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A novel model of small intestine cancer in hCYP1A-db/db mice and the inhibitory effect of delta-tocopherol on colorectal cancer in hCYP1A mice

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Title
A novel model of small intestine cancer in hCYP1A-db/db mice and the inhibitory effect of delta-tocopherol on colorectal cancer in hCYP1A mice
Name (type = personal)
NamePart (type = family)
Kuo
NamePart (type = given)
Ying-Yi
NamePart (type = date)
1988-
DisplayForm
Ying-Yi Kuo
Role
RoleTerm (authority = RULIB)
author
Name (type = personal)
NamePart (type = family)
Yang
NamePart (type = given)
Chung S.
DisplayForm
Chung S. Yang
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
chair
Name (type = personal)
NamePart (type = family)
Suh
NamePart (type = given)
Nanjoo
DisplayForm
Nanjoo Suh
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Shapses
NamePart (type = given)
Sue
DisplayForm
Sue Shapses
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = corporate)
NamePart
Rutgers University
Role
RoleTerm (authority = RULIB)
degree grantor
Name (type = corporate)
NamePart
Graduate School - New Brunswick
Role
RoleTerm (authority = RULIB)
school
TypeOfResource
Text
Genre (authority = marcgt)
theses
OriginInfo
DateCreated (qualifier = exact)
2014
DateOther (qualifier = exact); (type = degree)
2014-10
CopyrightDate (encoding = w3cdtf)
2014
Place
PlaceTerm (type = code)
xx
Language
LanguageTerm (authority = ISO639-2b); (type = code)
eng
Abstract (type = abstract)
In the digestive tract, cancer is common in colon and rectum but rare in small intestine. However, during the last 30 years, small intestine cancer has increased from 1% to 3% in the newly diagnosed digestive tract cancers for unknown reasons, whereas colorectal cancer has dropped by about 10%. In our experimental study, we used a humanized mouse model by replacing the mouse Cyp1a with human CYP1A to mimic human metabolism of the dietary carcinogen, 2-amino-1-methyl-6- phenylimidazo [4,5-b] pyridine (PhIP) to study PhIP-induced carcinogenesis. We bred hCYP1A mice with db/+ mice to investigate cancer promotion by obesity. Remarkably, we found that all PhIP-treated hCYP1A-db/db mice develop tumors in small intestine at the ages of Week 28-44. The tumor region of small intestine showed overexpression of COX-2 and nitrotyrosine. In contrast, we have not observed tumor in small intestine in PhIP-treated hCYP1A mice. This result strongly suggests the promotion of small intestine cancer by obesity. Our finding provides a model for further exploration of small intestine carcinogenesis and related preventive studies. Many chemoprevention studies of colorectal cancer have been done. However, the results of the inhibitory effect of α -tocopherol on carcinogenesis were inconsistent. Our recent studies showed δ-tocopherol has strong inhibitory effect on different type of cancer such as lung and prostate cancer. In my experiment, hCYP1A mice were fed AIN93M (control) diet or diet supplement with 0.3% δ-tocopherol. All mice were administrated 200 mg/kg PhIP by oral gavage and one week later, administered 1.5% DSS in drinking water for 4 days. All mice were sacrificed 8 week after PhIP administration. The results showed decreased tumor multiplicity, tumor volume, expression of COX-2 and 8-oxo-dG, and increased expression of cleaved caspase-3, in the 0.3% δ-tocopherol treated group. Our findings suggest that δ-tocopherol inhibits tumorigenesis by decreasing inflammation and increasing cell apoptosis in colorectal cancer in hCYP1A mice.
Subject (authority = RUETD)
Topic
Nutritional Sciences
RelatedItem (type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier (type = RULIB)
ETD
Identifier
ETD_5787
PhysicalDescription
Form (authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
1 online resource (xiii, 63 p. : ill.)
Note (type = degree)
M.S.
Note (type = bibliography)
Includes bibliographical references
Subject (authority = ETD-LCSH)
Topic
Colon (Anatomy)--Cancer
Subject (authority = ETD-LCSH)
Topic
Rectum--Cancer
Subject (authority = ETD-LCSH)
Topic
Tocotrienol
Note (type = statement of responsibility)
by Ying-Yi Kuo
RelatedItem (type = host)
TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier (type = local)
rucore19991600001
Location
PhysicalLocation (authority = marcorg); (displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier (type = doi)
doi:10.7282/T3ZS2TZZ
Genre (authority = ExL-Esploro)
ETD graduate
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The author owns the copyright to this work.
RightsHolder (type = personal)
Name
FamilyName
Kuo
GivenName
Ying-Yi
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2014-08-20 15:01:20
AssociatedEntity
Name
Ying-Yi Kuo
Role
Copyright holder
Affiliation
Rutgers University. Graduate School - New Brunswick
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License
Name
Author Agreement License
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I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
Copyright
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Copyright protected
Availability
Status
Open
Reason
Permission or license
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ContentModel
ETD
OperatingSystem (VERSION = 5.1)
windows xp
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