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Article ; Online: Vitamin D receptor absence does not enhance intestinal tumorigenesis in ApcPirc/+rats.

Irving, Amy A / Waters, Bayley J / Seeman, Jeremy R / Plum, Lori A / DeLuca, Hector F

2022 Volume 11, Issue 7

Abstract: Epidemiological observations have prompted some to posit that elevated circulating vitamin D is responsible for reduced colon cancer in individuals residing near the equator. We have previously demonstrated that vitamin D has no effect on colon cancer in ...

Abstract	Epidemiological observations have prompted some to posit that elevated circulating vitamin D is responsible for reduced colon cancer in individuals residing near the equator. We have previously demonstrated that vitamin D has no effect on colon cancer in two rodent models of intestinal tumorigenesis. We have now extended this line of inquiry to ask whether ablation of vitamin D receptor (VDR) affects tumorigenesis. A VDR null rat was developed using Cas9-CRISPR technology, which allowed us to investigate whether 1,25(OH)D3 signaling through its receptor plays a role in intestinal tumorigenesis. Loss of VDR expression alone did not induce tumorigenesis, even in animals exposed to the inflammatory agent dextran sodium sulfate. These VDR-/- rats were then crossed with ApcPirc/+ rats, which are predisposed to the development of intestinal neoplasms. In combination with the Pirc/+ mutation, VDR loss did not enhance tumor multiplicity, growth, or progression in the colon or small intestine. This study demonstrates that the vitamin D receptor does not impact tumor development, and strongly supports previous findings that vitamin D itself does not play a role in colon cancer development or progression. Alternative explanations are needed for the original latitude hypothesis, as well as observational data in humans. This article has an associated First Person interview with the first author of the paper.
MeSH term(s)	Animals ; Animals, Genetically Modified ; Carcinogenesis/genetics ; Cell Transformation, Neoplastic ; Colonic Neoplasms/genetics ; Colonic Neoplasms/metabolism ; Humans ; Rats ; Receptors, Calcitriol/genetics ; Receptors, Calcitriol/metabolism ; Vitamin D/metabolism
Chemical Substances	Receptors, Calcitriol ; Vitamin D (1406-16-2)
Language	English
Publishing date	2022-07-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2632264-X
ISSN	2046-6390 ; 2046-6390
ISSN (online)	2046-6390
ISSN	2046-6390
DOI	10.1242/bio.059290
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Article ; Online: UV light suppression of EAE (a mouse model of multiple sclerosis) is independent of vitamin D and its receptor.

Irving, Amy A / Marling, Steven J / Seeman, Jeremy / Plum, Lori A / DeLuca, Hector F

Proceedings of the National Academy of Sciences of the United States of America

2019 Volume 116, Issue 45, Page(s) 22552–22555

Abstract: Vitamin D and sunlight have each been reported to protect against the development of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS). To date, the contribution of each has been unclear as ultra violet (UV) ... ...

Abstract	Vitamin D and sunlight have each been reported to protect against the development of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS). To date, the contribution of each has been unclear as ultra violet (UV) exposure also causes the generation of vitamin D in the skin. To examine whether the UV based suppression of EAE results, at least, in part from the production of vitamin D, we studied the effect of UV light on EAE in mice unable to produce 7-dehydroxycholesterol (7-DHC), the required precursor of vitamin D. Furthermore, we examined UV suppression of EAE in mice devoid of the vitamin D receptor (VDR). Our results demonstrate that UV light suppression of EAE occurs in the absence of vitamin D production and in the absence of VDR. Future investigations will focus on identifying the pathway responsible for the protective action of UV in EAE and presumably human MS.
MeSH term(s)	Animals ; Cholecalciferol/analogs & derivatives ; Cholecalciferol/metabolism ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/genetics ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Encephalomyelitis, Autoimmune, Experimental/therapy ; Female ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Multiple Sclerosis/genetics ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/therapy ; Phototherapy ; Receptors, Calcitriol/genetics ; Receptors, Calcitriol/metabolism ; Skin/metabolism ; Skin/radiation effects ; Ultraviolet Rays ; Vitamin D/metabolism
Chemical Substances	Receptors, Calcitriol ; Vitamin D (1406-16-2) ; Cholecalciferol (1C6V77QF41) ; previtamin D(3) (HDA46400N5)
Language	English
Publishing date	2019-10-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1913294116
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Article ; Online: Vitamin D deficiency in the

Irving, Amy A / Duchow, Elizabeth G / Plum, Lori A / DeLuca, Hector F

Disease models & mechanisms

2018 Volume 11, Issue 3

Abstract: Human studies have shown that individuals with colon cancer tend to have lower serum 25-hydroxy-vitamin ... ...

