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1
adenomatous polyposis coli of large intestine 2005:2010[pubdate] *count=100
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adenomatous polyposis coli of large intestine
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Items 1 to 100 of about 7608
1.
Tanaka A, Minoguchi K, Chen X, Oda N, Yokoe T, Yamamoto Y, Yamamoto M, Watanabe Y, Ohta S, Xu X, Adachi M:
Activated protein C attenuates leukocyte elastase-induced lung injury in mice.
Shock
; 2008 Aug;30(2):153-8
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[Title]
Activated
protein C
attenuates leukocyte elastase-induced lung injury in mice.
The purpose of the current study was to (1) examine the relationship between LE-induced lung injury and specific markers of inflammation and cytokine/chemokine, and to (2) determine
the potential
of activated
protein C
(
APC
), a potent immunomodulator, to block the inflammatory response to LE.
Total cells, total
protein
, and neutrophils were increased and peaked at 16 h in bronchial alveolar lavage fluid.
Administration of LE up-regulated the synthesis of proinflammatory cytokines, IL-1beta and IL-6, chemokines, keratinocyte-derived chemokine, and macrophage inflammatory
protein
2 in bronchial alveolar lavage fluid, and their peaks were at 6 h.
Furthermore, the mice were treated with
APC
at 0.2, 2.0, and 10 mg/kg (i.v.) after instillation of LE.
Therapeutic treatment of
APC
at 2.0 and 10 mg/kg significantly attenuated the increases in all these parameters.
Lung histology revealed that, in addition to inflammation, alveolar hemorrhage and alveolar wall destruction induced by LE were also attenuated by
APC
.
Finally, the expression of tissue plasminogen activator and plasminogen activator inhibitor in whole lung of mice exposed to LE, detected by means of reverse-transcriptase-polymerase chain reaction, were
not
influenced by the treatment with
APC
.
These data demonstrate that intratracheal administration of LE to mice causes a transient inflammatory response,
and APC
can play a protective role against LE-induced lung injury.
[MeSH-major]
Inflammation Mediators / therapeutic use. Leukocyte Elastase / toxicity. Lung Diseases / chemically induced. Lung Diseases / pathology.
Protein C
/ metabolism.
Protein C
/ therapeutic use
[MeSH-minor]
Animals. Enzyme
Activation
/ physiology. Female. Fibrinolysis. Intubation, Intratracheal. Mice. Mice, Inbred C57BL. Neutrophil
Activation
/ physiology. Neutrophil Infiltration / physiology. Neutrophils / pathology.
Pulmonary
Alveoli / drug effects.
Pulmonary
Alveoli / metabolism.
Pulmonary
Alveoli / pathology
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consumer health - Lung Diseases
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 18628688.001).
[ISSN]
1073-2322
[Journal-full-title]
Shock (Augusta, Ga.)
[ISO-abbreviation]
Shock
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Inflammation Mediators; 0 / Protein C; EC 3.4.21.37 / Leukocyte Elastase
2.
Berkhout M, Nagtegaal ID, Cornelissen SJ, Dekkers MM, van de Molengraft FJ, Peters WH, Nagengast FM, van Krieken JH, Jeuken JW:
Chromosomal and methylation alterations in sporadic and familial adenomatous polyposis-related duodenal carcinomas.
Mod Pathol
; 2007 Dec;20(12):1253-62
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[Title]
Chromosomal and methylation alterations in sporadic
and familial
adenomatous polyposis
-related duodenal carcinomas.
Primary carcinomas of the small
intestine
are rare and the mechanism of their pathogenesis is poorly understood.
Patients with
familial
adenomatous polyposis
(
FAP
) have a high risk of developing duodenal carcinomas.
Therefore, five
FAP
-related duodenal carcinomas were characterized for chromosomal and methylation alterations, which were compared to those observed in sporadic duodenal carcinomas.
Comparative genomic hybridization (CGH) and methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) was performed in 10 primary sporadic and five primary
FAP
-related duodenal carcinomas.
In
the FAP
-related carcinomas, frequent gains were observed on chromosomes 8, 17 and 19, whereas in sporadic carcinomas they occurred on chromosomes 8, 12, 13 and 20.
In 60% of the sporadic carcinomas, gains in the regions of chromosome 12 were observed which were absent in
the FAP
-related carcinomas (P=0.04).
Hypermethylation was observed in the immunoglobulin superfamily genes member 4 (IGSF4), TIMP metallopeptidase inhibitor 3 (TIMP3), Estrogen receptor 1 (ESR1),
adenomatous polyposis coli
(
APC
), H-cadherin (CDH13) and paired box gene 6 (PAX6) genes.
Hypermethylation of PAX6 was only observed in
FAP
-related carcinomas (3/5)
and not
in sporadic carcinomas (P=0.02).
In conclusion, in contrast to sporadic duodenal carcinomas, gains on chromosome 12 were
not
observed in duodenal carcinomas of patients with
FAP
.
Identification of the genes in these regions of chromosome 12 could lead to a better understanding of the carcinogenesis pathways leading to sporadic
and FAP
-related duodenal carcinomas.
Furthermore, hypermethylation seems to be a general feature of both
FAP
-related duodenal carcinomas as well as sporadic duodenal carcinomas with the exception of the PAX6 gene, which is methylated only in
FAP
-related carcinomas.
[MeSH-major]
Adenocarcinoma / genetics.
Adenomatous Polyposis Coli
/ genetics. Chromosome Aberrations. DNA Methylation. Duodenal Neoplasms / genetics
Genetic Alliance.
consumer health - Familial Adenomatous Polyposis (FAP)
.
Genetic Alliance.
consumer health - Familial Polyposis
.
MedlinePlus Health Information.
consumer health - Intestinal Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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(PMID = 17873900.001).
[ISSN]
0893-3952
[Journal-full-title]
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
[ISO-abbreviation]
Mod. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
3.
Lee SH, Kang HJ, Shin DH, Cho DY, Song JM, Lee HC, Kim GH, Song GA, Sol MY, Kim JY, Choi KU, Lee CH, Huh GY, Park DY:
Expression of beta-catenin and its mechanism of delocalization in intestinal-type early gastric cancer based on mucin expression.
Histol Histopathol
; 2009 07;24(7):831-8
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[Title]
Expression of beta-catenin and its mechanism of delocalization in
intestinal
-
type
early gastric cancer based on mucin expression.
The biological characteristics of
intestinal
-
type
early gastric cancers (ICs) differ based on mucin phenotypes.
There was increased cytoplasmic and nuclear beta-catenin expression (delocalization) in ICs with a predominant
intestinal
mucin phenotype (ICIP; 46.3% [25/54 cases]) compared to ICs with a predominant gastric mucin phenotype (ICGP; 20% [11/55 cases]).
There were no beta-catenin or
APC
mutations in ICs.
APC
promoter hypermethylation was present in 49 of 105 (46.7%) cases of ICs.
There was a significant relationship between
APC
promoter hypermethylation and beta-catenin delocalization in ICs, especially in ICIPs.
There was no relationship between beta-catenin delocalization
and APC
gene loss of heterozygosity in ICs.
In conclusion, we showed that beta-catenin delocalization was more evident in ICIPs,
and APC
promoter hypermethylation might play a role in delocalization of beta-catenin, especially in ICIPs.
[MeSH-minor]
Adult. Aged. Alleles. Base Sequence. Cell Nucleus / metabolism. DNA Methylation. DNA Mutational Analysis. DNA, Neoplasm / genetics. DNA, Neoplasm / isolation & purification. Female. Gastrectomy. Gastric Mucosa / metabolism. Gastric Mucosa / pathology. Genes,
APC
. Humans. Immunohistochemistry. Loss of Heterozygosity. Male. Middle Aged. Molecular Sequence Data. Mutation. Polymerase Chain Reaction. Polymorphism, Restriction Fragment Length. Polymorphism, Single-Stranded Conformational. Promoter Regions, Genetic. Retrospective Studies. Sequence Analysis, DNA. Time Factors
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(PMID = 19475529.001).
[ISSN]
1699-5848
[Journal-full-title]
Histology and histopathology
[ISO-abbreviation]
Histol. Histopathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Spain
[Chemical-registry-number]
0 / CTNNB1 protein, human; 0 / DNA, Neoplasm; 0 / Mucins; 0 / beta Catenin
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4.
Hull MA, Faluyi OO, Ko CW, Holwell S, Scott DJ, Cuthbert RJ, Poulsom R, Goodlad R, Bonifer C, Markham AF, Coletta PL:
Regulation of stromal cell cyclooxygenase-2 in the ApcMin/+ mouse model of intestinal tumorigenesis.
Carcinogenesis
; 2006 Mar;27(3):382-91
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[Title]
Regulation of stromal cell cyclooxygenase-2 in the ApcMin/+ mouse model of
intestinal
tumorigenesis.
Cyclooxygenase-2 (Cox-2) is expressed predominantly by stromal cells in
intestinal
adenomas from
the Apc
(Min/+) mouse model of
familial
adenomatous polyposis
.
We investigated the mechanistic basis of stromal cell Cox-2 expression in
Apc
(Min/+) mouse adenomas, as well as Cox-2 expression and activity in histologically normal (HN)
Apc
(Min/+) mouse
intestine
, in order to gain further insights into regulation of Cox-2 as
a potential
chemoprevention target.
Upregulation of Cox-2 in
intestinal
tumours is
not
an intrinsic feature of
Apc
(Min/+) macrophages as bone marrow-derived
Apc
(Min/+) macrophages did
not
exhibit an
abnormality
in Cox-2 expression or activity.
Intestinal
permeability to lactulose or mannitol was similar in
Apc
(Min/+) mice and wild-
type
littermates, implying that macrophage
activation
by luminal antigen is unlikely to explain stromal cell Cox-2 induction.
Moreover, stromal cells exhibited differential expression of Cox-2 and inducible nitric oxide synthase, suggesting 'alternative' (M2) rather than 'classical' (M1) macrophage
activation
.
SMNCs from HN
Apc
(Min/+)
intestinal
mucosa exhibited similar levels of Cox-2 mRNA
and protein
, but produced more Cox-2-derived PGE(2) than wild-
type
cells at 70 days of age.
There was an age-dependent decline in PGE(2) synthesis by
Apc
(Min/+) SMNCs, despite tumour progression.
These data suggest that other Cox-2-independent factors also control PGE(2) levels during
Apc
(Min/+) mouse
intestinal
tumorigenesis.
[MeSH-major]
Adenoma
/ genetics.
Adenomatous Polyposis Coli
Protein
/ genetics. Cyclooxygenase 2 / biosynthesis.
Intestinal
Neoplasms / genetics
[MeSH-minor]
Animals. Cell Transformation, Neoplastic. Chemoprevention. Dinoprostone / biosynthesis.
Disease
Models,
Animal
. Flow Cytometry. Gene Expression Regulation. Macrophages. Mice. Mice, Inbred C57BL. Permeability. Stromal Cells / enzymology
COS Scholar Universe.
author profiles
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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(PMID = 16219637.001).
[ISSN]
0143-3334
[Journal-full-title]
Carcinogenesis
[ISO-abbreviation]
Carcinogenesis
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G116/146
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Adenomatous Polyposis Coli Protein; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone
5.
Leal RF, Ayrizono Mde L, Milanski M, Fagundes JJ, Moraes JC, Meirelles LR, Velloso LA, Coy CS:
Detection of epithelial apoptosis in pelvic ileal pouches for ulcerative colitis and familial adenomatous polyposis.
J Transl Med
; 2010;8:11
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[Title]
Detection of epithelial apoptosis in pelvic ileal pouches for ulcerative colitis
and familial
adenomatous polyposis
.
BACKGROUND: Ileal pouch-anal anastomosis (IPAA) is the surgical
procedure
of choice for patients with refractory ulcerative colitis (UC) and for
familial
adenomatous polyposis
(
FAP
) with many rectal polyps.
Pouchitis is one of the more frequent complications after IPAA in UC patients; however, it is rare in
FAP
.
OBJECTIVE: Evaluate pro-apoptotic activity in endoscopically and histological normal mucosa of the ileal pouch in patients with UC
and FAP
.
METHODS: Eighteen patients (nine with UC and nine with
FAP
) with J pouch after total rectocolectomy were studied.
The specimens were snap-
frozen and
the expressions of Bax and Bcl-2 were determined by immunoblot of
protein
extracts and by immunohistochemistry analysis.
FADD, Caspase-8, APAF-
1 and
Caspase-9 were evaluated by immunoprecipitation and immunoblot.
RESULTS: Patients with UC had significantly higher
protein
levels of Bax and APAF-1, Caspase-9 than patients with
FAP
, but were similar to controls.
Immunohistochemistry for Bax showed less intensity of immunoreactions in
FAP
than in UC and Controls.
CONCLUSION: Patients with
FAP
present lower levels of pro-apoptotic
proteins
in all methods applied, even in the absence of clinical and endoscopic pouchitis and dysplasia in the histological analysis.
However,
FAP
patients had low pro-apoptotic activity in the mucosa, and it could explain the tendency to low cell turn over and presence of adenomas in this
syndrome
.
[MeSH-major]
Adenomatous Polyposis Coli
/ surgery. Apoptosis / physiology. Colitis, Ulcerative / surgery. Colonic Pouches / pathology.
Intestinal
Mucosa / pathology
[MeSH-minor]
Animals. Apoptosis Regulatory
Proteins
/ metabolism. Apoptotic Protease-Activating Factor 1 / metabolism. Caspase 8 / metabolism. Caspase 9 / metabolism. Humans. Ileum / anatomy & histology. Ileum / pathology. Proto-Oncogene
Proteins c
-bcl-2 / metabolism. bcl-2-
Associated
X
Protein
/ metabolism
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[Cites]
Curr Opin Cell Biol. 2003 Dec;15(6):691-9
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]
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[
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]
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]
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Clin Gastroenterol Hepatol. 2006 Jan;4(1):81-9; quiz 2-3
[
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]
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World J Gastroenterol. 2006 Feb 21;12(7):1056-62
[
16534846.001
]
[Cites]
Gut. 2006 Jun;55(6):833-41
[
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]
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[
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]
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Fam Cancer. 2006;5(3):241-60; discussion 261-2
[
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]
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]
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]
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[
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]
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[
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]
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[
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]
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10961587.001
]
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]
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]
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]
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[
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]
[Cites]
Anal Biochem. 1976 May 7;72:248-54
[
942051.001
]
(PMID = 20113505.001).
[ISSN]
1479-5876
[Journal-full-title]
Journal of translational medicine
[ISO-abbreviation]
J Transl Med
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / APAF1 protein, human; 0 / Apoptosis Regulatory Proteins; 0 / Apoptotic Protease-Activating Factor 1; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9
[Other-IDs]
NLM/ PMC2843649
6.
Aizu K, Li W, Yajima T, Arai T, Shimoda K, Nimura Y, Yoshikai Y:
An important role of Tyk2 in APC function of dendritic cells for priming CD8+ T cells producing IFN-gamma.
Eur J Immunol
; 2006 Nov;36(11):3060-70
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[Title]
An important role of Tyk2 in
APC
function of dendritic cells for priming CD8+ T cells producing IFN-gamma.
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(PMID = 17048270.001).
[ISSN]
0014-2980
[Journal-full-title]
European journal of immunology
[ISO-abbreviation]
Eur. J. Immunol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antigens, Bacterial; 0 / Cytokines; 0 / HLA-A Antigens; 0 / HLA-B Antigens; 0 / OVA-8; 0 / Peptide Fragments; 82115-62-6 / Interferon-gamma; 9006-59-1 / Ovalbumin; EC 2.7.10.2 / TYK2 Kinase; EC 2.7.10.2 / Tyk2 protein, mouse
7.
Takamori N, Shimomura A, Senda T:
Microtubule-bundling activity of APC is stimulated by interaction with PSD-95.
Neurosci Lett
; 2006 Jul 31;403(1-2):68-72
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[Title]
Microtubule-bundling activity of
APC
is stimulated by interaction with PSD-95.
Adenomatous polyposis coli
(
APC
) tumor suppressor
protein
binds to microtubules, leading to microtubule bundling and stabilization.
The protein
also interacts with postsynaptic density (PSD)-95, a major scaffolding
protein
in neurons.
Here, we analyzed the effects of PSD-95 on the microtubule-bundling activity of
APC
.
The coexpression of
APC and
PSD-95 in COS-7 cells enhanced microtubule-bundle formation compared with the expression of
APC
alone.
A mutant
APC
variant that does
not
associate with PSD-95 did
not
enhance microtubule bundling, despite coexpression with PSD-95.
Immunoelectron microscopy showed that
the APC
-PSD-95 complex sometimes colocalized on microtubules in processes of cultured neurons.
These results suggest that the microtubule-bundling activity of
APC
is regulated by its interaction with PSD-95, which might modulate microtubule architecture and dynamics in neurons.
[MeSH-major]
Adenomatous Polyposis Coli
Protein
/ physiology. Microtubules / metabolism. Nerve Tissue
Proteins
/ physiology
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(PMID = 16701944.001).
[ISSN]
0304-3940
[Journal-full-title]
Neuroscience letters
[ISO-abbreviation]
Neurosci. Lett.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Ireland
[Chemical-registry-number]
0 / Adenomatous Polyposis Coli Protein; 0 / Nerve Tissue Proteins; 0 / postsynaptic density proteins
8.
Nielsen M, de Miranda NF, van Puijenbroek M, Jordanova ES, Middeldorp A, van Wezel T, van Eijk R, Tops CM, Vasen HF, Hes FJ, Morreau H:
Colorectal carcinomas in MUTYH-associated polyposis display histopathological similarities to microsatellite unstable carcinomas.
BMC Cancer
; 2009;9:184
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[Title]
Colorectal carcinomas in MUTYH-
associated
polyposis
display histopathological similarities to microsatellite unstable carcinomas.
BACKGROUND: MUTYH-
associated
polyposis
(
MAP
) is a recessively inherited
disorder
which predisposes biallelic carriers for a high risk
of polyposis
and colorectal carcinoma (CRC).
Since about one third of the biallelic
MAP
patients in population based CRC series has no adenomas, this study aimed to identify specific clinicopathological characteristics of
MAP
CRCs and compare these with reported data on sporadic and Lynch CRCs.
METHODS: From 44
MAP
patients who developed > or = 1 CRCs, 42 of 58 tumours were analyzed histologically and 35 immunohistochemically for p53 and beta-catenin.
KRAS2, the mutation cluster region (MCR) of
APC
, p53, and SMAD4 were analyzed for somatic mutations.
RESULTS:
MAP
CRCs frequently localized to the proximal
colon
(69%, 40/58), were mucinous in 21% (9/42), and had a conspicuous Crohn's like infiltrate reaction in 33% (13/40); all of these parameters occurred at a higher rate than reported for sporadic CRCs.
Tumour infiltrating lymphocytes (TILs) were also highly prevalent in
MAP
CRCs.
Somatic
APC
MCR mutations occurred in 14% (5/36) while 64% (23/36) had KRAS2 mutations (22/23 c.34G>T).
CONCLUSION:
MAP
CRCs show some similarities to micro-satellite unstable cancers, with a preferential proximal location, a high rate of mucinous histotype and increased presence of TILs.
These features should direct the practicing pathologist towards
a MAP
aetiology of CRC as an alternative for a mismatch repair deficient cause.
High frequent G>T transversions in
APC and
KRAS2 (mutated in early tumour development) but
not
in P53 and SMAD4 (implicated in tumour progression) might indicate a predominant MUTYH effect in early carcinogenesis.
[MeSH-major]
Adenomatous Polyposis Coli
/ genetics.
Adenomatous Polyposis Coli
/ pathology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. DNA Glycosylases / genetics. Microsatellite Instability
[MeSH-minor]
Adult. Aged. Alleles. Cohort Studies. Female. Genetic Predisposition to
Disease
. Humans. Immunohistochemistry. Lymphocytes, Tumor-Infiltrating / immunology. Male. Middle Aged. Mutation. Tissue Array Analysis
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Am J Pathol. 2001 Feb;158(2):527-35
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[
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]
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Am J Pathol. 2001 Jul;159(1):297-304
[
11438476.001
]
(PMID = 19527492.001).
[ISSN]
1471-2407
[Journal-full-title]
BMC cancer
[ISO-abbreviation]
BMC Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
[Other-IDs]
NLM/ PMC2706846
9.
Inoue K, Koike E, Takano H, Yanagisawa R, Ichinose T, Yoshikawa T:
Effects of diesel exhaust particles on antigen-presenting cells and antigen-specific Th immunity in mice.
