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1
adenocarcinoma basal cell 2005:2010[pubdate] *count=100
464 results
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adenocarcinoma
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Items 1 to 100 of about 464
1.
Montironi R, Mazzucchelli R, Lopez-Beltran A, Cheng L, Scarpelli M:
Mechanisms of disease: high-grade prostatic intraepithelial neoplasia and other proposed preneoplastic lesions in the prostate.
Nat Clin Pract Urol
; 2007 Jun;4(6):321-32
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[Title]
Mechanisms of
disease
: high-grade prostatic intraepithelial
neoplasia
and other proposed preneoplastic lesions in the prostate.
High-grade prostatic intraepithelial
neoplasia
(HGPIN) is the most likely precursor of prostatic
adenocarcinoma
according to virtually all available evidence.
This lesion is characterized by cellular proliferations within pre-existing ducts and acini, with nuclear and nucleolar enlargements similar to those seen in prostate cancer, although unlike cancer HGPIN retains a
basal
-
cell
layer.
The recognition of HGPIN is clinically important because of the strong association between this
disease
and prostatic carcinoma.
The predictive value for cancer of an initial
diagnosis
of HGPIN on needle biopsy has substantially declined, with values falling from 36% to 21%.
Other possible findings in the prostate might indicate premalignant
disease
(low-grade prostatic intraepithelial
neoplasia
, atrophy, malignancy-associated changes, and atypical
adenomatous
hyperplasia or adenosis), but the data for these premalignant diseases are much less convincing than those for HGPIN.
[MeSH-major]
Precancerous Conditions. Prostatic Intraepithelial
Neoplasia
/
diagnosis
. Prostatic Intraepithelial
Neoplasia
/ pathology. Prostatic Neoplasms /
diagnosis
. Prostatic Neoplasms / pathology
[MeSH-minor]
Adenocarcinoma
/
diagnosis
.
Adenocarcinoma
/ pathology. Biopsy, Needle. Humans. Male. Predictive Value of Tests
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(PMID = 17551536.001).
[ISSN]
1743-4289
[Journal-full-title]
Nature clinical practice. Urology
[ISO-abbreviation]
Nat Clin Pract Urol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
78
2.
Lal DR, Clark I, Shalkow J, Downey RJ, Shorter NA, Klimstra DS, La Quaglia MP:
Primary epithelial lung malignancies in the pediatric population.
Pediatr Blood Cancer
; 2005 Oct 15;45(5):683-6
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We reviewed the Memorial Sloan-Kettering Cancer Center experience with these tumors to better understand their histology, time to
diagnosis
, treatment, and outcome.
PROCEDURE: A retrospective review was performed on all patients 21 years of age or younger at
diagnosis
, treated for primary epithelial lung malignancies at Memorial Sloan-Kettering Cancer Center between 1980 and 2001.
The median age at
diagnosis
was 19 (range: 12-21) years.
The most common radiographic
abnormality
was a mass (55%) on chest imaging.
Seven patients (64%) were initially diagnosed as having pneumonia which contributed to a delay in
diagnosis
.
Final pathologic diagnoses included
adenocarcinoma
(four), carcinoid tumor (three typical, one atypical), basaloid carcinoma (two), and mucoepidermoid carcinoma (one).
A majority of patients presented with advanced
disease
(two stage III, four stage IV).
Patients with localized
disease
were treated with surgical resection and all but one remains
disease
free with a median follow-up of 60 months (range: 13-286).
Patients with either advanced locoregional or distant metastatic
disease
were treated with multimodal therapy and a majority had rapid progression of
disease
.
CONCLUSIONS: When children and adolescents present with primary epithelial lung malignancy a majority will have advanced
disease
and experience a delay in
diagnosis
.
Patients with carcinoid tumors seem to have the best prognosis, followed by
adenocarcinoma
.
[MeSH-major]
Carcinoma /
diagnosis
. Lung Neoplasms /
diagnosis
[MeSH-minor]
Adenocarcinoma
/
diagnosis
.
Adenocarcinoma
/ pathology. Adolescent. Adult. Carcinoid Tumor /
diagnosis
. Carcinoid Tumor / pathology. Carcinoma,
Basal Cell
/
diagnosis
. Carcinoma,
Basal Cell
/ pathology. Child. Diagnostic Errors. Female. Humans. Male. Pneumonia /
diagnosis
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(PMID = 15714450.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
3.
Sitterding SM, Wiseman WR, Schiller CL, Luan C, Chen F, Moyano JV, Watkin WG, Wiley EL, Cryns VL, Diaz LK:
AlphaB-crystallin: a novel marker of invasive basal-like and metaplastic breast carcinomas.
Ann Diagn Pathol
; 2008 Feb;12(1):33-40
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[Title]
AlphaB-crystallin: a novel marker of invasive
basal
-like and metaplastic breast carcinomas.
Basal
-like tumors are a newly recognized estrogen receptor (ER) negative and HER2 negative breast cancer
subtype
that express
basal
epithelial genes and are associated with poor survival.
Metaplastic carcinomas are thought to belong within the
basal
-like group.
We have recently demonstrated that the small heat shock protein alphaB-crystallin is commonly expressed in
basal
-like tumors and contributes to their aggressive phenotype.
The current study examined the rates and patterns of alphaB-crystallin expression in whole tissue sections of human breast, including normal tissue, proliferative lesions, in situ and invasive carcinomas (ER positive, HER2 positive,
basal
-like, and metaplastic cancers).
In normal breast tissue, proliferative lesions and in situ carcinomas, alphaB-crystallin expression was restricted to the myoepithelial
cell
compartment of ductal and lobular units.
Most
basal
-like and metaplastic carcinomas demonstrated cytoplasmic expression of alphaB-crystallin (81% and 86%, respectively).
Taken together, our results indicate that alphaB-crystallin is a sensitive (81%) and specific (100%) marker for
basal
-like breast carcinomas.
Moreover, the high rates of expression of alphaB-crystallin in metaplastic breast carcinomas (86%) suggest that these tumors may represent a histologically distinctive subset of
basal
-like breast tumors with a similar underlying molecular etiology.
[MeSH-major]
Adenocarcinoma
/ metabolism. Biomarkers, Tumor / metabolism. Breast Neoplasms / metabolism.
Neoplasm
Proteins / metabolism. alpha-Crystallin B Chain / metabolism
[MeSH-minor]
Breast Cyst / metabolism. Breast Cyst / pathology. Carcinoma, Intraductal, Noninfiltrating / metabolism. Carcinoma, Intraductal, Noninfiltrating / pathology.
Cell
Proliferation. Female. Fibrocystic Breast
Disease
/ metabolism. Fibrocystic Breast
Disease
/ pathology. Fluorescent Antibody Technique, Indirect. Humans. Immunoenzyme Techniques. Metaplasia.
Neoplasm
Invasiveness. Predictive Value of Tests
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(PMID = 18164413.001).
[ISSN]
1092-9134
[Journal-full-title]
Annals of diagnostic pathology
[ISO-abbreviation]
Ann Diagn Pathol
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P50CA89018; United States / NCI NIH HHS / CA / R01CA097198
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / alpha-Crystallin B Chain
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4.
Adley BP, Yang XJ:
Alpha-methylacyl coenzyme A racemase immunoreactivity in partial atrophy of the prostate.
Am J Clin Pathol
; 2006 Dec;126(6):849-55
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In addition, 82 (67.2%) showed patchy to negative distribution of
basal
cells
.
Compounding this problem, focal lack of
basal
cells
may be seen.
However, the AMACR staining pattern of partial atrophy is usually comparable to that of adjacent benign glands and substantially different from
adenocarcinoma
.
[MeSH-minor]
Adenocarcinoma
/ enzymology.
Adenocarcinoma
/ pathology. Adult. Aged. Atrophy / enzymology. Atrophy / pathology. Biomarkers / metabolism. Biopsy, Needle. Humans. Immunoenzyme Techniques. Male. Middle Aged. Prostatic Neoplasms / enzymology. Prostatic Neoplasms / pathology
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.
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(PMID = 17074684.001).
[ISSN]
0002-9173
[Journal-full-title]
American journal of clinical pathology
[ISO-abbreviation]
Am. J. Clin. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
5.
Mukherjee S, Bhattacharya RK, Roy M:
Targeting protein kinase C (PKC) and telomerase by phenethyl isothiocyanate (PEITC) sensitizes PC-3 cells towards chemotherapeutic drug-induced apoptosis.
J Environ Pathol Toxicol Oncol
; 2009;28(4):269-82
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[Title]
Targeting protein kinase C (PKC) and telomerase by phenethyl isothiocyanate (PEITC) sensitizes PC-3
cells
towards chemotherapeutic drug-induced apoptosis.
Telomerase, a reverse transcriptase, is highly activated in prostate cancer
cells
.
The present study investigates the effects of natural isothiocyanate phenethyl isothiocyanate (PEITC) in modulating the activities of PKC and telomerase in the androgen-independent human prostate
adenocarcinoma
(PC-3)
cell
line.
Basal
level of PKC delta, a proapoptotic form, was very poor and its modulation was not significant.
Studies were conducted to measure the degree of apoptotic
cell
death induced either by PEITC alone or in combination with adriamycin or etoposide.
PEITC exhibited remarkable efficacy in sensitizing PC-3
cells
to undergo
cell
death by adriamycin and etoposide, which might prove to be of considerable value in synergistic therapy of cancer.
[MeSH-minor]
Antineoplastic Combined Chemotherapy Protocols / pharmacology. Biomarkers, Tumor / metabolism. Caspases / metabolism.
Cell
Line, Tumor. Cytochromes c / metabolism. Down-Regulation / drug effects. Doxorubicin / pharmacology. Drug Resistance,
Neoplasm
. Etoposide / pharmacology. Humans. Male
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.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
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(PMID = 20102325.001).
[ISSN]
2162-6537
[Journal-full-title]
Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer
[ISO-abbreviation]
J. Environ. Pathol. Toxicol. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Isothiocyanates; 6PLQ3CP4P3 / Etoposide; 6U7TFK75KV / phenethyl isothiocyanate; 80168379AG / Doxorubicin; 9007-43-6 / Cytochromes c; EC 2.7.11.13 / Protein Kinase C; EC 2.7.7.49 / Telomerase; EC 3.4.22.- / Caspases
6.
Paquette J, Bessette B, Ledru E, Deal C:
Identification of upstream stimulatory factor binding sites in the human IGFBP3 promoter and potential implication of adjacent single-nucleotide polymorphisms and responsiveness to insulin.
Endocrinology
; 2007 Dec;148(12):6007-18
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Functionality of these SNPs was further explored in hepatic
adenocarcinoma
-derived SK-HEP-1
cells
using transient transfections of luciferase constructs driven by different haplotypes of the IGFBP3 promoter.
Basal
luciferase activity revealed a significant haplotype-dependent transcriptional activity (at nucleotides -202 and -185, AC > CC, P < 0.001; AC > CT, P < 0.001; AC > AT, P < 0.001).
Chromatin immunoprecipitation with anti-USF-1/-2 showed an enrichment of IGFBP3 promoter in insulin-treated
cells
compared with unstimulated
cells
.
In summary, we report a methylation-dependent USF binding site influencing the
basal
and insulin-stimulated transcriptional activity of the IGFBP3 promoter.
[MeSH-minor]
Base Sequence. Binding Sites / genetics.
Cell
Line, Tumor. Chromatin Immunoprecipitation. DNA Methylation. Electrophoretic Mobility Shift Assay. Haplotypes. Humans. Insulin-Like Growth Factor Binding Protein 3. Luciferases / genetics. Luciferases / metabolism. Molecular Sequence Data. Mutagenesis, Site-Directed. Mutation. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Transcription, Genetic / drug effects
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(PMID = 17823260.001).
[ISSN]
0013-7227
[Journal-full-title]
Endocrinology
[ISO-abbreviation]
Endocrinology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / IGFBP3 protein, human; 0 / Insulin; 0 / Insulin-Like Growth Factor Binding Protein 3; 0 / Insulin-Like Growth Factor Binding Proteins; 0 / Recombinant Fusion Proteins; 0 / Upstream Stimulatory Factors; EC 1.13.12.- / Luciferases
7.
Sanchis García JM, Dualde Beltrán D, Ramírez Sabio JB, Vera González A, Palmero da Cruz J:
[Well-differentiated basal cell adenocarcinoma of the lacrimal sac: a case report].
Radiologia
; 2007 May-Jun;49(3):201-4
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[Title]
[Well-differentiated
basal cell adenocarcinoma
of the lacrimal sac: a case report].
[Transliterated title]
Adenocarcinoma
de
células basales del saco lacrimal bien diferenciado. A propósito
de
un caso.
Basal cell adenocarcinoma
is a rare tumor first considered to be a separate entity by the WHO in 1991.
We present a case of
adenocarcinoma
of the lacrimal sac diagnosed at histological study.
We discuss the differential
diagnosis
and treatment for this tumor.
[MeSH-major]
Adenocarcinoma
/
diagnosis
. Lacrimal Apparatus
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(PMID = 17524341.001).
[ISSN]
0033-8338
[Journal-full-title]
Radiología
[ISO-abbreviation]
Radiologia
[Language]
spa
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Spain
8.
Forest V, Campos L, Péoc'h M, Guyotat D, Vergnon JM:
[Development of an experimental model for the study of the effects of cryotherapy on lung tumours].
Pathol Biol (Paris)
; 2005 May;53(4):199-203
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Adenocarcinomas
are today the most frequent lung cancers.
MATERIALS AND METHODS: A xenograft system was used:
cells
from the A549
cell
line were injected subcutaneously into SCID mice.
The histological study showed that these tumours faithfully reproduced the morphological features of
adenocarcinoma
, and developed an intratumoral neovascularization.
RESULTS: The
basal
expression of cleaved caspase-3 in untreated tumours (23%) increased after cryotherapy.
The increase was maximal eight hours after treatment (up to 47% of positive
cells
) and was less important with the first protocol, suggesting a lesser efficiency in the induction of apoptosis.
[MeSH-major]
Adenocarcinoma
/ therapy. Cryotherapy. Lung Neoplasms / therapy. Neoadjuvant Therapy. Neoplasms, Experimental / therapy
[MeSH-minor]
Animals.
Cell
Line, Tumor / transplantation. Humans. Male. Mice. Mice, SCID.
Neoplasm
Transplantation. Xenograft Model Antitumor Assays
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(PMID = 15850952.001).
[ISSN]
0369-8114
[Journal-full-title]
Pathologie-biologie
[ISO-abbreviation]
Pathol. Biol.
[Language]
fre
[Publication-type]
English Abstract; Evaluation Studies; Journal Article
[Publication-country]
France
9.
Li Y, Wo JM, Su RR, Ray MB, Jones W, Martin RC:
Esophageal injury with external esophageal perfusion.
J Surg Res
; 2005 Nov;129(1):107-13
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BACKGROUND: External esophageal perfusion (EEP) with the idea that esophageal perfusion can be controlled with a single ingredient at a constant rate and concentration, might be used to dissect the injurious role of gastro-duodenal secretions for the progression from esophagitis to Barrett's esophagus (BE) and esophageal
adenocarcinoma
(EAC).
Histological changes,
cell
proliferation, apoptosis, 8-hydroxy-deoxyguanosine (8-OH-dG) and Manganese superoxide dismutase (MnSOD) were observed after perfusion and compared.
RESULTS: The bile perfusion for 1 week, 2 weeks, and 4 weeks induced mucosa infiltration of inflammatory
cells
,
basal cell
hyperproliferation, and papillae hypertrophy in all animals.
Further studies are needed to induce Barrett's esophagus and esophageal
adenocarcinoma
.
[MeSH-minor]
Animals. Apoptosis.
Cell
Division. Deoxyguanosine / analogs & derivatives. Deoxyguanosine / analysis. Gastric Juice / chemistry. Hypertrophy. Immunohistochemistry. In Situ Nick-End Labeling. Mucous Membrane / pathology. Rats. Rats, Sprague-Dawley. Superoxide Dismutase / analysis. Time Factors
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(PMID = 15921698.001).
[ISSN]
0022-4804
[Journal-full-title]
The Journal of surgical research
[ISO-abbreviation]
J. Surg. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; EC 1.15.1.1 / Superoxide Dismutase; G9481N71RO / Deoxyguanosine
10.
Quintyn-Ranty ML, Escourrou G, Guilbeau C, Rimailho J, Delisle MB:
[Vaginal adenoid cystic carcinoma: a case report].
Ann Pathol
; 2008 Apr;28(2):135-7
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[Transliterated title]
Carcinome
adénoïde kystique vaginal: à propos d'un cas.
Differential
diagnosis
includes adenoid
basal
carcinoma, polymorphous low-grade
adenocarcinoma
and basaloid squamous
cell
carcinoma.