Abstract	Human studies have shown that individuals with colon cancer tend to have lower serum 25-hydroxy-vitamin D
MeSH term(s)	Adenomatous Polyposis Coli Protein/genetics ; Adenomatous Polyposis Coli Protein/metabolism ; Animals ; Calcitriol/blood ; Calcium/blood ; Calcium, Dietary/pharmacology ; Calcium, Dietary/therapeutic use ; Carcinogenesis/drug effects ; Carcinogenesis/genetics ; Carcinogenesis/pathology ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; Colonic Neoplasms/genetics ; Colonic Neoplasms/pathology ; Colonic Neoplasms/prevention & control ; Dextran Sulfate ; Disease Models, Animal ; Disease Progression ; Gene Expression Regulation, Neoplastic/drug effects ; Ki-67 Antigen/genetics ; Ki-67 Antigen/metabolism ; Limit of Detection ; Protective Agents/pharmacology ; Protective Agents/therapeutic use ; Rats ; Vitamin D Deficiency/complications ; Weight Gain/drug effects
Chemical Substances	Adenomatous Polyposis Coli Protein ; Calcium, Dietary ; Ki-67 Antigen ; Mki67 protein, mouse ; Protective Agents ; Dextran Sulfate (9042-14-2) ; Calcitriol (FXC9231JVH) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2018-03-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1754-8411
ISSN (online)	1754-8411
DOI	10.1242/dmm.032300
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Article ; Online: Suppression of experimental autoimmune encephalomyelitis by ultraviolet light is not mediated by isomerization of urocanic acid.

Irving, Amy A / Marling, Steven J / Plum, Lori A / DeLuca, Hector F

BMC neuroscience

2017 Volume 18, Issue 1, Page(s) 8

Abstract: Background: Ultraviolet B irradiation confers strong resistance against experimental autoimmune encephalomyelitis, a model of multiple sclerosis. This protection by ultraviolet B is independent of vitamin D production but causes isomerization of ... ...

Abstract	Background: Ultraviolet B irradiation confers strong resistance against experimental autoimmune encephalomyelitis, a model of multiple sclerosis. This protection by ultraviolet B is independent of vitamin D production but causes isomerization of urocanic acid, a naturally occurring immunosuppressant. Methods: To determine whether UCA isomerization from trans to cis is responsible for the protection against experimental autoimmune encephalomyelitis afforded by ultraviolet B, trans- or cis-urocanic acid was administered to animals and their disease progression was monitored. Results: Disease incidence was reduced by 74% in animals exposed to ultraviolet B, and skin cis-urocanic acid levels increased greater than 30%. However, increasing skin cis-urocanic acid levels independent of ultraviolet B was unable to alter disease onset or progression. Conclusions: It is unlikely that urocanic acid isomerization is responsible for the ultraviolet B-mediated suppression of experimental autoimmune encephalomyelitis. Additional work is needed to investigate alternative mechanisms by which UVB suppresses disease.
MeSH term(s)	Animals ; Disease Progression ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Encephalomyelitis, Autoimmune, Experimental/therapy ; Female ; Isomerism ; Mice ; Mice, Inbred C57BL ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/therapy ; Ultraviolet Rays ; Ultraviolet Therapy ; Urocanic Acid/administration & dosage ; Urocanic Acid/chemistry ; Urocanic Acid/radiation effects
Chemical Substances	Urocanic Acid (G8D26XJJ3B)
Language	English
Publishing date	2017-01-05
Publishing country	England
Document type	Journal Article
ISSN	1471-2202
ISSN (online)	1471-2202
DOI	10.1186/s12868-016-0323-2
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Article ; Online: The conserved protective cyclic AMP-phosphodiesterase function PDE4B is expressed in the adenoma and adjacent normal colonic epithelium of mammals and silenced in colorectal cancer.

Pleiman, Jennifer K / Irving, Amy A / Wang, Zhishi / Toraason, Erik / Clipson, Linda / Dove, William F / Deming, Dustin A / Newton, Michael A

PLoS genetics

2018 Volume 14, Issue 9, Page(s) e1007611

Abstract: Conservation over three mammalian genera-the mouse, rat, and human-has been found for a subset of the transcripts whose level differs between the adenoma and normal epithelium of the colon. Pde4b is one of the triply conserved transcripts whose level is ... ...