Exp Biol Med (Maywood)
; 2009 Feb;234(2):200-9
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The present study characterized more precisely which pathways and cellular events of the allergic response are amplified by DEP in view of the maturation/
activation
/function of antigen-presenting cells (
APC
) and the antigen-specific Th response.
We evaluated the effects of DEP on the phenotype and function of bone marrow-derived dendritic cells (BMDC) in vitro and on the expression pattern of
APC
-related molecules in the murine lung in the presence or absence of antigen in vivo.
In addition, an in vivo experiment showed that repetitive
pulmonary
exposure to DEP plus antigen (OVA) increased the numbers of MHC class II+cells and those expressing CD11c, DEC205 (DC markers), CD80, CD86 (co-stimulatory molecules), F4/80 (a macrophage marker), and CD19 (a B-cell differentiation antigen) in the lung as compared to that of others (vehicle, DEP, or OVA).
In conclusion, enhancement of allergic responses by DEP can be explained via two novel mechanisms, i.e., enhancement effects on
APC
including DC and on antigen-specific Th response, which culminate in the promotion of local and systemic dysregulated Th immunity.
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(PMID = 19064938.001).
[ISSN]
1535-3702
[Journal-full-title]
Experimental biology and medicine (Maywood, N.J.)
[ISO-abbreviation]
Exp. Biol. Med. (Maywood)
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Adjuvants, Immunologic; 0 / Antigens; 0 / Epitopes; 0 / Histocompatibility Antigens Class II; 0 / Immunoglobulins; 0 / Particulate Matter; 0 / Vehicle Emissions; 9006-59-1 / Ovalbumin
10.
Wu YM, Yan J, Chen LL, Gu ZY:
Association between infection of different strains of Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans in subgingival plaque and clinical parameters in chronic periodontitis.
J Zhejiang Univ Sci B
; 2007 Feb;8(2):121-31
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METHODS: Two multiplex polymerase chain reaction (PCR) assays were developed to detect the 16SrDNA, collagenase (prtC) and fimbria (fimA) genes of P. gingivalis and the 16SrDNA, leukotoxin (lktA) and fimbria-
associated protein
(
fap
) genes of A. actinomycetemcomitans in 60 sulcus samples from 30 periodontal healthy subjects and in 122 subgingival plaque samples from 61 patients with CP.
RESULTS: The 16SrDNA, prtC and fimA genes of P. gingivalis were detected in 92.6%, 85.2% and 80.3% of the subgingival plaque samples respectively, while the 16SrDNA, lktA
and fap
genes of A. actinomycetemcomitans were in 84.4%, 75.4% and 50.0% respectively.
Nucleotide sequence analysis showed 98.62%~100% homology of the PCR products in these genes with the reported sequences. P. gingivalis strains with prtC+/fimA+
and A
. actinomycetemcomitans with lktA+ were predominant in deep pockets (>6 mm) or in sites with
attachment
loss > or =5 mm than in shallow pockets (3~4 mm) or in sites with
attachment
loss < or =2 mm (P<0.05). P. gingivalis strains with prtC+/fimA+ also showed higher frequency in gingival index (GI)=3 than in GI=1 group (P<0.05).
CONCLUSION: Infection of P. gingivalis with prtC+/fimA+
and A
. actinomycetemcomitans with lktA+ correlates with periodontal destruction of CP in Chinese.
Nonetheless P. gingivalis fimA, prtC genes
and A
. actinomycetemcomitans lktA gene are closely
associated
with periodontal destruction, while A. actinomycetemcomitans
fap
gene is
not
.
[MeSH-minor]
Adult. Aged. China / epidemiology. Chronic
Disease
. Female. Humans. Male. Middle Aged. Prevalence. Risk Assessment / methods. Risk Factors. Species Specificity. Statistics as Topic
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J Clin Periodontol. 2001 Sep;28(9):886-90
[
11493360.001
]
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J Periodontol. 2001 Oct;72(10):1354-63
[
11699477.001
]
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J Clin Periodontol. 2001 Dec;28(12):1163-71
[
11737515.001
]
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Eur J Oral Sci. 2002 Jun;110(3):212-7
[
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]
[Cites]
J Periodontol. 2003 Jan;74(1):90-6
[
12593602.001
]
[Cites]
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[
12753365.001
]
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Acta Odontol Scand. 2003 Apr;61(2):115-22
[
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]
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[
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]
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[
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]
[Cites]
FEMS Microbiol Lett. 2004 Mar 12;232(1):31-7
[
15019731.001
]
(PMID = 17266188.001).
[ISSN]
1673-1581
[Journal-full-title]
Journal of Zhejiang University. Science. B
[ISO-abbreviation]
J Zhejiang Univ Sci B
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Other-IDs]
NLM/ PMC1791058
11.
Tanaka M, Jin G, Yamazaki Y, Takahara T, Takuwa M, Nakamura T:
Identification of candidate cooperative genes of the Apc mutation in transformation of the colon epithelial cell by retroviral insertional mutagenesis.
Cancer Sci
; 2008 May;99(5):979-85
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[Title]
Identification of candidate cooperative genes of
the Apc
mutation in transformation of
the colon
epithelial cell by retroviral insertional mutagenesis.
The mutation of
Apc
is an important early genetic event in
colon
carcinogenesis.
To identify cooperative genes for
the Apc
(Min) mutation the authors carried out retroviral insertional mutagenesis (RIM) using Min mouse-derived IMCE
colon
epithelial cells.
Anchorage-independent transformed colonies were induced by retroviral infection only in IMCE cells, while no transformation was found in young adult mouse
colon
(YAMC) cells that are normal for
Apc
.
These data suggest the importance of cytoskeletal function in
Apc
-related tumor development and the usefulness of RIM in non-hematopoietic tissues, providing new insight into the early stage of
colon
carcinogenesis.
[MeSH-major]
Cell Transformation, Neoplastic / genetics.
Colon
/ pathology. Genes,
APC
. Mutagenesis, Insertional. Mutation. Retroviridae / genetics
[MeSH-minor]
Animals. Cell Line. Dyneins / genetics. Epithelial Cells / pathology. Membrane
Proteins
/ genetics. Mice. Microtubules / metabolism. Neoplasm
Proteins
/ genetics. Up-Regulation
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(PMID = 18294281.001).
[ISSN]
1349-7006
[Journal-full-title]
Cancer science
[ISO-abbreviation]
Cancer Sci.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Ahnak protein, mouse; 0 / Membrane Proteins; 0 / Neoplasm Proteins; EC 3.6.4.2 / Dnah3 protein, mouse; EC 3.6.4.2 / Dyneins
12.
Tighe A, Ray-Sinha A, Staples OD, Taylor SS:
GSK-3 inhibitors induce chromosome instability.
BMC Cell Biol
; 2007 Aug 14;8:34
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While several lines of evidence suggest that mutations in
adenomatous polyposis coli
(
APC
) may promote chromosome instability, at least in
colon
cancer, the underlying mechanisms remain unclear.
Here, we turn our attention to GSK-3 -
a protein
kinase, which in concert with
APC
, targets beta-catenin for proteolysis - and ask whether GSK-3 is required for accurate chromosome segregation.
Analysis of synchronised HeLa cells shows that GSK-3 inhibitors
do not
prevent G1/S progression or cell division.
CONCLUSION: Thus,
not
only do our observations indicate a role for GSK-3 in accurate chromosome segregation, but they also raise the possibility that, if used as therapeutic agents, GSK-3 inhibitors may induce unwanted side effects by inducing chromosome instability.
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.
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.
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.
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[ISSN]
1471-2121
[Journal-full-title]
BMC cell biology
[ISO-abbreviation]
BMC Cell Biol.
[Language]
ENG
[Grant]
United Kingdom / Wellcome Trust / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Protein Kinase Inhibitors; 0 / beta Catenin; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
[Other-IDs]
NLM/ PMC1976608
13.
Gaspar C, Cardoso J, Franken P, Molenaar L, Morreau H, Möslein G, Sampson J, Boer JM, de Menezes RX, Fodde R:
Cross-species comparison of human and mouse intestinal polyps reveals conserved mechanisms in adenomatous polyposis coli (APC)-driven tumorigenesis.
Am J Pathol
; 2008 May;172(5):1363-80
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[Title]
Cross-species comparison of human and mouse
intestinal
polyps reveals conserved mechanisms in
adenomatous polyposis coli
(
APC
)-driven tumorigenesis.
The majority of sporadic colorectal cancers are triggered by mutations in the
adenomatous polyposis coli
(
APC
) tumor suppressor gene, leading to the constitutive
activation
of the Wnt/beta-catenin signaling pathway and formation of adenomas.
Despite this common genetic basis, colorectal cancers are very heterogeneous in their degree of differentiation, growth rate, and malignancy
potential
.
Here, we applied a cross-species comparison of expression profiles of
intestinal
polyps derived from
hereditary
colorectal cancer patients carrying
APC
germline mutations and from mice carrying a targeted inactivating mutation in the mouse homologue
Apc
.
This comparative approach resulted in the establishment of a conserved signature of 166 genes that were differentially expressed between adenomas and normal
intestinal
mucosa in both species.
Functional analyses of the conserved genes revealed a general increase in cell proliferation and the
activation
of the Wnt/beta-catenin signaling pathway.
Moreover, the conserved signature was able to resolve expression profiles from
hereditary
polyposis
patients carrying
APC
germline mutations from those with bi-allelic inactivation of
the MYH
gene, supporting the usefulness of such comparisons to discriminate among patients with distinct genetic defects.
[MeSH-major]
Adenomatous Polyposis Coli
/ metabolism.
Adenomatous Polyposis Coli
Protein
/ metabolism. Cell Transformation, Neoplastic / metabolism. Colorectal Neoplasms / pathology.
Intestinal
Polyps / metabolism
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.
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consumer health - Colorectal Cancer
.
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(subscription/membership/fee required).
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Mouse Genome Informatics (MGI)
.
SciCrunch.
ArrayExpress: Data: Microarray
.
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[ISSN]
1525-2191
[Journal-full-title]
The American journal of pathology
[ISO-abbreviation]
Am. J. Pathol.
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G0301154
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Adenomatous Polyposis Coli Protein
[Other-IDs]
NLM/ PMC2329845
14.
De Groot CO, Jelesarov I, Damberger FF, Bjelić S, Schärer MA, Bhavesh NS, Grigoriev I, Buey RM, Wüthrich K, Capitani G, Akhmanova A, Steinmetz MO:
Molecular insights into mammalian end-binding protein heterodimerization.
J Biol Chem
; 2010 Feb 19;285(8):5802-14
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[Title]
Molecular insights into mammalian end-binding
protein
heterodimerization.
Microtubule plus-end tracking
proteins
(+TIPs) are involved in many microtubule-based processes.
End binding (EB)
proteins
constitute a highly conserved family of +TIPs.
Here we used a combination of methods to investigate the dimerization properties of the three human EB
proteins
EB1, EB2, and EB3.
Based on Förster resonance energy transfer, we demonstrate that
the C
-terminal dimerization domains of EBs (EBc) can readily exchange their chains in solution.
We further document that EB1c and EB3c preferentially form heterodimers, whereas EB2c does
not
participate significantly in the formation of heterotypic complexes.
Fluorescence spectroscopy and nuclear magnetic resonance studies in the presence of the cytoskeleton-
associated protein
-glycine-rich domains of either CLIP-170 or p150(glued) or of a fragment derived from the
adenomatous polyposis coli
tumor suppressor
protein
show that chain exchange of EBc domains can be controlled by binding partners.
Extension of these studies of the EBc domains to full-length EBs demonstrate that heterodimer formation between EB1 and EB3, but
not
between EB2 and the other two EBs, occurs both in vitro and in cells as revealed by live cell imaging.
[MeSH-major]
Microtubule-
Associated Proteins
/ metabolism. Models, Molecular.
Protein
Multimerization / physiology
[MeSH-minor]
Animals. CHO Cells. Cell Line. Cricetinae. Cricetulus. Humans. Kinetics. Magnetic Resonance Spectroscopy. Neoplasm
Proteins
/ chemistry. Neoplasm
Proteins
/ genetics. Neoplasm
Proteins
/ metabolism.
Protein
Structure, Quaternary.
Protein
Structure, Tertiary. Recombinant
Proteins
/ chemistry. Recombinant
Proteins
/ genetics. Recombinant
Proteins
/ metabolism. Spectrometry, Fluorescence
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Nature. 2003 Apr 17;422(6933):753-8
[
12700769.001
]
(PMID = 20008324.001).
[ISSN]
1083-351X
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MAPRE1 protein, human; 0 / MAPRE3 protein, human; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Recombinant Proteins; 144198-36-7 / dynactin; 148349-95-5 / cytoplasmic linker protein 170
[Other-IDs]
NLM/ PMC2820806
15.
Sinicrope FA:
Targeting cyclooxygenase-2 for prevention and therapy of colorectal cancer.
Mol Carcinog
; 2006 Jun;45(6):447-54
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A causal link for COX-2 in epithelial tumorigenesis was shown in genetically manipulated
animal
models of
colon and
breast carcinoma.
COX enzymes are targets for cancer prevention as shown by the observation that nonselective COX and selective COX-2 inhibitors have been reported to effectively prevent experimental
colon
cancer and can regress colorectal polyps in patients with
familial
adenomatous polyposis
.
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.
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consumer health - Colorectal Cancer
.
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(PMID = 16688727.001).
[ISSN]
0899-1987
[Journal-full-title]
Molecular carcinogenesis
[ISO-abbreviation]
Mol. Carcinog.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Cyclooxygenase Inhibitors; 0 / Prostaglandins; EC 1.14.99.1 / Cyclooxygenase 2
[Number-of-references]
53
16.
Hendrix ND, Wu R, Kuick R, Schwartz DR, Fearon ER, Cho KR:
Fibroblast growth factor 9 has oncogenic activity and is a downstream target of Wnt signaling in ovarian endometrioid adenocarcinomas.
Cancer Res
; 2006 Feb 1;66(3):1354-62
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[Title]
Fibroblast
growth factor 9 has oncogenic activity and is a downstream target of Wnt signaling in ovarian endometrioid adenocarcinomas.
Roughly 40% of ovarian endometrioid adenocarcinomas (OEA) have constitutive
activation
of Wnt signaling as a result of oncogenic mutations in the beta-catenin
protein
or inactivating mutations in key negative regulators of beta-catenin, such as the
adenomatous polyposis coli
and Axin tumor suppressor
proteins
.
Using microarray and quantitative PCR-based approaches, we found that
fibroblast
growth factor (FGF9) expression was increased >6-fold in primary OEAs with Wnt/beta-catenin pathway defects compared with OEAs lacking such defects.
[MeSH-major]
Carcinoma, Endometrioid / genetics.
Fibroblast
Growth Factor 9 / genetics. Ovarian Neoplasms / genetics. Wnt1
Protein
/ metabolism
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consumer health - Ovarian Cancer
.
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(PMID = 16452189.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / PHS HHS / / NIH P30 46952; United States / NCI NIH HHS / CA / R01 CA 85463; United States / NCI NIH HHS / CA / R01 CA 94172; United States / NCI NIH HHS / CA / U19 CA 84953
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / FGF9 protein, human; 0 / Fibroblast Growth Factor 9; 0 / RNA, Messenger; 0 / Wnt1 Protein; 0 / beta Catenin
17.
Wu JQ, Kornbluth S:
Not-so-pseudo a substrate: Acm1-mediated inhibition of the APC.
Mol Cell
; 2008 Jun 6;30(5):543-4
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[Title]
Not
-so-pseudo a substrate: Acm1-mediated inhibition of
the APC
.
In a recent issue of Molecular Cell, Enquist-Newman et
al
. (2008) demonstrate that Acm1 is ubiquitinated by
APC
(Cdc20).
By contrast, the high-affinity interaction between Acm1
and APC
(Cdh1) renders it a poor substrate, but a specific inhibitor, of
the APC
(Cdh1) complex.
[MeSH-major]
Repressor
Proteins
/ metabolism. Saccharomyces cerevisiae / metabolism. Saccharomyces cerevisiae
Proteins
/ metabolism. Ubiquitin-
Protein
Ligase Complexes / antagonists & inhibitors. Ubiquitin-
Protein
Ligase Complexes / metabolism
[MeSH-minor]
Anaphase-Promoting Complex-Cyclosome. Cdc20
Proteins
. Cdh1
Proteins
. Cell Cycle
Proteins
/ metabolism. Mitosis. Substrate Specificity. Ubiquitination
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
Saccharomyces Genome Database.
Saccharomyces Genome Database
.
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[CommentOn]
Mol Cell. 2008 May 23;30(4):437-46
[
18498748.001
]
(PMID = 18538651.001).
[ISSN]
1097-4164
[Journal-full-title]
Molecular cell
[ISO-abbreviation]
Mol. Cell
[Language]
eng
[Publication-type]
Comment; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Acm1 protein, S cerevisiae; 0 / CDC20 protein, S cerevisiae; 0 / CDH1 protein, S cerevisiae; 0 / Cdc20 Proteins; 0 / Cdh1 Proteins; 0 / Cell Cycle Proteins; 0 / Repressor Proteins; 0 / Saccharomyces cerevisiae Proteins; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes
18.
Fouladkhah A, Avens JS:
Effects of combined heat and acetic acid on natural microflora reduction on cantaloupe melons.
J Food Prot
; 2010 May;73(5):981-4
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High level of nutrients and water activity, direct contact with soil, and lack of thermal
procedures
during primary processing make fresh produce
a potential
food safety hazard.
Aerobic plate counts (
APC
) of dilutions were determined.
Statistical analysis (least significant difference-based analysis of variance) showed that there were no significant (P > 0.05) differences in
APC
among control, water at 25 degrees C, and 5% acetic acid at 25 degrees C.
Thermal treatments with water at 95 degrees C, and 5% acetic acid at 95 degrees C, were both significantly (P < 0.05) more effective in
APC
reduction than were nonthermal treatments, but were
not
significantly different from each other.
Results indicated that a thermal water immersion intervention in primary processing of fresh melons can result in a 3-log reduction of natural microflora surface contamination, but 5% acetic acid will
not
significantly augment this reduction.
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.
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(PMID = 20501053.001).
[ISSN]
0362-028X
[Journal-full-title]
Journal of food protection
[ISO-abbreviation]
J. Food Prot.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Anti-Infective Agents, Local; Q40Q9N063P / Acetic Acid
19.
Hosseini BH, Louban I, Djandji D, Wabnitz GH, Deeg J, Bulbuc N, Samstag Y, Gunzer M, Spatz JP, Hämmerling GJ:
Immune synapse formation determines interaction forces between T cells and antigen-presenting cells measured by atomic force microscopy.
Proc Natl Acad Sci U S A
; 2009 Oct 20;106(42):17852-7
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This recognition results in the formation of a so-called immune synapse (IS) at the T-cell/
APC
interface, which is crucial for T-cell
activation
.
Dynamic analysis of T-cell/
APC
interaction by AFM revealed that in the presence of antigen interaction forces increased from 1 to 2 nN at early time-points to a maximum of approximately 14 nN after 30 min and decreased again after 60 min.
BIRT377 almost completely abolish the interaction forces, emphasizing the importance of LFA-1/ICAM-1-interactions for firm T-cell/
APC
adhesion.
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NCI CPTAC Assay Portal
.
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]
[ErratumIn]
Proc Natl Acad Sci U S A. 2010 Feb 2;107(5):2373
(PMID = 19822763.001).
[ISSN]
1091-6490
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
ENG
[Grant]
United States / NEI NIH HHS / EY / PN2 EY016586
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / BIRT 377; 0 / Imidazolidines; 0 / Lymphocyte Function-Associated Antigen-1; 0 / Peptide Fragments; 126547-89-5 / Intercellular Adhesion Molecule-1; EC 3.2.1.- / hen egg lysozyme; EC 3.2.1.17 / Muramidase
[Other-IDs]
NLM/ PMC2764924
20.
Lyons LC, Collado MS, Khabour O, Green CL, Eskin A:
The circadian clock modulates core steps in long-term memory formation in Aplysia.
J Neurosci
; 2006 Aug 23;26(34):8662-71
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We investigated whether the circadian clock modulated core molecular processes necessary for memory formation in vivo by analyzing circadian regulation of basal and LTS-induced levels of phosphorylated mitogen-activated
protein
kinase (P-MAPK) and Aplysia CCAAT/enhancer binding
protein
(
ApC
/EBP).