Histological examination revealed nests of
cells
with peripheral palisading organisation and glandular lumina containing material produced by the tumor
cells
.
[MeSH-minor]
Actins / analysis. Epithelial
Cells
/ pathology. Female. Humans. Middle Aged. Papillomavirus Infections / pathology
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(PMID = 18675169.001).
[ISSN]
0242-6498
[Journal-full-title]
Annales de pathologie
[ISO-abbreviation]
Ann Pathol
[Language]
fre
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
France
[Chemical-registry-number]
0 / Actins
11.
Teulière J, Faraldo MM, Deugnier MA, Shtutman M, Ben-Ze'ev A, Thiery JP, Glukhova MA:
Targeted activation of beta-catenin signaling in basal mammary epithelial cells affects mammary development and leads to hyperplasia.
Development
; 2005 Jan;132(2):267-77
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[Title]
Targeted activation of beta-catenin signaling in
basal
mammary epithelial
cells
affects mammary development and leads to hyperplasia.
Wnt/beta-catenin signaling pathway is involved in the maintenance of the progenitor
cell
population in the skin, intestine and other tissues, and its aberrant activation caused by stabilization of beta-catenin contributes to tumorigenesis.
In the mammary gland, constitutive activation of Wnt/beta-catenin signaling in luminal secretory
cells
results in precocious lobuloalveolar differentiation and induces
adenocarcinomas
, whereas the impact of this signaling pathway on the function of the second major mammary epithelial
cell
lineage, the
basal
myoepithelial
cells
, has not been analyzed.
We have used the keratin (K) 5 promoter to target the expression of stabilized N-terminally truncated beta-catenin to the
basal cell
layer of mouse mammary epithelium.
Nulliparous transgenic females developed mammary hyperplasia that comprised undifferentiated
basal
(K5/14-positive, K8- and alpha-smooth muscle-actin-negative)
cells
.
Multiparous mice, in addition, developed invasive
basal
-type carcinomas.
Thus, activation of beta-catenin signaling in
basal
mammary epithelial
cells
affects the entire process of mammary gland development and induces amplification of
basal
-type
cells
that lack lineage markers, presumably, a subpopulation of mammary progenitors able to give rise to tumors.
[MeSH-major]
Cytoskeletal Proteins / genetics. Cytoskeletal Proteins / metabolism. Epithelial
Cells
/ metabolism. Gene Expression Regulation, Developmental. Mammary Glands, Animal / metabolism. Trans-Activators / genetics. Trans-Activators / metabolism
[MeSH-minor]
Adenocarcinoma
/ metabolism. Animals. Blotting, Southern. Blotting, Western.
Cell
Differentiation.
Cell
Lineage.
Cell
Proliferation. DNA Primers / chemistry. Epithelium / pathology. Female. Hyperplasia / metabolism. Immunohistochemistry. In Situ Nick-End Labeling. Mice. Mice, Inbred C57BL. Mice, Transgenic. Microscopy, Fluorescence. Phosphoproteins / genetics. Polymerase Chain Reaction. Promoter Regions, Genetic. Protein Structure, Tertiary. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Time Factors. beta Catenin
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SciCrunch.
Marmoset Gene list: Data: Gene Annotation
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(PMID = 15590737.001).
[ISSN]
0950-1991
[Journal-full-title]
Development (Cambridge, England)
[ISO-abbreviation]
Development
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / CTNNB1 protein, mouse; 0 / Cytoskeletal Proteins; 0 / DNA Primers; 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / Trans-Activators; 0 / Trp63 protein, mouse; 0 / beta Catenin
12.
Epstein JI:
An update of the Gleason grading system.
J Urol
; 2010 Feb;183(2):433-40
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RESULTS: Since the introduction of the Gleason grading system more than 40 years ago many aspects of prostate cancer have changed, including prostate specific antigen testing, transrectal ultrasound guided prostate needle biopsy with greater sampling, immunohistochemistry for
basal
cells
that changed the classification of prostate cancer and new prostate cancer variants.
The grading of variants and subtypes of acinar
adenocarcinoma
of the prostate, including cancer with vacuoles, foamy gland carcinoma, ductal
adenocarcinoma
, pseudohyperplastic carcinoma and small
cell
carcinoma have also been modified.
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[Copyright]
Copyright 2010 American Urological Association. Published by Elsevier Inc. All rights reserved.
(PMID = 20006878.001).
[ISSN]
1527-3792
[Journal-full-title]
The Journal of urology
[ISO-abbreviation]
J. Urol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
43
13.
Ihemelandu CU, Naab TJ, Mezghebe HM, Makambi KH, Siram SM, Leffall LD Jr, Dewitty RL Jr, Frederick WA:
Basal cell-like (triple-negative) breast cancer, a predictor of distant metastasis in African American women.
Am J Surg
; 2008 Feb;195(2):153-8
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[Title]
Basal cell
-like (triple-negative) breast cancer, a predictor of distant metastasis in African American women.
BACKGROUND: The aim of this study was to evaluate the prognostic significance of the
basal cell
-like molecular breast cancer
subtype
with respect to locoregional recurrence and distant metastasis in African American women treated for breast cancer.
Compared with the other molecular subtypes the
basal cell
-like
subtype
showed a statistically significant association to distant metastasis: 15 (42.9%) vs 13 (37.1%), 4 (11.4%), and 3 (8.6%) (P < .001), respectively, for luminal A, Her-2/neu, and luminal B subtypes.
The
basal cell
-like
subtype
was an independent predictor of distant metastasis (odds ratio, 5.8; 95% confidence interval, 1.5-22.0, P = .009).
The molecular subtypes showed no statistically significant difference with respect to locoregional treatment administered and tumor stage at time of
diagnosis
.
CONCLUSIONS: The
basal cell
-like molecular breast cancer
subtype
is an independent predictor of distant metastasis in African American women.
[MeSH-major]
Adenocarcinoma
/ ethnology.
Adenocarcinoma
/ secondary. African Americans / genetics. Breast Neoplasms / ethnology. Breast Neoplasms / genetics.
Neoplasm
Recurrence, Local / genetics
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(PMID = 18083134.001).
[ISSN]
1879-1883
[Journal-full-title]
American journal of surgery
[ISO-abbreviation]
Am. J. Surg.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
14.
Graveel CR, DeGroot JD, Su Y, Koeman J, Dykema K, Leung S, Snider J, Davies SR, Swiatek PJ, Cottingham S, Watson MA, Ellis MJ, Sigler RE, Furge KA, Vande Woude GF:
Met induces diverse mammary carcinomas in mice and is associated with human basal breast cancer.
Proc Natl Acad Sci U S A
; 2009 Aug 4;106(31):12909-14
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[Title]
Met induces diverse mammary carcinomas in mice and is associated with human
basal
breast cancer.
We describe a knockin mouse with mutationally activated Met (Met(mut)) that develops a high incidence of diverse mammary tumors with
basal
characteristics, including metaplasia, absence of progesterone receptor and ERBB2 expression, and expression of cytokeratin 5.
With gene expression and tissue microarray analysis, we show that high MET expression in human breast cancers significantly correlated with estrogen receptor negative/ERBB2 negative tumors and with
basal
breast cancers.
Few treatment options exist for breast cancers of the
basal
or trastuzumab-resistant ERBB2 subtypes.
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.
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.
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J Mammary Gland Biol Neoplasia. 1998 Jan;3(1):85-94
[
10819507.001
]
(PMID = 19567831.001).
[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 / NCI NIH HHS / CA / F32 CA105748; United States / NCI NIH HHS / CA / U01 CA114722; United States / NCI NIH HHS / CA / F32CA105748
[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 / Receptors, Progesterone; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Erbb2 protein, mouse; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; EC 2.7.10.1 / Receptor, ErbB-2
[Other-IDs]
NLM/ PMC2722304
15.
Donadelli M, Dalla Pozza E, Scupoli MT, Costanzo C, Scarpa A, Palmieri M:
Intracellular zinc increase inhibits p53(-/-) pancreatic adenocarcinoma cell growth by ROS/AIF-mediated apoptosis.
Biochim Biophys Acta
; 2009 Feb;1793(2):273-80
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[Title]
Intracellular zinc increase inhibits p53(-/-) pancreatic
adenocarcinoma cell
growth by ROS/AIF-mediated apoptosis.
We show that treatment with non-toxic doses of zinc in association to the ionophore compound pyrrolidine dithiocarbamate (PDTC) inhibits p53(-/-) pancreatic cancer
cell
growth much more efficiently than gemcitabine, the gold standard chemotherapeutic agent for pancreatic cancer.
Both the metal chelator N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine and the radical scavenger N-acetyl-l-cysteine are able to recover
cell
growth inhibition by Zn/PDTC, demonstrating that this effect depends on the increased levels of intracellular zinc and of reactive oxygen species (ROS).
Zn/PDTC treatment induces a strong apoptotic
cell
death that is associated to ROS-dependent nuclear translocation of the mitochondrial factor AIF, but not to the regulation of apoptotic genes and caspase activation.
Primary fibroblasts are more resistant than pancreatic cancer
cells
to Zn/PDTC treatment and exhibit a lower
basal
and Zn/PDTC-induced enhancement of intracellular zinc.
[MeSH-major]
Adenocarcinoma
/ pathology. Apoptosis. Apoptosis Inducing Factor / metabolism. Pancreatic Neoplasms / pathology. Reactive Oxygen Species / metabolism. Tumor Suppressor Protein p53 / deficiency. Zinc / metabolism
[MeSH-minor]
Caspases / metabolism.
Cell
Line, Tumor.
Cell
Nucleus / drug effects.
Cell
Nucleus / metabolism.
Cell
Proliferation / drug effects. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Ethylenediamines / pharmacology. Fibroblasts / cytology. Fibroblasts / drug effects. Humans. Intracellular Space / drug effects. Intracellular Space / metabolism. Leupeptins / pharmacology. Mitochondria / drug effects. Mitochondria / enzymology. Models, Biological. Protein Transport / drug effects. Pyrrolidines / pharmacology. Thiocarbamates / pharmacology
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.
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ZINC, ELEMENTAL
.
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(PMID = 18951928.001).
[ISSN]
0006-3002
[Journal-full-title]
Biochimica et biophysica acta
[ISO-abbreviation]
Biochim. Biophys. Acta
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Apoptosis Inducing Factor; 0 / Ethylenediamines; 0 / Leupeptins; 0 / Pyrrolidines; 0 / Reactive Oxygen Species; 0 / Thiocarbamates; 0 / Tumor Suppressor Protein p53; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 16858-02-9 / N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine; 25769-03-3 / pyrrolidine dithiocarbamic acid; EC 3.4.22.- / Caspases; J41CSQ7QDS / Zinc
16.
González-García R, Nam-Cha SH, Muñoz-Guerra MF, Gamallo-Amat C:
Basal cell adenoma of the parotid gland. Case report and review of the literature.
Med Oral Patol Oral Cir Bucal
; 2006 Mar;11(2):E206-9
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[Title]
Basal cell
adenoma
of the parotid gland. Case report and review of the literature.
Basal cell
adenoma
of the salivary glands is an uncommon type of monomorphous
adenoma
.
Histologically, isomorphic
cells
in nests and interlaced trabecules with a prominent
basal
membrane are observed.
In contrast to pleomorphic
adenoma
, it tends to be multiple and its recurrence rate after surgical excision is high.
Due to prognostic implications, differential
diagnosis
with
basal cell adenocarcinoma
, adenoid cystic carcinoma and basaloid squamous
cell
carcinoma is mandatory.
We describe a case of
basal cell
adenoma
of the parotid gland.
We also review the literature and discuss the
diagnosis
and management of this rare entity.
[MeSH-major]
Adenoma
/ pathology. Parotid Neoplasms / pathology
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(PMID = 16505803.001).
[ISSN]
1698-6946
[Journal-full-title]
Medicina oral, patología oral y cirugía bucal
[ISO-abbreviation]
Med Oral Patol Oral Cir Bucal
[Language]
eng; spa
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Spain
[Number-of-references]
21
17.
Fok JY, Mehta K:
Tissue transglutaminase induces the release of apoptosis inducing factor and results in apoptotic death of pancreatic cancer cells.
Apoptosis
; 2007 Aug;12(8):1455-63
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[Title]
Tissue transglutaminase induces the release of apoptosis inducing factor and results in apoptotic death of pancreatic cancer
cells
.
Pancreatic ductal
adenocarcinoma
(PDAC) is a highly lethal
malignant disease
with poor long-term survival rates.
Major reason for poor
disease
outcome is the profound intrinsic resistance of PDAC
cells
to currently available treatment regimens.
We recently found that a great majority of PDAC tumors and tumor
cell
lines express high
basal
level of tissue transglutaminase (TG2), a multifunctional protein implicated in apoptosis,
cell
attachment,
cell
survival, and
cell
motility functions.
Based on these observations, we hypothesized that activation of endogenous TG2 can induce spontaneous apoptosis in PDAC
cells
.
The results obtained suggested that activation of endogenous TG2 by calcium ionophore A23187 induced rapid and spontaneous apoptosis in PDAC
cells
.
The release of AIF from mitochondria led to its translocation to the nucleus and subsequent apoptosis of PDAC
cells
in caspase-independent manner.
In conclusion, our results provide first evidence that TG2 can induce apoptosis in PDAC
cells
in an AIF-dependent and caspase-independent manner.
[MeSH-minor]
Calcimycin / pharmacology. Calcium Channels / metabolism.
Cell
Death.
Cell
Differentiation. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology.
Disease
Progression. GTP-Binding Proteins. Gene Expression Regulation, Neoplastic. Humans. Ionophores / pharmacology. Models, Biological. Tumor
Cells
, Cultured
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(PMID = 17440814.001).
[ISSN]
1360-8185
[Journal-full-title]
Apoptosis : an international journal on programmed cell death
[ISO-abbreviation]
Apoptosis
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / AIFM1 protein, human; 0 / Apoptosis Inducing Factor; 0 / Calcium Channels; 0 / Ionophores; 0W860991D6 / Deoxycytidine; 37H9VM9WZL / Calcimycin; B76N6SBZ8R / gemcitabine; EC 2.3.2.- / transglutaminase 2; EC 2.3.2.13 / Transglutaminases; EC 3.6.1.- / GTP-Binding Proteins
18.
Yazgan S, Gürsoy S, Yaldiz S, Basok O:
Outcome of surgery for lung cancer in young and elderly patients.
Surg Today
; 2005;35(10):823-7
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We conducted this study to determine whether the
basal
characteristics and survival of young patients undergoing surgical resection of lung cancer differ from those of elderly patients.
The patients' medical records were reviewed with respect to age, gender, histological
diagnosis
, coexisting diseases, smoking history, postoperative staging, type of operation, and postoperative morbidity, mortality, and survival results.
However, the 5-year survival rates for patients who underwent surgery for non-small
cell
lung cancer did not differ between groups 1 and 2, at 33.3% versus 21.3%, respectively (P = 0.09).
CONCLUSIONS: The incidence of
adenocarcinoma
was higher in the young patients, whose prognosis was slightly better than that of the elderly patients.
[MeSH-major]
Carcinoma, Non-Small-
Cell
Lung / mortality. Carcinoma, Non-Small-
Cell
Lung / surgery. Carcinoma, Small
Cell
/ mortality. Carcinoma, Small
Cell
/ surgery. Lung Neoplasms / mortality. Lung Neoplasms / surgery
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(PMID = 16175462.001).
[ISSN]
0941-1291
[Journal-full-title]
Surgery today
[ISO-abbreviation]
Surg. Today
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
Japan
19.
Pires MM, Emmert D, Hrycyna CA, Chmielewski J:
Inhibition of P-glycoprotein-mediated paclitaxel resistance by reversibly linked quinine homodimers.
Mol Pharmacol
; 2009 Jan;75(1):92-100
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The designed agents were potent inhibitors of rhodamine 123 efflux in cultured cancer
cell
lines that display high levels of P-gp expression at the
cell
surface and in transfected
cells
expressing P-gp.
Further studies revealed that Q2 inhibited the efflux of a range of fluorescent substrates (rhodamine 123, doxorubicin, mitoxantrone, and BODIPY-FL-prazosin) from MCF-7/DX1
cells
.
The reversibility of the tether was confirmed in experiments showing that Q2 was readily hydrolyzed by esterases in vitro (t(1/2) approximately 20 h) while demonstrating high resistance to nonenzymatic hydrolysis in
cell
culture media (t(1/2) approximately 21 days).
In addition, low concentrations of Q2 stimulated
basal
P-gp ATPase levels.
Finally, Q2 was shown to inhibit the transport of radiolabeled paclitaxel (Taxol) in MCF-7/DX1
cells
, and it completely reversed the P-gp-mediated paclitaxel resistance phenotype.