Abstract	Conservation over three mammalian genera-the mouse, rat, and human-has been found for a subset of the transcripts whose level differs between the adenoma and normal epithelium of the colon. Pde4b is one of the triply conserved transcripts whose level is enhanced both in the colonic adenoma and in the normal colonic epithelium, especially adjacent to adenomas. It encodes the phosphodiesterase PDE4B, specific for cAMP. Loss of PDE4B function in the ApcMin/+ mouse leads to a significant increase in the number of colonic adenomas. Similarly, Pde4b-deficient ApcMin/+ mice are hypersensitive to treatment by the inflammatory agent DSS, becoming moribund soon after treatment. These observations imply that the PDE4B function protects against ApcMin-induced adenomagenesis and inflammatory lethality. The paradoxical enhancement of the Pde4b transcript in the adenoma versus this inferred protective function of PDE4B can be rationalized by a feedback model in which PDE4B is first activated by early oncogenic stress involving cAMP and then, as reported for frank human colon cancer, inactivated by epigenetic silencing.
MeSH term(s)	Adenoma/genetics ; Adenoma/mortality ; Adenoma/pathology ; Adenomatous Polyposis Coli Protein/genetics ; Animals ; Colon/pathology ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/mortality ; Colorectal Neoplasms/pathology ; Cyclic AMP/metabolism ; Cyclic Nucleotide Phosphodiesterases, Type 4/genetics ; Cyclic Nucleotide Phosphodiesterases, Type 4/metabolism ; Dextran Sulfate/toxicity ; Disease Models, Animal ; Female ; Gene Knockout Techniques ; Humans ; Inflammatory Bowel Diseases/chemically induced ; Inflammatory Bowel Diseases/pathology ; Intestinal Mucosa/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Rats ; Tissue Array Analysis
Chemical Substances	Adenomatous Polyposis Coli Protein ; adenomatous polyposis coli protein, mouse ; Dextran Sulfate (9042-14-2) ; Cyclic AMP (E0399OZS9N) ; Cyclic Nucleotide Phosphodiesterases, Type 4 (EC 3.1.4.17) ; PDE4B protein, human (EC 3.1.4.17) ; PDE4B protein, mouse (EC 3.1.4.17) ; PDE4B protein, rat (EC 3.1.4.17)
Language	English
Publishing date	2018-09-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1007611
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Article ; Online: The concentrations of EGFR, LRG1, ITIH4, and F5 in serum correlate with the number of colonic adenomas in ApcPirc/+ rats.

Ivancic, Melanie M / Irving, Amy A / Jonakin, Kelli G / Dove, William F / Sussman, Michael R

Cancer prevention research (Philadelphia, Pa.)

2014 Volume 7, Issue 11, Page(s) 1160–1169

Abstract: The development of noninvasive methods for early detection of colon cancer is critical for the successful management of this disease. Using a targeted quantitative proteomics technique, we assessed the ability of 12 serum proteins to detect the presence ... ...

Abstract	The development of noninvasive methods for early detection of colon cancer is critical for the successful management of this disease. Using a targeted quantitative proteomics technique, we assessed the ability of 12 serum proteins to detect the presence of colonic polyps in the Apc(Pirc) (/+) rat model of familial colon cancer. Serum protein candidates were selected from gene transcripts upregulated in colonic tumors of Apc(Pirc) (/+) rats and from a prior study of serum proteins differentially expressed in mice carrying intestinal adenomas. Proteins were quantified at early stages of polyp formation in a rat cohort monitored longitudinally by colonoscopy over a period of 75 days. Of the 12 proteins monitored at three distinct time points, seven showed differential expression in at least one time point in the serum from Apc(Pirc) (/+) rats compared with wild-type rats. Tumor multiplicity correlated with protein expression changes, and most tumors grew during the study. EGFR, LRG1, ITIH4, and F5 displayed the most robust tumor-associated protein expression changes over time. Receiver operator characteristic analysis using these four proteins resulted in a sensitivity of 100%, a specificity of 80%, and an area under the curve of 0.93 at 135 days of age, when the Pirc rats bore an average of 19 tumors in the colon and seven in the small intestine. The results of this study demonstrate that the quantitative analysis of a panel of serum proteins can detect the presence of early intestinal tumors in a rat model, and provides support for future measurements in humans.
MeSH term(s)	Adenoma/metabolism ; Animals ; Biomarkers, Tumor/blood ; Blood Proteins/analysis ; Calcium-Binding Proteins/blood ; Chromatography, Liquid ; Colonic Neoplasms/blood ; Colonoscopy ; Disease Models, Animal ; ErbB Receptors/blood ; Factor V/analysis ; False Positive Reactions ; Female ; Gene Expression Regulation, Neoplastic ; Glycoproteins/analysis ; Glycoproteins/blood ; Male ; Mass Spectrometry ; Oligonucleotide Array Sequence Analysis ; Proteinase Inhibitory Proteins, Secretory ; Proteomics ; RNA, Messenger/metabolism ; ROC Curve ; Rats ; Rats, Inbred F344 ; Rats, Transgenic
Chemical Substances	Biomarkers, Tumor ; Blood Proteins ; Calcium-Binding Proteins ; Glycoproteins ; ITIH4 protein, rat ; LRG1 protein, rat ; Proteinase Inhibitory Proteins, Secretory ; RNA, Messenger ; Factor V (9001-24-5) ; Egfr protein, rat (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2014-09-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2434717-6
ISSN	1940-6215 ; 1940-6207
ISSN (online)	1940-6215
ISSN	1940-6207
DOI	10.1158/1940-6207.CAPR-14-0056
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Zs.A 6766: Show issues