In contrast, the circadian clock regulated basal levels of
ApC
/EBP
protein
with peak levels at night, antiphase to the rhythm in LTS.
Importantly, LTS training during the (subjective) day produced greater increases in P-MAPK
and ApC
/EBP than training at night.
Thus, circadian modulation of LTS occurs, at least in part, by suppressing changes in key
proteins
at night.
Rescue of long-term memory formation at night required both facilitation of MAPK and transcription in conjunction with LTS training, confirming that the circadian clock at night actively suppresses MAPK
activation and
transcription involved in memory formation.
The circadian clock appears to modulate LTS at
multiple
levels.
Together, our studies suggest that the circadian clock modulates LTS at
multiple
steps and locations during the formation of long-term memory.
[MeSH-minor]
Animals. CCAAT-Enhancer-Binding
Proteins
/ metabolism. Electric Stimulation / methods. Enzyme
Activation
/ physiology. Ganglia, Invertebrate / enzymology. Hemolymph / metabolism. Mitogen-Activated
Protein
Kinases / metabolism. Phosphorylation. Serotonin / metabolism
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(PMID = 16928854.001).
[ISSN]
1529-2401
[Journal-full-title]
The Journal of neuroscience : the official journal of the Society for Neuroscience
[ISO-abbreviation]
J. Neurosci.
[Language]
eng
[Grant]
United States / NINDS NIH HHS / NS / NS050589
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / CCAAT-Enhancer-Binding Proteins; 333DO1RDJY / Serotonin; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
21.
Favory R, Lancel S, Maréchal X, Tissier S, Neviere R:
Cardiovascular protective role for activated protein C during endotoxemia in rats.
Intensive Care Med
; 2006 Jun;32(6):899-905
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[Title]
Cardiovascular protective role for activated
protein C
during endotoxemia in rats.
OBJECTIVE: We examined whether activated
protein C
(
APC
) treatment improves cardiovascular inflammation and dysfunction in endotoxemic rats.
INTERVENTIONS: Internal carotid
artery and
external jugular vein were catheterized under sterile conditions in rats.
Instrumented rats infused or
not
with
APC
(240 microg/kg per hour) were challenged with E.
coli
endotoxin (10 mg/kg).
MEASUREMENTS AND RESULTS: Endotoxin administration induced systemic hypotension, depression of myocardial systolic performance and reduction in capillary density of the small
intestine
muscularis layer.
Plasma levels of nitrite/nitrate, tumor necrosis factor alpha and macrophage migration inhibitory factor, mesentery venule leukocyte-endothelium interactions, heart and small
intestine
myeloperoxidase activities were increased in endotoxin-treated rats.
APC
largely prevented endotoxin-induced cardiovascular dysfunction with improved systemic hemodynamics, functional capillary density, and myocardial contractile performance.
Beneficial cardiovascular effects of
APC
were
associated
with attenuation of entotoxin-induced inflammatory response in terms of plasma levels of nitrite/nitrate, tumor necrosis factor alpha, macrophage migration inhibitory factor, and endothelial cell-leukocyte
activation
.
CONCLUSION:
APC
reduces systemic and tissue inflammation and preserves cardiovascular function during experimental endotoxemia.
[MeSH-major]
Cardiovascular System / drug effects. Endotoxemia.
Protein C
Inhibitor / pharmacology. Serine Proteinase Inhibitors / pharmacology
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12563316.001
]
[Cites]
Crit Care Med. 2003 Mar;31(3):834-40
[
12626993.001
]
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N Engl J Med. 2001 Mar 8;344(10 ):699-709
[
11236773.001
]
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Biochem Soc Trans. 2005 Apr;33(Pt 2):401-5
[
15787615.001
]
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Crit Care Med. 2005 Feb;33(2):368-72
[
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]
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J Am Coll Cardiol. 2004 Jun 16;43(12):2348-58
[
15193704.001
]
(PMID = 16601957.001).
[ISSN]
0342-4642
[Journal-full-title]
Intensive care medicine
[ISO-abbreviation]
Intensive Care Med
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Protein C Inhibitor; 0 / Serine Proteinase Inhibitors
22.
Kalchayanand N, Arthur TM, Bosilevac JM, Brichta-Harhay DM, Guerini MN, Shackelford SD, Wheeler TL, Koohmaraie M:
Microbiological characterization of lamb carcasses at commercial processing plants in the United States.
J Food Prot
; 2007 Aug;70(8):1811-9
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To address this missing information, a total of 2,548 sponge samples from pelts, preevisceration carcasses, and postintervention carcasses were collected from
multiple
large
commercial lamb processing plants to determine aerobic plate counts, the prevalences of Escherichia
coli
O157:H7, non-O157 Shiga toxin-producing E.
coli
(STEC), and Salmonella.
The prevalences of E.
coli
O157:H7 from the pelts, the preevisceration carcasses, and the postintervention carcasses were 12.8, 1.6, and 2.9%, respectively.
The average Salmonella prevalences were 14.4, 4.3,
and 1
.8% for pelts, preevisceration carcasses, and postintervention carcasses, respectively.
A small number of STEC serotypes
associated
with severe human illness were isolated from postintervention carcasses.
The results of this study establish a baseline for microbiological quality and prevalences of Salmonella, E.
coli
O157:H7, and STEC in U.S. lamb processing plants.
[MeSH-major]
Escherichia
coli
/ isolation & purification. Food Contamination / analysis. Food-Processing Industry / standards. Salmonella / isolation & purification. Sheep / microbiology
[MeSH-minor]
Abattoirs. Animals. Colony Count, Microbial. Consumer Product Safety. Escherichia
coli
O157 / isolation & purification. Food Microbiology. Humans. Meat / microbiology. Prevalence. Serotyping. United States
MedlinePlus Health Information.
consumer health - Foodborne Illness
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(PMID = 17803136.001).
[ISSN]
0362-028X
[Journal-full-title]
Journal of food protection
[ISO-abbreviation]
J. Food Prot.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
23.
Lefevre JH, Parc Y, Svrcek M, Kernéis S, Colas C, Shields C, Flejou JF, Parc R, Tiret E:
APC, MYH, and the correlation genotype-phenotype in colorectal polyposis.
Ann Surg Oncol
; 2009 Apr;16(4):871-7
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[Title]
APC
,
MYH
, and the correlation genotype-phenotype in colorectal
polyposis
.
BACKGROUND:
Familial
adenomatous polyposis
(
FAP
) has been divided into two entities: classical (CFAP) and attenuated (AFAP).
With the discovery of
MYH associated
polyposis
(
MAP
)
syndrome
, the clinical differences have become unclear.
The aim of our study was to investigate patients with
polyposis
treated in our institution for a correlation between genotype and phenotype.
Four groups were identified: AFAP, CFAP,
MAP
, and no-mutation patients.
RESULTS: Patient breakdown was CFAP patients (n = 322/294), AFAP patients (n = 13/41),
MYH
patients (n = 17) and no-mut patients (n = 32).
Patients
not
tested for
APC
mutation (n = 131) were excluded.
Major differences were found for
MYH
patients: later age at
diagnosis
, more cancers, fewer polyps, and more located in the right part of
the colon
.
For phenotype/genotype correlation, patients aged more than 35 years at the time of colectomy and with fewer than 100 polyps had significantly more mutation found on
MYH
.
CONCLUSIONS: This two-way analysis did
not
show any correlation that might help to identify a subgroup of patients with
APC
mutation that may be considered attenuated.
It is more likely that
the MAP syndrome
is the real AFAP.
[MeSH-major]
Adenomatous Polyposis Coli
/ genetics. DNA Glycosylases / genetics. Genes,
APC
[MeSH-minor]
Adolescent. Adult. Female. Genetic Predisposition to
Disease
. Genotype. Humans. Male. Middle Aged. Mutation. Phenotype.
Syndrome
. Young Adult
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(PMID = 19169759.001).
[ISSN]
1534-4681
[Journal-full-title]
Annals of surgical oncology
[ISO-abbreviation]
Ann. Surg. Oncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
24.
Cheah PY, Wong YH, Loi C, Koh PK, Eu KW:
Novel human pathological mutations. Gene symbol: APC. Disease: adenomatous polyposis coli.
Hum Genet
; 2009 Apr;125(3):352
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[Title]
Novel human pathological mutations. Gene symbol:
APC
.
Disease
:
adenomatous polyposis coli
.
[MeSH-major]
Adenomatous Polyposis Coli
/ genetics. Genes,
APC
. INDEL Mutation
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(PMID = 19320041.001).
[ISSN]
1432-1203
[Journal-full-title]
Human genetics
[ISO-abbreviation]
Hum. Genet.
[Language]
eng
[Databank-accession-numbers]
GENBANK/ HX080001
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Codon; 0 / Codon, Nonsense
25.
Holler E, Landfried K, Meier J, Hausmann M, Rogler G:
The role of bacteria and pattern recognition receptors in GVHD.
Int J Inflam
; 2010;2010:814326
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Graft-versus-Host
Disease
(GvHD) is the most serious complication of allogeneic stem cell transplantation (SCT) and results from an
activation
of donor lymphocytes by recipient antigen-presenting cells (APCs).
For a long time, it has been postulated that
the intestinal
microflora and endotoxin exert a crucial step in this
APC activation
, as there is early and severe gastrointestinal damage induced by pretransplant conditioning.
With the detailed description of pathogen-
associated
molecular patterns and pathogen recognition receptors single nucleotide polymorphisms of TLRs and especially NOD2 have been identified as
potential
risk factors of GvHD and transplant related complications thus further supporting the crucial role of innate immunity in SCT, related complications.
Gastrointestinal decontamination and neutralization of endotoxin have been used to interfere with this early axis of
activation
with some success but more specific approaches of modulation of innate immunity are needed for further improvement of clinical outcome.
ClinicalTrials.gov.
clinical trials - ClinicalTrials.gov
.
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(PMID = 21188220.001).
[ISSN]
2042-0099
[Journal-full-title]
International journal of inflammation
[ISO-abbreviation]
Int J Inflam
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC3003997
26.
Marrocco K, Bergdoll M, Achard P, Criqui MC, Genschik P:
Selective proteolysis sets the tempo of the cell cycle.
Curr Opin Plant Biol
; 2010 Dec;13(6):631-9
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This is achieved by
the action
of ubiquitin ligases (E3s), which remove both negative and positive regulators of the cell cycle.
Though our current understanding of the plant cell cycle has improved a lot these recent years, the identity of the E3s regulating it and their mode of
action
is still in its infancy.
Thus the anaphase promoting complex/cyclosome (
APC
/C)
not
only controls mitotic events, but is also important in post-mitotic cells for normal plant development and cell differentiation.
[MeSH-minor]
Anaphase-Promoting Complex-Cyclosome. Models, Biological. Plant Growth Regulators / metabolism. Ubiquitin-
Protein
Ligase Complexes / genetics. Ubiquitin-
Protein
Ligase Complexes / metabolism. Ubiquitin-
Protein
Ligases / genetics. Ubiquitin-
Protein
Ligases / metabolism
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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[Copyright]
Copyright © 2010 Elsevier Ltd. All rights reserved.
(PMID = 20810305.001).
[ISSN]
1879-0356
[Journal-full-title]
Current opinion in plant biology
[ISO-abbreviation]
Curr. Opin. Plant Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Plant Growth Regulators; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes; EC 6.3.2.19 / Ubiquitin-Protein Ligases
27.
Yoshida K:
Cell-cycle-dependent regulation of the human and mouse Tome-1 promoters.
FEBS Lett
; 2005 Feb 28;579(6):1488-92
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In turn, Tome-1 itself is targeted for degradation by
APC
in the G1 phase of the cell cycle.
[MeSH-major]
Cell Cycle / genetics. Cell Cycle
Proteins
/ genetics. Promoter Regions, Genetic / genetics
[MeSH-minor]
5' Flanking Region / genetics. Animals. Base Sequence. Cell Division. Down-Regulation / genetics. G2 Phase. Humans. Mice. Molecular Sequence Data. Mutation / genetics. NIH 3T3 Cells. Sequence Alignment. Transcriptional
Activation
/ genetics
The Lens.
Cited by Patents in
.
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(PMID = 15733861.001).
[ISSN]
0014-5793
[Journal-full-title]
FEBS letters
[ISO-abbreviation]
FEBS Lett.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / CDCA3 protein, human; 0 / Cell Cycle Proteins; 0 / Tome-1 protein, mouse
28.
Chambers WM, McC Mortensen NJ:
Should ileal pouch-anal anastomosis include mucosectomy?
Colorectal Dis
; 2007 Jun;9(5):384-92
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OBJECTIVE: Debate exists as to the benefits of performing mucosectomy as part of pouch surgery for ulcerative colitis (UC)
and familial
adenomatous polyposis
(
FAP
).
Potential
reasons for functional problems were investigated, as were rates of 'cuffitis', dysplasia,
polyposis
and cancer in the ileal pouch and anal canal.
Meta-analysis suggested that nighttime seepage of stool and resting and squeeze
pressure
were worse after mucosectomy.
Mucosectomy does seem to confer benefit in terms of
disease
control but this benefit does
not
reach statistical significance.
Performing mucosectomy results in some clinical benefits in terms of lower rates of inflammation and dysplasia in the retained mucosa in UC patients and lower rates of cuff
polyposis
in
FAP
patients.
However, on the basis of available evidence mucosectomy is only indicated in those cases where the patient is at a high risk of
disease
in the retained rectal cuff.
[MeSH-major]
Colonic Pouches / adverse effects.
Intestinal
Mucosa / surgery. Proctocolectomy, Restorative / adverse effects
[MeSH-minor]
Adenocarcinoma / prevention & control.
Adenomatous Polyposis Coli
/ surgery. Anastomosis, Surgical / adverse effects. Anastomosis, Surgical / methods. Anus Neoplasms / prevention & control. Arsenates. Colitis, Ulcerative / surgery. Humans. Ileal Neoplasms / prevention & control. Randomized Controlled Trials as Topic
Hazardous Substances Data Bank.
ARSENIC ACID
.
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(PMID = 17504334.001).
[ISSN]
1462-8910
[Journal-full-title]
Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland
[ISO-abbreviation]
Colorectal Dis
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Arsenates; N7CIZ75ZPN / arsenic acid
[Number-of-references]
70
29.
Mozaffarian N, Wiedeman AE, Stevens AM:
Active systemic lupus erythematosus is associated with failure of antigen-presenting cells to express programmed death ligand-1.
Rheumatology (Oxford)
; 2008 Sep;47(9):1335-41
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[Title]
Active systemic lupus erythematosus is
associated
with failure of antigen-presenting cells to express programmed death ligand-1.
OBJECTIVE: Antigen-presenting cells (
APC
) play critical roles in establishing and maintaining peripheral tolerance.
This is accomplished in part via expression of negative co-stimulatory molecules such as programmed death ligand-1 (PD-L1) on tolerogenic
APC
, such as immature myeloid dendritic cells (mDC).
Several studies have strongly linked dysfunction of
APC
, including mDC, to the pathogenesis of SLE.
The objective of this study was to determine whether
APC
expressed PD-L1
protein
at normal levels during active lupus.
In contrast, both mDC and Mo from patients with active SLE failed to up-regulate PD-L1 over a 5 day time course, expressing this
protein
only during
disease
remissions.
CONCLUSIONS: These data are the first to link active lupus with reversibly decreased PD-L1 expression on professional
APC
, suggesting a novel mechanism for loss of peripheral tolerance in SLE.
Genetic Alliance.
consumer health - Lupus
.
Genetic Alliance.
consumer health - Systemic lupus erythematosus
.
MedlinePlus Health Information.
consumer health - Lupus
.
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(PMID = 18650228.001).
[ISSN]
1462-0332
[Journal-full-title]
Rheumatology (Oxford, England)
[ISO-abbreviation]
Rheumatology (Oxford)
[Language]
ENG
[Grant]
United States / NCRR NIH HHS / RR / M01 RR000037; United States / NIAMS NIH HHS / AR / T32 AR007108; United States / NCRR NIH HHS / RR / M01-RR-00037
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD274; 0 / CD274 protein, human
[Other-IDs]
NLM/ PMC2722808
30.
Alferez DG, Ryan AJ, Goodlad RA, Wright NA, Wilkinson RW:
Effects of vandetanib on adenoma formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model.
Int J Oncol
; 2010 Oct;37(4):767-72
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[Title]
Effects of vandetanib on
adenoma
formation in a dextran sodium sulphate enhanced
Apc
(MIN/+) mouse model.
The Apc
(MIN/+) mouse is a well-characterised model of
intestinal
tumourigenesis in which animals develop macroscopically detectable adenomas.
However, most of the adenomas are formed in the small
intestine
and resolution of events in
the colon
, the most relevant site for human
disease
, is limited.
Inducing colitis with dextran sodium sulphate (DSS) can selectively enhance the development of lesions in
the colon
.
We demonstrated that a DSS pre-treatment is well tolerated and effective at inducing
colon
adenomas in an
Apc
(MIN/+) mouse model.
We then investigated the effect of inhibiting vascular endothelial growth factor (VEGFR)- and epidermal growth factor receptor (EGFR)-dependent signalling pathways on the development of adenomas induced in DSS-pretreated (DSS/
Apc
(MIN/+)) or non-DSS-pretreated (
Apc
(MIN/+)) mice using vandetanib (ZD6474), a potent and selective inhibitor of VEGFR and EGFR tyrosine kinase activity.
Eight-week old
Apc
(MIN/+) mice were given either drinking water or 1.8% DSS and then vandetanib (ZD6474) (50 mg/kg/day) or vehicle by oral gavage for 28 days and sacrificed 24 h after the last dose and assessed for
adenoma
formation in the intestines.
DSS pre-treatment was well tolerated and significantly enhanced formation of adenomas in
the colon
of control
Apc
(MIN/+) mice.
Vandetanib treatment significantly reduced
adenoma
formation in the small
intestine
by 68% (P=0.001) and the
colon
by 77% (from 13.8 to 3.1, P=0.01) of DSS-pretreated
Apc
(MIN/+) mice.
In
the Apc
(MIN/+) group, vandetanib also reduced the mean number of adenomas in the small
intestine
by 76% (P<0.001) and in
the colon
by 60% (from 3.9 to 1.5, P=0.1).
DSS-pre-treatment increased the resolution of the model, allowing us to confirm statistically significant effects of vandetanib on the development and growth of
colon
adenomas in
the Apc
(MIN/+) mouse.
Moreover these preclinical data provide a rationale for studying the effects of vandetanib in early stages of
intestinal
cancer in the clinic.
[MeSH-major]
Adenoma
/ prevention & control. Antineoplastic Agents / pharmacology. Colitis / chemically induced. Colonic Neoplasms / prevention & control. Dextran Sulfate. Genes,
APC
. Piperidines / pharmacology.
Protein
Kinase Inhibitors / pharmacology. Quinazolines / pharmacology
[MeSH-minor]
Animals.
Disease
Models,
Animal
.
Intestine
, Small / drug effects.
Intestine
, Small / enzymology.
Intestine
, Small / pathology. Mice. Mice, Inbred C57BL. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors. Vascular Endothelial Growth Factor Receptor-2 / metabolism. beta Catenin / metabolism
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.
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(PMID = 20811697.001).
[ISSN]
1791-2423
[Journal-full-title]
International journal of oncology
[ISO-abbreviation]
Int. J. Oncol.
[Language]
eng
[Grant]
United Kingdom / Cancer Research UK / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / CTNNB1 protein, mouse; 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Piperidines; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / beta Catenin; 9042-14-2 / Dextran Sulfate; EC 2.7.10.1 / EGFR protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
31.
Voutsadakis IA:
Pathogenesis of colorectal carcinoma and therapeutic implications: the roles of the ubiquitin-proteasome system and Cox-2.
J Cell Mol Med
; 2007 Mar-Apr;11(2):252-85
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Pathways of the molecular pathogenesis of colorectal carcinoma have been extensively studied and molecular lesions during the development of
the disease
have been revealed.
High up in the list of colorectal cancer lesions are
APC
(
adenomatous polyposis coli
), K-ras, Smad4 (or DPC4-deleted in pancreatic cancer 4) and p53 genes.
The ubiquitin-proteasome system (UPS) is comprised of a multi-unit cellular protease system that regulates several dozens of cell
proteins
after their ligation with
the protein
ubiquitin.
Given that among these
proteins
are regulators of the cell cycle, apoptosis, angiogenesis, adhesion and cell signalling, this system plays a significant role in cell fate and carcinogenesis.
