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Article ; Online: Dendritic Cell Vaccination in Non-Small Cell Lung Cancer: Remodeling the Tumor Immune Microenvironment.

Abascal, Jensen / Oh, Michael S / Liclican, Elvira L / Dubinett, Steven M / Salehi-Rad, Ramin / Liu, Bin

2023 Volume 12, Issue 19

Abstract: Non-small-cell lung cancer (NSCLC) remains one of the leading causes of death worldwide. While NSCLCs possess antigens that can potentially elicit T cell responses, defective tumor antigen presentation and T cell activation hinder host anti-tumor immune ... ...

Abstract	Non-small-cell lung cancer (NSCLC) remains one of the leading causes of death worldwide. While NSCLCs possess antigens that can potentially elicit T cell responses, defective tumor antigen presentation and T cell activation hinder host anti-tumor immune responses. The NSCLC tumor microenvironment (TME) is composed of cellular and soluble mediators that can promote or combat tumor growth. The composition of the TME plays a critical role in promoting tumorigenesis and dictating anti-tumor immune responses to immunotherapy. Dendritic cells (DCs) are critical immune cells that activate anti-tumor T cell responses and sustain effector responses. DC vaccination is a promising cellular immunotherapy that has the potential to facilitate anti-tumor immune responses and transform the composition of the NSCLC TME via tumor antigen presentation and cell-cell communication. Here, we will review the features of the NSCLC TME with an emphasis on the immune cell phenotypes that directly interact with DCs. Additionally, we will summarize the major preclinical and clinical approaches for DC vaccine generation and examine how effective DC vaccination can transform the NSCLC TME toward a state of sustained anti-tumor immune signaling.
MeSH term(s)	Humans ; Carcinoma, Non-Small-Cell Lung/metabolism ; Lung Neoplasms/metabolism ; Tumor Microenvironment ; Antigens, Neoplasm/metabolism ; Vaccination ; Dendritic Cells
Chemical Substances	Antigens, Neoplasm
Language	English
Publishing date	2023-10-04
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12192404
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Erratum: Describing the dynamic translational science landscape through core voucher utilization - ERRATUM.

Liclican, Elvira L / Filler, Scott G / Kaye, Jonathan / Denny, Christopher T

Journal of clinical and translational science

2019 Volume 4, Issue 1, Page(s) 73

Abstract: This corrects the article DOI: 10.1017/cts.2019.4.]. ...

Abstract	[This corrects the article DOI: 10.1017/cts.2019.4.].
Language	English
Publishing date	2019-11-27
Publishing country	England
Document type	Published Erratum
ISSN	2059-8661
ISSN (online)	2059-8661
DOI	10.1017/cts.2019.420
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Article ; Online: Describing the dynamic translational science landscape through Core Voucher utilization.

Liclican, Elvira L / Filler, Scott G / Kaye, Jonathan / Denny, Christopher T

Journal of clinical and translational science

2019 Volume 3, Issue 2-3, Page(s) 105–112

Abstract: Introduction: Core facilities play crucial roles in carrying out the academic research mission by making available to researchers advanced technologies, facilities, or expertise that are unfeasible for most investigators to obtain on their own. To ... ...

Abstract	Introduction: Core facilities play crucial roles in carrying out the academic research mission by making available to researchers advanced technologies, facilities, or expertise that are unfeasible for most investigators to obtain on their own. To facilitate translational science through support of core services, the University of California, Los Angeles Clinical and Translational Science Institute (UCLA CTSI) created a Core Voucher program. The underlying premise is that by actively promoting interplay between researchers and core facilities, a dynamic feedback loop could be established that could enhance both groups, the productivity of the former and the relevance of the latter. Our primary goal was to give translational investigators what they need to pursue their immediate projects at hand. Methods: To implement this system across four noncontiguous campuses, open-source web-accessible software applications were created that were scalable and could efficiently administer investigator submissions and subsequent reviews in a multicampus fashion. Results: In the past five years, we have processed over 1400 applications submitted by over 750 individual faculty members across both clinical and nonclinical departments. In total, 1926 core requests were made in conjunction with 1467 submitted proposals. The top 10 most popular cores accounted for 50% of all requests, and the top half of the most popular cores accounted for 90% of all requests. Conclusion: Tracking investigator demand provides a unique window into what are the high- and low-priority core services that best support translational research.
Language	English
Publishing date	2019-06-14
Publishing country	England
Document type	Journal Article
ISSN	2059-8661
ISSN (online)	2059-8661
DOI	10.1017/cts.2019.4
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Article ; Online: Describing the dynamic translational science landscape through core voucher utilization — ERRATUM