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Hazardous Substances Data Bank.
QUININE
.
Hazardous Substances Data Bank.
VERAPAMIL HYDROCHLORIDE
.
Hazardous Substances Data Bank.
PRAZOSIN HYDROCHLORIDE
.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
TAXOL
.
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(PMID = 18945821.001).
[ISSN]
1521-0111
[Journal-full-title]
Molecular pharmacology
[ISO-abbreviation]
Mol. Pharmacol.
[Language]
ENG
[Grant]
United States / NEI NIH HHS / EY / R21 EY018481; United States / NCI NIH HHS / CA / 2P30-CA23168; United States / NEI NIH HHS / EY / EY018481
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Affinity Labels; 0 / Fluorescent Dyes; 0 / P-Glycoprotein; 1N3CZ14C5O / Rhodamine 123; 80168379AG / Doxorubicin; A7V27PHC7A / Quinine; CJ0O37KU29 / Verapamil; EC 3.6.1.- / Adenosine Triphosphatases; P88XT4IS4D / Paclitaxel; XM03YJ541D / Prazosin
[Other-IDs]
NLM/ PMC2685053
20.
Vasudev P, Boutross-Tadross O, Radhi J:
Basaloid squamous cell carcinoma: two case reports.
Cases J
; 2009;2:9351
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[Title]
Basaloid squamous
cell
carcinoma: two case reports.
Basaloid squamous
cell
carcinoma (BSCC) is a rare and aggressive variant of squamous
cell
carcinoma (SCC) that occurs preferentially in the upper aerodigestive tract.
BSCC of the head and neck should be distinguished from adenoid cystic carcinoma, small
cell
neuroendocrine carcinoma,
basal cell adenocarcinoma
, adenosquamous carcinoma, squamous
cell
carcinoma, spindle
cell
squamous carcinoma, mucoepidermoid carcinoma, and adenoid cystic carcinoma.
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[Cites]
Eur J Cancer. 2008 Jan;44(2):244-50
[
18096379.001
]
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]
(PMID = 20062602.001).
[ISSN]
1757-1626
[Journal-full-title]
Cases journal
[ISO-abbreviation]
Cases J
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC2804002
21.
Liu YL, Matsuzaki T, Nakazawa T, Murata S, Nakamura N, Kondo T, Iwashina M, Mochizuki K, Yamane T, Takata K, Katoh R:
Expression of aquaporin 3 (AQP3) in normal and neoplastic lung tissues.
Hum Pathol
; 2007 Jan;38(1):171-8
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To investigate the expression of AQP3 in normal and neoplastic lung tissues, we studied a series of 149 lung carcinoma tissues and 2
cell
lines by immunohistochemistry, Western blotting, and reverse transcriptase-polymerase chain reaction.
In normal lung tissues, immunohistochemical expression of AQP3 was demonstrated in bronchial
basal
cells
, alveolar type II
cells
, bronchiolar epithelial
cells
, and secretory
cells
of submucosal glands.
In lung carcinomas, AQP3 expression was observed in 59 (70.2%) of 84
adenocarcinomas
.
Squamous
cell
carcinoma and large
cell
carcinoma had rather low positive ratios (35.8% and 13.4%, respectively).
No AQP3 expression was demonstrated in small
cell
carcinoma, pleomorphic carcinoma, or metastatic colon
adenocarcinoma
.
In
adenocarcinomas
, AQP3 was detected in all tumors of bronchioloalveolar
subtype
.
Papillary
subtype
also showed a higher positive ratio of AQP3 compared with that in acinar and solid with mucin subtypes.
In addition, AQP3 expression was related to tumor differentiation and clinical stage in
adenocarcinomas
.
Western blotting and reverse transcriptase-polymerase chain reaction analyses confirmed the expression of AQP3 protein and messenger RNA in
cell
lines and tissues of lung
adenocarcinoma
.
In addition, lung carcinomas, especially
adenocarcinomas
, can produce AQP3, possibly in connection with their functional and/or biological nature, although the detailed mechanism of AQP3 expression in lung carcinomas remains to be clarified.
[MeSH-minor]
Adenocarcinoma
/ genetics.
Adenocarcinoma
/ metabolism.
Adenocarcinoma
/ pathology. Blotting, Western.
Cell
Line, Tumor. Female. Gene Expression. Humans. Immunohistochemistry. Male. Reverse Transcriptase Polymerase Chain Reaction
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(PMID = 17056099.001).
[ISSN]
0046-8177
[Journal-full-title]
Human pathology
[ISO-abbreviation]
Hum. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
158801-98-0 / Aquaporin 3
22.
Wei J, Yan W, Li X, Chang WC, Tai HH:
Activation of thromboxane receptor alpha induces expression of cyclooxygenase-2 through multiple signaling pathways in A549 human lung adenocarcinoma cells.
Biochem Pharmacol
; 2007 Sep 1;74(5):787-800
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[Title]
Activation of thromboxane receptor alpha induces expression of cyclooxygenase-2 through multiple signaling pathways in A549 human lung
adenocarcinoma
cells
.
Human lung
adenocarcinoma
A549
cells
stably transfected with TPalpha (A549-TPalpha) were used to study agonist I-BOP-induced expression of cyclooxygenase-2 (COX-2) and the related mechanisms of induced expression.
I-BOP, a TP agonist, induced a time- and dose-dependent expression of COX-2 in A549-TPalpha
cells
.
Distal NF-kappaB site is essential for the
basal
induction of the COX-2 transcription, whereas CRE and proximal NF-kappaB sites are important for the induced transcription.
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10860826.001
]
(PMID = 17632087.001).
[ISSN]
1873-2968
[Journal-full-title]
Biochemical pharmacology
[ISO-abbreviation]
Biochem. Pharmacol.
[Language]
ENG
[Grant]
United States / NHLBI NIH HHS / HL / HL046296-11; United States / NHLBI NIH HHS / HL / R01 HL046296-07; United States / NHLBI NIH HHS / HL / R01 HL046296; United States / NHLBI NIH HHS / HL / HL046296-06; United States / NHLBI NIH HHS / HL / HL046296-07; United States / NHLBI NIH HHS / HL / HL-46296; United States / NHLBI NIH HHS / HL / R01 HL046296-09; United States / NHLBI NIH HHS / HL / HL046296-08; United States / NHLBI NIH HHS / HL / R01 HL046296-11; United States / NHLBI NIH HHS / HL / R01 HL046296-08; United States / NHLBI NIH HHS / HL / HL046296-09; United States / NHLBI NIH HHS / HL / R01 HL046296-10; United States / NHLBI NIH HHS / HL / HL046296-10; United States / NHLBI NIH HHS / HL / R01 HL046296-06
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Bicyclo Compounds, Heterocyclic; 0 / Fatty Acids, Unsaturated; 0 / Protein Isoforms; 0 / Receptors, Thromboxane; 0 / Receptors, Thromboxane A2, Prostaglandin H2; 124924-85-2 / 7-(3-(3-hydroxy-4-(4'-iodophenoxy)-1-butenyl)-7-oxabicyclo(2.2.1)heptan-2-yl)-5-heptenoic acid; EC 1.14.99.1 / Cyclooxygenase 2
[Other-IDs]
NLM/ NIHMS28713; NLM/ PMC1995664
23.
Uphoff J, Woziwodzki J, Schattka SO, Kollias A:
[Loss of differentiation of a prostate adenocarcinoma after hormone therapy: the example of a metastasis in the spongy body of the penis].
Aktuelle Urol
; 2008 Sep;39(5):373-7
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[Title]
[Loss of differentiation of a prostate
adenocarcinoma
after hormone therapy: the example of a metastasis in the spongy body of the penis].
Metastases in the penis only occur at an advanced state of the tumour and with a high dedifferentiation, e. g., ductal
adenocarcinoma
.
Changes in the morphology of the prostate carcinoma are specially known for the occurrence of small-
cell
neuroendocrine and undifferentiated carcinomas.
At this state of the
disease
, there is only the possibility of a palliative therapy with a poor prognosis.
[MeSH-major]
Adenocarcinoma
/ secondary. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma,
Basal Cell
/ secondary. Carcinoma, Transitional
Cell
/ secondary.
Cell
Transformation, Neoplastic / pathology. Diphosphonates / therapeutic use. Gonadotropin-Releasing Hormone / antagonists & inhibitors. Neoplasms, Multiple Primary / drug therapy. Penile Neoplasms / secondary. Prostatic Neoplasms / drug therapy
[MeSH-minor]
Aged. Biomarkers, Tumor / analysis. Biopsy. Bone Neoplasms / drug therapy. Bone Neoplasms / pathology. Bone Neoplasms / secondary. Bone Neoplasms / surgery. Combined Modality Therapy. Cystectomy.
Diagnosis
, Differential.
Disease
Progression. Humans. Lymphatic Metastasis. Male.
Neoplasm
Staging. Penis / pathology. Penis / surgery. Prostate / pathology. Prostate / surgery. Prostatectomy
MedlinePlus Health Information.
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.
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(PMID = 18798127.001).
[ISSN]
0001-7868
[Journal-full-title]
Aktuelle Urologie
[ISO-abbreviation]
Aktuelle Urol
[Language]
ger
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Diphosphonates; 33515-09-2 / Gonadotropin-Releasing Hormone
24.
Peng Y, Jiang Y, Chuang ST, Yang XJ:
Computer-aided detection of prostate cancer on tissue sections.
Appl Immunohistochem Mol Morphol
; 2009 Oct;17(5):442-50
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The first set of images consisted of 20 training images (10
malignant
) used for developing the computer technique and 15 test images (7
malignant
) used for testing and optimizing the technique.
The second set of images consisted of 299 images (114
malignant
) used for evaluation of the performance of the computer technique.
The computer technique identified image segments of alpha-methylacyl-CoA racemase-labeled
malignant
epithelial
cells
(red), p63, and high-molecular-weight cytokeratin-labeled benign
basal
cells
(brown), and secretory and stromal
cells
(blue) for identifying prostate cancer automatically.
If high-grade prostatic intraepithelial
neoplasia
, which is a precursor of cancer, and atypical cases were included, the sensitivity and specificity were 85% (97/114) and 89% (165/185), respectively.
These results show that the novel automated computer technique can accurately identify prostatic
adenocarcinoma
in the triple-antibody cocktail-stained prostate sections.
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.
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[Cites]
Radiology. 2001 Sep;220(3):781-6
[
11526282.001
]
[Cites]
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[
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[
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]
[Cites]
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[
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]
[Cites]
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[
18300803.001
]
[Cites]
AJR Am J Roentgenol. 2008 Apr;190(4):854-9
[
18356428.001
]
(PMID = 19417626.001).
[ISSN]
1533-4058
[Journal-full-title]
Applied immunohistochemistry & molecular morphology : AIMM
[ISO-abbreviation]
Appl. Immunohistochem. Mol. Morphol.
[Language]
ENG
[Grant]
United States / NIBIB NIH HHS / EB / R21 EB006466; United States / NCI NIH HHS / CA / R21 CA97308; United States / NCI NIH HHS / CA / R21 CA097308-01; United States / NCI NIH HHS / CA / CA097308-02; United States / NCI NIH HHS / CA / R01 CA092361; United States / NCI NIH HHS / CA / CA097308-01; United States / NIBIB NIH HHS / EB / EB006466-02; United States / NIBIB NIH HHS / EB / EB006466-01A1; United States / NIBIB NIH HHS / EB / R21 EB006466-01A1; United States / NIBIB NIH HHS / EB / R21 EB006466-02; United States / NCI NIH HHS / CA / R21 CA097308; United States / NCI NIH HHS / CA / R21 CA097308-02
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS100571; NLM/ PMC2836393
25.
Koshimizu TA, Fujiwara Y, Sakai N, Shibata K, Tsuchiya H:
Oxytocin stimulates expression of a noncoding RNA tumor marker in a human neuroblastoma cell line.
Life Sci
; 2010 Mar 13;86(11-12):455-60
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[Title]
Oxytocin stimulates expression of a noncoding RNA tumor marker in a human neuroblastoma
cell
line.
AIMS: A noncoding RNA, metastasis-associated lung
adenocarcinoma
transcript 1 (MALAT1), is upregulated in several
malignant
tumors.
The aim of this study is to clarify how MALAT1 gene expression is altered by extracellular signals in the SK-N-SH neuroblastoma
cell
line and to define its proximal promoter in order to study the mechanism of MALAT1 gene expression.
Although the expression of immediate early genes returned to
basal
levels after 3h, MALAT1 transcript levels peaked 6-24h after stimulation.
SIGNIFICANCE: The expression of the tumor marker MALAT1 ncRNA is sensitive to
cell
surface receptor activation by oxytocin in a neuroblastoma
cell
line.
[MeSH-major]
Biomarkers, Tumor / biosynthesis. Oxytocin / pharmacology. RNA,
Neoplasm
/ biosynthesis
[MeSH-minor]
Brain Neoplasms / metabolism. Calcium / metabolism.
Cell
Line, Tumor. Cyclic AMP Response Element-Binding Protein / biosynthesis. Cyclic AMP Response Element-Binding Protein / genetics. Humans. Informatics. Neuroblastoma / metabolism. Oligonucleotide Array Sequence Analysis. Receptors, Oxytocin / agonists. Reverse Transcriptase Polymerase Chain Reaction
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.
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culture/stock collections - NBRP resources
.
Hazardous Substances Data Bank.
Oxytocin
.
Hazardous Substances Data Bank.
CALCIUM, ELEMENTAL
.
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[Copyright]
Copyright (c) 2010 Elsevier Inc. All rights reserved.
(PMID = 20149803.001).
[ISSN]
1879-0631
[Journal-full-title]
Life sciences
[ISO-abbreviation]
Life Sci.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Cyclic AMP Response Element-Binding Protein; 0 / RNA, Neoplasm; 0 / Receptors, Oxytocin; 50-56-6 / Oxytocin; SY7Q814VUP / Calcium
26.
Colucci R, Blandizzi C, Ghisu N, Florio T, Del Tacca M:
Somatostatin inhibits colon cancer cell growth through cyclooxygenase-2 downregulation.
Br J Pharmacol
; 2008 Sep;155(2):198-209
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[Title]
Somatostatin inhibits colon cancer
cell
growth through cyclooxygenase-2 downregulation.
BACKGROUND AND PURPOSE: Cyclooxygenase-2 (COX-2) is expressed in colonic neoplasms, where it supports
cell
proliferation via prostaglandin E(2) (PGE(2)) production.
This study investigated the effects of somatostatin-14 on COX-2 expression, PGE(2) production and proliferation in colon cancer
cells
.
EXPERIMENTAL APPROACH: Human colon
adenocarcinoma cell
lines Caco-2, HT-29 and HCT116 were used.
The following techniques were employed: colourimetric assay for
cell
growth; 5-bromo-2'-deoxyuridine assay for DNA synthesis; enzyme immunoassay for PGE(2); COX-2 mRNA silencing; RT-PCR or Western blot for somatostatin receptor subtypes, cyclooxygenase isoforms, phosphorylated-ERK-1/ERK-2 and phosphorylated-Akt.
KEY RESULTS: HT-29 and Caco-2
cells
expressed COX-2 and somatostatin receptors (sst(3/4/5) and sst(3/5), respectively).
HCT116
cells
did express somatostatin receptors (sst(2/3/5)), but not COX-2.
Somatostatin-14 inhibited
basal
COX-2 expression, PGE(2) production, DNA synthesis and growth in Caco-2
cells
and these effects were prevented by BN81658 (sst(3) receptor antagonist).
Basal
proliferation of HT-29, HCT116 and COX-2-silenced Caco-2
cells
was not affected by somatostatin-14.
Stimulation of HT-29
cells
with gastrin-17 elicited increments of ERK-1/ERK-2 and Akt phosphorylation, COX-2 expression, PGE(2) production, DNA synthesis and
cell
growth, which were all counteracted by somatostatin-14.
CONCLUSIONS AND IMPLICATIONS: Somatostatin decreases COX-2 expression and function in colon cancer
cells
via activation of sst(3) or sst(5) receptors, and these effects contribute to the inhibitory action of somatostatin on
cell
proliferation.
[MeSH-major]
Cell
Proliferation / drug effects. Colonic Neoplasms / pathology. Cyclooxygenase 2 / metabolism. Cyclooxygenase 2 Inhibitors / pharmacology. Somatostatin / pharmacology
[MeSH-minor]
Caco-2
Cells
. Colon / pathology. Down-Regulation / drug effects. Down-Regulation / physiology. Gastrins / metabolism. HT29
Cells
. Humans. Mitogen-Activated Protein Kinase 1 / metabolism. Oligopeptides / metabolism. Protein Kinase C / metabolism. Protein Tyrosine Phosphatases / metabolism
NCI CPTAC Assay Portal.
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NCI CPTC Antibody Characterization Program
.