UPS inhibition has been found to be a pre-requisite for apoptosis and is already clinically exploited with the proteasome inhibitor bortezomib in
multiple
myeloma.
Inhibition of Cox-2 by
aspirin and
other non-steroidal anti-inflammatory drugs (NSAIDs) has been found to inhibit proliferation of colorectal cancer cells and in epidemiologic studies has been shown to reduce
colon polyp
formation in genetically predisposed populations and in the general population.
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(PMID = 17488476.001).
[ISSN]
1582-1838
[Journal-full-title]
Journal of cellular and molecular medicine
[ISO-abbreviation]
J. Cell. Mol. Med.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Romania
[Chemical-registry-number]
0 / Cyclooxygenase Inhibitors; 0 / Ubiquitin; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.4.25.1 / Proteasome Endopeptidase Complex
[Number-of-references]
298
[Other-IDs]
NLM/ PMC3822826
32.
Heng W, Huang JA, Shen WH, Dai L, Bai X, Wang ZY:
[Expression of endothelial protein C receptor in tumor cell lines and It's significance].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
; 2010 Aug;26(8):761-3
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[Title]
[Expression of endothelial
protein C
receptor in tumor cell lines and It's significance].
AIM: To detect the role of activated
protein C
(
APC
) on proliferation of endothelial cell and investigate the expression of endothelial
protein C
receptor( EPCR) in variety of tumor cell lines.
METHODS: The effect of
APC
on endotheliocyte proliferation was determined by MTT colorimetry.
RESULTS:
APC
can increase the proliferation of EC significantly.
CONCLUSION:
APC
can stimulate the proliferation of endothelial cell.
High expression of EPCR in tumor cell lines provides
a potential
biological marker for malignancies.
[MeSH-minor]
Cell Line, Tumor. Cell Proliferation. Humans. Interleukin-6 / metabolism. Interleukin-8 / metabolism.
Protein C
/ metabolism
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(PMID = 20619102.001).
[ISSN]
1007-8738
[Journal-full-title]
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology
[ISO-abbreviation]
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Antigens, CD; 0 / Interleukin-6; 0 / Interleukin-8; 0 / PROCR protein, human; 0 / Protein C; 0 / Receptors, Cell Surface
33.
Kryczek I, Wei S, Gong W, Shu X, Szeliga W, Vatan L, Chen L, Wang G, Zou W:
Cutting edge: IFN-gamma enables APC to promote memory Th17 and abate Th1 cell development.
J Immunol
; 2008 Nov 1;181(9):5842-6
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[Title]
Cutting edge: IFN-gamma enables
APC
to promote memory Th17 and abate Th1 cell development.
However, Th1, Th17, and memory but
not
naive T cells are colocalized in an inflammatory environment.
We show that IFN-gamma stimulates B7-H1 expression on
APC
subsets and abates their Th1 polarization capacity in a B7-H1-dependent manner.
Interestingly, IFN-gamma triggers APCs to produce IL-
1 and
IL-23 and enables them to induce memory Th17 expansion via IL-
1 and
IL-23 in a B7-H1-independent manner.
We propose a novel dynamic between Th1 and Th17 in the course of inflammation as follows: Th1-mediated inflammation is attenuated by IFN-gamma-induced B7-H1 on APCs and is evolved toward Th17-mediated chronic inflammation by IFN-gamma-induced,
APC
-derived IL-
1 and
IL-23.
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(PMID = 18941172.001).
[ISSN]
1550-6606
[Journal-full-title]
Journal of immunology (Baltimore, Md. : 1950)
[ISO-abbreviation]
J. Immunol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA099985; United States / NCI NIH HHS / CA / CA123088
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD274; 0 / CD274 protein, human; 0 / Growth Inhibitors; 0 / Interleukin-1; 0 / Interleukin-17; 0 / Interleukin-23; 82115-62-6 / Interferon-gamma
34.
Samuel MS, Suzuki H, Buchert M, Putoczki TL, Tebbutt NC, Lundgren-May T, Christou A, Inglese M, Toyota M, Heath JK, Ward RL, Waring PM, Ernst M:
Elevated Dnmt3a activity promotes polyposis in Apc(Min) mice by relaxing extracellular restraints on Wnt signaling.
Gastroenterology
; 2009 Sep;137(3):902-13, 913.e1-11
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[Title]
Elevated Dnmt3a activity promotes
polyposis
in
Apc
(Min) mice by relaxing extracellular restraints on Wnt signaling.
Here we use knock-in transgenic mice to investigate the consequences of
intestinal
epithelium-specific overexpression of
de
novo Dnmt3a.
METHODS: A novel gene targeting strategy, based on
the intestinal
epithelium-specific, uniform expression of the A33 glycoprotein, is employed to restrict Dnmt3a overexpression in homozygous A33(Dnmt3a) mutant mice.
RESULTS: A33(Dnmt3a) mice infrequently develop spontaneous
intestinal
polyps.
However, when genetically challenged, tumor multiplicity in A33(Dnmt3a);
Apc
(Min) compound mice is 3-fold higher than in
Apc
(Min) mice.
Although we observe a requirement for spontaneous loss of heterozygosity of the
adenomatous polyposis coli
(
Apc
) gene to trigger tumorigenesis in
Apc
(Min) mice, lesions in A33(Dnmt3a);
Apc
(Min) mice frequently retain the wild-
type Apc
allele.
However, epithelia from normal mucosa and polyps of A33(Dnmt3a);
Apc
(Min) mice show hypermethylation-mediated transcriptional silencing of the Wnt antagonists Sfrp5, and to a lesser extent, Sfrp1 and increased nuclear beta-catenin alongside
activation
of the Wnt-target gene Axin2/Conductin.
Conversely, enforced Sfrp5 expression suppresses canonical Wnt-signaling more effectively in wild-
type
than in
Apc
(Min) cells.
CONCLUSIONS: Aberrant
activation
of the canonical Wnt pathway, either by mono-allelic
Apc
loss or transcriptional silencing of Sfrp5 is largely insufficient to promote
polyposis
, but epistatic interactions between these genetic and epigenetic events enables initiation and promotion of
disease
.
[MeSH-major]
Adenomatous Polyposis Coli
/ metabolism. DNA (Cytosine-5-)-Methyltransferase / metabolism. Genes,
APC
.
Intestinal
Mucosa / metabolism. Signal Transduction. Wnt
Proteins
/ metabolism
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(PMID = 19454286.001).
[ISSN]
1528-0012
[Journal-full-title]
Gastroenterology
[ISO-abbreviation]
Gastroenterology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Gpa33 protein, mouse; 0 / Membrane Glycoproteins; 0 / Wnt Proteins; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA methyltransferase 3A
35.
Walker A, Acquaviva C, Matsusaka T, Koop L, Pines J:
UbcH10 has a rate-limiting role in G1 phase but might not act in the spindle checkpoint or as part of an autonomous oscillator.
J Cell Sci
; 2008 Jul 15;121(Pt 14):2319-26
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[Title]
UbcH10 has a rate-limiting role in G1 phase but might
not
act in the spindle checkpoint or as part of an autonomous oscillator.
Ubiquitin-dependent proteolysis mediated by the anaphase-promoting complex/cyclosome (
APC
/C) ubiquitin ligase lies at the heart of the cell cycle.
The APC
/C targets mitotic cyclins for destruction in mitosis and G1 phase and is then inactivated at S phase, thereby generating the alternating states of high and low cyclin-Cdk activity required for the alternation of mitosis and DNA replication.
Two key questions are how
the APC
/C is held in check by the spindle-assembly checkpoint to delay cells in mitosis in the presence of improperly attached chromosomes, and how
the APC
/C is inactivated once cells exit mitosis.
The ubiquitin-conjugating
protein
UbcH10 has been proposed to be crucial in the answers to both questions.
However, here we show that the behaviour of UbcH10 is inconsistent with both a crucial role in the spindle checkpoint and in inactivating
the APC
/C as part of an autonomous oscillator.
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(PMID = 18559889.001).
[ISSN]
0021-9533
[Journal-full-title]
Journal of cell science
[ISO-abbreviation]
J. Cell. Sci.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Cyclin A; EC 6.3.2.19 / UBE2C protein, human; EC 6.3.2.19 / Ubiquitin-Conjugating Enzymes
36.
Tojo K, Sekijima Y, Kelly JW, Ikeda S:
Diflunisal stabilizes familial amyloid polyneuropathy-associated transthyretin variant tetramers in serum against dissociation required for amyloidogenesis.
Neurosci Res
; 2006 Dec;56(4):441-9
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[Title]
Diflunisal stabilizes
familial
amyloid
polyneuropathy
-
associated
transthyretin variant tetramers in serum against dissociation required for amyloidogenesis.
Transthyretin (TTR) tetramer dissociation, misfolding and misassembly are required for the process of amyloid fibril formation
associated
with
familial
amyloid
polyneuropathy
(
FAP
).
Here, we investigated the feasibility of using these molecules for the treatment of
FAP
utilizing serum samples from 37
FAP
patients with 10 different mutations.
We demonstrated that the TTR heterotetramer structures in
FAP
patients serum are significantly less stable than that in normal subjects, indicating the instability of the variant TTR structure is a fundamental cause of TTR amyloidosis.
Trivalent chromium at levels obtained by oral supplementation did
not
stabilize TTR in a statistically significant fashion.
Importantly, diflunisal increased serum TTR stability in
FAP
patients beyond the level of normal controls.
[MeSH-major]
Amyloid Neuropathies,
Familial
/ metabolism. Amyloid beta-Peptides / biosynthesis. Amyloid beta-Peptides / genetics. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Diflunisal / pharmacology. Prealbumin / biosynthesis. Prealbumin / genetics
[MeSH-minor]
Adult. Aged. Chromium / pharmacology. Female. Flufenamic Acid / pharmacology. Humans. Hydrogen-Ion Concentration. Iron / physiology. Male. Middle Aged. Mutation / physiology.
Protein
Denaturation
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(PMID = 17028027.001).
[ISSN]
0168-0102
[Journal-full-title]
Neuroscience research
[ISO-abbreviation]
Neurosci. Res.
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / DK046335
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
Ireland
[Chemical-registry-number]
0 / Amyloid beta-Peptides; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Prealbumin; 0R0008Q3JB / Chromium; 60GCX7Y6BH / Flufenamic Acid; 7C546U4DEN / Diflunisal; E1UOL152H7 / Iron
37.
Langelaar MF, Hope JC, Rutten VP, Noordhuizen JP, van Eden W, Koets AP:
Mycobacterium avium ssp. paratuberculosis recombinant heat shock protein 70 interaction with different bovine antigen-presenting cells.
Scand J Immunol
; 2005 Mar;61(3):242-50
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[Title]
Mycobacterium avium ssp. paratuberculosis recombinant heat shock
protein
70 interaction with different bovine antigen-presenting cells.
Abstract Heat shock
proteins
(Hsp) can deliver antigen into the major histocompatibility complex class I presentation pathway of antigen-presenting cells (
APC
), a process called cross priming, thus stimulating antigen-specific CD8+ T-cell reactions.
Hsp were shown to elicit proinflammatory responses in
APC
.
Both processes require interaction of Hsp with
APC
via specific receptors.
Characterized monocyte-derived macrophages, monocyte-derived dendritic cells (DC) and BoMac, an immortalized bovine macrophage cell line, were used to investigate the interaction of rHsp70 with different bovine
APC
.
Involvement of CD91 as a cellular receptor for rHsp70 was demonstrated; however, competition studies with immature DC demonstrated that other receptors exist on bovine
APC
.
[MeSH-major]
Antigen-Presenting Cells / immunology. Bacterial
Proteins
/ immunology. HSP70 Heat-Shock
Proteins
/ immunology. Mycobacterium avium subsp. paratuberculosis / immunology
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(PMID = 15787741.001).
[ISSN]
0300-9475
[Journal-full-title]
Scandinavian journal of immunology
[ISO-abbreviation]
Scand. J. Immunol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD14; 0 / Bacterial Proteins; 0 / Bacterial Vaccines; 0 / HSP70 Heat-Shock Proteins; 0 / alpha-Macroglobulins
38.
Yamashita T, Ando Y, Ueda M, Okamoto S, Misumi Y, Nakamura M, Takashi O, Uchino M:
A rapid and sensitive prenatal diagnosis of familial amyloidotic polyneuropathy ATTR Val30Met by mass spectrometry.
Prenat Diagn
; 2009 Oct;29(10):930-3
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[Title]
A rapid and sensitive prenatal
diagnosis
of
familial amyloidotic polyneuropathy
ATTR Val30Met by mass spectrometry.
OBJECTIVE: To make a prenatal
diagnosis
of
familial amyloidotic polyneuropathy
(
FAP
) by mass spectrometry with the amniotic fluid.
METHODS: Amniotic-fluid samples of three non-
FAP
pregnant women and six amniotic-fluid samples of fetal mice whose mother was a heterozygotic
FAP
amyloidgenic transthyretin (ATTR) Val30Met gene carrier were collected.
CONCLUSION: Mass spectrometry analysis of the amniotic fluid might be a useful tool to make a prenatal
diagnosis
of
FAP
ATTR Val30Met.
[MeSH-major]
Amyloid Neuropathies,
Familial
/
diagnosis
. Mass Spectrometry / methods. Prealbumin / analysis. Prenatal
Diagnosis
/ methods
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(PMID = 19609897.001).
[ISSN]
1097-0223
[Journal-full-title]
Prenatal diagnosis
[ISO-abbreviation]
Prenat. Diagn.
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antibodies; 0 / Prealbumin; AE28F7PNPL / Methionine; HG18B9YRS7 / Valine
39.
Dalby M, Kharbanda R, Ghimire G, Spiro J, Moore P, Roughton M, Lane R, Al-Obaidi M, Teoh M, Hutchison E, Whitbread M, Fountain D, Grocott-Mason R, Mitchell A, Mason M, Ilsley C:
Achieving routine sub 30 minute door-to-balloon times in a high volume 24/7 primary angioplasty center with autonomous ambulance diagnosis and immediate catheter laboratory access.
Am Heart J
; 2009 Nov;158(5):829-35
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[Title]
Achieving routine sub 30 minute door-to-balloon times in a high volume 24/7 primary angioplasty center with autonomous ambulance
diagnosis and
immediate catheter laboratory access.
Using autonomous ambulance
diagnosis
with open access to the myocardial infarction center catheter laboratory, we compared reperfusion times and clinical outcomes for the final 2 years of TL with the first 3 years of PPCI.
RESULTS: Comparison was made between TL (2002-2004, n = 185) and PPCI (2004-2007, n = 704); all times are medians in minutes (interquartile range): for TL, symptom to needle 153 (85-225), call to needle 58 (49-73), first professional contact (
FPC
) to needle 47 (39-63), door to needle 18 (12-30) (mortality: 7.6% at 30 days, 9.2% at 1 year); for interhospital transfer PPCI (n = 227), symptom to balloon 226 (175-350), call to balloon 135 (117-188),
FPC
to balloon 121 (102-166), first door-to-balloon 100 (80-142) (mortality: 7.0% at 30 days, 12.3% at 1 year); for direct-access PPCI (n = 477), symptom to balloon 142 (101-238), call to balloon 79 (70-93),
FPC
to balloon 69 (59-82), door to balloon 20 (16-29) (mortality: 4.6% at 30 days, 8.6% at 1 year).
With autonomous ambulance
diagnosis and
open access direct to the catheter laboratory, a median door-to-balloon time of <30 minutes day and night was achieved, and >95% of patients were reperfused within 1 hour.
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[ErratumIn]
Am Heart J. 2010 Feb;159(2):330
(PMID = 19853705.001).
[ISSN]
1097-6744
[Journal-full-title]
American heart journal
[ISO-abbreviation]
Am. Heart J.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Fibrinolytic Agents
40.
Wen K, Azevedo MS, Gonzalez A, Zhang W, Saif LJ, Li G, Yousef A, Yuan L:
Toll-like receptor and innate cytokine responses induced by lactobacilli colonization and human rotavirus infection in gnotobiotic pigs.
Vet Immunol Immunopathol
; 2009 Feb 15;127(3-4):304-15
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We demonstrated that LAB induced strong TLR2-expressing
APC
responses in blood and spleen, HRV induced a TLR3 response in spleen, and TLR9 responses were induced by either HRV (in spleen) or LAB (in blood).
LAB and HRV have an additive effect on TLR2- and TLR9-expressing
APC
responses, consistent with the adjuvant effect of LAB.
LAB enhanced the IFN-gamma and IL-4 responses in serum, but it had a suppressive effect on the TLR3- and TLR9-expressing CD14-
APC
responses in spleen and the serum IFN-alpha response induced by HRV.
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Vaccine. 2008 Jul 4;26(29-30):3655-61
[
18524434.001
]
(PMID = 19054578.001).
[ISSN]
0165-2427
[Journal-full-title]
Veterinary immunology and immunopathology
[ISO-abbreviation]
Vet. Immunol. Immunopathol.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / R01 AI033561-11; United States / NIAID NIH HHS / AI / R01 AI033561; United States / NCCIH NIH HHS / AT / R21 AT002524-02; United States / NCCIH NIH HHS / AT / R21 AT002524; United States / NIAID NIH HHS / AI / AI033561-11; United States / NCCIH NIH HHS / AT / 1R21AT002524; United States / NIAID NIH HHS / AI / R01AI033561
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Cytokines; 0 / Toll-Like Receptors
[Other-IDs]
NLM/ NIHMS89734; NLM/ PMC2653198
41.
Zurbuchen U, Kroesen AJ, Buhr HJ:
[Continent ileoanal reservoir--a surgical challenge].
Urologe A
; 2008 Jan;47(1):18-24
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Nowadays, patients with ulcerative colitis or
familial
adenomatous polyposis
of
the colon
undergo proctocolectomy as the definitive treatment for their underlying
disease
.
This contribution describes the surgical indications and pathophysiological changes for
the colon
J-pouch and ileoanal reservoir.
In addition, explanations of the surgical techniques for both
procedures
are presented.
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(PMID = 18210064.001).
[ISSN]
1433-0563
[Journal-full-title]
Der Urologe. Ausg. A
[ISO-abbreviation]
Urologe A
[Language]
ger
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Germany
[Number-of-references]
40
42.
Bobe G, Wang B, Seeram NP, Nair MG, Bourquin LD:
Dietary anthocyanin-rich tart cherry extract inhibits intestinal tumorigenesis in APC(Min) mice fed suboptimal levels of sulindac.
J Agric Food Chem
; 2006 Dec 13;54(25):9322-8
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[Title]
Dietary anthocyanin-rich tart cherry extract inhibits
intestinal
tumorigenesis in
APC
(Min) mice fed suboptimal levels of sulindac.
A promising approach for cancer chemoprevention might be a combination therapy utilizing dietary phytochemicals and anticarcinogenic pharmaceuticals at a suboptimal dosage to minimize any
potential
adverse side effects.
Mice that were fed anthocyanin-rich extract (at any dose) in combination with sulindac had fewer tumors
and a
smaller total tumor burden (total tumor area per mouse) in the small
intestine
when compared to mice fed sulindac alone.
These results suggest that a dietary combination of tart cherry anthocyanins and sulindac is more protective against
colon
cancer than sulindac alone.
[MeSH-major]
Anthocyanins / administration & dosage. Antineoplastic Agents / administration & dosage. Fruit / chemistry.
Intestinal
Neoplasms / prevention & control. Prunus / chemistry. Sulindac / administration & dosage
[MeSH-minor]
Adenomatous Polyposis Coli
/ genetics. Animals. Diet. Female. Male. Mice. Mice, Inbred C57BL. Mice, Mutant Strains. Mutation. Plant Extracts / administration & dosage. Plant Extracts / chemistry
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(PMID = 17147414.001).
[ISSN]
0021-8561
[Journal-full-title]
Journal of agricultural and food chemistry
[ISO-abbreviation]
J. Agric. Food Chem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Anthocyanins; 0 / Antineoplastic Agents; 0 / Plant Extracts; 184SNS8VUH / Sulindac
43.
Terazaki H, Ando Y, Fernandes R, Yamamura K, Maeda S, Saraiva MJ:
Immunization in familial amyloidotic polyneuropathy: counteracting deposition by immunization with a Y78F TTR mutant.
Lab Invest
; 2006 Jan;86(1):23-31
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[Title]
Immunization in
familial amyloidotic polyneuropathy
: counteracting deposition by immunization with a Y78F TTR mutant.