Elvira L. Liclican / Scott G. Filler / Jonathan Kaye / Christopher T. Denny

Journal of Clinical and Translational Science, Vol 4, Pp 73-

2020 Volume 73

Keywords	Medicine ; R
Language	English
Publishing date	2020-02-01T00:00:00Z
Publisher	Cambridge University Press
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Describing the dynamic translational science landscape through Core Voucher utilization

Elvira L. Liclican / Scott G. Filler / Jonathan Kaye / Christopher T. Denny

Journal of Clinical and Translational Science, Vol 3, Pp 105-

2019 Volume 112

Abstract: AbstractIntroduction:Core facilities play crucial roles in carrying out the academic research mission by making available to researchers advanced technologies, facilities, or expertise that are unfeasible for most investigators to obtain on their own. To ...

Abstract	AbstractIntroduction:Core facilities play crucial roles in carrying out the academic research mission by making available to researchers advanced technologies, facilities, or expertise that are unfeasible for most investigators to obtain on their own. To facilitate translational science through support of core services, the University of California, Los Angeles Clinical and Translational Science Institute (UCLA CTSI) created a Core Voucher program. The underlying premise is that by actively promoting interplay between researchers and core facilities, a dynamic feedback loop could be established that could enhance both groups, the productivity of the former and the relevance of the latter. Our primary goal was to give translational investigators what they need to pursue their immediate projects at hand.Methods:To implement this system across four noncontiguous campuses, open-source web-accessible software applications were created that were scalable and could efficiently administer investigator submissions and subsequent reviews in a multicampus fashion.Results:In the past five years, we have processed over 1400 applications submitted by over 750 individual faculty members across both clinical and nonclinical departments. In total, 1926 core requests were made in conjunction with 1467 submitted proposals. The top 10 most popular cores accounted for 50% of all requests, and the top half of the most popular cores accounted for 90% of all requests.Conclusion:Tracking investigator demand provides a unique window into what are the high- and low-priority core services that best support translational research.
Keywords	Core facility ; Core Voucher ; translational science ; UCLA CTSI ; request for application ; Medicine ; R
Subject code	001
Language	English
Publishing date	2019-06-01T00:00:00Z
Publisher	Cambridge University Press
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Molecular circuits of resolution in the eye.

Liclican, Elvira L / Gronert, Karsten

TheScientificWorldJournal

2010 Volume 10, Page(s) 1029–1047

Abstract: Lipid autacoids have well-established key roles in physiology and pathophysiology. Eicosanoids derived from omega-6 arachidonic acid (AA) have long been recognized for their roles in cardiovascular and renal functions, and vascular tone, as well as ... ...

Abstract	Lipid autacoids have well-established key roles in physiology and pathophysiology. Eicosanoids derived from omega-6 arachidonic acid (AA) have long been recognized for their roles in cardiovascular and renal functions, and vascular tone, as well as regulating inflammatory and immune functions. It is now appreciated that AA is a substrate for generating lipid mediators with anti-inflammatory and proresolving properties, namely lipoxins (i.e., LXA4), which are an integral component for the successful execution of beneficial and essential acute inflammatory responses. In addition to AA, the omega-3 polyunsaturated fatty acids (PUFAs) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) also serve as substrates to generate potent and protective autacoids, such as resolvins and neuroprotectin (i.e., NPD1), respectively. These omega-3-derived signals may mediate the remarkable protective action of essential dietary omega-3 PUFAs. Formation and bioactivity of lipid mediators in the eye are relatively unexplored and of considerable interest, as the eye contains highly specialized tissues, including the transparent avascular and immune-privileged cornea, and the neuro-retina. A rapidly emerging field has identified key biosynthetic enzymes, receptors, and temporally defined endogenous formation of omega-3- and omega-6-derived protective lipid circuits in the eye. Protective endogenous roles of LXA4 and NPD1 have been established utilizing lipidomic analysis, knockout mice, and pharmacological, genetic, and dietary manipulation, providing compelling evidence that these intrinsic lipid autacoid circuits play essential roles in restraining inflammation, promoting wound healing, inhibiting pathological angiogenesis, and providing neuroprotection in the delicate visual axis.
MeSH term(s)	Animals ; Eye/metabolism ; Humans ; Lipid Metabolism
Language	English
Publishing date	2010-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2075968-X
ISSN	1537-744X ; 1537-744X
ISSN (online)	1537-744X
ISSN	1537-744X
DOI	10.1100/tsw.2010.99
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Article ; Online: Molecular Circuits of Resolution in the Eye