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[Cites]
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[
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(PMID = 18587421.001).
[ISSN]
0007-1188
[Journal-full-title]
British journal of pharmacology
[ISO-abbreviation]
Br. J. Pharmacol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / BIM 23056; 0 / Cyclooxygenase 2 Inhibitors; 0 / Gastrins; 0 / Oligopeptides; 51110-01-1 / Somatostatin; 60748-06-3 / gastrin 17; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 3.1.3.48 / Protein Tyrosine Phosphatases
[Other-IDs]
NLM/ PMC2538699
27.
Seethala RR, Pasha TL, Raghunath PN, Livolsi VA, Zhang PJ:
The selective expression of CD43 in adenoid cystic carcinoma.
Appl Immunohistochem Mol Morphol
; 2008 Mar;16(2):165-72
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CD43, a sialoglycoprotein expressed on hematopoietic
cells
, has only rarely been reported in nonhematopoietic tumors, mostly of colon.
CD43 immunoreactivity with 2 different antibodies was detected mainly in ACC but also 1 membranous type
basal cell adenocarcinoma
and 1 colonic
adenocarcinoma
.
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(PMID = 18227725.001).
[ISSN]
1541-2016
[Journal-full-title]
Applied immunohistochemistry & molecular morphology : AIMM
[ISO-abbreviation]
Appl. Immunohistochem. Mol. Morphol.
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD43; 0 / RNA, Messenger; 0 / UN1 sialoglycoprotein, human
28.
Devaney KO, Boschman CR, Willard SC, Ferlito A, Rinaldo A:
Tumours of the external ear and temporal bone.
Lancet Oncol
; 2005 Jun;6(6):411-20
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The external ear can be the site of development of squamous carcinomas and
basal
-
cell
carcinomas; the middle ear and inner ear can host metastatic deposits, and primary squamous carcinomas and
adenocarcinomas
.
Most auricular
malignant
diseases occur in adulthood; only the rhabdomyosarcomas of the middle ear arise in children.
Most
malignant
diseases of the auricular apparatus are treated by a combination of surgery (commonly including radical excision of temporal bone), radiotherapy, and chemotherapy.
[MeSH-major]
Ear Neoplasms /
diagnosis
. Ear Neoplasms / therapy. Ear, External. Skull Neoplasms /
diagnosis
. Skull Neoplasms / therapy. Temporal Bone
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(PMID = 15925819.001).
[ISSN]
1470-2045
[Journal-full-title]
The Lancet. Oncology
[ISO-abbreviation]
Lancet Oncol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Number-of-references]
76
29.
Osunkoya AO, Hansel DE, Sun X, Netto GJ, Epstein JI:
Aberrant diffuse expression of p63 in adenocarcinoma of the prostate on needle biopsy and radical prostatectomy: report of 21 cases.
Am J Surg Pathol
; 2008 Mar;32(3):461-7
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[Title]
Aberrant diffuse expression of p63 in
adenocarcinoma
of the prostate on needle biopsy and radical prostatectomy: report of 21 cases.
Aberrant diffuse expression of p63 in prostate carcinoma
cells
is a rare and poorly understood phenomenon.
The presence of p63 positive atypical glands with an infiltrative pattern and perineural invasion on radical prostatectomy confirmed the needle biopsy
diagnosis
of carcinoma.
Rarely, prostate cancer can aberrantly express diffuse p63 staining in a nonbasal
cell
distribution leading to the erroneous
diagnosis
of atrophy or atypical
basal cell
proliferation.
The
diagnosis
of prostate cancer is based on the morphology and confirmed by the absence of high molecular weight cytokeratin staining and positivity for alpha-methylacyl-CoA racemase in the atypical glands.
Pathologists need to be aware of this rare and unusual phenomenon, which is a potential pitfall in prostate cancer
diagnosis
.
[MeSH-major]
Adenocarcinoma
/ chemistry. Biopsy, Needle. Membrane Proteins / analysis. Prostatectomy. Prostatic Neoplasms / chemistry
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(PMID = 18300803.001).
[ISSN]
0147-5185
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / CKAP4 protein, human; 0 / Membrane Proteins
30.
Kurvinen K, Rantanen V, Syrjänen S, Johansson B:
Radiation-induced effects on telomerase in gynecological cancer cell lines with different radiosensitivity and repair capacity.
Int J Radiat Biol
; 2006 Dec;82(12):859-67
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[Title]
Radiation-induced effects on telomerase in gynecological cancer
cell
lines with different radiosensitivity and repair capacity.
PURPOSE: Telomerase activation in response to irradiation might enhance the radioresistance of
cells
.
Thus, we have investigated radiation-induced effects on telomerase in six gynecological cancer
cell
lines, with different intrinsic radiosensitivity and capacity for sublethal damage repair (SLDR).
MATERIALS AND METHODS: Three endometrial
adenocarcinoma
(UM-EC-1, UT-EC-2B and UT-EC-3) and three vulvar squamous
cell
carcinoma (A431, UM-SCV-2 and UM-SCV-7)
cell
lines were irradiated with doses of 5, 10 and 25 Gy and the effects on telomerase were evaluated at 0.5, 6, 24 and 48 h post-irradiation.
RESULTS: The most radioresistant
cell
line A431 had the strongest stimulatory effects (approximately 2.0 - 2.5-fold) on telomerase activity 24 and 48 h post-irradiation with the highest radiation doses.
In contrast to that, telomerase activities in the highly radiosensitive
cell
line UT-EC-2B remained below the
basal
level throughout the 48-h period of post-irradiation with the highest doses, and even a decline to approximately 50% of the
basal
level was found 24 h after exposure.
In other
cell
lines being either moderately or highly radiation resistant, telomerase activity levels in response to irradiation remained mainly at the
basal
level or gradually increased.
However, no correlation was found between the radiation-induced effects on telomerase and the sublethal damage repair capacity of the
cells
.
[MeSH-major]
DNA Repair. DNA,
Neoplasm
/ radiation effects. Genital Neoplasms, Female / enzymology. Genital Neoplasms, Female / genetics. Radiation Tolerance. Telomerase / metabolism. Telomerase / radiation effects
[MeSH-minor]
Cell
Line, Tumor. DNA Damage. Dose-Response Relationship, Radiation. Enzyme Activation / radiation effects. Female. Humans. Radiation Dosage
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(PMID = 17178626.001).
[ISSN]
0955-3002
[Journal-full-title]
International journal of radiation biology
[ISO-abbreviation]
Int. J. Radiat. Biol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DNA, Neoplasm; EC 2.7.7.49 / Telomerase
31.
Final report on the safety assessment of capsicum annuum extract, capsicum annuum fruit extract, capsicum annuum resin, capsicum annuum fruit powder, capsicum frutescens fruit, capsicum frutescens fruit extract, capsicum frutescens resin, and capsaicin.
Int J Toxicol
; 2007;26 Suppl 1:3-106
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Weanling rats fed
basal
diets supplemented with whole red pepper at concentrations up to 5.0% for up to 8 weeks had no pathology of the large intestines, livers, and kidneys, but destruction of the taste buds and keratinization and erosion of the gastrointestinal (GI) tract were noted in groups fed 0.5% to 5.0% red pepper.
A rabbit skin irritation test of Capsicum Annuum Fruit Extract at concentrations ranging from 0.1% to 1.0% produced no irritation, but Capsicum Frutescens Fruit Extract induced concentration-dependent (at 25 to 500 microg/ml) cytotoxicity in a human buccal mucosa fibroblast
cell
line.
Adenocarcinoma
of the abdomen was observed in 7/20 mice fed 100 mg red chilies per day for 12 months; no tumors were seen in control animals.
Other feeding studies evaluated the effect of red chili peppers on the incidence of stomach tumors produced by N-methyl-N'-nitro-N-nitrosoguanidine,
finding
that red pepper had a promoting effect.
Capsaicin inhibits protein synthesis in Vero kidney
cells
and human neuroblastoma SHSY-5Y
cells
in vitro, and inhibits growth of E. coli, Pseudomonas solanacearum, and Bacillus subtilis bacterial cultures, but not Saccharomyces cerevisiae.
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(PMID = 17365137.001).
[ISSN]
1091-5818
[Journal-full-title]
International journal of toxicology
[ISO-abbreviation]
Int. J. Toxicol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Cosmetics; 0 / Plant Extracts; 0 / Resins, Plant; S07O44R1ZM / Capsaicin
[Number-of-references]
462
32.
Trauzold A, Röder C, Sipos B, Karsten K, Arlt A, Jiang P, Martin-Subero JI, Siegmund D, Müerköster S, Pagerols-Raluy L, Siebert R, Wajant H, Kalthoff H:
CD95 and TRAF2 promote invasiveness of pancreatic cancer cells.
FASEB J
; 2005 Apr;19(6):620-2
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[Title]
CD95 and TRAF2 promote invasiveness of pancreatic cancer
cells
.
Pancreatic
adenocarcinoma
represents a tumor type with extremely poor prognosis.
High apoptosis resistance and a strong invasive and early metastatic potential contribute to its highly
malignant
phenotype.
Using immunohistochemistry and Western blot analysis we found TRAF2 overexpressed in 34 of 36 pancreatic tumor samples as well as in pancreatic tumor
cell
lines resistant to CD95-mediated apoptosis.
Introduction of a TRAF2 expression vector in CD95-sensitive Colo357
cells
resulted in (i) resistance to CD95-induced apoptosis;.
(ii) increased constitutive NF-kappaB and AP-1 activity; and (iii) higher
basal
secretion of matrix metalloproteinases (MMPs), urokinase-type plasminogen activator (uPA), and IL-8, leading to increased invasiveness.
Stimulation of TRAF2-overexpressing
cells
with CD95 ligand led to induction of NF-kappaB and AP-1, enhanced IL-8- and uPA-secretion, and a further increased invasiveness.
[MeSH-major]
Adenocarcinoma
/ pathology. Antigens, CD95 / physiology.
Neoplasm
Invasiveness. Pancreatic Neoplasms / pathology. TNF Receptor-Associated Factor 2 / physiology
[MeSH-minor]
Apoptosis.
Cell
Line, Tumor. Electrophoretic Mobility Shift Assay. Gene Expression. Humans. In Situ Hybridization, Fluorescence. Interleukin-8 / analysis. Mitogen-Activated Protein Kinase Kinases / metabolism. NF-kappa B / physiology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Transfection. Urokinase-Type Plasminogen Activator / analysis
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(PMID = 15670977.001).
[ISSN]
1530-6860
[Journal-full-title]
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
[ISO-abbreviation]
FASEB J.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD95; 0 / Interleukin-8; 0 / NF-kappa B; 0 / TNF Receptor-Associated Factor 2; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator
33.
Trivunić S, Budakov P, Vucković N, Zivojinov M:
[Morphological parameters of prostatic adenocarcinoma].
Med Pregl
; 2007 Nov-Dec;60(11-12):549-52
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[Title]
[Morphological parameters of prostatic
adenocarcinoma
].
The following histologic changes are associated with prostatic carcinomas. prostatic acini are close to one another and present with linear infiltrates in the fibromuscular tissue;
cells
lining the acini often consist of a single layer, and the
basal cell
layer is absent; prominent large eosinophilic nucleoli are usually present in
malignant cells
; nuclear hyperchromatism is rare and it depends on the quality of the tissue fixation; perineural invasion is often observed.
Immunohistochemistry is widely used in pathology and clinical
diagnosis
of prostatic carcinoma, metastases of prostatic origin in staging
malignant
tumors and in the prognosis.
[MeSH-major]
Adenocarcinoma
/ pathology. Prostatic Neoplasms / pathology
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(PMID = 18666594.001).
[ISSN]
0025-8105
[Journal-full-title]
Medicinski pregled
[ISO-abbreviation]
Med. Pregl.
[Language]
srp
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Serbia
34.
Bozdogan O, Atasoy P, Bozdogan N, Erekul S, Batislam E, Yilmaz E, Başar MM:
BAG-1 expression in hyperplastic and neoplastic prostate tissue: is there any relationship with BCL-related proteins and androgen receptor status?
Tumori
; 2005 Nov-Dec;91(6):539-45
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METHODS: Twenty-eight prostatic
adenocarcinomas
and 16 prostate hyperplasias were included in this retrospective study.
The M30 antibody was used to identify preapoptotic and apoptotic
cells
.
BAG-1 showed the same specific
basal cell
localization as BCL-2 in hyperplastic and normal glands.
BAG-1 in association with BCL-2 inhibits apoptosis and may prolong the life of neoplastic
cells
and give them a chance to gain new oncogenic features in early carcinogenesis.
[MeSH-major]
Adenocarcinoma
/ chemistry. Biomarkers, Tumor / analysis. DNA-Binding Proteins / analysis. Prostatic Hyperplasia / metabolism. Prostatic Neoplasms / chemistry. Receptors, Androgen / analysis. Transcription Factors / analysis
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(PMID = 16457154.001).
[ISSN]
0300-8916
[Journal-full-title]
Tumori
[ISO-abbreviation]
Tumori
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / BCL2-associated athanogene 1 protein; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Receptors, Androgen; 0 / Transcription Factors
35.
Zheng HC, Saito H, Masuda S, Wang ZG, Takano Y:
Cytoplasmic and nuclear maspin expression in lung carcinomas: an immunohistochemical study using tissue microarrays.
Appl Immunohistochem Mol Morphol
; 2008 Oct;16(5):459-65
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Here, maspin expression was examined on tissue microarrays containing lung carcinoma (n=155) and adjacent noncancerous tissue (n=20) and also 4 lung carcinoma
cell
lines (LC-1/Sq, LC-IF, PC-14, and AoI) by immunohistochemistry.
Maspin expression showed positive nuclear staining in
basal
cells
, LC-IF, and PC-14
cell
lines, and also cytoplasmic immunoreactivity in secretory and ciliated
cells
, LC-1/Sq
cell
line.
Cytoplasmic staining was the lowest in
adenocarcinoma
(
AD
) and the highest in squamous
cell
carcinoma as compared with other types of lung carcinoma (P<0.05), and positively correlated with expression of p53 and caspase-3 (P<0.05).
The nuclear maspin expression gradually increased through squamous
cell
carcinoma,
AD
, large
cell
carcinoma to small
cell
carcinoma (P<0.05) and was also positively associated with the levels of vascular epithelial growth factor and extracellular matrix metalloproteinase inducer expression (P<0.05).
Kaplan-Meier analysis indicated that the cytoplasmic or nuclear maspin expression was not a good prognostic marker for lung carcinomas overall (P>0.05), but the cytoplasmic pattern pointed to good survival for
AD
cases (P<0.05).
The cytoplasmic maspin may play an important role in lung carcinomas by regulating apoptosis and thus is a favorable prognostic marker for
AD
patients, whereas the nuclear location may be linked to promotion of angiogenesis.
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(PMID = 18665036.001).
[ISSN]
1533-4058
[Journal-full-title]
Applied immunohistochemistry & molecular morphology : AIMM
[ISO-abbreviation]
Appl. Immunohistochem. Mol. Morphol.
[Language]
ENG
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / SERPIN-B5; 0 / Serpins
36.
Wietfeldt ED, Thiele J:
Malignancies of the anal margin and perianal skin.
Clin Colon Rectal Surg
; 2009 May;22(2):127-35
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Commonly included in this group of cancers are Bowen's
disease
(intraepithelial squamous
cell
cancer), perianal Paget's
disease
(intraepithelial
adenocarcinoma
), invasive squamous
cell
cancer,
basal cell
cancer, and
malignant
melanoma.
Proper
diagnosis
requires a high index of suspicion on the part of the surgeon.
Innocent local irritations will resolve in a short time with appropriate therapy; those that persist must be biopsied for tissue
diagnosis
.
All have met with a fair amount of success in controlling local
disease
; however, the number of patients treated in each instance is small, making it difficult to design an evidence-based treatment strategy.
Invasion and metastasis are relatively rare in this group of neoplasms; perianal Paget's
disease
has the highest risk of associated underlying
neoplasm
.
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[Cites]
Dis Colon Rectum. 2008 Dec;51(12):1842-5
[
18584248.001
]
[Cites]
J Am Acad Dermatol. 2007 Aug;57(2 Suppl):S36-7
[
17637368.001
]
[Cites]
Dermatol Surg. 2007 Apr;33(4):427-31; discussion 431-2
[
17430376.001
]
[Cites]
Br J Dermatol. 2007 Jan;156(1):11-21
[
17199561.001
]
[Cites]
Dermatol Surg. 2001 Jun;27(6):587-90
[
11442599.001
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[Cites]
Dis Colon Rectum. 2004 Oct;47(10):1655-60; discussion 1660-1
[
15540295.001
]
(PMID = 20436838.001).