The mechanism of amyloid formation in
familial amyloidotic polyneuropathy
(
FAP
),
a hereditary disorder associated
with mutant transthyretin (TTR), is still unknown.
To test whether TTR deposition in
FAP
can be counteracted by antibodies for cryptic epitopes, we immunized with TTR Y78F, transgenic mice carrying the most common
FAP
-
associated
TTR mutant--V30M (transthyretin mutant with methionine replacing valine at position 30)--at selected ages that present normally with either nonfibrillar or TTR amyloid deposition.
Compared to age-matched control nonimmunized mice, Y78F-immunized mice had a significant reduction in TTR deposition usually found in this strain, in particular in stomach and
intestine
; by contrast, animals immunized with V30M did
not
show differences in deposition in comparison with nonimmunized mice.
Immunohistochemical analyses of tissues revealed that immunization with Y78F lead to infiltration by lymphocytes and macrophages at common deposition sites, but
not
in tissues such as liver, choroid plexus, and Langerhans islets, in which TTR is produced.
Therefore, TTR immunization with selected TTR mutants has
potential
application in immune therapy for
FAP
.
[MeSH-major]
Amyloid Neuropathies,
Familial
/ prevention & control. Mutation. Prealbumin / administration & dosage
NCI CPTAC Assay Portal.
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(PMID = 16357867.001).
[ISSN]
0023-6837
[Journal-full-title]
Laboratory investigation; a journal of technical methods and pathology
[ISO-abbreviation]
Lab. Invest.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Prealbumin
44.
Dietrich KA, Schwarz R, Liska M, Grass S, Menke A, Meister M, Kierschke G, Längle C, Genze F, Giehl K:
Specific induction of migration and invasion of pancreatic carcinoma cells by RhoC, which differs from RhoA in its localisation and activity.
Biol Chem
; 2009 Oct;390(10):1063-77
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These differences are
not
mediated by a different interaction with RhoGDIs.
[MeSH-major]
Cell Movement. Neoplasm Invasiveness. Pancreatic Neoplasms / pathology. rho GTP-Binding
Proteins
/ metabolism. rhoA GTP-Binding
Protein
/ metabolism
[MeSH-minor]
Cell Line, Tumor. Deep Brain Stimulation. Humans.
Protein
Isoforms / chemistry.
Protein
Isoforms / genetics.
Protein
Isoforms / metabolism. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. rap GTP-Binding
Proteins
/ chemistry. rap GTP-Binding
Proteins
/ genetics. rap GTP-Binding
Proteins
/ metabolism
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(PMID = 19642867.001).
[ISSN]
1437-4315
[Journal-full-title]
Biological chemistry
[ISO-abbreviation]
Biol. Chem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Protein Isoforms; 0 / RHOC protein, human; 0 / RNA, Messenger; EC 3.6.5.2 / rap GTP-Binding Proteins; EC 3.6.5.2 / rho GTP-Binding Proteins; EC 3.6.5.2 / rhoA GTP-Binding Protein
45.
Chen D, Kennedy A, Wang JY, Zeng W, Zhao Q, Pearl M, Zhang M, Suo Z, Nesland JM, Qiao Y, Ng AK, Hirashima N, Yamane T, Mori Y, Mitsumata M, Ghersi G, Chen WT:
Activation of EDTA-resistant gelatinases in malignant human tumors.
Cancer Res
; 2006 Oct 15;66(20):9977-85
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[Title]
Activation
of EDTA-resistant gelatinases in malignant human tumors.
Among the many proteases
associated
with human cancer, seprase or
fibroblast activation protein
alpha,
a type
II transmembrane glycoprotein, has two types of EDTA-resistant protease activities: dipeptidyl peptidase
and a
170-kDa gelatinase activity.
To test if
activation
of gelatinases
associated
with seprase could be involved in malignant tumors, we used a mammalian expression system to generate a soluble recombinant seprase (r-seprase).
Proteins
purified from experimental xenografts and malignant tumors using antibody- or lectin-affinity columns in the presence of 5 mmol/L EDTA were assayed for seprase
activation
in vivo.
Seprase expression
and activation
occur most prevalently in ovarian carcinoma but were also detected in four other malignant tumor types, including adenocarcinoma of
the colon
and stomach, invasive ductal carcinoma of the breast, and malignant melanoma.
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Disodium EDTA
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ETHYLENEDIAMINE TETRAACETIC ACID
.
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DISODIUM CALCIUM EDTA
.
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[Cites]
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Proc Natl Acad Sci U S A. 1990 Nov;87(21):8296-300
[
2172980.001
]
(PMID = 17047060.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA039077; United States / NIBIB NIH HHS / EB / R01EB002065; United States / NIBIB NIH HHS / EB / R01 EB002065; United States / NCRR NIH HHS / RR / M01 RR010710; United States / NCRR NIH HHS / RR / M01RR10710; United States / NCI NIH HHS / CA / R01CA0039077
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Membrane Proteins; 0 / Recombinant Proteins; 9G34HU7RV0 / Edetic Acid; EC 3.4.14.- / Dipeptidyl-Peptidases and Tripeptidyl-Peptidases; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
[Other-IDs]
NLM/ NIHMS11890; NLM/ PMC1626657
46.
Morais-de-Sá E, Neto-Silva RM, Pereira PJ, Saraiva MJ, Damas AM:
The binding of 2,4-dinitrophenol to wild-type and amyloidogenic transthyretin.
Acta Crystallogr D Biol Crystallogr
; 2006 May;62(Pt 5):512-9
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[Title]
The binding of 2,4-dinitrophenol to wild-
type and
amyloidogenic transthyretin.
Systemic deposition of transthyretin (TTR) amyloid fibrils is always observed in
familial amyloidotic polyneuropathy
, senile systemic amyloidosis
and familial amyloidotic
cardiomyopathy patients.
The destabilization of a native
protein
with consequent conformational changes appears to be a common link in several human amyloid diseases.
Intensive research has been directed towards
finding
small molecules that could work as therapeutic agents for the prevention/inhibition of amyloid diseases through stabilization of the native fold of the potentially amyloidogenic
protein
.
This work provides insight into the structural determinants of the highly stabilizing effects of 2,4-dinitrophenol on wild-
type
TTR.
As a result of 2,4-dinitrophenol binding, the two dimers in the TTR tetramer become closer, increasing the stability of
the protein
.
MedlinePlus Health Information.
consumer health - Amyloidosis
.
Hazardous Substances Data Bank.
2,4-Dinitrophenol
.
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.
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(PMID = 16627944.001).
[ISSN]
0907-4449
[Journal-full-title]
Acta crystallographica. Section D, Biological crystallography
[ISO-abbreviation]
Acta Crystallogr. D Biol. Crystallogr.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Peptides; 0 / Prealbumin; Q13SKS21MN / 2,4-Dinitrophenol
47.
Inoue K, Hiraoka T, Kanemitsu K, Takamori H, Tsuji T, Kawasuji M:
Onset of liver metastasis after histologically curative resection of pancreatic cancer.
Surg Today
; 2006;36(3):252-6
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[Title]
Onset of liver metastasis after histologically curative resection of pancreatic cancer.
PURPOSE: We assessed the possibility of predicting the time of onset of liver metastases by measuring the postoperative changes in serum carbohydrate antigen (CA)19-9 after curative resection of pancreatic cancers.
METHODS: Among 28 patients who underwent histologically defined curative resection of pancreatic cancer between 1984 and 1999, liver metastasis developed in 11 patients with elevated serum CA19-9 levels.
We plotted the serum CA19-9 levels against time on a semilogarithmic graph.
Over the linear part of the curve, the time when log[CA19-9] equaled zero was defined as the time of onset of liver metastases.
The log[CA19-9] level doubling time was then calculated and evaluated in relation to the survival period.
RESULTS: The serum CA19-9 levels increased linearly in 10 of the 11 patients.
The predicted time of onset of liver metastasis ranged from preoperative day 163.0 to postoperative day 27.1, being preoperative in eight patients.
The doubling time until death correlated strongly with survival in the eight patients with maintained log[CA19-9] linearity.
CONCLUSION: The onset of liver metastases might be preoperative in patients with advanced pancreatic cancer.
Therefore, neoadjuvant chemotherapy should be mandatory even if there is no sign of liver metastases.
[MeSH-major]
Biomarkers, Tumor / blood. CA-19-9 Antigen / blood. Liver Neoplasms / secondary. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery
[MeSH-minor]
Adult. Aged. Female. Humans. Male. Middle Aged. Prognosis. Time Factors
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[ISSN]
0941-1291
[Journal-full-title]
Surgery today
[ISO-abbreviation]
Surg. Today
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen
48.
Cai H, Hua B, Fan L, Wang Q, Wang S, Zhao Y:
A novel mutation (g2172-->c) in the factor V gene in a Chinese family with hereditary activated protein C resistance.
Thromb Res
; 2010 Jun;125(6):545-8
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[Title]
A novel mutation (g2172-->c) in the factor V gene in a Chinese family with
hereditary
activated
protein C
resistance.
BACKGROUND: Activated
protein C
resistance (
APC
-R) was a major risk factor for venous thromboembolism(VTE) in Caucasians, and at least 90% of
APC
-R were
associated
with the point mutation of factor V (FV) gene (Arg506-->Gln, FV Leiden).
OBJECTIVE: To identify the genetic defect of FV in a Chinese family with
APC
-
R associated
with VTE.
Blood samples were obtained from five family members (including the proband) for screening
APC
-R by coagulation assay and the genetic defect of FV using direct sequencing.
RESULTS: Four out of five members had
APC
-R.
We identified a novel mutation (G2172-->C) in exon 13 of the FV gene, which was present in all the individuals with
APC
-R but was absent in the individual without
APC
-R.
This mutation is predicted to result in the replacement of glutamate by aspartate at position 666, close to one of
the APC
cleavage sites.
CONCLUSIONS: We have identified, for the first time, a novel mutation (G2172-->C) of FV that was
associated
with
APC
-R in a Chinese family with VTE.
We speculate that this mutation interferes with cleavage at Arg679 by
APC
.
[MeSH-major]
Activated
Protein C
Resistance / genetics. Factor V / genetics. Point Mutation
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[Copyright]
Copyright 2010 Elsevier Ltd. All rights reserved.
(PMID = 20304467.001).
[ISSN]
1879-2472
[Journal-full-title]
Thrombosis research
[ISO-abbreviation]
Thromb. Res.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
9001-24-5 / Factor V
49.
Sangha S, Yao M, Wolfe MM:
Non-steroidal anti-inflammatory drugs and colorectal cancer prevention.
Postgrad Med J
; 2005 Apr;81(954):223-7
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Currently, the most effective strategy available for
colon
cancer prevention is endoscopic screening, with polypectomy or surgical resection for advanced lesions.
Data obtained from
animal and
epidemiological studies and most recently from randomised, placebo controlled trials, suggest that non-steroidal anti-inflammatory drugs may prove effective chemopreventive agents in different groups of people, from patients with
familial
adenomatous polyposis
to those with sporadic adenomas.
[MeSH-minor]
Colorectal Neoplasms,
Hereditary
Nonpolyposis / prevention & control. Humans. Randomized Controlled Trials as Topic. Treatment Outcome
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(PMID = 15811884.001).
[ISSN]
0032-5473
[Journal-full-title]
Postgraduate medical journal
[ISO-abbreviation]
Postgrad Med J
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents
[Other-IDs]
NLM/ PMC1743256
51.
Wick EC, Sears CL:
Bacteroides spp. and diarrhea.
Curr Opin Infect Dis
; 2010 Oct;23(5):470-4
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RECENT FINDINGS: Bacteroides fragilis is the only strain of Bacteroides spp.
associated
with diarrheal
disease
.
Toxin-producing strains of B. fragilis, termed enterotoxigenic Bacteroides fragilis (ETBF), are an established cause of diarrheal
disease
in people.
The clinical
syndrome associated
with ETBF diarrheal
disease
encompasses abdominal pain, tenesmus and inflammatory diarrhea.
Two new studies conducted in mice have further defined the chronic inflammatory response
associated
with ETBF infection and observed that in
the multiple intestinal
neoplasia mouse strain, heterozygotes for the
adenomatous polyposis coli
gene, ETBF infection enhances development of colonic tumors.
SUMMARY: B. fragilis remains the leading anaerobe in human
disease
.
ETBF is emerging as an important cause of human diarrheal
disease
but additional epidemiologic studies are needed to better understand the role of ETBF human
disease
.
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]
(PMID = 20697287.001).
[ISSN]
1473-6527
[Journal-full-title]
Current opinion in infectious diseases
[ISO-abbreviation]
Curr. Opin. Infect. Dis.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / R01 DK045496-16; United States / NIDDK NIH HHS / DK / DK059655-01; United States / NIDDK NIH HHS / DK / R01 DK059655-03; United States / NIDDK NIH HHS / DK / R01 DK045496-13; United States / NIDDK NIH HHS / DK / DK045496-15; United States / NIDDK NIH HHS / DK / DK059655-02; United States / NIDDK NIH HHS / DK / R01 DK080817-01; United States / NIDDK NIH HHS / DK / DK080817-04; United States / NIDDK NIH HHS / DK / DK080817-01; United States / NIDDK NIH HHS / DK / R01 DK045496; United States / NIDDK NIH HHS / DK / R01 DK059655-02; United States / NIDDK NIH HHS / DK / R01 DK045496-17; United States / NIDDK NIH HHS / DK / R01 DK080817-02; United States / NIDDK NIH HHS / DK / DK045496-16; United States / NIDDK NIH HHS / DK / DK059655-03; United States / NIDDK NIH HHS / DK / DK045496-18; United States / NIDDK NIH HHS / DK / DK080817-02; United States / NIDDK NIH HHS / DK / DK045496-14; United States / NIDDK NIH HHS / DK / R01 DK080817-03; United States / NIDDK NIH HHS / DK / R01 DK059655; United States / NIDDK NIH HHS / DK / R01 DK045496-14; United States / NIDDK NIH HHS / DK / R01 DK045496-15; United States / NIDDK NIH HHS / DK / DK045496-13; United States / NIDDK NIH HHS / DK / R01 DK080817; United States / NIDDK NIH HHS / DK / R01 DK059655-01; United States / NIDDK NIH HHS / DK / DK080817-03; United States / NIDDK NIH HHS / DK / DK045496-17; United States / NIDDK NIH HHS / DK / R01 DK045496-18; United States / NIDDK NIH HHS / DK / R01 DK080817-04
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Adenomatous Polyposis Coli Protein; 0 / Bacterial Toxins; 0 / Virulence Factors
[Other-IDs]
NLM/ NIHMS262792; NLM/ PMC3079340
52.
Winship IM, Dudding TE:
Lessons from the skin--cutaneous features of familial cancer.
Lancet Oncol
; 2008 May;9(5):462-72
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[Title]
Lessons from the skin--cutaneous features of
familial
cancer.
As the molecular basis of
disease
continues to be elucidated,
familial
cancer
syndromes
, which consist of a range of neoplastic and non-neoplastic features, are emerging.
The usual pathway of referral to a genetics clinic or
familial
cancer centre is via an oncologist, when high-risk features that suggest a possible
hereditary
basis for the presenting cancer are recognised.
These features are effective in ascertaining a substantial proportion of families with
hereditary
breast and ovarian cancer due to a BRCA mutation, or the more common bowel-cancer predisposition
syndromes
, such as
hereditary
non-
polyposis
colon
cancer
and familial
adenomatous polyposis
.
However, there are a range of
familial
cancer
syndromes
that are
not
easily detected and that can remain undiagnosed when history and examination are
not
extended to include non-malignant features.
The identification of cutaneous signs
associated
with rare
familial
-cancer
syndromes
provides individuals and their families with the opportunity to undertake early surveillance for malignant and non-malignant complications that might in time be shown to improve outcomes.
[MeSH-major]
Colonic Neoplasms / pathology. Endocrine Gland Neoplasms / pathology. Kidney Neoplasms / pathology. Neoplastic
Syndromes
,
Hereditary
/ pathology. Skin / pathology. Skin Neoplasms / pathology
[MeSH-minor]
Adenomatous Polyposis Coli
/ pathology. Basal Cell Nevus
Syndrome
/ pathology. Carcinoma, Renal Cell / pathology. Colorectal Neoplasms,
Hereditary
Nonpolyposis / pathology.
Disease
Progression. Gene Expression Regulation, Neoplastic. Genetic Testing. Hamartoma
Syndrome
,
Multiple
/ pathology. Humans. Leiomyomatosis / pathology.
Multiple
Endocrine Neoplasia / pathology.
Multiple
Endocrine Neoplasia
Type
2a / pathology.
Multiple
Endocrine Neoplasia
Type
2b / pathology. Mutation. Neurofibromatosis 1 / pathology. Neurofibromatosis 2 / pathology. Pedigree. Peutz-Jeghers
Syndrome
/ pathology. Tuberous Sclerosis / pathology
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(PMID = 18452857.001).
[ISSN]
1474-5488
[Journal-full-title]
The Lancet. Oncology
[ISO-abbreviation]
Lancet Oncol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Number-of-references]
75
53.
Giles RH, Lolkema MP, Snijckers CM, Belderbos M, van der Groep P, Mans DA, van Beest M, van Noort M, Goldschmeding R, van Diest PJ, Clevers H, Voest EE:
Interplay between VHL/HIF1alpha and Wnt/beta-catenin pathways during colorectal tumorigenesis.
Oncogene
; 2006 May 18;25(21):3065-70
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Activation
of the Wnt signaling pathway initiates the transformation of colorectal epithelial cells, although the transition to metastatic cancer requires angiogenesis.
Here, we show that VHL expression is regulated by TCF4 and is restricted to the proliferative compartment at the bottom of
intestinal
crypts.
Accordingly, VHL is completely absent from the proliferative
intestinal
pockets of Tcf4(-/-) perinatal mice.
We observed complementary staining of the hypoxia-inducible factor (HIF) 1alpha to VHL in normal
intestinal
epithelium as well as in all stages of colorectal cancer (CRC).
Although we observed upregulated levels of VHL in very early CRC lesions from sporadic
and familial
adenomatous polyposis
patients - presumably due to activated Wnt signaling - a clear reduction of VHL expression is observed in later stages of CRC progression, coinciding with stabilization of HIF1alpha.
[MeSH-major]
Adenocarcinoma / etiology. Cell Transformation, Neoplastic / genetics. Colorectal Neoplasms / etiology. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Nerve Tissue
Proteins
/ physiology. TCF Transcription Factors / physiology. Von Hippel-Lindau Tumor Suppressor
Protein
/ physiology. Wnt
Proteins
/ physiology. beta Catenin / physiology
[MeSH-minor]
Adenoma
/ genetics.
Adenoma
/ metabolism.
Adenoma
/ pathology.
Adenomatous Polyposis Coli
/ genetics.
Adenomatous Polyposis Coli
/ metabolism.
Adenomatous Polyposis Coli
/ pathology. Animals. Basic Helix-Loop-Helix Leucine Zipper Transcription Factors. Cell Line.
Colon
/ cytology.
Colon
/ metabolism.
Colon
/ pathology. Colonic Polyps / genetics. Colonic Polyps / metabolism. Colonic Polyps / pathology.
Disease
Progression. Epithelial Cells / metabolism. Erythropoietin / genetics. Gene Expression Regulation, Neoplastic. Genes, Reporter. Humans.
Intestinal
Mucosa / cytology.
Intestinal
Mucosa / metabolism.
Intestinal
Mucosa / pathology. Kidney. L Cells (Cell Line). Mice. Mice, Knockout. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / metabolism. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Promoter Regions, Genetic. Recombinant Fusion
Proteins
/ biosynthesis. Recombinant Fusion
Proteins
/ genetics. Signal Transduction / physiology. Transcription Factor 7-Like 2
Protein
. Wnt3
Protein
MedlinePlus Health Information.
consumer health - Colorectal Cancer
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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(PMID = 16407833.001).
[ISSN]
0950-9232
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / CTNNB1 protein, human; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Nerve Tissue Proteins; 0 / Recombinant Fusion Proteins; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Tcf4 protein, mouse; 0 / Tcf7l2 protein, mouse; 0 / Transcription Factor 7-Like 2 Protein; 0 / Wnt Proteins; 0 / Wnt3 Protein; 0 / beta Catenin; 11096-26-7 / Erythropoietin; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Vhlh protein, mouse; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
54.