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Article ; Online: Cholecalciferol or 25-hydroxycholecalciferol neither prevents nor treats adenomas in a rat model of familial colon cancer.

Irving, Amy A / Plum, Lori A / Blaser, William J / Ford, Madeline R / Weng, Chao / Clipson, Linda / DeLuca, Hector F / Dove, William F

The Journal of nutrition

2014 Volume 145, Issue 2, Page(s) 291–298

Abstract: Background: Epidemiologic studies in humans have shown associations between greater sunlight exposure, higher serum 25-hydroxycholecalciferol [25(OH)D3] concentrations, and reduced colon cancer risk. However, results from a limited number of vitamin D ... ...

Abstract	Background: Epidemiologic studies in humans have shown associations between greater sunlight exposure, higher serum 25-hydroxycholecalciferol [25(OH)D3] concentrations, and reduced colon cancer risk. However, results from a limited number of vitamin D supplementation trials in humans have not shown a protective effect. Objective: We sought to determine whether adding to the diet increasing amounts of either 25(OH)D3, the stable metabolite measured in serum and associated with cancer risk, or cholecalciferol (vitamin D3), the compound commonly used for supplementation in humans, could reduce emergent adenomas (chemoprevention) or decrease the growth of existing adenomas (treatment) in the colons of vitamin D-sufficient rats carrying a truncation mutation of adenomatous polyposis coli (Apc), a model of early intestinal cancer. Methods: Apc(Pirc/+) rats were supplemented with either vitamin D3 over a range of 4 doses [6-1500 μg/(kg body weight · d)] or with 25(OH)D3 over a range of 6 doses [60-4500 μg/(kg body weight · d)] beginning after weaning. Rats underwent colonoscopy every other week to assess effects on adenoma number and size. At termination (140 d of age), the number of tumors in the small intestine and colon and the size of tumors in the colon were determined, and serum calcium and 25(OH)D3 measurements were obtained. Results: At lower doses (those that did not affect body weight), neither of the vitamin D compounds reduced the number of existing or emergent colonic tumors (P-trend > 0.24). By contrast, supplementation at higher doses (those that caused a suppression in body weight gain) with either 25(OH)D3 or vitamin D3 caused a dose-dependent increase in colonic tumor number in both males and females (P-trend < 0.003). Conclusions: No evidence for protection against colon tumor development was seen with lower dose supplementation with either cholecalciferol or 25-hydroxycholecalciferol. Thus, the association between sunlight exposure and the incidence of colon cancer may involve factors other than vitamin D concentrations. Alternative hypotheses warrant investigation. Furthermore, this study provides preliminary evidence for the need for caution regarding vitamin D supplementation of humans at higher doses, especially in individuals with sufficient serum 25(OH)D3 concentrations.
MeSH term(s)	Adenoma/drug therapy ; Adenoma/prevention & control ; Animals ; Calcifediol/blood ; Calcifediol/pharmacology ; Calcium, Dietary/blood ; Cholecalciferol/blood ; Cholecalciferol/pharmacology ; Colon/drug effects ; Colon/metabolism ; Colonic Neoplasms/drug therapy ; Colonic Neoplasms/prevention & control ; Diet ; Dietary Supplements ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Female ; Male ; Rats ; Rats, Inbred F344 ; Vitamin D Deficiency/drug therapy
Chemical Substances	Calcium, Dietary ; Cholecalciferol (1C6V77QF41) ; Calcifediol (P6YZ13C99Q)
Language	English
Publishing date	2014-12-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218373-0
ISSN	1541-6100 ; 0022-3166
ISSN (online)	1541-6100
ISSN	0022-3166
DOI	10.3945/jn.114.204396
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Article ; Online: Candidate serum biomarkers for early intestinal cancer using 15N metabolic labeling and quantitative proteomics in the ApcMin/+ mouse.