[ISSN]
1530-9681
[Journal-full-title]
Clinics in colon and rectal surgery
[ISO-abbreviation]
Clin Colon Rectal Surg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2780245
[Keywords]
NOTNLM ; Anal margin cancer / diagnosis / local excision / radiation therapy / treatment options
37.
Pornpanich K, Chindasub P:
Eyelid tumors in Siriraj Hospital from 2000-2004.
J Med Assoc Thai
; 2005 Nov;88 Suppl 9:S11-4
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RESULTS: There were 53 (17.8%) inflammatory conditions, 212 (71.4%) benign eyelid tumors and 32 (10.8%)
malignant
eyelid tumors.
These 32
malignant
eyelid tumors included 13 sebaceous gland carcinomas, 12
basal cell
carcinomas, 3
malignant
melanomas, 2 squamous
cell
carcinomas, 1 apocrine
adenocarcinoma
and 1 metastatic carcinoma.
CONCLUSION: The majority of eyelid lesions were benign eyelid tumors while
malignant
eyelid tumors contributed 10.8% of the total eyelid lesions.
[MeSH-major]
Carcinoma,
Basal Cell
/ epidemiology. Carcinoma, Squamous
Cell
/ epidemiology. Eyelid Neoplasms / epidemiology. Sebaceous Gland Neoplasms / epidemiology
[MeSH-minor]
Adolescent. Adult. Age Distribution. Aged. Aged, 80 and over. Biopsy, Needle. Child. Child, Preschool. Female. Humans. Immunohistochemistry. Incidence. Male. Middle Aged.
Neoplasm
Staging. Prognosis. Retrospective Studies. Risk Assessment. Sex Distribution. Thailand / epidemiology
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(PMID = 16681045.001).
[ISSN]
0125-2208
[Journal-full-title]
Journal of the Medical Association of Thailand = Chotmaihet thangphaet
[ISO-abbreviation]
J Med Assoc Thai
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Thailand
38.
Yu N, Kozlowski JM, Park II, Chen L, Zhang Q, Xu D, Doll JA, Crawford SE, Brendler CB, Lee C:
Overexpression of transforming growth factor β1 in malignant prostate cells is partly caused by a runaway of TGF-β1 auto-induction mediated through a defective recruitment of protein phosphatase 2A by TGF-β type I receptor.
Urology
; 2010 Dec;76(6):1519.e8-13
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[Title]
Overexpression of transforming growth factor β1 in
malignant
prostate
cells
is partly caused by a runaway of TGF-β1 auto-induction mediated through a defective recruitment of protein phosphatase 2A by TGF-β type I receptor.
OBJECTIVES: To elucidate the mechanism of transforming growth factor (TGF)-β1 overexpression in prostate cancer
cells
.
METHODS:
Malignant
(PC3, DU145) and benign (RWPE1, BPH1) prostate epithelial
cells
were used.
Blockade of TGF-β1 signaling in
cells
was accomplished either by using TGF-β-neutralizing monoclonal antibody or by transduction of a dominant negative TGF-β type II receptor retroviral vector.
RESULTS:
Basal
levels of TGF-β1 in
malignant cells
were significantly higher than those in benign
cells
.
Blockade of TGF-β signaling resulted in a significant decrease in TGF-β1 expression in
malignant cells
, but not in benign
cells
.
Upon TGF-β1 treatment (10 ng/mL), TGF-β1 expression was increased in
malignant cells
, but not in benign
cells
.
This differential TGF-β1 auto-induction between benign and
malignant cells
correlated with differential activation of extracellular signal-regulated kinase (ERK).
Following TGF-β1 treatment, the activity of serine/threonine phosphatase and recruitment of PP2A-Bα by TβRI increased in benign
cells
, but not in
malignant cells
.
Inhibition of PP2A in benign
cells
resulted in an increase in ERK activation and in TGF-β1 auto-induction after TGF-β1 (10 ng/mL) treatment.
CONCLUSIONS: These results suggest that TGF-β1 overexpression in
malignant cells
is caused, at least in part, by a runaway of TGF-β1 auto-induction through ERK activation because of a defective recruitment of PP2A-Bα by TβRI.
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[Copyright]
Copyright © 2010 Elsevier Inc. All rights reserved.
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17643425.001
]
(PMID = 21030067.001).
[ISSN]
1527-9995
[Journal-full-title]
Urology
[ISO-abbreviation]
Urology
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA090386-06A2; United States / NCI NIH HHS / CA / P50 CA090386; United States / NCI NIH HHS / CA / P50 CA090386-06A2; United States / NCI NIH HHS / CA / P50CA90386
[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 / Neoplasm Proteins; 0 / PPP2R2A protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; EC 2.7.1.11 / TGF-beta type I receptor; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.1.3.16 / Protein Phosphatase 2
[Other-IDs]
NLM/ NIHMS194313; NLM/ PMC2997920
39.
Adamski H, Le Lan J, Chevrier S, Cribier B, Watier E, Chevrant-Breton J:
Primary cutaneous cribriform carcinoma: a rare apocrine tumour.
J Cutan Pathol
; 2005 Sep;32(8):577-80
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This
neoplasm
is often located on the limbs.
The histopathological
diagnosis
is difficult, mainly because this tumour is exceptional.
The aggregations of neoplastic
cells
were interconnected and varied in size and shape.
The
cells
were arranged in solid nests or tubular structures.
In the lumina of tubules, some papillary protrusion of basophilic
cells
was seen.
The ductal elements were lined by cuboidal or cylindric
cells
with images of decapitation secretion.
The nuclei of the neoplastic
cells
were pleomorphic.
Differential diagnoses, including cutaneous metastasis of
adenocarcinoma
, adenoid
basal cell
carcinoma and adenoid cystic carcinoma, are discussed.
[MeSH-major]
Adenocarcinoma
/ pathology. Apocrine Glands / pathology. Sweat Gland Neoplasms / pathology
[MeSH-minor]
Adult. Carcinoma, Adenoid Cystic /
diagnosis
. Carcinoma,
Basal Cell
/
diagnosis
.
Diagnosis
, Differential. Humans. Male. Treatment Outcome
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(PMID = 16115058.001).
[ISSN]
0303-6987
[Journal-full-title]
Journal of cutaneous pathology
[ISO-abbreviation]
J. Cutan. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Denmark
40.
Scholz N, Krugmann J, Scholtz A, Höllrigl A, Verdorfer I:
Genetic alterations in a basal cell adenocarcinoma of the glandula submandibularis.
Cancer Genet Cytogenet
; 2007 Jan 1;172(1):87-9
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[Title]
Genetic alterations in a
basal cell adenocarcinoma
of the glandula submandibularis.
[MeSH-major]
Adenocarcinoma
/ genetics. Submandibular Gland Neoplasms / genetics
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(PMID = 17175388.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Letter; Research Support, Non-U.S. Gov't
[Publication-country]
United States
41.
Trevino JG, Gray MJ, Nawrocki ST, Summy JM, Lesslie DP, Evans DB, Sawyer TK, Shakespeare WC, Watowich SS, Chiao PJ, McConkey DJ, Gallick GE:
Src activation of Stat3 is an independent requirement from NF-kappaB activation for constitutive IL-8 expression in human pancreatic adenocarcinoma cells.
Angiogenesis
; 2006;9(2):101-10
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[Title]
Src activation of Stat3 is an independent requirement from NF-kappaB activation for constitutive IL-8 expression in human pancreatic
adenocarcinoma
cells
.
Human pancreatic tumors often overexpress the angiogenesis-promoting factor Interleukin 8 (IL-8), in part due to overexpression of NF-kappaB, a frequent occurrence in pancreatic
adenocarcinoma
.
Pharmacologic inhibition of NF-kappaB activity significantly reduced
basal
IL-8 expression and tumor necrosis factor-induced IL-8 expression (P < 0.05 for both), yet NF-kappaB activity was not dependent on Src.
We therefore suggest that Src activation, through phosphorylation of STAT3, and NF-kappaB are all required for expression of IL-8 a critical angiogenic-promoting factor in pancreatic
adenocarcinomas
.
[MeSH-major]
Adenocarcinoma
/ metabolism. Interleukin-8 / metabolism. NF-kappa B / metabolism. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins pp60(c-src) / metabolism. STAT3 Transcription Factor / metabolism
[MeSH-minor]
Cell
Line, Tumor. Genes, Reporter. Humans. Immunohistochemistry. Luciferases / metabolism. Microscopy, Confocal. Phosphorylation. RNA, Small Interfering / metabolism
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(PMID = 16871430.001).
[ISSN]
0969-6970
[Journal-full-title]
Angiogenesis
[ISO-abbreviation]
Angiogenesis
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / 2R01-1 CA65527; United States / NCI NIH HHS / CA / T32 CA 09599; United States / NCI NIH HHS / CA / U54 CA 090810-01
[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]
Netherlands
[Chemical-registry-number]
0 / Interleukin-8; 0 / NF-kappa B; 0 / RNA, Small Interfering; 0 / STAT3 Transcription Factor; EC 1.13.12.- / Luciferases; EC 2.7.10.2 / Proto-Oncogene Proteins pp60(c-src)
42.
Seo JO, Han SI, Lim SC:
Role of CDK8 and beta-catenin in colorectal adenocarcinoma.
Oncol Rep
; 2010 Jul;24(1):285-91
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[Title]
Role of CDK8 and beta-catenin in colorectal
adenocarcinoma
.
Colorectal
adenocarcinoma
is a major cause of morbidity and mortality.
CDK8 is a cyclin-dependent kinase (CDK) member of the mediator complex that couples transcriptional regulators to the
basal
transcriptional machinery, and is implicated in the transcriptional regulation of key pathways involved in colon cancers.
To determine the relationship between CDK8 and beta-catenin expressions, a population-based study was conducted for immunohistochemical staining analysis of tumor tissues, and Western blot analysis and CDK8 interference studies of colon cancer
cell
lines.
However, beta-catenin expression was not completely suppressed by CDK8 interference in the colon cancer
cell
lines HCT-116, HT-29 and SNU-C5.
[MeSH-major]
Adenocarcinoma
/ metabolism. Colorectal Neoplasms / metabolism. Cyclin-Dependent Kinase 8 / physiology. beta Catenin / physiology
[MeSH-minor]
Case-Control Studies. Drug Evaluation, Preclinical. Female. HCT116
Cells
. HT29
Cells
. Humans. Male. Prognosis. RNA, Small Interfering / pharmacology. Survival Analysis. Tumor
Cells
, Cultured
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(PMID = 20514474.001).
[ISSN]
1791-2431
[Journal-full-title]
Oncology reports
[ISO-abbreviation]
Oncol. Rep.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / RNA, Small Interfering; 0 / beta Catenin; EC 2.7.11.22 / CDK8 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 8
43.
Epstein JI:
Precursor lesions to prostatic adenocarcinoma.
Virchows Arch
; 2009 Jan;454(1):1-16
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[Title]
Precursor lesions to prostatic
adenocarcinoma
.
High-grade prostatic intraepithelial
neoplasia
(PIN) is the one well-documented precursor to
adenocarcinoma
of the prostate.
Benign lesions that may be confused with high-grade PIN, including central zone histology, clear
cell
cribriform hyperplasia, and
basal cell
hyperplasia are described and illustrated.
High-grade PIN is also differentiated from invasive acinar (usual) and ductal
adenocarcinoma
.
[MeSH-major]
Adenocarcinoma
/ pathology. Precancerous Conditions / pathology. Prostatic Neoplasms / pathology
[MeSH-minor]
Diagnosis
, Differential. Humans. Male. Prostatic Hyperplasia /
diagnosis
. Prostatic Hyperplasia / pathology. Prostatic Intraepithelial
Neoplasia
/
diagnosis
. Prostatic Intraepithelial
Neoplasia
/ pathology. Risk Factors
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[ISSN]
0945-6317
[Journal-full-title]
Virchows Archiv : an international journal of pathology
[ISO-abbreviation]
Virchows Arch.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Germany
[Number-of-references]
85
44.
Iwase H, Kurebayashi J, Tsuda H, Ohta T, Kurosumi M, Miyamoto K, Yamamoto Y, Iwase T:
Clinicopathological analyses of triple negative breast cancer using surveillance data from the Registration Committee of the Japanese Breast Cancer Society.
Breast Cancer
; 2010 Apr;17(2):118-24
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BACKGROUND: Triple negative (TN) breast cancer is defined as
a subtype
that is negative for estrogen receptor (ER), progesterone receptor (PgR), and human epidermal growth factor receptor 2 (HER2).
Of these, the most prevalent (53.8%) was a hormone-responsive
subtype
with ER positive/PgR positive/HER2 negative, followed by TN
subtype
(15.5%).
RESULTS: The proportion of postmenopausal patients was relatively high in the TN
subtype
.
Morphologically, the TN
subtype
was more frequently classified as solid-tubular carcinoma.
Mucinous, tubular, or secretary carcinomas were frequently found in the hormone receptor positive/HER2 negative
subtype
, while squamous
cell
carcinoma, spindle
cell
carcinoma, and metaplastic carcinoma with bone/cartilage metaplasia were very frequently found in the TN group.
CONCLUSIONS: Although TN types are similar to
basal
-like breast tumor, as determined by gene profiling, their
diagnosis
needs verification by determination of the level of epidermal growth factor receptor or cytokeratin 5/6 expression.
[MeSH-minor]
Adenocarcinoma
/ metabolism.
Adenocarcinoma
/ pathology.
Adenocarcinoma
, Scirrhous / metabolism.
Adenocarcinoma
, Scirrhous / pathology. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / metabolism. Carcinoma / metabolism. Carcinoma / pathology. Carcinoma, Intraductal, Noninfiltrating / metabolism. Carcinoma, Intraductal, Noninfiltrating / pathology. Carcinoma, Lobular / metabolism. Carcinoma, Lobular / pathology. Female. Humans. Japan. Middle Aged. Prognosis. Receptor, ErbB-2 / metabolism. Registries. Societies, Medical / statistics & numerical data. Young Adult
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(PMID = 19466512.001).
[ISSN]
1880-4233
[Journal-full-title]
Breast cancer (Tokyo, Japan)
[ISO-abbreviation]
Breast Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
45.
Xue LY, Zou SM, Zheng S, Xie YQ, Wen P, Liu XY, Lin DM, Lü N:
[Expression of fascin and CK14 in different histological types of cancer and its differential diagnostic significance].
Zhonghua Zhong Liu Za Zhi
; 2010 Nov;32(11):838-44
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OBJECTIVE: To investigate and analyze the expression of fascin and CK14 in multiple histological types of cancer and to explore the potential value of the two proteins as markers in
diagnosis
and differential
diagnosis
of various cancer types.
METHODS: Tissue microarray containing esophageal squamous
cell
carcinoma (SCC), lung SCC, larynx SCC, uterine cervical SCC, SCC of external genital organs, lung
adenocarcinoma
, gastric
adenocarcinoma
, colorectal
adenocarcinoma
, heptocellular carcinoma, pancreatic ductal
adenocarcinoma
, breast infiltrating ductal carcinoma, thyroid papillary carcinoma, uterine endometrioid
adenocarcinoma
, ovarian serous
adenocarcinoma
and renal clear
cell
carcinoma, 30 cases each, as well as corresponding normal controls was constructed.
RESULTS: In normal esophagus, bronchus, larynx, uterine cervix and skin, fascin was mainly expressed in the
basal
cells
or reserve
cells
, but the expression was diffuse in esophageal SCC, lung SCC, larynx SCC, uterine cervical SCC and SCC of external genital organs, with a positive rate of 90.0%, 90.0%, 96.7%, 78.6% and 89.7%, respectively.
In lung
adenocarcinoma
, gastric
adenocarcinoma
, colorectal
adenocarcinoma
, hepatocellular carcinoma, pancreatic ductal
adenocarcinoma
, breast infiltrating dutal
adenocarcinoma
, thyroid papillary carcinoma, uterine endometrioid
adenocarcinoma
, ovarian serous
adenocarcinoma
and renal clear
cell
carcinoma, the positive rates were 38.0%, 23.3%, 14.3%, 10.3%, 73.3%, 13.3%, 6.7%, 60.0%, 66.7% and 10.0%, respectively.
CK14 was mainly expressed in the
basal
cells
, reserve
cells
or myoepithelia of normal tissues.
It was weak and focal in lung
adenocarcinoma
, gastric
adenocarcinoma
, colorectal
adenocarcinoma
, hepatocellular carcinoma, pancreatic ductal
adenocarcinoma
, breast infiltrating dutal
adenocarcinoma
, thyroid papillary carcinoma, uterine endometrioid
adenocarcinoma
, ovarian serous
adenocarcinoma
, and renal clear
cell
carcinoma, with a positive rate of 13.3%, 13.3%, 20.7%, 41.4%, 46.7%, 6.7%, 40.0%, 13.3%, 20.0% and 6.7%, respectively.