Li JM, Southerland LT, Lu Y, Darlak KA, Giver CR, McMillin DW, Harris WA, Jaye DL, Waller EK:
Activation, immune polarization, and graft-versus-leukemia activity of donor T cells are regulated by specific subsets of donor bone marrow antigen-presenting cells in allogeneic hemopoietic stem cell transplantation.
J Immunol
; 2009 Dec 15;183(12):7799-809
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[Title]
Activation
, immune polarization, and graft-versus-leukemia activity of donor T cells are regulated by specific subsets of donor bone marrow antigen-presenting cells in allogeneic hemopoietic stem cell transplantation.
We investigated the roles of specific subsets of donor APCs purified from bone marrow in donor T cell
activation and
graft-vs-leukemia (GvL) activity in murine models of hemopoietic stem cell transplantation.
Lineage(-)CD11c(+)
APC
precursors were separated from donor bone marrow based on expression of CD11b.
Transplanting lineage(-)CD11c(+)CD11b(-)
APC
(CD11b(-)
APC
) in combination with c-kit(+)Sca-1(+)lineage(-) hemopoietic stem cells (HSC) and congenic donor T cells led to increased donor CD4(+) and CD8(+) T cell proliferation and higher donor T cell chimerism than with transplanting grafts containing HSC, T cells, and lineage(-)CD11c(+)CD11b(+) APCs (CD11b(+)
APC
), or grafts containing only HSC and T cells.
Transplanting CD11b(-) APCs induced Th1/
type 1
cytotoxic T lymphocyte donor T cell immune polarization and enhanced GvL activity of donor T cells without increased graft-vs-host
disease
in both MHC- and minor histocompatibility Ag-mismatched murine hemopoietic stem cell transplantation models, whereas CD11b(+) APCs led to Th2/
type
2 cytotoxic T lymphocyte donor T cell immune polarization.
Donor CD11b(-) APCs were plasmacytoid dendritic cell progenitors (>90% CD317; PDCA-1(+)) and up-regulated CD80, CD86, and IL-12 during alloantigen presentation, whereas CD11b(+) APCs expressed Gr-
1 and
up-regulated expression of programmed death ligands-
1 and
2 after
activation
.
These results are the first to show that manipulation of the content of donor APCs in allogeneic HSC grafts can regulate donor T cell immunity and enhance GvL without increasing graft-vs-host
disease
activity.
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[ISSN]
1550-6606
[Journal-full-title]
Journal of immunology (Baltimore, Md. : 1950)
[ISO-abbreviation]
J. Immunol.
[Language]
ENG
[Grant]
United States / NHLBI NIH HHS / HL / P01 HL086773; United States / NCI NIH HHS / CA / R01 CA074364; United States / PHS HHS / / NHLBI P01HL086773; United States / NCI NIH HHS / CA / R01 CA-74364-03
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Isoantigens
[Other-IDs]
NLM/ NIHMS549152; NLM/ PMC3908652
55.
Bauer S, Adrian N, Siebenborn U, Fadle N, Plesko M, Fischer E, Wüest T, Stenner F, Mertens JC, Knuth A, Ritter G, Old LJ, Renner C:
Sequential cancer immunotherapy: targeted activity of dimeric TNF and IL-8.
Cancer Immun
; 2009;9:2
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Polymorphonuclear neutrophils (PMNs) are potent effectors of inflammation and their attempts to respond to cancer are suggested by their systemic, regional and intratumoral
activation
.
We previously reported on the recruitment of CD11b+ leukocytes due to tumor site-specific enrichment of TNF activity after intravenous administration of a dimeric TNF immunokine with specificity for
fibroblast activation protein
(
FAP
).
With the aim to amplify the TNF-induced and IL-8-mediated chemotactic response, we generated immunocytokines by N-terminal fusion of a human anti-
FAP
scFv fragment with human IL-8 (IL-8(72)) and its N-terminally truncated form IL-8(3-72).
Due to the dramatic difference in chemotaxis induction in vitro, we favored the mature chemokine fused to the anti-
FAP
scFv for further investigation in vivo.
BALB/c nu/nu mice were simultaneously xenografted with
FAP
-positive or -negative tumors and extended chemo-attraction of PMNs was only detectable in
FAP
-expressing tissue after intravenous administration of the anti-
FAP
scFv-IL-8(72) construct.
As TNF-activated PMNs are likewise producers and primary targets for IL-8, we investigated the therapeutic efficacy of co-administration of both effectors: Sequential application of scFv-IL-8(72) and dimeric IgG1-TNF fusion
proteins
significantly enhanced anti-tumor activity when compared either to a single effector treatment regimen or sequential application of non-targeted cytokines, indicating that the tumor-restricted sequential application of IL-8(72) and TNF is a promising approach for cancer therapy.
[MeSH-major]
Immunotherapy. Interleukin-8 / therapeutic use. Neoplasms / drug therapy. Neoplasms / immunology.
Protein
Multimerization. Tumor Necrosis Factor-alpha / therapeutic use
[MeSH-minor]
Animals. Antigens. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / metabolism. Chemotaxis / drug effects. Gelatinases. Humans. Kinetics. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / metabolism. Membrane
Proteins
. Mice. Recombinant Fusion
Proteins
/ pharmacology. Recombinant Fusion
Proteins
/ therapeutic use. Serine Endopeptidases / metabolism. Transfection. Treatment Outcome. Xenograft Model Antitumor Assays
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(PMID = 19267427.001).
[ISSN]
1424-9634
[Journal-full-title]
Cancer immunity
[ISO-abbreviation]
Cancer Immun.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Interleukin-8; 0 / Membrane Proteins; 0 / Recombinant Fusion Proteins; 0 / Tumor Necrosis Factor-alpha; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
[Other-IDs]
NLM/ PMC2935764
56.
Crane CH, Winter K, Regine WF, Safran H, Rich TA, Curran W, Wolff RA, Willett CG:
Phase II study of bevacizumab with concurrent capecitabine and radiation followed by maintenance gemcitabine and bevacizumab for locally advanced pancreatic cancer: Radiation Therapy Oncology Group RTOG 0411.
J Clin Oncol
; 2009 Sep 01;27(25):4096-102
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PURPOSE: The primary objective of this study was to assess
the 1
-year survival of patients with locally advanced, unresectable pancreatic cancer treated with the combination of bevacizumab, capecitabine, and radiation.
The median
and 1
-year survival rates were 11.9 months (95%
CI
, 9.9 to 14.0 months) and 47% (95%
CI
, 36% to 57%).
Median PFS was 8.6 months (95%
CI
, 6.9 to 10.5), and RR was 26%.
Unacceptable radiotherapy protocol deviations (ie, inappropriately generous volume contoured) correlated with grade 3 or greater gastrointestinal toxicity during chemoradiotherapy (45% v 18%; adjusted odds ratio, 3.7; 95%
CI
, 0.98 to 14.1; P = .05).
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Angiogenesis Inhibitors / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Antimetabolites, Antineoplastic / administration & dosage. Bevacizumab. Capecitabine. Chemotherapy, Adjuvant. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives.
Disease
-Free Survival. Female. Fluorouracil / administration & dosage. Fluorouracil / analogs & derivatives. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Pancreatectomy. Pancreaticoduodenectomy. Radiotherapy, Adjuvant. Time Factors. Treatment Outcome
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.
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CAPECITABINE
.
Hazardous Substances Data Bank.
FLUOROURACIL
.
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[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00114179
[Grant]
United States / NCI NIH HHS / CA / U10 CA32115; United States / NCI NIH HHS / CA / U10 CA21661; United States / NCI NIH HHS / CA / U10 CA37422; United States / NCI NIH HHS / CA / U10 CA037422; United States / NCI NIH HHS / CA / U10 CA021661; United States / NCI NIH HHS / CA / U10 CA032115
[Publication-type]
Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 2S9ZZM9Q9V / Bevacizumab; 6804DJ8Z9U / Capecitabine; B76N6SBZ8R / gemcitabine; U3P01618RT / Fluorouracil
[Other-IDs]
NLM/ PMC2734421
57.
Al-Sukhni W, Aronson M, Gallinger S:
Hereditary colorectal cancer syndromes: familial adenomatous polyposis and lynch syndrome.
Surg Clin North Am
; 2008 Aug;88(4):819-44, vii
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[Title]
Hereditary
colorectal cancer
syndromes
:
familial
adenomatous polyposis
and lynch
syndrome
.
Familial
colorectal cancer (CRC) accounts for 10% to 20% of all cases of CRC.
Two major autosomal dominant forms of heritable CRC are
familial
adenomatous polyposis
(
FAP
) and Lynch
syndrome
(also known as
hereditary
nonpolyposis colorectal cancer).
Along with the risk for CRC, both
syndromes
are
associated
with elevated risk for other tumors.
Improved understanding of the genetic basis of these diseases has
not
only facilitated the identification and screening of at-risk individuals and the development of prophylactic or early-stage intervention strategies but also provided better insight into sporadic CRC.
This article reviews the clinical and genetic characteristics of
FAP and
Lynch
syndrome
, recommended screening and surveillance practices, and appropriate surgical and nonsurgical interventions.
[MeSH-major]
Adenomatous Polyposis Coli
/ genetics. Colorectal Neoplasms,
Hereditary
Nonpolyposis / genetics. Genetic Predisposition to
Disease
[MeSH-minor]
Diagnosis
, Differential. Humans
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.
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.
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.
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(PMID = 18672142.001).
[ISSN]
0039-6109
[Journal-full-title]
The Surgical clinics of North America
[ISO-abbreviation]
Surg. Clin. North Am.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
124
58.
Mirabella D, Spena R, Scognamiglio G, Luca L, Gracco A, Siciliani G:
LED vs halogen light-curing of adhesive-precoated brackets.
Angle Orthod
; 2008 Sep;78(5):935-40
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OBJECTIVE: To test the hypothesis that bonding with a blue light-emitting diode (LED) curing unit produces no more failures in adhesive-precoated (
APC
) orthodontic brackets than bonding carried out by a conventional halogen lamp.
MATERIALS AND METHODS: Sixty-five patients were selected for this randomized clinical trial, in which a total of 1152 stainless steel
APC
brackets were employed.
In order to carry out a valid comparison of the bracket failure rate following use of each
type
of curing unit, each patient's mouth was divided into four quadrants.
In 34 of the randomly selected patients, designated group A,
the APC
brackets of the right maxillary and left mandibular quadrants were bonded using a halogen light, while the remaining quadrants were treated with an LED curing unit.
In the other 31 patients, designated group B, halogen light was used to cure the left maxillary and right mandibular quadrants, whereas
the APC
brackets in the remaining quadrants were bonded using an LED dental curing light.
The bonding date,
the type
of light used for curing, and the date of any bracket failures over a mean period of 8.9 months were recorded for each bracket and, subsequently, the chi-square test, the Yates-corrected chi-square test, the Fisher exact test, Kaplan-Meier survival estimates, and the log-rank test were employed in statistical analyses of the results.
RESULTS: No statistically significant difference in bond failure rate was found between
APC
brackets bonded with the halogen light-curing unit and those cured with LED light.
CONCLUSIONS: The hypothesis cannot be rejected since use of an LED curing unit produces similar
APC
bracket failure rates to use of conventional halogen light, with the advantage of a far shorter curing time (10 seconds).
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(PMID = 18298197.001).
[ISSN]
0003-3219
[Journal-full-title]
The Angle orthodontist
[ISO-abbreviation]
Angle Orthod
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Randomized Controlled Trial
[Publication-country]
United States
[Chemical-registry-number]
0 / Composite Resins; 0 / Resin Cements; 0 / Transbond XT; 12597-68-1 / Stainless Steel
59.
Baum P, Müller D, Rüger R, Kontermann RE:
Single-chain Fv immunoliposomes for the targeting of fibroblast activation protein-expressing tumor stromal cells.
J Drug Target
; 2007 Jul;15(6):399-406
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[Title]
Single-chain Fv immunoliposomes for the targeting of
fibroblast activation protein
-expressing tumor stromal cells.
Fibroblast activation protein
(
FAP
) represents a cell surface antigen selectively expressed by reactive tumor stromal fibroblasts of various cancers.
Here, we describe anti-
FAP
immunoliposomes as carrier systems for active targeting of
FAP
-expressing cells.
As targeting ligand we used single-chain Fv (scFv) molecules cross-reacting with human and mouse
FAP
.
These scFv molecules were genetically modified to express an additional cysteine residue at
the C
-terminus allowing a defined and site-directed conjugation.
Coupling to Mal-PEG(2000)-DSPE containing liposomes resulted in sterically stabilized scFv immunoliposomes showing strong and specific binding to
FAP
-expressing cells.
In addition, we could show that binding to
FAP
-expressing cells leads to internalization of intact liposomes into the endosomal compartment.
Thus, these anti-
FAP
scFv immunoliposomes should be suitable for target cell-specific delivery and uptake of encapsulated drugs.
[MeSH-major]
Antigens, Neoplasm / immunology. Biomarkers, Tumor / immunology. Immunoglobulin Fragments / chemistry. Immunoglobulin Variable Region / chemistry. Liposomes / chemistry. Membrane
Proteins
/ immunology. Serine Endopeptidases / immunology. Stromal Cells / metabolism
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(PMID = 17613658.001).
[ISSN]
1061-186X
[Journal-full-title]
Journal of drug targeting
[ISO-abbreviation]
J Drug Target
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Drug Carriers; 0 / Immunoglobulin Fragments; 0 / Immunoglobulin Variable Region; 0 / Liposomes; 0 / Membrane Proteins; 0 / Phosphatidylethanolamines; 0 / immunoglobulin Fv; 1G4B5265CQ / 1,2-distearoylphosphatidylethanolamine; 30IQX730WE / Polyethylene Glycols; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
60.
Imanaka H, Tanaka S, Feng B, Imamura K, Nakanishi K:
Cultivation characteristics and gene expression profiles of Aspergillus oryzae by membrane-surface liquid culture, shaking-flask culture, and agar-plate culture.
J Biosci Bioeng
; 2010 Mar;109(3):267-73
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We cultivated a filamentous fungus, Aspergillus oryzae IAM 2706 by three different cultivation methods, i.e., shaking-flask culture (SFC), agar-plate culture (
APC
), and membrane-surface liquid culture (MSLC), to elucidate the differences of its behaviors by different cultivation methods under the same media, by measuring the growth, secretion of proteases and alpha-amylase, secreted
protein
level, and gene transcriptional profile by the DNA microarray analysis.
The protease activities detected by MSLC
and APC
were much higher than that by SFC, using both modified Czapek-Dox (mCD) and dextrin-peptone-yeast extract (DPY) media.
The alpha-amylase activity was detected in MSLC
and APC
in a much larger extent than that in SFC when DPY medium was used.
On the basis of SDS-PAGE analyses
and N
-terminal amino acid sequences, 6
proteins
were identified in the supernatants of the culture broths using DPY medium, among which oryzin (alkaline protease) and alpha-amylase were detected at a much higher extent for
APC and
MSLC than those for SFC while only oryzin was detected in mCD medium, in accordance with the activity measurements.
A microarray analysis for the fungi cultivated by SFC,
APC
, and MSLC using mCD medium was carried out to elucidate the differences in the gene transcriptional profile by the cultivation methods.
The gene transcriptional profile obtained for the MSLC sample showed a similar tendency to
the APC
sample while it was quite different from that for the SFC sample.
Most of the genes specifically transcribed in the MSLC sample versus those in the SFC sample with a 10-fold up-regulation or higher were unknown or predicted
proteins
.
[MeSH-major]
Agar / metabolism. Aspergillus oryzae / metabolism. Bioreactors / microbiology. Cell Culture Techniques / methods. Cell Membrane / metabolism. Culture Media / metabolism. Fungal
Proteins
/ metabolism. Gene Expression Regulation, Fungal / physiology
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[Copyright]
Copyright 2009 The Society for Biotechnology, Japan. Published by Elsevier B.V. All rights reserved.
(PMID = 20159576.001).
[ISSN]
1347-4421
[Journal-full-title]
Journal of bioscience and bioengineering
[ISO-abbreviation]
J. Biosci. Bioeng.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Culture Media; 0 / Fungal Proteins; 0 / Solutions; 9002-18-0 / Agar
61.
Kretschmer B, Lüthje K, Ehrlich S, Osterloh A, Piedavent M, Fleischer B, Breloer M:
CD83 on murine APC does not function as a costimulatory receptor for T cells.
Immunol Lett
; 2008 Oct 30;120(1-2):87-95
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[Title]
CD83 on murine
APC
does
not
function as a costimulatory receptor for T cells.
The transmembrane glycoprotein CD83 is rapidly upregulated on murine and human DC upon maturation and therefore a costimulatory function for T cell
activation
has been suggested.
Studies employing human
APC
indeed showed that CD83 expression was positively correlated to the stimulatory capacity of
the APC
.
Murine
APC
that were CD83 deficient however, did
not
display a reduced capacity to activate T cells.
To elucidate this contradiction, we thoroughly compared the stimulatory capacity of CD83-overexpressing and CD83-deficient
APC
.
Here we show that CD83 expression levels on
APC
did
not
affect the capacity of
the APC
to activate CD8(+) T cells.
CD83 expression levels did
not
significantly affect CD4(+) T cell
activation
in vivo, but a weak positive correlation of CD83 expression with CD4(+) T cell
activation
was observed in vitro under suboptimal stimulation conditions.
As CD83 expression also positively correlated with MHC-II but
not
with MHC-I expression, this differential stimulation specifically of CD4(+) T cells could be explained by a higher density of MHC-II peptide complexes on
the APC
surface.
Taken together, our results strongly suggest that CD83 does
not
deliver crucial costimulatory signals to murine T cells.
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(PMID = 18675848.001).
[ISSN]
0165-2478
[Journal-full-title]
Immunology letters
[ISO-abbreviation]
Immunol. Lett.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD86; 0 / CD83 antigen; 0 / Cd86 protein, mouse; 0 / Histocompatibility Antigens Class II; 0 / Immunoglobulins; 0 / Membrane Glycoproteins; 0 / Receptors, Antigen, T-Cell
62.
Clarke DJ, Bachant J:
Kinetochore structure and spindle assembly checkpoint signaling in the budding yeast, Saccharomyces cerevisiae.
Front Biosci
; 2008;13:6787-819
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Here we review recent developments in our understanding of SAC control with particular emphasis on the role of the kinetochore, the nature of the tension sensing mechanism and the possibility that the SAC encompasses more than just stabilization of securin and/or cyclin-B via inhibition of
the APC
/C to delay anaphase initiation.
[MeSH-minor]
Cell Cycle. Chromatids / physiology. Chromosomes, Fungal / genetics. Chromosomes, Fungal / physiology. DNA Topoisomerases,
Type
II / metabolism. Saccharomyces cerevisiae
Proteins
/ metabolism. Stress, Mechanical
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(PMID = 18508695.001).
[ISSN]
1093-9946
[Journal-full-title]
Frontiers in bioscience : a journal and virtual library
[ISO-abbreviation]
Front. Biosci.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA099033; United States / NIGMS NIH HHS / GM / GM-66190
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Chromatin; 0 / Saccharomyces cerevisiae Proteins; EC 5.99.1.3 / DNA Topoisomerases, Type II
[Number-of-references]
326
63.
Lin H, Yamada Y, Nguyen S, Linhart H, Jackson-Grusby L, Meissner A, Meletis K, Lo G, Jaenisch R:
Suppression of intestinal neoplasia by deletion of Dnmt3b.
Mol Cell Biol
; 2006 Apr;26(8):2976-83
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[Title]
Suppression of
intestinal
neoplasia by deletion of Dnmt3b.
Aberrant gene silencing accompanied by DNA methylation is
associated
with neoplastic progression in many tumors that also show global loss of DNA methylation.
Using conditional inactivation of
de
novo methyltransferase Dnmt3b in
Apc
(Min/+) mice, we demonstrate that the loss of Dnmt3b has no impact on microadenoma formation, which is considered the earliest stage of
intestinal
tumor formation.
Interestingly, many
large
adenomas showed regions with Dnmt3b inactivation, indicating that Dnmt3b is required for initial outgrowth of macroscopic adenomas but is
not
required for their maintenance.
These results support a role for Dnmt3b in the transition stage between microadenoma formation and macroscopic colonic tumor growth and further suggest that Dnmt3b, and by extension
de
novo methylation, is
not
required for maintaining tumor growth after this transition stage has occurred.
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Cell. 1999 Oct 29;99(3):247-57
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(PMID = 16581773.001).
