhibition of Stearoyl-CoA Desaturase 1 expression in human lung adenocarcinoma cells impairs tumorigenesis.

    Scaglia, Natalia / Igal, R Ariel

    International journal of oncology

    2008  Volume 33, Issue 4, Page(s) 839–850

    Abstract: Saturated (SFA) and monounsaturated (MUFA) fatty acids, the most abundant fatty acid species, have many divergent biological effects including the regulation of cell proliferation, programmed cell death and lipid-mediated cytotoxicity. Their distribution ...

    Abstract Saturated (SFA) and monounsaturated (MUFA) fatty acids, the most abundant fatty acid species, have many divergent biological effects including the regulation of cell proliferation, programmed cell death and lipid-mediated cytotoxicity. Their distribution is regulated by Stearoyl-CoA Desaturases (SCD), the enzymes that convert SFA into MUFA. A positive correlation between high levels of tissue MUFA and several types of cancer has been reported, but a causal relationship between the function of SCD1, the main human SCD isoform, and cancer development has not yet been firmly established. Here we report that the stable knockdown of SCD1 gene expression in A549 human lung adenocarcinoma cells decreased the ratio MUFA/SFA in total lipids and inhibited the incorporation of glucose into cell lipids. Cell proliferation and anchorage-independent growth were considerably decreased in SCD1-depleted cells, whereas the rate of apoptosis was elevated, with respect to control A549 cells. In addition, phosphorylation of Akt-Ser473 and GSK-3beta-Ser9 was found notably impaired in SCD1-ablated A549 cells. Interestingly, the effects of SCD1 blockade on Akt activation, cancer cell growth and apoptosis could not be reversed by exogenously added oleic acid. Remarkably, the reduction of SCD1 expression in lung cancer cells significantly delayed the formation of tumors and reduced the growth rate of tumor xenografts in mice. Our study demonstrates that SCD1 activity regulates Akt activation and determines the rate of cell proliferation, survival and invasiveness in A549 cancer cells and shows, for the first time, that SCD1 is a key factor in the regulation of tumorigenesis in vivo.
    MeSH term(s) Animals ; Cell Line, Tumor ; Cell Proliferation ; Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Neoplastic ; Humans ; Lipids/chemistry ; Lung Neoplasms/drug therapy ; Mice ; Mice, Nude ; Oleic Acid/metabolism ; Phenotype ; Protein Isoforms ; Proto-Oncogene Proteins c-akt/metabolism ; Stearoyl-CoA Desaturase/antagonists & inhibitors ; Stearoyl-CoA Desaturase/biosynthesis
    Chemical Substances Lipids ; Protein Isoforms ; Oleic Acid (2UMI9U37CP) ; Stearoyl-CoA Desaturase (EC 1.14.19.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2008-10
    Publishing country Greece
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1154403-x
    ISSN 1019-6439
    ISSN 1019-6439
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3690: Show issues Location:
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  10. Article ; Online: Stearoyl-CoA desaturase activity modulates the activation of epidermal growth factor receptor in human lung cancer cells.

    Nashed, Mary / Chisholm, Jeffrey W / Igal, R Ariel

    Experimental biology and medicine (Maywood, N.J.)

    2012  Volume 237, Issue 9, Page(s) 1007–1017

    Abstract: Stearoyl-CoA desaturase-1 (SCD1), the main enzyme that converts saturated fatty acids into monounsaturated fatty acids, is a key factor in the mechanisms of cancer cell proliferation, survival and tumorigenesis. Evidence indicates that SCD1 activity ... ...

    Abstract Stearoyl-CoA desaturase-1 (SCD1), the main enzyme that converts saturated fatty acids into monounsaturated fatty acids, is a key factor in the mechanisms of cancer cell proliferation, survival and tumorigenesis. Evidence indicates that SCD1 activity regulates these events in part by targeting the phosphatidylinositol-3 phosphate kinase/Akt and Ras/extracellular signal-regulated kinase (ERK) pathways, but the molecular mechanisms remain unknown. We now show that in H460 lung cancer cells, the suppression of SCD activity with CVT-11127, a specific small molecule SCD inhibitor, impairs the ligand-induced phosphorylation of epidermal growth factor (EGF) receptor, causing the inactivation of its downstream targets Akt, ERK and mammalian target of rapamycin. Importantly, the mitogenic response to EGF was markedly defective in SCD-depleted cancer cells. The inactivation of EGF receptor (EGFR) promoted by SCD inhibition may be caused by perturbations in the lipid microenvironment surrounding the receptor, since we detected significant alterations in the lateral mobility of plasma lipid microdomains. Finally, incubation of lung cancer cells with SCD blockers potentiated the antigrowth effect of gefitinib, an EGFR inhibitor employed in cancer treatment. Altogether, our data indicate that SCD activity may control cancer cell metabolism, proliferation and survival by modulating the EGFR→Akt/ERK signaling platforms. Our studies also suggest a value for SCD inhibitors as novel pharmacological agents in lung cancer, one of the most common and lethal forms of cancer for which therapeutic options remain very limited.
    MeSH term(s) Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell Proliferation ; Cell Survival ; Cell Transformation, Neoplastic ; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Humans ; Lung Neoplasms/enzymology ; Lung Neoplasms/metabolism ; MAP Kinase Signaling System/drug effects ; Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation/drug effects ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors ; Proto-Oncogene Proteins c-akt/metabolism ; Quinazolines/pharmacology ; Receptor, Epidermal Growth Factor/antagonists & inhibitors ; Receptor, Epidermal Growth Factor/metabolism ; Stearoyl-CoA Desaturase/antagonists & inhibitors ; Stearoyl-CoA Desaturase/metabolism ; TOR Serine-Threonine Kinases/antagonists & inhibitors
    Chemical Substances Antineoplastic Agents ; Quinazolines ; Stearoyl-CoA Desaturase (EC 1.14.19.1) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Receptor, Epidermal Growth Factor (EC 2.7.10.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; gefitinib (S65743JHBS)
    Language English
    Publishing date 2012-09
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 4015-0
    ISSN 1535-3699 ; 1525-1373 ; 0037-9727
    ISSN (online) 1535-3699 ; 1525-1373
    ISSN 0037-9727
    DOI 10.1258/ebm.2012.012126
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