Combination of fascin and CK14 should be a valuable marker in
diagnosis
and differential
diagnosis
of carcinoma.
[MeSH-major]
Adenocarcinoma
/ metabolism. Carcinoma, Squamous
Cell
/ metabolism. Carrier Proteins / metabolism. Keratin-14 / metabolism. Laryngeal Neoplasms / metabolism. Microfilament Proteins / metabolism
[MeSH-minor]
Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Colorectal Neoplasms / metabolism. Colorectal Neoplasms / pathology. Cystadenocarcinoma, Serous / metabolism. Cystadenocarcinoma, Serous / pathology.
Diagnosis
, Differential. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / pathology. Female. Humans. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Male. Ovarian Neoplasms / metabolism. Ovarian Neoplasms / pathology. Stomach Neoplasms / metabolism. Stomach Neoplasms / pathology. Uterine Cervical Neoplasms / metabolism. Uterine Cervical Neoplasms / pathology
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(PMID = 21223690.001).
[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 / Carrier Proteins; 0 / Keratin-14; 0 / Microfilament Proteins; 146808-54-0 / fascin
46.
McCormick DL, Rao KV, Johnson WD, Bosland MC, Lubet RA, Steele VE:
Null activity of selenium and vitamin e as cancer chemopreventive agents in the rat prostate.
Cancer Prev Res (Phila)
; 2010 Mar;3(3):381-92
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After stimulation of prostate epithelial
cell
proliferation by a sequential regimen of cyproterone acetate followed by testosterone propionate, male Wistar-Unilever rats received a single i.v. injection of N-methyl-N-nitrosourea (MNU) followed by chronic androgen stimulation via subcutaneous implantation of testosterone pellets.
At 1 week post-MNU, groups of carcinogen-treated rats (39-44/group) were fed either a
basal
diet or a
basal
diet supplemented with l-selenomethionine (3 or 1.5 mg/kg diet; study 1), dl-alpha-tocopherol (vitamin E, 4,000 or 2,000 mg/kg diet; study 2), l-selenomethionine + vitamin E (3 + 2,000 mg/kg diet or 3 + 500 mg/kg diet; study 3), or selenized yeast (target selenium levels of 9 or 3 mg/kg diet; study 4).
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Hazardous Substances Data Bank.
SELENIUM COMPOUNDS
.
Hazardous Substances Data Bank.
SELENIUM METHIONINE
.
Hazardous Substances Data Bank.
CYPROTERONE ACETATE
.
Hazardous Substances Data Bank.
TESTOSTERONE
.
Hazardous Substances Data Bank.
VITAMIN E
.
Hazardous Substances Data Bank.
N-NITROSO-N-METHYLUREA
.
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[Cites]
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Pathol Res Pract. 1995 Sep;191(9):838-41
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]
(PMID = 20145190.001).
[ISSN]
1940-6215
[Journal-full-title]
Cancer prevention research (Philadelphia, Pa.)
[ISO-abbreviation]
Cancer Prev Res (Phila)
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CN / N01-CN-95113; United States / NCI NIH HHS / CA / P30 CA016087; United States / NCI NIH HHS / CN / N01 CN095113; United States / NIEHS NIH HHS / ES / P30-ES-00260; United States / NCI NIH HHS / CN / N01 CN065120; United States / NIEHS NIH HHS / ES / P30 ES000260; United States / NCI NIH HHS / CA / P30-CA-16087; United States / NCI NIH HHS / CA / N01 CN35566; United States / NCI NIH HHS / CN / CN35566-02; United States / NCI NIH HHS / CN / N01-CN-65120; United States / NCI NIH HHS / CN / N01 CN35566-02; United States / NCI NIH HHS / CN / N01-CN-35566-02
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Alkylating Agents; 0 / Androgens; 0 / Antioxidants; 0 / Selenium Compounds; 1406-18-4 / Vitamin E; 3XMK78S47O / Testosterone; 4KM2BN5JHF / Cyproterone Acetate; 684-93-5 / Methylnitrosourea; 964MRK2PEL / Selenomethionine; H4N855PNZ1 / alpha-Tocopherol
[Other-IDs]
NLM/ NIHMS161245; NLM/ PMC2945242
47.
Leinonen T, Pirinen R, Böhm J, Johansson R, Rinne A, Weber E, Kosma VM:
Biological and prognostic role of acid cysteine proteinase inhibitor (ACPI, cystatin A) in non-small-cell lung cancer.
J Clin Pathol
; 2007 May;60(5):515-9
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[Title]
Biological and prognostic role of acid cysteine proteinase inhibitor (ACPI, cystatin A) in non-small-
cell
lung cancer.
BACKGROUND: Acid cysteine protease inhibitor (ACPI) is an intracellular protein, often linked to neoplastic changes in epithelium and thought to have an inhibitory role in
malignant
transformation.
AIM: To analyse the expression and prognostic role of ACPI in non-small-
cell
lung cancer (NSCLC).
RESULTS: A normal bronchial epithelium showed positive staining for ACPI in the
basal
cells
, whereas the upper two-thirds of the dysplastic epithelium was ACPI positive.
High staining for ACPI was found in 74% (91/123) of squamous-
cell
carcinomas, whereas 16% (8/49) of
adenocarcinomas
and 30% of (8/27) large-
cell
carcinomas showed the high expression of ACPI (p<0.001).
Among squamous-
cell
carcinomas, low expression of ACPI was correlated with poor tumour differentiation (p=0.032).
In overall survival (OS) and
disease
-free survival (DFS) analyses, the histological type of the tumour (both p<0.001) and stage of the tumour (p=0.001, p=0.013, respectively) were related to patient outcome.
Low expression of ACPI in tumour
cells
was associated with poor OS and DFS (p<0.041, p=0.004, respectively).
CONCLUSIONS: ACPI expression is linked with the
malignant
transformation of the bronchial epithelium and predicts a risk of tumour recurrence as well as poor rate of survival for the patients.
[MeSH-major]
Biomarkers, Tumor / metabolism. Carcinoma, Non-Small-
Cell
Lung / metabolism. Cystatins / metabolism. Cysteine Proteinase Inhibitors / metabolism. Lung Neoplasms / metabolism
[MeSH-minor]
Adenocarcinoma
/ metabolism.
Adenocarcinoma
/ pathology. Adult. Aged. Carcinoma, Large
Cell
/ metabolism. Carcinoma, Large
Cell
/ pathology. Carcinoma, Squamous
Cell
/ metabolism. Carcinoma, Squamous
Cell
/ pathology. Follow-Up Studies. Humans. Immunoenzyme Techniques. Middle Aged.
Neoplasm
Staging. Precancerous Conditions / metabolism. Prognosis. Survival Analysis
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.
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consumer health - Lung Cancer
.
NCI CPTC Antibody Characterization Program.
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.
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(PMID = 16790691.001).
[ISSN]
0021-9746
[Journal-full-title]
Journal of clinical pathology
[ISO-abbreviation]
J. Clin. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Cystatins; 0 / Cysteine Proteinase Inhibitors
[Other-IDs]
NLM/ PMC1994551
48.
Xu XL, Li B, Sun XL, Li LQ, Ren RJ, Gao F:
[Clinical and pathological analysis of 2639 cases of eyelid tumors].
Zhonghua Yan Ke Za Zhi
; 2008 Jan;44(1):38-41
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The 5 leading eyelid
malignant
tumors were
basal cell
carcinoma, sebaceous gland carcinoma, lymphoma, squamous
cell
carcinoma and melanoma.
The mean age at
diagnosis
was 61 years for
basal cell
carcinoma and sebaceous gland carcinoma, 57 years and 52 years for squamous
cell
carcinoma and melanoma, respectively, and 48 years for lymphoma.
There was no significant sex predilection in
basal cell
carcinoma and sebaceous gland carcinoma.
Melanoma and lymphoma occurred more commonly in women, whereas squamous
cell
carcinoma occurred more commonly in men.
CONCLUSIONS:
Basal cell
carcinoma and sebaceous gland carcinoma were the most common
malignant
eyelid tumors, and lymphoma ranked third and had an increasing trend.
The
malignant
tumors occurred predominantly in the elderly of 60 years and above.
[MeSH-major]
Adenocarcinoma
, Sebaceous / pathology. Carcinoma,
Basal Cell
/ pathology. Eyelid Neoplasms / pathology. Lymphoma / pathology
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(PMID = 18510241.001).
[ISSN]
0412-4081
[Journal-full-title]
[Zhonghua yan ke za zhi] Chinese journal of ophthalmology
[ISO-abbreviation]
Zhonghua Yan Ke Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
49.
Akrish S, Peled M, Ben-Izhak O, Nagler RM:
Malignant salivary gland tumors and cyclo-oxygenase-2: a histopathological and immunohistochemical analysis with implications on histogenesis.
Oral Oncol
; 2009 Dec;45(12):1044-50
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[Title]
Malignant
salivary gland tumors and cyclo-oxygenase-2: a histopathological and immunohistochemical analysis with implications on histogenesis.
The classification system for
malignant
salivary gland tumors (MST) is largely dependent on its histogenesis.
The histogenesis is uncertain but the "bicellular theory of origin" has been accepted by most and states that
malignant
transformation of reserve
cells
from either the intercalated or excretory duct are responsible for the development of MST.
Fifty six primary major and minor gland MST were stained with anti-cox-2 antibody and rated with a combined score that added a scale of intensity to the percentage of tumor
cells
that overexpressed the cox-2 protein.
Strong cox-2 overexpression was noted in all MST of proposed excretory duct origin: salivary duct carcinoma (100%), mucoepidermoid carcinoma (MEC) (92%), and
adenocarcinoma
nos
(AdC
nos
) (83%).
Primary squamous
cell
carcinoma (PSCC) was the exception.
Negative expression was noted in all tumors of proposed intercalated duct origin (adenoid cystic carcinoma,
basal cell adenocarcinoma
and acinic
cell
carcinoma) with the exception of one case of polymorphous low grade
adenocarcinoma
.
Strong cox-2 overexpression was noted in the epidermoid
cells
of MEC, abluminal duct
cells
surrounding the duct-like structures and ductal
cells
of AdC
nos
and salivary duct carcinoma.
Myoepithelial and acinar
cells
were unreactive.
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(PMID = 19729335.001).
[ISSN]
1879-0593
[Journal-full-title]
Oral oncology
[ISO-abbreviation]
Oral Oncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 1.14.99.1 / Cyclooxygenase 2
50.
Deng J, Fujimoto J, Ye XF, Men TY, Van Pelt CS, Chen YL, Lin XF, Kadara H, Tao Q, Lotan D, Lotan R:
Knockout of the tumor suppressor gene Gprc5a in mice leads to NF-kappaB activation in airway epithelium and promotes lung inflammation and tumorigenesis.
Cancer Prev Res (Phila)
; 2010 Apr;3(4):424-37
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Examination of normal lung tissue and tumors from 51 Gprc5a(+/+) (
adenoma
incidence, 9.8%;
adenocarcinoma
, 0%) and 38 Gprc5a(-/-) mice (
adenoma
, 63%;
adenocarcinoma
, 21%) revealed macrophage infiltration into lungs of 45% of the Gprc5a(-/-) mice and 8% of Gprc5a(+/+) mice and the direct association of macrophages with 42% of
adenomas
and 88% of
adenocarcinomas
in the knockout mice.
Studies with epithelial
cells
cultured from tracheas of Gprc5a(-/-) and Gprc5a(+/+) mice revealed that Gprc5a loss is associated with increased
cell
proliferation, resistance to
cell
death in suspension, and increased
basal
, tumor necrosis factor alpha-induced, and lipopolysaccharide-induced NF-kappaB activation, which were reversed partially in Gprc5a(-/-)
adenocarcinoma
cells
by reexpression of Gprc5a.
Compared with Gprc5a(+/+)
cells
, the Gprc5a(-/-)
cells
produced higher levels of chemokines and cytokines and their conditioned medium induced more extensive macrophage migration.
Silencing Gprc5a and the p65 subunit of NF-kappaB in Gprc5a(+/+) and Gprc5a(-/-)
cells
, respectively, reversed these effects.
Thus, Gprc5a loss enhances NF-kappaB activation in lung epithelial
cells
, leading to increased autocrine and paracrine interactions,
cell
autonomy, and enhanced inflammation, which may synergize in the creation of a tumor-promoting microenvironment.
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[Copyright]
(c) 2010 AACR.
[CommentIn]
Cancer Prev Res (Phila). 2010 Apr;3(4):403-5
[
20354166.001
]
(PMID = 20354164.001).
[ISSN]
1940-6215
[Journal-full-title]
Cancer prevention research (Philadelphia, Pa.)
[ISO-abbreviation]
Cancer Prev Res (Phila)
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P30 CA16672
[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 / NF-kappa B; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Receptors, G-Protein-Coupled
51.
Lin Z, Liu M, Li Z, Kim C, Lee E, Kim I:
DeltaNp63 protein expression in uterine cervical and endometrial cancers.
J Cancer Res Clin Oncol
; 2006 Dec;132(12):811-6
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MATERIALS AND METHODS: DeltaNp63 protein expression was studied in a variety of 127 cases of uterine cervical lesions (20 non-neoplastic cervices, 43 cervical intraepithelial
neoplasia
[CIN], 54 squamous
cell
carcinomas (SCCs), 40
adenocarcinomas
, and 13 other histologic types) and 30 endometrioid type of endometrial
adenocarcinomas
by using immunohistochemistry.
One SCC
cell
line (ME-180) and one
adenocarcinoma cell
line (HeLa) were also included.
RESULTS: In uterine cervix, the expression of DeltaNp63 was increased with progression of CIN, and positive in all SCCs, transitional
cell
carcinomas, and adenoid
basal
carcinoma, but negative in all
adenocarcinomas
.
Adenosquamous
cell
carcinoma and mixed neuroendocrine and squamous
cell
carcinoma were positive in squamous component, but not in
adenocarcinoma
and neuroendocrine carcinoma components.
ME-180
cell
line was positive, whereas HeLa
cell
line was negative.
Endometrioid type of endometrial
adenocarcinomas
showed a positive staining in glandular (26.7%) and squamous component.
[MeSH-major]
Adenocarcinoma
/ metabolism. Carcinoma, Squamous
Cell
/ metabolism. DNA-Binding Proteins / biosynthesis. Endometrial Neoplasms / metabolism. Trans-Activators / biosynthesis. Tumor Suppressor Proteins / biosynthesis. Uterine Cervical Neoplasms / metabolism
[MeSH-minor]
Antigens, Differentiation / biosynthesis.
Cell
Line, Tumor. Cervix Uteri / cytology. Cervix Uteri / metabolism. Female. HeLa
Cells
. Humans. Immunohistochemistry. Transcription Factors
MedlinePlus Health Information.
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.
International Agency for Research on Cancer - Screening Group.
diagnostics - Histopathology and cytopathology of the uterine cervix - digital atlas
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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[Cites]
Gynecol Oncol. 2001 Jan;80(1):24-9
[
11136565.001
]
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J Histochem Cytochem. 2003 Aug;51(8):1097-9
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Carcinogenesis. 2004 Jun;25(6):857-64
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]
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]
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(PMID = 16804722.001).
[ISSN]
0171-5216
[Journal-full-title]
Journal of cancer research and clinical oncology
[ISO-abbreviation]
J. Cancer Res. Clin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antigens, Differentiation; 0 / DNA-Binding Proteins; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
52.
Shieh JJ, Liu KT, Huang SW, Chen YJ, Hsieh TY:
Modification of alternative splicing of Mcl-1 pre-mRNA using antisense morpholino oligonucleotides induces apoptosis in basal cell carcinoma cells.
J Invest Dermatol
; 2009 Oct;129(10):2497-506
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[Title]
Modification of alternative splicing of Mcl-1 pre-mRNA using antisense morpholino oligonucleotides induces apoptosis in
basal cell
carcinoma
cells
.
Myeloid
cell
leukemia-1 (Mcl-1, Mcl-1L) is an anti-apoptotic protein of the Bcl-2 family that acts as a critical molecule in apoptosis control.
In this study, we found an imbalance between the expression levels of Mcl-1L and Mcl-1S in the skin
basal cell
carcinoma (BCC)
cell
line when compared with primary keratinocytes.
We showed that overexpression of Mcl-1S induces apoptosis in BCC
cells
.
This shift increases the level of pro-apoptotic Mcl-1S and reduces the level of anti-apoptotic Mcl-1L, which induces apoptosis in BCC
cells
and AGS
cells
, a human gastric
adenocarcinoma
epithelial
cell
line.