Ivancic, Melanie M / Huttlin, Edward L / Chen, Xiaodi / Pleiman, Jennifer K / Irving, Amy A / Hegeman, Adrian D / Dove, William F / Sussman, Michael R

Journal of proteome research

2013 Volume 12, Issue 9, Page(s) 4152–4166

Abstract: Current screening procedures for colorectal cancer are imperfect and highly invasive and result in increased mortality rates due to low compliance. The goal of the experiments reported herein is to identify potential blood-based biomarkers indicative of ... ...

Abstract	Current screening procedures for colorectal cancer are imperfect and highly invasive and result in increased mortality rates due to low compliance. The goal of the experiments reported herein is to identify potential blood-based biomarkers indicative of early stage intestinal cancers using the ApcMin/+ mouse model of intestinal cancer as an experimental system. Serum proteins from tumor-bearing ApcMin/+ mice were quantitatively compared to tumor-free Apc+/+ wild-type mice via in anima metabolic labeling with 14N/15N-labeled Spirulina algae and an LTQ Orbitrap mass spectrometer. Out of 1116 total serum proteins quantified, this study identified 40 that were differentially expressed and correlated with the increase in intestinal neoplasms. A subset of these differentially expressed proteins underwent a secondary quantitative screen using selected reaction monitoring-mass spectrometry with stable isotope-labeled peptides. Using both quantitative techniques, we identified MGAM and COL1A1 as downregulated and ITIH3 and F5 as upregulated in serum. All but COL1A1 were similarly differentially expressed in the mRNA of neoplastic colonic tissues of ApcMin/+ mice compared to normal wild-type tissue. These differentially expressed proteins identified in the ApcMin/+ mouse model have provided a set of candidate biomarkers for future validation screens in humans.
MeSH term(s)	Animals ; Biomarkers, Tumor/blood ; Colorectal Neoplasms/blood ; Colorectal Neoplasms/diagnosis ; Early Detection of Cancer ; Female ; Genes, APC ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nitrogen Isotopes ; Protein Interaction Maps ; Proteomics ; Staining and Labeling ; Up-Regulation
Chemical Substances	Biomarkers, Tumor ; Nitrogen Isotopes
Language	English
Publishing date	2013-08-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2078618-9
ISSN	1535-3907 ; 1535-3893
ISSN (online)	1535-3907
ISSN	1535-3893
DOI	10.1021/pr400467c
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Article: Candidate Serum Biomarkers for Early Intestinal Cancer Using 15N Metabolic Labeling and Quantitative Proteomics in the ApcMin/+ Mouse

Ivancic, Melanie M / Huttlin, Edward L / Chen, Xiaodi / Pleiman, JenniferK / Irving, Amy A / Hegeman, AdrianD / Dove, William F / Sussman, Michael R