Elvira L. Liclican / Karsten Gronert

The Scientific World Journal, Vol 10, Pp 1029-

2010 Volume 1047

Abstract: Lipid autacoids have well-established key roles in physiology and pathophysiology. Eicosanoids derived from ω-6 arachidonic acid (AA) have long been recognized for their roles in cardiovascular and renal functions, and vascular tone, as well as ... ...

Abstract	Lipid autacoids have well-established key roles in physiology and pathophysiology. Eicosanoids derived from ω-6 arachidonic acid (AA) have long been recognized for their roles in cardiovascular and renal functions, and vascular tone, as well as regulating inflammatory and immune functions. It is now appreciated that AA is a substrate for generating lipid mediators with anti-inflammatory and proresolving properties, namely lipoxins (i.e., LXA4), which are an integral component for the successful execution of beneficial and essential acute inflammatory responses. In addition to AA, the ω-3 polyunsaturated fatty acids (PUFAs) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) also serve as substrates to generate potent and protective autacoids, such as resolvins and neuroprotectin (i.e., NPD1), respectively. These ω-3–derived signals may mediate the remarkable protective action of essential dietary ω-3 PUFAs. Formation and bioactivity of lipid mediators in the eye are relatively unexplored and of considerable interest, as the eye contains highly specialized tissues, including the transparent avascular and immune-privileged cornea, and the neuro-retina. A rapidly emerging field has identified key biosynthetic enzymes, receptors, and temporally defined endogenous formation of ω-3– and ω-6–derived protective lipid circuits in the eye. Protective endogenous roles of LXA4 and NPD1 have been established utilizing lipidomic analysis, knockout mice, and pharmacological, genetic, and dietary manipulation, providing compelling evidence that these intrinsic lipid autacoid circuits play essential roles in restraining inflammation, promoting wound healing, inhibiting pathological angiogenesis, and providing neuroprotection in the delicate visual axis.
Keywords	Technology ; T ; Medicine ; R ; Science ; Q
Language	English
Publishing date	2010-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Selective activation of the prostaglandin E2 circuit in chronic injury-induced pathologic angiogenesis.

Liclican, Elvira L / Nguyen, Van / Sullivan, Aaron B / Gronert, Karsten

Investigative ophthalmology & visual science

2010 Volume 51, Issue 12, Page(s) 6311–6320

Abstract: Purpose: Cyclooxygenase (COX)-derived prostaglandin E(2) (PGE(2)) is a prevalent and established mediator of inflammation and pain in numerous tissues and diseases. Distribution and expression of the four PGE(2) receptors (EP1-EP4) can dictate whether ... ...