[MeSH-major]
Alternative Splicing / drug effects. Apoptosis / drug effects. Carcinoma,
Basal Cell
/ pathology. Oligonucleotides, Antisense / pharmacology. Proto-Oncogene Proteins c-bcl-2 / genetics. RNA, Messenger / genetics. Skin Neoplasms / pathology
[MeSH-minor]
Adenocarcinoma
/ metabolism.
Adenocarcinoma
/ pathology.
Cell
Line, Tumor. Humans. Keratinocytes / metabolism. Keratinocytes / pathology. Myeloid
Cell
Leukemia Sequence 1 Protein. Stomach Neoplasms / metabolism. Stomach Neoplasms / pathology
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.
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(PMID = 19369967.001).
[ISSN]
1523-1747
[Journal-full-title]
The Journal of investigative dermatology
[ISO-abbreviation]
J. Invest. Dermatol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger
53.
Guo RX, Wei LH, Zhao D, Wang JL, Li XP:
[Effects of ICI182780 (Faslodex) on proliferation and apoptosis induced by 17beta-estradiol in endometrial carcinoma cells].
Beijing Da Xue Xue Bao
; 2006 Oct 18;38(5):470-4
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[Title]
[Effects of ICI182780 (Faslodex) on proliferation and apoptosis induced by 17beta-estradiol in endometrial carcinoma
cells
].
OBJECTIVE: To observe the influence of estrogen receptor, ICI182780, on proleferation,
cell
cycle progression and apoptosis in estrogen receptor (ER)-positive and ER-poor endometrial carcinoma
cells
and to explore the possible preliminary value of ICI182780 treating endometrial carcinoma.
METHODS: The effects of ICI182780 on proliferation, apoptosis and
cell
cycle distribution of endometrial cancer
cells
costimulated with 10(-6) mol/L E2 was detected by monotetrazolium (MTT) assay and fluorescence-activated
cell
sorting technique.
Cell
cycle distribution analysis revealed that percentage of Ishikawa
cells
at G0-G1 phase decreased and percentage at S phase increased significantly, whereas that of HEC-1A
cells
did not show significant alteration.
In cotreatment of endometrial cancer
cells
with ICI182780, values of OD 570 nm and numbers of apoptotic
cells
of Ishikawa
cells
decreased to
basal
levels, G0-G1 phase proportion increased, percentage of S phase increased in a time or time-dependent manner.
But there was no such alteration in HEC-1A
cells
.
CONCLUSION: The specific ER antagonist, ICI182780, can inhibit Ishikawa
cell
propagation induced by E2, make
cells
apoptosis and block Ishikawa
cells
at the G1/S transition.
[MeSH-major]
Apoptosis / drug effects.
Cell
Proliferation / drug effects. Estradiol / analogs & derivatives. Estradiol / pharmacology
[MeSH-minor]
Adenocarcinoma
/ pathology.
Adenocarcinoma
/ physiopathology.
Cell
Cycle / drug effects.
Cell
Line, Tumor.
Cell
Survival / drug effects. Dose-Response Relationship, Drug. Endometrial Neoplasms / pathology. Endometrial Neoplasms / physiopathology. Estrogen Antagonists / pharmacology. Female. Flow Cytometry. Humans
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.
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ESTRADIOL
.
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(PMID = 17068616.001).
[ISSN]
1671-167X
[Journal-full-title]
Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
[ISO-abbreviation]
Beijing Da Xue Xue Bao
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / Estrogen Antagonists; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol
54.
Gubbay O, Guo W, Rae MT, Niven D, Langdon SP, Hillier SG:
Inflammation-associated gene expression is altered between normal human ovarian surface epithelial cells and cell lines derived from ovarian adenocarcinomas.
Br J Cancer
; 2005 May 23;92(10):1927-33
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[Title]
Inflammation-associated gene expression is altered between normal human ovarian surface epithelial
cells
and
cell
lines derived from ovarian
adenocarcinomas
.
The process of ovulation is synonymous with inflammation and inflammatory cytokines such as interleukin-1alpha (IL-1alpha) have recently been shown to induce both inflammatory and anti-inflammatory responses in human OSE (HOSE)
cells
.
In this study we directly compared levels of IL-1alpha-induced gene expression by analysing the levels of 11beta-hydroxysteroid dehydrogenase (11betaHSD) types 1 (11betaHSD-1) and 2 (11betaHSD-2), cyclooxygenase-2 (COX-2), IL-1 receptor (IL-1R) and glucocorticoid receptor alpha (GRalpha) mRNA between normal HOSE
cells
and
cell
lines derived from poorly differentiated (SKOV-3, BG-1, PEO-4) and well-differentiated (PEO-14) ovarian
adenocarcinoma
.
In HOSE
cell
cultures, and to a lesser extent PEO-14
cells
, the
basal
mRNA levels of COX-2 and 11betaHSD-1 were relatively high and further shown to be induced in response to IL-1alpha (for HOSE
cells
; >20-fold, P<0.05 and PEO-14
cells
; >3fold, P<0.05).
However, whereas HOSE
cells
expressed a low level of 11betaHSD-2 mRNA that was only mildly responsive to IL-1alpha (1.3-fold, P<0.001), all
cell
lines exhibited a higher
basal
level of 11betaHSD-2 mRNA that was in some cases further stimulated in PEO-4
cells
(five-fold; P<0.05) or suppressed in SKOV-3
cells
(two-fold; P<0.01) in response to IL-1alpha.
All
cells
tested expressed IL-1R and, with the exception of BG-1, GRalpha.
These results indicate that
cell
lines derived from ovarian cancers have lost the ability to respond normally to inflammatory cytokines such as IL-1alpha.
The
finding
that normal OSE
cells
, in contrast to
cell
lines derived from patients with ovarian
adenocarcinoma
, abundantly express 11betaHSD-1 mRNA but are essentially devoid of 11betaHSD-2 mRNA supports the concept that the pattern of 11betaHSD isoform gene expression is a defining feature of neoplastic cellular transformation, which might have particular relevance to the ovary.
[MeSH-major]
Adenocarcinoma
/ genetics.
Adenocarcinoma
/ immunology. Cytokines / biosynthesis. Cytokines / genetics. Gene Expression Regulation. Inflammation. Ovarian Neoplasms / genetics. Ovarian Neoplasms / immunology
[MeSH-minor]
11-beta-Hydroxysteroid Dehydrogenases / biosynthesis.
Cell
Differentiation.
Cell
Transformation, Neoplastic. Cyclooxygenase 2. Epithelial
Cells
. Female. Humans. Interleukin-1 / pharmacology. Membrane Proteins. Ovulation. Prostaglandin-Endoperoxide Synthases / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction
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.
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.
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[ISSN]
0007-0920
[Journal-full-title]
British journal of cancer
[ISO-abbreviation]
Br. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Cytokines; 0 / Interleukin-1; 0 / Membrane Proteins; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenases; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
[Other-IDs]
NLM/ PMC2361768
55.
Bi S, Liu JR, Li Y, Wang Q, Liu HK, Yan YG, Chen BQ, Sun WG:
gamma-Tocotrienol modulates the paracrine secretion of VEGF induced by cobalt(II) chloride via ERK signaling pathway in gastric adenocarcinoma SGC-7901 cell line.
Toxicology
; 2010 Jul-Aug;274(1-3):27-33
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[Title]
gamma-Tocotrienol modulates the paracrine secretion of VEGF induced by cobalt(II) chloride via ERK signaling pathway in gastric
adenocarcinoma
SGC-7901
cell
line.
Hypoxia is a common characteristic feature of solid tumors, and carcinoma
cells
are known to secrete many growth factors.
In this study, the effect of gamma-tocotrienol, a natural product commonly found in palm oil and rice bran, on the accumulation of HIF-1alpha protein and the paracrine secretion of VEGF in human gastric
adenocarcinoma
SGC-7901
cell
line induced by cobalt(II) chloride (as a hypoxia mimic) was investigated.
These results showed that cobalt(II) chloride induced the high expression of VEGF in SGC-7901
cells
at dose of 150 micromol/L for 24h.
Both
basal
level and cobalt(II) chloride-induced HIF-1alpha protein accumulation and VEGF paracrine secretion were inhibited in SGC-7901
cells
treated with gamma-tocotrienol at 60 micromol/L treatment for 24 h.
[MeSH-minor]
Adenocarcinoma
.
Cell
Line. Chromans. Cobalt / pharmacology. Guanylate Cyclase. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / pharmacology. Mitogen-Activated Protein Kinase 3 / metabolism. Mitogen-Activated Protein Kinase 3 / pharmacology. Neovascularization, Pathologic. Phosphorylation. Receptors, Cytoplasmic and Nuclear. Signal Transduction / drug effects. Vascular Endothelial Growth Factors / metabolism. Vascular Endothelial Growth Factors / pharmacology. Vitamin E / analogs & derivatives
MedlinePlus Health Information.
consumer health - Stomach Cancer
.
Hazardous Substances Data Bank.
COBALT, ELEMENTAL
.
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 CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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[Copyright]
2010 Elsevier Ireland Ltd. All rights reserved.
(PMID = 20452389.001).
[ISSN]
1879-3185
[Journal-full-title]
Toxicology
[ISO-abbreviation]
Toxicology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Ireland
[Chemical-registry-number]
0 / Chromans; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Proteins; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 1406-18-4 / Vitamin E; 3G0H8C9362 / Cobalt; 4382-43-8 / plastochromanol 8; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 4.6.1.2 / Guanylate Cyclase; EC 4.6.1.2 / soluble guanylyl cyclase
56.
Kong CS, Beck AH, Longacre TA:
A panel of 3 markers including p16, ProExC, or HPV ISH is optimal for distinguishing between primary endometrial and endocervical adenocarcinomas.
Am J Surg Pathol
; 2010 Jul;34(7):915-26
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[Title]
A panel of 3 markers including p16, ProExC, or HPV ISH is optimal for distinguishing between primary endometrial and endocervical
adenocarcinomas
.
Endometrial and endocervical
adenocarcinomas
may seem histologically identical and it can be difficult to determine primary site of origin based on morphology alone.
The TMA consisted of 214 endometrial carcinomas, 33 endocervical
adenocarcinomas
, and 36 problematic cases.
The endometrial and endocervical carcinomas represented usual endometrioid and mucinous types, and special variants (uterine serous carcinoma, uterine clear
cell
carcinoma, minimal deviation endocervical
adenocarcinoma
, cervical small
cell
carcinoma, adenoid
basal cell
carcinoma, mesonephric carcinoma).
Using a script written in R, the diagnostic accuracy of all possible combinations of markers was evaluated and it was shown that a 3 marker panel including vimentin, ER, or PR, and an HPV marker (p16, ProExC, or HPV ISH) is optimal for determining site of origin for usual endometrial and endocervical
adenocarcinomas
.
[MeSH-major]
Adenocarcinoma
/
diagnosis
. Biomarkers, Tumor / analysis. Cyclin-Dependent Kinase Inhibitor p16 / analysis. DNA, Viral / analysis. Endometrial Neoplasms /
diagnosis
. Papillomaviridae / genetics. Uterine Cervical Neoplasms /
diagnosis
[MeSH-minor]
Diagnosis
, Differential. Female. Humans. Immunoenzyme Techniques. In Situ Hybridization. Papillomavirus Infections /
diagnosis
. Reproducibility of Results. Tissue Array Analysis. Vimentin / metabolism
MedlinePlus Health Information.
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.
International Agency for Research on Cancer - Screening Group.
diagnostics - A practical manual on visual screening for cervical neoplasia
.
The Lens.
Cited by Patents in
.
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(PMID = 20534993.001).
[ISSN]
1532-0979
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Grant]
United States / NLM NIH HHS / LM / T15 LM007033
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Viral; 0 / Vimentin
[Other-IDs]
NLM/ NIHMS775595; NLM/ PMC4847142
57.
Sanchez-Salazar AJ, Basler JW, Nicolas MM:
Intraductal carcinoma of the prostate in the ejaculatory duct.
Int J Surg Pathol
; 2010 Aug;18(4):298-9
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Intraductal carcinoma of the prostate (IDCP) involving prostatic ducts and acini is a well-known phenomenon typically seen in a background of high-grade invasive prostatic
adenocarcinoma
.
The current case of prostatic
adenocarcinoma
with Gleason score of 9 (4 + 5) invades the ejaculatory ducts, left seminal vesicle, and extraprostatic tissue.
The tumor involving the left ejaculatory duct spans the lumen with preservation of native duct architecture, including
basal
cells
, similar features described in IDCP involving prostatic ducts and acini.
[MeSH-minor]
Aged. Biomarkers, Tumor / metabolism. Humans. Male. Neoplasms, Multiple Primary. Prognosis. Prostatectomy. Prostatic Intraepithelial
Neoplasia
/ metabolism. Prostatic Intraepithelial
Neoplasia
/ pathology. Prostatic Intraepithelial
Neoplasia
/ surgery
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(PMID = 20444733.001).
[ISSN]
1940-2465
[Journal-full-title]
International journal of surgical pathology
[ISO-abbreviation]
Int. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor
58.
Luebke AM, Schlomm T, Gunawan B, Bonkhoff H, Füzesi L, Erbersdobler A:
Simultaneous tumour-like, atypical basal cell hyperplasia and acinar adenocarcinoma of the prostate: a comparative morphological and genetic approach.
Virchows Arch
; 2005 Mar;446(3):338-41
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[Title]
Simultaneous tumour-like, atypical
basal cell
hyperplasia and acinar
adenocarcinoma
of the prostate: a comparative morphological and genetic approach.
Basal cell
tumours of the prostatic gland are rare, and the classification is difficult.
In the present case report, a large, tumour-like proliferation of atypical basaloid
cells
was found incidentally in a prostatectomy specimen that otherwise contained a conventional acinar
adenocarcinoma
.
The basaloid
cells
displayed a solid or adenoid-cystic growth pattern and strongly expressed high-molecular-weight cytokeratins and bcl-2.
A high Ki-67 index was recorded within the atypical basaloid
cells
, by far exceeding the one counted in the conventional
adenocarcinoma
.
However, there were no definite criteria for
a malignant
behaviour of the
basal cell
tumour.
Comparative genomic hybridisation from microdissected tumour
cells
yielded losses at the short arms of chromosomes 8 and 12 in the conventional
adenocarcinoma
and a normal karyotype in the
basal cell
tumour.
The pathological findings favoured the
diagnosis
of an atypical
basal cell
hyperplasia.
[MeSH-major]
Carcinoma, Acinar
Cell
/ complications. Carcinoma, Acinar
Cell
/ pathology. Prostatic Hyperplasia / complications. Prostatic Hyperplasia / pathology. Prostatic Neoplasms / complications. Prostatic Neoplasms / pathology
[MeSH-minor]
Diagnosis
, Differential. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasms,
Basal Cell
/ genetics. Neoplasms,
Basal Cell
/ pathology. Nucleic Acid Hybridization
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[Cites]
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8343043.001
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Hum Pathol. 1998 Dec;29(12):1447-50
[
9865831.001
]
(PMID = 15726402.001).
[ISSN]
0945-6317
[Journal-full-title]
Virchows Archiv : an international journal of pathology
[ISO-abbreviation]
Virchows Arch.
[Language]
eng
[Publication-type]
Case Reports; Comparative Study; Journal Article
[Publication-country]
Germany
59.
Fleming JC, Linder JS, Karcioglu ZA:
Orbital hyperostosis following exenteration.
Ophthal Plast Reconstr Surg
; 2008 Sep-Oct;24(5):378-82
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The histopathology revealed necrotic destruction of the trabeculae mixed with randomly distributed chronic inflammatory
cells
and fibrosis and inflamed overlying granulation tissue.
[MeSH-major]
Adenocarcinoma
, Sebaceous / surgery. Carcinoma,
Basal Cell
/ surgery. Eyelid Neoplasms / surgery. Hyperostosis / etiology. Orbital Diseases / etiology. Postoperative Complications
[MeSH-minor]
Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged.
Neoplasm
Invasiveness.
Neoplasm
Recurrence, Local / surgery. Orbit / pathology. Orbit / radiography. Orbit Evisceration. Tomography, X-Ray Computed
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(PMID = 18806659.001).
[ISSN]
1537-2677
[Journal-full-title]
Ophthalmic plastic and reconstructive surgery
[ISO-abbreviation]
Ophthal Plast Reconstr Surg
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
60.
Mayes DC, Patterson JW, Ramnani DM, Mills SE:
alpha-methylacyl coenzyme A racemase is immunoreactive in extramammary Paget disease.
Am J Clin Pathol
; 2007 Apr;127(4):567-71
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[Title]
alpha-methylacyl coenzyme A racemase is immunoreactive in extramammary Paget
disease
.
alpha-Methylacyl-coenzyme A racemase (AMACR) has become a common tool in the
diagnosis
of morphologically difficult prostatic carcinoma and often is used in combination with the
basal cell
markers p63 and 34betaE12.