[ISSN]
0270-7306
[Journal-full-title]
Molecular and cellular biology
[ISO-abbreviation]
Mol. Cell. Biol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R37 CA 84198; United States / NICHD NIH HHS / HD / R01 HD050760; United States / NCI NIH HHS / CA / R01 CA 87869; United States / NCI NIH HHS / CA / R37 CA084198; United States / NICHD NIH HHS / HD / R01 HD 0445022; United States / NCI NIH HHS / CA / R01 CA087869
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Neoplasm; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA methyltransferase 3B
[Other-IDs]
NLM/ PMC1446955
64.
Chen WT, Khazaie K, Zhang G, Weissleder R, Tung CH:
Detection of dysplastic intestinal adenomas using a fluorescent folate imaging probe.
Mol Imaging
; 2005 Jan-Mar;4(1):67-74
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[Title]
Detection of dysplastic
intestinal
adenomas using a fluorescent folate imaging probe.
Activated macrophages overexpress folate receptors and we used this phenomenon to image inflammatory reactions in
colon
dysplasia using a fluorescent folate probe (FFP).
APC
(Delta468) mice injected with FFP showed fluorescent adenomas (target-to-background ratio,
adenoma
vs. adjacent normal mucosa, of 2.46 +/- 0.41), significantly higher (p < .001) than adenomas in animals injected with a non-folate-containing control probe.
Taken together, these results indicate that probe potentially can be used to image dysplastic
intestinal
adenomas in vivo.
[MeSH-major]
Adenoma
/ pathology. Flow Cytometry / methods. Folic Acid / analysis.
Intestinal
Neoplasms / pathology
[MeSH-minor]
Animals. Antigens, Differentiation / metabolism. Carrier
Proteins
/ metabolism. Fluorescent Dyes. Folate Receptors, GPI-Anchored. Genes,
APC
. Macrophage-1 Antigen / metabolism. Macrophages / metabolism. Macrophages / pathology. Mice. Mice, Mutant Strains. Receptors, Cell Surface / metabolism
MedlinePlus Health Information.
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.
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(PMID = 15967128.001).
[ISSN]
1535-3508
[Journal-full-title]
Molecular imaging
[ISO-abbreviation]
Mol Imaging
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P50 CA 86355; United States / NCI NIH HHS / CA / R01 CA 104547-01A1; United States / NCI NIH HHS / CA / R01 CA 99385; United States / NCI NIH HHS / CA / R33 CA 88365
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Differentiation; 0 / Carrier Proteins; 0 / Fluorescent Dyes; 0 / Folate Receptors, GPI-Anchored; 0 / Macrophage-1 Antigen; 0 / Receptors, Cell Surface; 0 / monocyte-macrophage differentiation antigen; 935E97BOY8 / Folic Acid
65.
Loeffler M, Krüger JA, Niethammer AG, Reisfeld RA:
Targeting tumor-associated fibroblasts improves cancer chemotherapy by increasing intratumoral drug uptake.
J Clin Invest
; 2006 Jul;116(7):1955-62
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[Title]
Targeting tumor-
associated
fibroblasts improves cancer chemotherapy by increasing intratumoral drug uptake.
Tumor-
associated
fibroblasts are key regulators of tumorigenesis.
These cells are also the primary source of collagen
type
I, which contributes to decreased chemotherapeutic drug uptake in tumors and plays a significant role in regulating tumor sensitivity to a variety of chemotherapies.
To specifically kill tumor-
associated
fibroblasts, we constructed an oral DNA vaccine targeting
fibroblast activation protein
(
FAP
), which is specifically overexpressed by fibroblasts in the tumor stroma.
Through CD8+ T cell-mediated killing of tumor-
associated
fibroblasts, our vaccine successfully suppressed primary tumor cell growth and metastasis of multidrug-resistant murine
colon and
breast carcinoma.
Furthermore, tumor tissue of
FAP
-vaccinated mice revealed markedly decreased collagen
type
I expression and up to 70% greater uptake of chemotherapeutic drugs.
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[ErratumIn]
J Clin Invest. 2009 Feb;119(2):421
(PMID = 16794736.001).
[ISSN]
0021-9738
[Journal-full-title]
The Journal of clinical investigation
[ISO-abbreviation]
J. Clin. Invest.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA083856; United States / NCI NIH HHS / CA / CA83856
[Publication-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.
[Publication-country]
United States
[Chemical-registry-number]
0 / Cancer Vaccines; 0 / Collagen Type I; 0 / Membrane Proteins; 0 / Recombinant Fusion Proteins; 0 / Vaccines, DNA; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
[Other-IDs]
NLM/ PMC1481657
66.
Saito T, Oda Y, Yamamoto H, Kawaguchi K, Tanaka K, Matsuda S, Iwamoto Y, Tsuneyoshi M:
Nuclear beta-catenin correlates with cyclin D1 expression in spindle and pleomorphic sarcomas but not in synovial sarcoma.
Hum Pathol
; 2006 Jun;37(6):689-97
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[Title]
Nuclear beta-catenin correlates with cyclin D1 expression in spindle and pleomorphic sarcomas but
not
in synovial sarcoma.
Frequent
activation
of Wnt signaling pathway has been also shown in synovial sarcoma (SS), suggesting a specific role of this pathway in SS.
Immunohistochemical detection of nuclear beta-catenin accumulation correlated with cyclin D1 overexpression in spindle cell and pleomorphic sarcomas (P = .037), and the expression of these
proteins
evenly distributed throughout each section.
Cyclin D1 mRNA expression levels were statistically higher in tumors with cyclin D1 overexpression than in tumors without (P = .037), suggesting that cyclin D1 overexpression is due to transcriptional
activation
.
However, these correlations could
not
be detected in SS.
Mutations in exon 3 of the beta-catenin gene and in the mutation cluster region
of adenomatous polyposis coli
gene were absent in this series of cases.
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(PMID = 16733209.001).
[ISSN]
0046-8177
[Journal-full-title]
Human pathology
[ISO-abbreviation]
Hum. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / RNA, Messenger; 0 / beta Catenin; 136601-57-5 / Cyclin D1
67.
Kroboth K, Newton IP, Kita K, Dikovskaya D, Zumbrunn J, Waterman-Storer CM, Näthke IS:
Lack of adenomatous polyposis coli protein correlates with a decrease in cell migration and overall changes in microtubule stability.
Mol Biol Cell
; 2007 Mar;18(3):910-8
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[Title]
Lack
of adenomatous polyposis coli
protein
correlates with a decrease in cell migration and overall changes in microtubule stability.
Most sporadic colorectal tumors carry truncation mutations in the
adenomatous polyposis coli
(
APC
) gene.
The APC protein
is involved in many processes that govern gut tissue.
In addition to its involvement in the regulation of beta-catenin,
APC
is a cytoskeletal regulator with direct and indirect effects on microtubules.
Cancer-related truncation mutations lack direct and indirect binding sites for microtubules in
APC
, suggesting that loss of this function contributes to defects in
APC
-mutant cells.
In this study, we show that loss of
APC
results in disappearance of cellular protrusions and decreased cell migration.
Consistent with the ability of
APC
to affect cell shape, the overexpression of
APC
in cells can induce cellular protrusions.
These data demonstrate that cell migration and microtubule stability are linked to
APC
status, thereby revealing a weakness in
APC
-deficient cells with
potential
therapeutic implications.
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]
(PMID = 17192415.001).
[ISSN]
1059-1524
[Journal-full-title]
Molecular biology of the cell
[ISO-abbreviation]
Mol. Biol. Cell
[Language]
ENG
[Grant]
United States / NIGMS NIH HHS / GM / R01 GM061804; United States / NIGMS NIH HHS / GM / GM-61804
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Adenomatous Polyposis Coli Protein
[Other-IDs]
NLM/ PMC1805109
68.
Romero-Giménez J, Dopeso H, Blanco I, Guerra-Moreno A, Gonzalez S, Vogt S, Aretz S, Schwartz S Jr, Capella G, Arango D:
Germline hypermethylation of the APC promoter is not a frequent cause of familial adenomatous polyposis in APC/MUTYH mutation negative families.
Int J Cancer
; 2008 Mar 15;122(6):1422-5
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[Title]
Germline hypermethylation of
the APC
promoter is
not a
frequent cause of
familial
adenomatous polyposis
in
APC
/MUTYH mutation negative families.
Familial
adenomatous polyposis
(
FAP
) is an autosomal dominant
syndrome
predisposing to colorectal cancer and affects 1 in 5-10,000 births.
Inheritance of a mutant allele of the
adenomatous polyposis coli
(
APC
) gene is the cause of approximately 80% of
FAP and
20-30% of an attenuated form of
FAP
(AFAP), whereas mutations in MUTYH account for a small proportion of the remaining cases.
However, the genetic cause of
FAP
/AFAP in a significant number of families is
not
known, and cancer risk for individual members of these families cannot be assessed.
There is, therefore, an acute need to identify the underlying genetic cause responsible for
FAP
/AFAP in
APC
/MUTYH mutation negative families.
Moreover,
APC
promoter hypermethylation is observed in approximately 20% of sporadic colorectal tumors and correlates with the loss of gene expression.
In our study, we used bisulfite treatment and direct sequencing of 2 regulatory regions of
APC
containing a total of 25 CpG dinucleotides, to investigate the possible role of germline hypermethylation of
the APC
promoter in
FAP and
AFAP families that were negative for
APC and
MUTYH mutations.
Analysis of 21
FAP and
39 AFAP families did
not
identify signs of abnormal promoter methylation, indicating that this form of epigenetic silencing is
not a
common cause of
FAP
/AFAP.
These results substantially contribute to clarify
the potential
role of germline epimutations as a cause of inherited predisposition to cancer.
[MeSH-major]
Adenomatous Polyposis Coli
/ genetics. DNA Glycosylases / genetics. DNA Methylation. Genes,
APC
. Germ-Line Mutation. Promoter Regions, Genetic
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[Copyright]
(c) 2007 Wiley-Liss, Inc.
(PMID = 18027849.001).
[ISSN]
1097-0215
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA Primers; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase
69.
Walker LR, Bülow S:
[Restorative proctocolectomy with an ileoanal pouch. Postoperative course and long-term functional results].
Ugeskr Laeger
; 2008 May 12;170(20):1721-5
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INTRODUCTION: Over the last 25 years restorative proctocolectomy with an ileoanal pouch has been the gold standard in the surgical treatment of ulcerative colitis and in selected patients with
familial
adenomatous polyposis
.
MATERIALS AND METHODS: A prospective cohort analysis
and a
questionnaire in 178 consecutive patients operated since 1987 in Hvidovre Hospital.
The late complications comprised reoperation for
intestinal
bowel obstruction in 10 (6%), pouch fistula in 6 (3%), pouchitis in 22 (12%), and anastomotic stricture in 8 (5%).
In our opinion restorative proctocolectomy with an ileoanal pouch is still the gold standard for patients with ulcerative colitis and for selected patients with
familial
adenomatous polyposis
.
[MeSH-major]
Adenomatous Polyposis Coli
/ surgery. Colitis, Ulcerative / surgery. Colonic Pouches. Proctocolectomy, Restorative
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(PMID = 18489884.001).
[ISSN]
1603-6824
[Journal-full-title]
Ugeskrift for laeger
[ISO-abbreviation]
Ugeskr. Laeg.
[Language]
dan
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Denmark
70.
Wu R, Hendrix-Lucas N, Kuick R, Zhai Y, Schwartz DR, Akyol A, Hanash S, Misek DE, Katabuchi H, Williams BO, Fearon ER, Cho KR:
Mouse model of human ovarian endometrioid adenocarcinoma based on somatic defects in the Wnt/beta-catenin and PI3K/Pten signaling pathways.
Cancer Cell
; 2007 Apr;11(4):321-33
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Deregulation of these two pathways in the murine ovarian surface epithelium by conditional inactivation of the Pten
and Apc
tumor suppressor genes results in the formation of adenocarcinomas morphologically similar to human OEAs with 100% penetrance, short latency, and rapid progression to metastatic
disease
in upwards of 75% of mice.
[MeSH-major]
Disease
Models,
Animal
. Ovarian Neoplasms / genetics. PTEN Phosphohydrolase / genetics. Phosphatidylinositol 3-Kinases / genetics. Signal Transduction. Wnt1
Protein
/ genetics. beta Catenin / genetics
[MeSH-minor]
Adenocarcinoma, Clear Cell / genetics. Adenocarcinoma, Clear Cell / metabolism. Adenocarcinoma, Clear Cell / pathology. Adenocarcinoma, Mucinous / genetics. Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Mucinous / pathology.
Adenomatous Polyposis Coli
Protein
/ genetics.
Adenomatous Polyposis Coli
Protein
/ physiology. Animals. Carcinoma, Endometrioid / genetics. Carcinoma, Endometrioid / metabolism. Carcinoma, Endometrioid / pathology. Cystadenocarcinoma, Serous / genetics. Cystadenocarcinoma, Serous / metabolism. Cystadenocarcinoma, Serous / pathology. Epithelium / metabolism. Epithelium / pathology. Female. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Mice. Mutation. Neoplasm Staging. Oligonucleotide Array Sequence Analysis. Ovary / metabolism. Ovary / pathology. Survival Rate. Tumor Suppressor
Protein
p53 / genetics. Tumor Suppressor
Protein
p53 / metabolism
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(PMID = 17418409.001).
[ISSN]
1535-6108
[Journal-full-title]
Cancer cell
[ISO-abbreviation]
Cancer Cell
[Language]
eng
[Databank-accession-numbers]
GEO/ GSE5987/ GSE6008
[Grant]
United States / NCI NIH HHS / CA / P30 CA46592; United States / NCI NIH HHS / CA / R01 CA85463; United States / NCI NIH HHS / CA / R01 CA94172; United States / NCI NIH HHS / CA / U19 CA84953
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Adenomatous Polyposis Coli Protein; 0 / Tumor Suppressor Protein p53; 0 / Wnt1 Protein; 0 / beta Catenin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.3.67 / PTEN Phosphohydrolase
71.
Wang D, Wang H, Guo Y, Ning W, Katkuri S, Wahli W, Desvergne B, Dey SK, DuBois RN:
Crosstalk between peroxisome proliferator-activated receptor delta and VEGF stimulates cancer progression.
Proc Natl Acad Sci U S A
; 2006 Dec 12;103(50):19069-74
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Here, we present genetic and pharmacologic evidence demonstrating that deletion of PPARdelta decreases
intestinal adenoma
growth in
Apc
(Min/+) mice and inhibits tumor-promoting effects of a PPARdelta agonist GW501516.
More importantly, we found that
activation
of PPARdelta up-regulated VEGF in
colon
carcinoma cells.
VEGF directly promotes
colon
tumor epithelial cell survival through
activation
of PI3K-Akt signaling.
These results
not
only highlight concerns about the use of PPARdelta agonists for treatment of metabolic disorders in patients who are at high risk for colorectal cancer, but also support the rationale for developing PPARdelta antagonists for prevention and/or treatment of cancer.
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]
(PMID = 17148604.001).
[ISSN]
0027-8424
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P01 CA 77839; United States / NIDDK NIH HHS / DK / R01 DK 62112; United States / NICHD NIH HHS / HD / R37 HD 12304; United States / NIDDK NIH HHS / DK / R37 DK 47297; United States / NICHD NIH HHS / HD / P30 HD033994; United States / NICHD NIH HHS / HD / R37 HD012304; United States / NCI NIH HHS / CA / P01 CA077839; United States / NCI NIH HHS / CA / P30 CA 068485; United States / NCI NIH HHS / CA / P30 CA068485; United States / NIDDK NIH HHS / DK / R37 DK047297; United States / NIDDK NIH HHS / DK / R01 DK062112; United States / NICHD NIH HHS / HD / U54 HD033994
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / GW 501516; 0 / PPAR delta; 0 / Thiazoles; 0 / Vascular Endothelial Growth Factor A; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
[Other-IDs]
NLM/ PMC1748178
72.
Schönthal AH, Chen TC, Hofman FM, Louie SG, Petasis NA:
Celecoxib analogs that lack COX-2 inhibitory function: preclinical development of novel anticancer drugs.
Expert Opin Investig Drugs
; 2008 Feb;17(2):197-208
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In addition, it was more recently approved as an oral adjunct to prevent
colon
cancer development in patients with
familial
adenomatous polyposis
and is presently being investigated for its chemotherapeutic
potential
in the therapy of advanced cancers.
However, in laboratory studies it was discovered that celecoxib was able to suppress tumor growth in the absence of any apparent involvement of COX-2, and additional pharmacologic activities
associated
with this drug were found.
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(PMID = 18230053.001).
[ISSN]
1744-7658
[Journal-full-title]
Expert opinion on investigational drugs
[ISO-abbreviation]
Expert Opin Investig Drugs
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / 2,5-dimethylcelecoxib; 0 / Antineoplastic Agents; 0 / OSU 03012; 0 / Pyrazoles; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 2; JCX84Q7J1L / Celecoxib
[Number-of-references]
91
73.
Quyn AJ, Steele RJ, Carey FA, Näthke IS:
Prognostic and therapeutic implications of Apc mutations in colorectal cancer.
Surgeon
; 2008 Dec;6(6):350-6
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[Title]
Prognostic and therapeutic implications of
Apc
mutations in colorectal cancer.
The
adenomatous polyposis coli
gene (
Apc
) is mutated in most colorectal cancers.
The multifunctional character of
the Apc protein
in the regulation of beta-catenin-mediated gene transcription and cytoskeletal
proteins
has been well described.
An important question is how this
protein
affects the behaviour of cells within a tumour and how its mutational status influences the prognosis for these tumours.
Here we provide an overview of the functions of
Apc and
examine how this information can be used in the prognosis and development of directed therapy in colorectal cancer.
[MeSH-major]
Colorectal Neoplasms / genetics. Genes,
APC
/ physiology
[MeSH-minor]
Anti-Inflammatory Agents, Non-Steroidal / pharmacology.
Aspirin
/ pharmacology. Cytoskeleton / genetics. Humans. Prognosis. Signal Transduction / drug effects. Signal Transduction / genetics. Wnt
Proteins
/ genetics. beta Catenin / metabolism
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[CommentIn]
Surgeon. 2008 Dec;6(6):324
[
19110817.001
]
(PMID = 19110823.001).
[ISSN]
1479-666X
[Journal-full-title]
The surgeon : journal of the Royal Colleges of Surgeons of Edinburgh and Ireland
[ISO-abbreviation]
Surgeon
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Scotland
[Chemical-registry-number]
0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Wnt Proteins; 0 / beta Catenin; R16CO5Y76E / Aspirin
[Number-of-references]
87
74.
Saif MW, Podoltsev NA, Rubin MS, Figueroa JA, Lee MY, Kwon J, Rowen E, Yu J, Kerr RO:
Phase II clinical trial of paclitaxel loaded polymeric micelle in patients with advanced pancreatic cancer.
Cancer Invest
; 2010 Feb;28(2):186-94
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PURPOSE: To determine in patients, with locally advanced or metastatic pancreatic cancer (
APC
), efficacy and safety of treatment with intravenous paclitaxel loaded polymeric micelle (GPM).
Patients with
APC
, ECOG performance status < or = 2, no prior chemotherapy and adequate organ function were treated with 3-hour GPM infusions every 3 weeks.
Median TTP for patients treated with 300 or 350 mg/m(2) doses was 3.2 months (95%
CI
, 2.6-4.2).
Median progression free survival (PFS) was 2.8 months (95%
CI
, 1.4-4.0).
Median overall survival (OS) was 6.5 months (95%
CI
, 5.1-7.9).
Disease
control rate (CR + PR + stable
disease
) was 60.0%.
CONCLUSIONS: Treatment of
APC
with GPM at a dose of 300 mg/m(2) q 3 weeks was well tolerated and common toxicities were qualitatively similar to Cremophor-based paclitaxel.
Future studies of GPM in combination with other agents for treatment of
APC
are warranted.
[MeSH-minor]
Adult. Aged. Aged, 80 and over.
Disease
-Free Survival. Drug Administration Schedule. Female. Humans. Male. Middle Aged. Neoplasm Metastasis
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(PMID = 19968498.001).
[ISSN]
1532-4192
[Journal-full-title]
Cancer investigation
[ISO-abbreviation]
Cancer Invest.
[Language]
eng
[Publication-type]
Clinical Trial, Phase II; Journal Article; Multicenter Study
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents, Phytogenic; 0 / Micelles; P88XT4IS4D / Paclitaxel
75.