Abstract	Purpose: Cyclooxygenase (COX)-derived prostaglandin E(2) (PGE(2)) is a prevalent and established mediator of inflammation and pain in numerous tissues and diseases. Distribution and expression of the four PGE(2) receptors (EP1-EP4) can dictate whether PGE(2) exerts an anti-inflammatory or a proinflammatory and/or a proangiogenic effect. The role and mechanism of endogenous PGE(2) in the cornea, and the regulation of EP expression during a dynamic and complex inflammatory/reparative response remain to be clearly defined. Methods: Chronic or acute self-resolving inflammation was induced in mice by corneal suture or epithelial abrasion, respectively. Reepithelialization was monitored by fluorescein staining and neovascularization quantified by CD31/PECAM-1 immunofluorescence. PGE(2) formation was analyzed by lipidomics and polymorphonuclear leukocyte (PMN) infiltration quantified by myeloperoxidase activity. Expression of EPs and inflammatory/angiogenic mediators was assessed by real-time PCR and immunohistochemistry. Mice eyes were treated with PGE(2) (100 ng topically, three times a day) for up to 7 days. Results: COX-2, EP-2, and EP-4 expression was upregulated with chronic inflammation that correlated with increased corneal PGE(2) formation and marked neovascularization. In contrast, acute abrasion injury did not alter PGE(2) or EP levels. PGE(2) treatment amplified PMN infiltration and the angiogenic response to chronic inflammation but did not affect wound healing or PMN infiltration after epithelial abrasion. Exacerbated inflammatory neovascularization with PGE(2) treatment was independent of the VEGF circuit but was associated with a significant induction of the eotaxin-CCR3 axis. Conclusions: These findings place the corneal PGE(2) circuit as an endogenous mediator of inflammatory neovascularization rather than general inflammation and demonstrate that chronic inflammation selectively regulates this circuit at the level of biosynthetic enzyme and receptor expression.
MeSH term(s)	Animals ; Cell Migration Assays, Leukocyte ; Chromatography, High Pressure Liquid ; Chronic Disease ; Corneal Injuries ; Corneal Neovascularization/metabolism ; Cyclooxygenase 2/metabolism ; Dinoprostone/metabolism ; Disease Models, Animal ; Epithelium, Corneal/physiology ; Eye Injuries/metabolism ; Female ; Fluorescent Antibody Technique, Indirect ; Keratitis/immunology ; Mice ; Mice, Inbred C57BL ; Neutrophils/physiology ; Peroxidase/metabolism ; Platelet Endothelial Cell Adhesion Molecule-1/metabolism ; RNA, Messenger/genetics ; Receptors, Prostaglandin E/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Tandem Mass Spectrometry ; Wound Healing/physiology ; Wounds, Nonpenetrating/metabolism
Chemical Substances	Platelet Endothelial Cell Adhesion Molecule-1 ; RNA, Messenger ; Receptors, Prostaglandin E ; Peroxidase (EC 1.11.1.7) ; Ptgs2 protein, mouse (EC 1.14.99.-) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2010-07-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.10-5455
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Article ; Online: The inflammatory tumor microenvironment, epithelial mesenchymal transition and lung carcinogenesis.

Heinrich, Eileen L / Walser, Tonya C / Krysan, Kostyantyn / Liclican, Elvira L / Grant, Jeanette L / Rodriguez, Nicole L / Dubinett, Steven M

Cancer microenvironment : official journal of the International Cancer Microenvironment Society

2011 Volume 5, Issue 1, Page(s) 5–18

Abstract: The inflammatory tumor microenvironment (TME) has many roles in tumor progression and metastasis, including creation of a hypoxic environment, increased angiogenesis and invasion, changes in expression of microRNAs (miRNAs) and an increase in a stem cell ...

Abstract	The inflammatory tumor microenvironment (TME) has many roles in tumor progression and metastasis, including creation of a hypoxic environment, increased angiogenesis and invasion, changes in expression of microRNAs (miRNAs) and an increase in a stem cell phenotype. Each of these has an impact on epithelial mesenchymal transition (EMT), particularly through the downregulation of E-cadherin. Here we review seminal work and recent findings linking the role of inflammation in the TME, EMT and lung cancer initiation, progression and metastasis. Finally, we discuss the potential of targeting aspects of inflammation and EMT in cancer prevention and treatment.
Language	English
Publishing date	2011-09-16
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2422345-1
ISSN	1875-2284 ; 1875-2292
ISSN (online)	1875-2284
ISSN	1875-2292
DOI	10.1007/s12307-011-0089-0
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Article: Failure to upregulate the adenosine2A receptor-epoxyeicosatrienoic acid pathway contributes to the development of hypertension in Dahl salt-sensitive rats.