Journal of Proteome Research. 2013 Sept. 06, v. 12, no. 9

2013

Abstract	Current screening procedures for colorectal cancer are imperfect and highly invasive and result in increased mortality rates due to low compliance. The goal of the experiments reported herein is to identify potential blood-based biomarkers indicative of early stage intestinal cancers using the ApcMin/+ mouse model of intestinal cancer as an experimental system. Serum proteins from tumor-bearing ApcMin/+ mice were quantitatively compared to tumor-free Apc+/+ wild-type mice via in anima metabolic labeling with 14N/15N-labeled Spirulina algae and an LTQ Orbitrap mass spectrometer. Out of 1116 total serum proteins quantified, this study identified 40 that were differentially expressed and correlated with the increase in intestinal neoplasms. A subset of these differentially expressed proteins underwent a secondary quantitative screen using selected reaction monitoring-mass spectrometry with stable isotope-labeled peptides. Using both quantitative techniques, we identified MGAM and COL1A1 as downregulated and ITIH3 and F5 as upregulated in serum. All but COL1A1 were similarly differentially expressed in the mRNA of neoplastic colonic tissues of ApcMin/+ mice compared to normal wild-type tissue. These differentially expressed proteins identified in the ApcMin/+ mouse model have provided a set of candidate biomarkers for future validation screens in humans.
Keywords	Spirulina ; algae ; animal models ; biomarkers ; blood proteins ; blood serum ; colorectal neoplasms ; gene expression regulation ; humans ; mass spectrometry ; messenger RNA ; mice ; mortality ; peptides ; protein synthesis ; proteome ; proteomics ; quantitative analysis ; screening ; spectrometers ; stable isotopes
Language	English
Dates of publication	2013-0906
Size	p. 4152-4166.
Publishing place	American Chemical Society
Document type	Article
ZDB-ID	2078618-9
ISSN	1535-3907 ; 1535-3893
ISSN (online)	1535-3907
ISSN	1535-3893
DOI	10.1021%2Fpr400467c
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Mitigation of late renal and pulmonary injury after hematopoietic stem cell transplantation.

Cohen, Eric P / Bedi, Manpreet / Irving, Amy A / Jacobs, Elizabeth / Tomic, Rade / Klein, John / Lawton, Colleen A / Moulder, John E

International journal of radiation oncology, biology, physics

2011 Volume 83, Issue 1, Page(s) 292–296

Abstract: Purpose: To update the results of a clinical trial that assessed whether the angiotensin-converting enzyme inhibitor captopril was effective in mitigating chronic renal failure and pulmonary-related mortality in subjects undergoing total body ... ...

Abstract	Purpose: To update the results of a clinical trial that assessed whether the angiotensin-converting enzyme inhibitor captopril was effective in mitigating chronic renal failure and pulmonary-related mortality in subjects undergoing total body irradiation (TBI) in preparation for hematopoietic stem cell transplantation (HSCT). Methods and materials: Updated records of the 55 subjects who were enrolled in this randomized controlled trial were analyzed. Twenty-eight patients received captopril, and 27 patients received placebo. Definitions of TBI-HSCT-related chronic renal failure (and relapse) were the same as those in the 2007 analysis. Pulmonary-related mortality was based on clinical or autopsy findings of pulmonary failure or infection as the primary cause of death. Follow-up data for overall and pulmonary-related mortality were supplemented by use of the National Death Index. Results: The risk of TBI-HSCT-related chronic renal failure was lower in the captopril group (11% at 4 years) than in the placebo group (17% at 4 years), but this was not statistically significant (p > 0.2). Analysis of mortality was greatly extended by use of the National Death Index, and no patients were lost to follow-up for reasons other than death prior to 67 months. Patient survival was higher in the captopril group than in the placebo group, but this was not statistically significant (p > 0.2). The improvement in survival was influenced more by a decrease in pulmonary mortality (11% risk at 4 years in the captopril group vs. 26% in the placebo group, p = 0.15) than by a decrease in chronic renal failure. There was no adverse effect on relapse risk (p = 0.4). Conclusions: Captopril therapy produces no detectable adverse effects when given after TBI. Captopril therapy reduces overall and pulmonary-related mortality after radiation-based HSCT, and there is a trend toward mitigation of chronic renal failure.
MeSH term(s)	Adult ; Angiotensin-Converting Enzyme Inhibitors/therapeutic use ; Captopril/therapeutic use ; Child ; Female ; Hematopoietic Stem Cell Transplantation ; Humans ; Kidney Failure, Chronic/etiology ; Kidney Failure, Chronic/mortality ; Kidney Failure, Chronic/prevention & control ; Lung Injury/etiology ; Lung Injury/mortality ; Lung Injury/prevention & control ; Male ; Prospective Studies ; Radiation Injuries/prevention & control ; Radiation-Protective Agents/therapeutic use ; Transplantation Conditioning/adverse effects ; Transplantation Conditioning/methods ; Whole-Body Irradiation/adverse effects ; Whole-Body Irradiation/methods
Chemical Substances	Angiotensin-Converting Enzyme Inhibitors ; Radiation-Protective Agents ; Captopril (9G64RSX1XD)
Language	English
Publishing date	2011-11-19
Publishing country	United States
Document type	Journal Article ; Randomized Controlled Trial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	197614-x
ISSN	1879-355X ; 0360-3016
ISSN (online)	1879-355X
ISSN	0360-3016
DOI	10.1016/j.ijrobp.2011.05.081
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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

Order via subito