Rajakannu M, Ananthakrishnan N, Madhavan M:
Isolated mesenteric fibromatosis.
Trop Gastroenterol
; 2008 Jul-Sep;29(3):179-80
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Fibromatosis is a rare, locally aggressive but non-metastasising fibrous mass often
associated
with
familial
adenomatous polyposis
in Gardner'
s Syndrome
(GS).
We report the case of a 40-year-old lady who underwent laparotomy for a
large
isolated abdominal mass three years after a Whipple'
s procedure
for adenocarcinoma of the distal common bile duct.
This case is peculiar in that mesenteric fibromatosis occurred in a patient with prior history of periampullary carcinoma and without history of
familial
adenomatous polyposis
.
[MeSH-major]
Fibroma /
diagnosis
. Jejunal Neoplasms /
diagnosis
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(PMID = 19115615.001).
[ISSN]
0250-636X
[Journal-full-title]
Tropical gastroenterology : official journal of the Digestive Diseases Foundation
[ISO-abbreviation]
Trop Gastroenterol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
India
76.
Szczepański M, Stelmachowska M, Stryczyński L, Golusiński W, Samara H, Mozer-Lisewska I, Zeromski J:
Assessment of expression of toll-like receptors 2, 3 and 4 in laryngeal carcinoma.
Eur Arch Otorhinolaryngol
; 2007 May;264(5):525-30
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Toll-like receptors 1-13 (TLRs) are crucial for
activation
of innate immunity and secondarily for the induction of acquired response.
Ligand binding to TLR leads to
the activation
of several genes, predominantly proinflammatory ones such as IL-
1 and
TNF-alpha and maturation of professional antigen presenting cells (
APC
) i.e., dendritic cells.
It can cause better tumor antigen presentation by
APC
.
Immunohistochemistry and indirect immunoflourescence on
frozen
tissue sections.
It is of interest that TLRs tested were expressed
not
only on cells of inflammatory infiltrate, but also on tumor cells.
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[Cites]
J Biol Chem. 2002 Apr 26;277(17):15028-34
[
11836257.001
]
[Cites]
J Immunol. 2000 Jan 15;164(2):558-61
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]
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Lab Invest. 2006 Jan;86(1):9-22
[
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]
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Nat Rev Immunol. 2004 Sep;4(9):675-87
[
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]
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Semin Cancer Biol. 2006 Feb;16(1):3-15
[
16153857.001
]
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Cancer Detect Prev. 1998;22(6):549-55
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]
[Cites]
Curr Opin Immunol. 2002 Jun;14(3):380-3
[
11973138.001
]
(PMID = 17165086.001).
[ISSN]
0937-4477
[Journal-full-title]
European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
[ISO-abbreviation]
Eur Arch Otorhinolaryngol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antigens, CD11; 0 / Antigens, CD3; 0 / HLA-DR Antigens; 0 / Interleukin-1; 0 / Toll-Like Receptor 2; 0 / Toll-Like Receptor 3; 0 / Toll-Like Receptor 4; 0 / Tumor Necrosis Factor-alpha
77.
Cai SR, Yu JK, Jiang WZ, Zhang SZ, Zheng S:
[Application of serum protein markers to distinguish familial adenomatous polyposis (FAP) and sporadic colorectal adenomas].
Zhonghua Zhong Liu Za Zhi
; 2009 Mar;31(3):192-5
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[Title]
[Application of serum
protein
markers to distinguish
familial
adenomatous polyposis
(
FAP
) and sporadic colorectal adenomas].
OBJECTIVE: To screen out specifically-expressed serum
protein
markers in
familial
adenomatous polyposis
(
FAP
) and to establish a serum
protein
fingerprint diagnostic model for distinguishing
FAP
from sporadic colorectal adenomas.
METHODS: Serum samples were collected from 19
FAP
cases and 16 sporadic colorectal adenomas with informed consent.
Serum
protein
fingerprint profiles were detected by SELDI-TOF-MS with CM 10
protein
chip to screen out
FAP adenoma
-related serum
protein
markers, and support vector machine (SVG) technique was used to establish the diagnostic model to distinguish
FAP
from sporadic colorectal adenomas.
RESULTS: Six differently-expressed
protein
peaks (P < 0.01) were detected.
Among them
proteins
of 5640, 3160, 4180 and 4290 m/z were highly expressed in
FAP
adenomas,
and proteins
of 3940 and 3400 m/z were highly expressed in sporadic colorectal adenomas.
The accuracy of diagnostic model established with SVG to distinguish
FAP
adenomas and sporadic colorectal adenomas was 94.7% and 93.7%, respectively.
CONCLUSION: SELDI-TOF-MS can be effectively used to screen out the differentially expressed serum
protein
markers in
FAP
adenomas and sporadic colorectal adenomas,
and a
diagnostic model build by SVG to distinguish them has been successfully established.
Therefore, a useful breakthrough point for research on molecular mechanisms of
FAP
pathogenesis is provided.
[MeSH-major]
Adenoma
/ metabolism.
Adenomatous Polyposis Coli
/ metabolism. Biomarkers, Tumor / metabolism. Colorectal Neoplasms / metabolism. Gene Expression Profiling
[MeSH-minor]
Adult. Aged.
Diagnosis
, Differential. Female. Humans. Male. Middle Aged.
Protein
Array Analysis. Proteomics. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
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(PMID = 19615258.001).
[ISSN]
0253-3766
[Journal-full-title]
Zhonghua zhong liu za zhi [Chinese journal of oncology]
[ISO-abbreviation]
Zhonghua Zhong Liu Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Biomarkers, Tumor
78.
Lee SH, Ahn BK, Chang HK, Baek SU:
Adenocarcinoma in ileal pouch after proctocolectomy for familial adenomatous polyposis: report of a case.
J Korean Med Sci
; 2009 Oct;24(5):985-8
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[Title]
Adenocarcinoma in ileal pouch after proctocolectomy for
familial
adenomatous polyposis
: report of a case.
Restorative proctocolectomy with ileal pouch-anal anastomosis is one of the surgical treatments of choice for patients with
familial
adenomatous polyposis
.
Although the risk of cancer developing in an ileal pouch is
not
yet clear, a few cases of adenocarcinoma arising in an ileal pouch have been reported.
A 56-yr-old woman was diagnosed as having
familial
adenomatous polyposis
.
[MeSH-major]
Adenocarcinoma /
diagnosis
.
Adenomatous Polyposis Coli
/ surgery. Colonic Pouches / pathology. Colorectal Neoplasms /
diagnosis
. Proctocolectomy, Restorative
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[Cites]
Gut. 2000 Nov;47(5):732-4
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11224623.001
]
(PMID = 19795007.001).
[ISSN]
1598-6357
[Journal-full-title]
Journal of Korean medical science
[ISO-abbreviation]
J. Korean Med. Sci.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Korea (South)
[Other-IDs]
NLM/ PMC2752792
[Keywords]
NOTNLM ; Adenocarcinoma / Adenomatous Polyposis Coli / Ileal Pouches
79.
Mahalingam D, Kelly KR, Swords RT, Carew J, Nawrocki ST, Giles FJ:
Emerging drugs in the treatment of pancreatic cancer.
Expert Opin Emerg Drugs
; 2009 Jun;14(2):311-28
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[Title]
Emerging drugs in the treatment of pancreatic cancer.
BACKGROUND: Pancreatic cancer is the fourth leading cause of cancer-related death in the US.
However, there is a growing belief that novel biological agents could improve survival of patients with this cancer.
Gemcitabine-based chemotherapy remains the cornerstone treatment for advanced pancreatic cancers.
So far, the current targeted agents that have been used in combination with gemcitabine have failed to improve clinical outcomes.
This failure may stem from the heterogeneous molecular pathogenesis of pancreatic cancers, which involves several oncogenic pathways and defined genetic mutations.
OBJECTIVE: The aims of this review are: i) to define the existing treatments available at present for patients with pancreatic cancers in the neo-adjuvant, adjuvant, locally advanced and metastatic settings;.
ii) to highlight the molecular heterogeneity of the cancers and the rationale for targeting specific oncogenic pathways;.
iii) to give an overview of targeted agents that may potentially have an impact in the treatment of pancreatic cancers.
CONCLUSIONS: Molecular pathogenesis of pancreatic cancer involves several pathways and defined genetic mutations.
Targeting these complex molecular pathways with a combination of novel biological and chemotherapeutic agents could potentially improve patient outcome.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Drugs, Investigational / therapeutic use. Pancreatic Neoplasms / drug therapy
[MeSH-minor]
Chemotherapy, Adjuvant / trends. Drug Delivery Systems. Humans. Mutation. Oncogenes / physiology. Signal Transduction / drug effects. Signal Transduction / physiology
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(PMID = 19466902.001).
[ISSN]
1744-7623
[Journal-full-title]
Expert opinion on emerging drugs
[ISO-abbreviation]
Expert Opin Emerg Drugs
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Drugs, Investigational
[Number-of-references]
169
80.
Ma JG, Yasue H, Eyer KE, Hiraiwa H, Shimogiri T, Meyers SN, Beever JE, Schook LB, Beattie CW, Liu WS:
An integrated RH map of porcine chromosome 10.
BMC Genomics
; 2009;10:211
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[Title]
An integrated RH
map
of porcine chromosome 10.
BACKGROUND: Whole genome radiation hybrid (WG-RH) maps serve as "scaffolds" to significantly improve the orientation of small bacterial artificial chromosome (BAC) contigs, order genes within the contigs and assist assembly of a sequence-ready
map
for virtually any species.
Here, we report the construction of a porcine: human comparative
map
for pig (Sus scrofa) chromosome 10 (SSC10) using the IMNpRH2(12,000-rad) porcine WG-RH panel, integrated with the IMpRH(7000-rad) WG-RH, genetic and BAC fingerprinted contig (
FPC
) maps.
RESULTS:
Map
vectors from the IMNpRH2(12,000-rad) and IMpRH(7,000-rad) panels were merged to construct parallel framework (FW) maps, within which FW markers common to both panels have an identical order.
This strategy reduced
map
discrepancies between the two panels and significantly improved
map
accuracy.
One linkage group covers SSC10p with accumulated
map
distances of 738.2 cR(7,000) and 1814.5 cR(12,000), respectively.
The second group covers SSC10q at
map
distances of 1336.9 cR(7,000) and 3353.6 cR(12,000), yielding an overall average
map
resolution of 16.4 kb/cR(12,000) or 393.5 kb per marker on SSC10.
This represents an approximately 2.5-fold increase in
map
resolution over the IMpRH(7,000-rad) panel.
Based on 127 porcine markers that have homologous sequences in the human genome, a detailed comparative
map
between SSC10 and human (Homo sapiens) chromosome (HSA) 1, 9 and 10 was built.
CONCLUSION: This initial comparative RH
map
of SSC10 refines the syntenic regions between SSC10 and HSA1, 9 and 10.
It integrates the IMNpRH2(12,000-rad) and IMpRH(7,000-rad), genetic and BAC
FPC
maps and provides a scaffold to close
potential
gaps between contigs prior to genome sequencing and assembly.
This
map
is also useful in fine mapping of QTLs on SSC10.
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(PMID = 19426492.001).
[ISSN]
1471-2164
[Journal-full-title]
BMC genomics
[ISO-abbreviation]
BMC Genomics
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
England
[Chemical-registry-number]
0 / Genetic Markers
[Other-IDs]
NLM/ PMC2689272
81.
Hara T, Nagata M, Yamashita Y, Fujimoto K, Muraki Y, Yasuda Y, Kurahashi T:
[Usefulness of S-1/gemcitabine combination therapy for advanced pancreatic cancer].
Gan To Kagaku Ryoho
; 2008 Jul;35(7):1233-7
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Combination chemotherapy with S-
1 and
gemcitabine(GEM)was given to patients with advanced pancreatic cancer and favorable results were obtained.
One course consisted of a 2-week treatment period
and a
recovery period; this course was repeated in all of these patients.
The 3 types of patients have survived for a year and five months, a year and three months, and nine months, respectively, after
diagnosis
.
Combination therapy with S-
1 and
GEM can be provided for a long-term treatment with few adverse reactions on an outpatient basis.
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(PMID = 18633271.001).
[ISSN]
0385-0684
[Journal-full-title]
Gan to kagaku ryoho. Cancer & chemotherapy
[ISO-abbreviation]
Gan To Kagaku Ryoho
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Drug Combinations; 0W860991D6 / Deoxycytidine; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; B76N6SBZ8R / gemcitabine
82.
Barone M, Scavo MP, Papagni S, Piscitelli D, Guido R, Di Lena M, Comelli MC, Di Leo A:
ERβ expression in normal, adenomatous and carcinomatous tissues of patients with familial adenomatous polyposis.
Scand J Gastroenterol
; 2010 Nov;45(11):1320-8
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[Title]
ERβ expression in normal,
adenomatous
and carcinomatous tissues of patients with
familial
adenomatous polyposis
.
OBJECTIVES:
The APC
gene mutation triggers
familial
adenomatous polyposis
(
FAP
) and approximately 80% of sporadic colorectal cancers.
FAP
summarizes the natural history of colorectal cancer because low- and high-grade dysplastic lesions and adenocarcinoma are simultaneously present in the same patients free from individual and environmental variability factors.
Estrogen receptor beta (ERβ) has recently been suggested as the most likely mediator of estrogen-related anti-carcinogenic effects in
Apc
(Min-/+) mice and humans.
In this study we assessed the ERβ expression in
the intestinal
mucosa of
FAP
patients to verify its possible involvement in tumor progression in colorectal cancer.
MATERIAL AND METHODS: ERβ and ERα expression, cell proliferation (Ki-67) and apoptosis (TUNEL), were evaluated on archival biopsy material from six patients with
FAP
who underwent colectomy.
RESULTS: A progressive significant decrease of ERβ expression was observed in the different stages of
the disease
as compared to normal mucosa (p < 0.001).
CONCLUSIONS: ERβ expression is related to the severity of
the disease
, supporting the role of ERβ as a relevant biomarker of tumor progression and possible chemopreventive target in patients at risk of colonic neoplasia.
[MeSH-major]
Adenocarcinoma / genetics.
Adenomatous Polyposis Coli
/ genetics.
Colon
, Descending / metabolism. Colorectal Neoplasms / genetics. DNA, Neoplasm. Estrogen Receptor beta / genetics. Gene Expression Regulation, Neoplastic
[MeSH-minor]
Adult. Apoptosis. Biopsy. Cell Proliferation.
Disease
Progression. Female. Humans. In Situ Nick-End Labeling.
Intestinal
Mucosa / metabolism.
Intestinal
Mucosa / pathology. Male. Prognosis. Severity of Illness Index
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(PMID = 20446826.001).
[ISSN]
1502-7708
[Journal-full-title]
Scandinavian journal of gastroenterology
[ISO-abbreviation]
Scand. J. Gastroenterol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / DNA, Neoplasm; 0 / Estrogen Receptor beta
83.
Moschos J, Tzilves D, Paikos D, Tagarakis G, Pilpilidis I, Antonopoulos Z, Kadis S, Katsos I, Tarpagos A:
Large mesenteric gastrointestinal stromal tumor in a patient with familial adenomatous polyposis syndrome.
Wien Klin Wochenschr
; 2006 Jun;118(11-12):355-7
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[Title]
Large
mesenteric gastrointestinal stromal tumor in a patient with
familial
adenomatous polyposis
syndrome
.
Colonoscopy revealed many (>100) polyps (
familial
adenomatous polyposis
syndrome
).
Abdominal CT scan showed a
large
mass at the left upper abdomen in conjunction with the splenic flexure.
We describe for the first time in medical literature the coexistence of
familial
adenomatous polyposis
syndrome and
GIST in a 30-year-old man.
[MeSH-major]
Adenomatous Polyposis Coli
/ complications.
Adenomatous Polyposis Coli
/
diagnosis
. Gastrointestinal Stromal Tumors / complications. Gastrointestinal Stromal Tumors /
diagnosis
. Mesentery / pathology
[MeSH-minor]
Adult. Humans. Male. Rare Diseases /
diagnosis
.
Syndrome
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[Cites]
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Zhonghua Bing Li Xue Za Zhi. 2005 Jan;34(1):11-4
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[ISSN]
0043-5325
[Journal-full-title]
Wiener klinische Wochenschrift
[ISO-abbreviation]
Wien. Klin. Wochenschr.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Austria
84.
Buckman SA, Heise CP:
Nutrition considerations surrounding restorative proctocolectomy.
Nutr Clin Pract
; 2010 Jun;25(3):250-6
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Restorative proctocolectomy with ileal pouch-anal anastomosis has become the surgical treatment of choice for patients with ulcerative colitis
and familial
polyposis coli
syndromes
.
Pouch construction uses the distal 30-40 cm of ileum, and there exists
a potential
for postoperative nutrition consequences.
Patients who have undergone an ileal pouch-anal anastomosis
procedure
often describe specific food sensitivities that may require diet alteration, even more so than do patients with permanent ileostomy.
[MeSH-minor]
Adenomatous Polyposis Coli
/ surgery. Anal Canal / surgery. Anemia, Iron-Deficiency / etiology. Colitis, Ulcerative / surgery. Diet. Dietary Supplements. Electrolytes / pharmacokinetics. Humans. Ileostomy.
Intestinal
Absorption. Pouchitis / etiology. Pouchitis / prevention & control. Probiotics. Trace Elements / pharmacokinetics. Vitamin B 12 Deficiency / etiology
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(PMID = 20581318.001).
[ISSN]
1941-2452
[Journal-full-title]
Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition
[ISO-abbreviation]
Nutr Clin Pract
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Electrolytes; 0 / Trace Elements
85.
Abdelrazeq AS, Scott N, Thorn C, Verbeke CS, Ambrose NS, Botterill ID, Jayne DG:
The impact of spontaneous tumour perforation on outcome following colon cancer surgery.
Colorectal Dis
; 2008 Oct;10(8):775-80
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[Title]
The impact of spontaneous tumour perforation on outcome following
colon
cancer surgery.
OBJECTIVE: The impact of spontaneous tumour perforation on survival following surgery for
colon
cancer is unclear.
METHOD: A prospective histological database was searched for all patients undergoing resection for adenocarcinoma of
the colon
between 1996 and 2002.
Patients with synchronous colonic and rectal cancers,
familial
polyposis
, inflammatory bowel
disease
, iatrogenic or remote colonic perforation were excluded.
Data were analysed for differences in demographics, histological variables, operative mortality,
disease
-free and overall survival.
Patients with perforated cancers were more likely to present with metastatic
disease and
undergo emergency surgery with a higher 30-day mortality.
There was a trend towards reduced overall survival in the perforated group (P = 0.06), but no difference in
disease
-free survival (P = 0.43).
CONCLUSION: Both perforated and nonperforated T4
colon
cancers have a poor prognosis.
Spontaneous perforation of the cancer is
associated
with reduced overall survival, due to higher 30-day mortality, but in itself does
not
appear to significantly impact on
disease
-free survival.
[MeSH-major]
Adenocarcinoma / mortality. Adenocarcinoma / surgery. Cause of Death. Colonic Neoplasms / mortality. Colonic Neoplasms / surgery.
Intestinal
Perforation / mortality
[MeSH-minor]
Adult. Age Factors. Aged. Aged, 80 and over. Biopsy, Needle. Cohort Studies. Colectomy / adverse effects. Colectomy / methods.
Disease
-Free Survival. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Multivariate Analysis. Neoplasm Staging. Postoperative Complications /
diagnosis
. Postoperative Complications / mortality. Probability. Prognosis. Proportional Hazards Models. Prospective Studies. Registries. Risk Assessment. Sex Factors. Statistics, Nonparametric. Survival Analysis
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(PMID = 18266887.001).
[ISSN]
1463-1318
[Journal-full-title]
Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland
[ISO-abbreviation]
Colorectal Dis
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
England
86.
Scott EN, Garcea G, Doucas H, Steward WP, Dennison AR, Berry DP:
Surgical bypass vs. endoscopic stenting for pancreatic ductal adenocarcinoma.
HPB (Oxford)
; 2009 Mar;11(2):118-24
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Methods of palliation in such patients with locally advanced
disease
comprise endoscopic placement of a biliary endoprosthesis or surgical bypass.
RESULTS: We identified a total of 56 patients, of whom 33 underwent endoscopic stenting and 23 underwent a surgical bypass consisting of a hepaticojejunostomy-en-Y
and a
gastrojejunostomy.
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