Liclican, Elvira L / McGiff, John C / Falck, John R / Carroll, Mairéad A

American journal of physiology. Renal physiology

2008 Volume 295, Issue 6, Page(s) F1696–704

Abstract: ... nitro-l-arginine methyl ester and preconstricted with phenylephrine. Bolus injections of the stable ...

Abstract	Adenosine-activated renovascular dilatation in Sprague-Dawley (SD) rats is mediated by stimulating adenosine(2A) receptors (A(2A)R), which is linked to epoxyeicosatrienoic acid (EET) synthesis. The A(2A)R-EET pathway is upregulated by high salt (HS) intake in normotensive SD rats. Because this pathway is antipressor, we examined the role of the A(2A)R-EET pathway in Dahl salt-sensitive (SS) rats. Male Dahl salt-resistant (SR) and SS rats were fed either HS (8.0% NaCl) or normal salt (NS; 0.4% NaCl) diet for 7 days. On day 8, isolated kidneys were perfused with Krebs-Henseleit buffer containing indomethacin and N(G)-nitro-l-arginine methyl ester and preconstricted with phenylephrine. Bolus injections of the stable adenosine analog 2-chloroadenosine (2-CA; 0.1-20 microg) elicited dose-dependent dilation in both Dahl SR and SS rats. Dahl SR rats fed a HS diet demonstrated a greater renal vasodilator response to 10 microg of 2-CA, as measured by the reduction in renal perfusion pressure, than that of Dahl SR rats fed a NS diet (-104 +/- 6 vs. -77 +/- 7 mmHg, respectively; P < 0.05). In contrast, Dahl SS rats did not exhibit a difference in the vasodilator response to 2-CA whether fed NS or HS diet (96 +/- 6 vs. 104 +/- 13 mmHg in NS- and HS-fed rats, respectively). In Dahl SR but not Dahl SS rats, HS intake significantly increased purine flux, augmented the protein expression of A(2A)R and the cytochrome P-450 2C23 and 2C11 epoxygenases, and elevated the renal efflux of EETs. Thus the Dahl SR rat is able to respond to HS intake by recruiting EET formation, whereas the Dahl SS rat appears to have exhausted its ability to increase EET synthesis above the levels observed on NS intake, and this inability of Dahl SS rats to upregulate the A(2A)R-EET pathway in response to salt loading may contribute to the development of salt-sensitive hypertension.
MeSH term(s)	8,11,14-Eicosatrienoic Acid/analogs & derivatives ; 8,11,14-Eicosatrienoic Acid/metabolism ; Animals ; Aryl Hydrocarbon Hydroxylases/genetics ; Cytochrome P-450 Enzyme System/genetics ; Cytochrome P450 Family 2 ; Hypertension/genetics ; Hypertension/physiopathology ; Hypertension/urine ; Purines/urine ; Rats ; Rats, Inbred Dahl/physiology ; Receptor, Adenosine A2A/genetics ; Receptor, Adenosine A2A/physiology ; Sodium Chloride/adverse effects ; Steroid 16-alpha-Hydroxylase/genetics ; Up-Regulation
Chemical Substances	Purines ; Receptor, Adenosine A2A ; Sodium Chloride (451W47IQ8X) ; 11,12-epoxy-5,8,14-eicosatrienoic acid (5DOQ38R4UW) ; 8,11,14-Eicosatrienoic Acid (7324-41-6) ; Cytochrome P-450 Enzyme System (9035-51-2) ; Aryl Hydrocarbon Hydroxylases (EC 1.14.14.1) ; CYP2C11 protein, rat (EC 1.14.14.1) ; Cytochrome P450 Family 2 (EC 1.14.14.1) ; Steroid 16-alpha-Hydroxylase (EC 1.14.14.1) ; arachidonate epoxygenase (EC 1.14.14.1)
Language	English
Publishing date	2008-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603837-2
ISSN	1522-1466 ; 1931-857X ; 0363-6127
ISSN (online)	1522-1466
ISSN	1931-857X ; 0363-6127
DOI	10.1152/ajprenal.90502.2008
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