We report findings in 21 cases of extramammary Paget
disease
(EMPD),
a neoplasm
not previously reported to show AMACR immunoreactivity.
AMACR immunoreactivity is a common
finding
in EMPD in men and women.
[MeSH-major]
Adenocarcinoma
/ complications. Biomarkers, Tumor / analysis. Paget
Disease
, Extramammary / complications. Paget
Disease
, Extramammary / metabolism. Prostatic Neoplasms / complications. Racemases and Epimerases / metabolism
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(PMID = 17369131.001).
[ISSN]
0002-9173
[Journal-full-title]
American journal of clinical pathology
[ISO-abbreviation]
Am. J. Clin. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
61.
Nasir S, Aydin MA:
Versatility of free SCIA/SIEA flaps in head and neck defects.
Ann Plast Surg
; 2010 Jul;65(1):32-7
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[MeSH-minor]
Adenocarcinoma
/ surgery. Adolescent. Adult. Aged. Bone Transplantation. Burns / surgery. Carcinoma,
Basal Cell
/ surgery. Carcinoma, Squamous
Cell
/ surgery. Child. Cicatrix / surgery. Facial Neoplasms / surgery. Female. Follow-Up Studies. Humans. Male. Maxilla / surgery. Maxillary Neoplasms / surgery. Middle Aged. Neck Injuries / surgery.
Neoplasm
Recurrence, Local / surgery. Reoperation. Scalp / surgery. Skin Neoplasms / surgery. Young Adult
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(PMID = 20574218.001).
[ISSN]
1536-3708
[Journal-full-title]
Annals of plastic surgery
[ISO-abbreviation]
Ann Plast Surg
[Language]
eng
[Publication-type]
Case Reports; Comparative Study; Journal Article
[Publication-country]
United States
62.
Parashar P, Baron E, Papadimitriou JC, Ord RA, Nikitakis NG:
Basal cell adenocarcinoma of the oral minor salivary glands: review of the literature and presentation of two cases.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod
; 2007 Jan;103(1):77-84
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[Title]
Basal cell adenocarcinoma
of the oral minor salivary glands: review of the literature and presentation of two cases.
Basal cell adenocarcinoma
(BCA) is an unusual salivary gland malignancy that very rarely affects the minor glands.
[MeSH-major]
Adenocarcinoma
/ pathology. Salivary Gland Neoplasms / pathology. Salivary Glands, Minor / pathology
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(PMID = 17178498.001).
[ISSN]
1528-395X
[Journal-full-title]
Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
[ISO-abbreviation]
Oral Surg Oral Med Oral Pathol Oral Radiol Endod
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Number-of-references]
35
63.
Mrena J, Wiksten JP, Nordling S, Kokkola A, Ristimäki A, Haglund C:
MMP-2 but not MMP-9 associated with COX-2 and survival in gastric cancer.
J Clin Pathol
; 2006 Jun;59(6):618-23
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BACKGROUND AND AIM: Matrix metalloproteinases (MMPs) MMP-2 and MMP-9 can degrade type IV collagen of extracellular matrix and
basal
membranes.
[MeSH-major]
Adenocarcinoma
/ enzymology. Biomarkers, Tumor / metabolism. Cyclooxygenase 2 / metabolism. Matrix Metalloproteinase 2 / metabolism. Stomach Neoplasms / enzymology
[MeSH-minor]
Age Distribution. Aged. Female. Humans. Lymphatic Metastasis. Male. Matrix Metalloproteinase 9 / metabolism. Middle Aged.
Neoplasm
Invasiveness.
Neoplasm
Staging. Prognosis. Survival Analysis
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(PMID = 16731602.001).
[ISSN]
0021-9746
[Journal-full-title]
Journal of clinical pathology
[ISO-abbreviation]
J. Clin. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
[Other-IDs]
NLM/ PMC1860392
64.
Fukui D, Bando G, Ishikawa Y, Kadota K:
Adenosquamous carcinoma with cilium formation, mucin production and keratinization in the nasal cavity of a red fox (Vulpes vulpes schrencki).
J Comp Pathol
; 2007 Aug-Oct;137(2-3):142-5
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A diagnosis
of adenosquamous carcinoma was made in an 11-year-old red fox.
The nasal and oral lesions were composed of adenocarcinomatous
cells
and squamous
cells
, the latter predominating in the oral lesions.
The marrow of the palatine bone also contained neoplastic tissue, which consisted of cysts and keratin masses surrounded by well-differentiated squamous
cells
.
Although inconspicuous in the oral cavity and marrow, ciliated
cells
with or without mucin were observed in the adenocarcinomatous and cystic elements.
Neoplastic
basal
cells
and less-differentiated
adenocarcinoma
cells
, which were identifiable by immunolabelling for cytokeratin 5 (CK5) and CK18, were considered to be pluripotential.
These
cells
, which lined tubular structures, were distinct from intermediate
cells
in mucoepidermoid carcinoma, which can differentiate into squamous and mucin-producing
cells
but have a nondescript appearance.
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(PMID = 17645890.001).
[ISSN]
0021-9975
[Journal-full-title]
Journal of comparative pathology
[ISO-abbreviation]
J. Comp. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Keratin-18; 0 / Keratin-5; 0 / Mucins; 68238-35-7 / Keratins
65.
Aust S, Brucker B, Graf J, Klimpfinger M, Thalhammer T:
Melatonin modulates acid/base transport in human pancreatic carcinoma cells.
Cell Physiol Biochem
; 2006;18(1-3):91-102
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[Title]
Melatonin modulates acid/base transport in human pancreatic carcinoma
cells
.
To study whether pancreatic bicarbonate secretion is stimulated by melatonin, investigations were done in two human ductal pancreatic
adenocarcinoma cell
lines MIA PaCa-2 (MIA) and PANC-1 (PANC).
Using the fluorescence pH-sensor BCECF-AM, we monitored melatonin effects on
basal
intracellular pH (pH(i)), and on pH(i) recovery after intracellular alkalinization produced by the removal of extracellular HCO(3) (-)/CO(2).
Exposure to 1 microM melatonin for 24 hrs and presence of the indoleamine during the experiment increases the
basal
pH(i).
In summary, we show a stimulatory effect of melatonin on bicarbonate secretion in the pancreatic cancer
cell
lines which may help to prevent duodenal damage.
[MeSH-minor]
Antiporters / genetics. Bicarbonates / metabolism. Biological Transport / drug effects.
Cell
Line, Tumor. Colforsin / pharmacology. Cyclic AMP / metabolism. Gene Expression / drug effects. Gene Expression / genetics. Humans. Hydrogen-Ion Concentration / drug effects. Models, Biological. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptor, Melatonin, MT1 / genetics. Receptor, Melatonin, MT2 / genetics. Reverse Transcriptase Polymerase Chain Reaction. Symporters / genetics
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(PMID = 16914894.001).
[ISSN]
1015-8987
[Journal-full-title]
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
[ISO-abbreviation]
Cell. Physiol. Biochem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Acids; 0 / Antiporters; 0 / Bicarbonates; 0 / RNA, Messenger; 0 / Receptor, Melatonin, MT1; 0 / Receptor, Melatonin, MT2; 0 / Symporters; 1F7A44V6OU / Colforsin; E0399OZS9N / Cyclic AMP; JL5DK93RCL / Melatonin
66.
Hirsch DL, Miles C, Dierks E:
Basal cell adenocarcinoma of the parotid gland: report of a case and review of the literature.
J Oral Maxillofac Surg
; 2007 Nov;65(11):2385-8
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[Title]
Basal cell adenocarcinoma
of the parotid gland: report of a case and review of the literature.
[MeSH-major]
Adenocarcinoma
/
diagnosis
. Parotid Neoplasms /
diagnosis
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(PMID = 17954345.001).
[ISSN]
0278-2391
[Journal-full-title]
Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons
[ISO-abbreviation]
J. Oral Maxillofac. Surg.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Number-of-references]
6
67.
Shimizu Y, Yoshida T, Kato M, Hirota J, Ono S, Nakagawa M, Kobayashi T, Kubota K, Asaka M:
Low-grade dysplasia component in early invasive squamous cell carcinoma of the esophagus.
J Gastroenterol Hepatol
; 2010 Feb;25(2):314-8
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[Title]
Low-grade dysplasia component in early invasive squamous
cell
carcinoma of the esophagus.
If LGD progresses to squamous
cell
carcinoma, early carcinoma lesions that have such a natural history might contain a remaining LGD component.
METHODS: The lesions in the 68 patients with early invasive squamous
cell
carcinoma who underwent endoscopic mucosal resection were examined for the presence of an LGD component.
RESULTS: Histological examination of resected specimens confirmed LGD components in 43% of the squamous
cell
carcinoma lesions.
CONCLUSION: Our results indicate the possibility that the lesion was formed by a combination of small lesions that arose as a multicentric occurrence of squamous
cell
carcinoma and dysplasia.
However, the concept of '
basal cell
layer type carcinoma in situ' may be suitable for squamous
cell
lesions with a high degree of cytological abnormalities confined to the lower half of the epithelium.
[MeSH-major]
Adenocarcinoma
/ pathology. Carcinoma in Situ / pathology. Carcinoma, Squamous
Cell
/ pathology. Esophageal Neoplasms / pathology. Esophagus / pathology. Precancerous Conditions / pathology
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Biopsy.
Cell
Transformation, Neoplastic / pathology.
Disease
Progression. Esophagoscopy. Female. Humans. Male. Middle Aged. Mucous Membrane / pathology.
Neoplasm
Invasiveness.
Neoplasm
Staging
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(PMID = 19968747.001).
[ISSN]
1440-1746
[Journal-full-title]
Journal of gastroenterology and hepatology
[ISO-abbreviation]
J. Gastroenterol. Hepatol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Australia
68.
Matsuzaki K, Okazaki K:
Transforming growth factor-beta during carcinogenesis: the shift from epithelial to mesenchymal signaling.
J Gastroenterol
; 2006 Apr;41(4):295-303
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While the TbetaRI/pSmad3C pathway inhibits growth of normal epithelial
cells
, JNK/pSmad3L-mediated signaling is involved in invasion by activated mesenchymal
cells
.
During sporadic human colorectal carcinogenesis, TGF-beta signaling confers a selective advantage on tumor
cells
by shifting from the TbetaRI/pSmad3C pathway characteristic of mature epithelial
cells
to the JNK/pSmad3L pathway, which is more characteristic of the state of flux shown by the activated mesenchymal
cells
.
JNK acts as a regulator of TGF-beta signaling by increasing the
basal
level of pSmad3L available for action in the nuclei of the invasive
adenocarcinoma
, in the meantime shutting down TGF-beta-dependent nuclear activity of pSmad3C.
From the viewpoint of TGF-beta signaling, a key therapeutic aim in cancer would be restoration of the lost tumor suppressor function observed in normal colorectal epithelial
cells
at the expense of effects promoting aggressive behavior of the
adenocarcinoma
.
[MeSH-minor]
Disease
Progression. Humans
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Sci STKE. 2000 Mar 14;2000(23):re1
[
11752591.001
]
(PMID = 16741607.001).
[ISSN]
0944-1174
[Journal-full-title]
Journal of gastroenterology
[ISO-abbreviation]
J. Gastroenterol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Japan
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Transforming Growth Factor beta
[Number-of-references]
41
69.
Prayaga AK, Loya AC, Gottimukkala SR, Digumarti RR, Maddali LS, Challa S:
Cytologic features of primary malignant tumors of skin and adnexae.
Acta Cytol
; 2008 Nov-Dec;52(6):702-9
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[Title]
Cytologic features of primary
malignant
tumors of skin and adnexae.
STUDY DESIGN: Cases of primary
malignant
tumors of skin and adnexae diagnosed on cytology with histopathology confirmation were retrieved from case records of 1998-2005.
RESULTS: Thirty primary
malignant
tumors of skin and adnexae were analyzed.
Melanoma was the most common (n=12), followed by squamous
cell
carcinoma (SCC) (n=5).
There were 3
basal cell
carcinomas and 2 cases each of sebaceous carcinoma, Paget's
disease
of the breast and lymphoma.
There were single cases of eccrine carcinoma,
malignant
trichilemmal tumor, undifferentiated carcinoma and extramedullary myeloid
cell
tumor.
CONCLUSION: Cytodiagnosis of primary
malignant
tumors of skin and adnexae is possible based on morphology and clinical presentation.
[MeSH-minor]
Adenocarcinoma
, Sebaceous / pathology. Breast Neoplasms / pathology. Carcinoma,
Basal Cell
/ pathology. Carcinoma, Squamous
Cell
/ pathology. Cytodiagnosis. Humans. Lymphatic Metastasis. Medical Records. Melanoma / pathology. Paget's
Disease
, Mammary / pathology
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(PMID = 19068675.001).
[ISSN]
0001-5547
[Journal-full-title]
Acta cytologica
[ISO-abbreviation]
Acta Cytol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
70.
Krajewska M, Olson AH, Mercola D, Reed JC, Krajewski S:
Claudin-1 immunohistochemistry for distinguishing malignant from benign epithelial lesions of prostate.
Prostate
; 2007 Jun 15;67(9):907-10
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[Title]
Claudin-1 immunohistochemistry for distinguishing
malignant
from benign epithelial lesions of prostate.
BACKGROUND: Claudins are a family of approximately 23 integral membrane tight junction (TJ) proteins that maintain
cell
polarity and paracellular barrier functions in epithelial and endothelial
cells
.
METHODS: Using immunohistochemistry, the expression of Claudin-1 was investigated in prostate tissue samples arranged in a tissue microarray (TMA) format and comprising elements of normal prostatic epithelium (n = 6), benign prostatic hyperplasia (BPH; n = 38), prostatic intraepithelial
neoplasia
(PIN; n = 11), and prostate
adenocarcinoma
(n = 48).
The Claudin-1 expression pattern was compared with that of the
basal cell
-specific markers, p63, and HMW cytokeratin (34betaE12), by employing double-labeling techniques in conjunction with image analysis methods utilizing color deconvolution algorithms.
RESULTS: In benign prostatic epithelium, pronounced Claudin-1 expression was observed in the
basal cell
layer with no staining in luminal
cells
.
Prostate
adenocarcinoma
specimens from 98% (47/48) patients lacked Claudin-1 immunostaining, and no cases contained >5% immunopositive tumor
cells
.
CONCLUSIONS: Claudin-1 immunohistochemistry should be considered for use as a new diagnostic tool for distinguishing
malignant
from benign lesions of the prostate.
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(PMID = 17440968.001).
[ISSN]
0270-4137
[Journal-full-title]
The Prostate
[ISO-abbreviation]
Prostate
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U01 CA114810; United States / NCI NIH HHS / CA / CA114810-02
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / CKAP4 protein, human; 0 / CLDN1 protein, human; 0 / Claudin-1; 0 / Membrane Proteins; 68238-35-7 / Keratins
71.
Marci V, Volante M, Cappia S, Righi L, Novello C, Scagliotti GV, Brambilla E, Papotti M:
Basaloid adenocarcinoma. A new variant of pulmonary adenocarcinoma.
Virchows Arch
; 2007 Sep;451(3):729-36
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[Title]
Basaloid
adenocarcinoma
. A new variant of pulmonary
adenocarcinoma
.
The 2004 WHO classification of lung tumours recognised basaloid carcinoma as a variant of squamous and large
cell
carcinoma.
We report a unique case of primary pulmonary
adenocarcinoma
with a basaloid component.
The patient is
disease
-free 13 months after
diagnosis
.
The former was an
adenocarcinoma
with mucus containing spaces lined by columnar mucinous
cells
and basaloid
cells
.
The solid component was an organoid proliferation of basaloid-type
cells
, as in cutaneous
basal cell
carcinoma.
Basaloid
cells
, but not mucinous
cells
, were immunoreactive for high molecular weight cytokeratins (CK), CK 7 and, focally, for TTF-1.
(1) The solid areas resemble a conventional basaloid carcinoma, except for the presence of small mucin-containing spaces. (2) The mucinous
adenocarcinoma
areas contain two layers of columnar and basaloid
cells
. (3) Both components are neoplastic based on
cell
morphology, invasive properties and phenotypic profile.
These findings indicate that a basaloid variant of
adenocarcinoma
is also existing in the spectrum of basaloid carcinomas of the lung.
[MeSH-major]
Adenocarcinoma
/ pathology. Lung Neoplasms / pathology
[MeSH-minor]
Aged, 80 and over. Carcinoma,
Basal Cell
. Humans. Keratins / analysis. Male. Mucins / analysis.
Neoplasm
Invasiveness. Phenotype. World Health Organization
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[Cites]
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Virchows Arch. 2005 Mar;446(3):338-41
[
15726402.001
]
(PMID = 17618455.001).
[ISSN]
0945-6317
[Journal-full-title]
Virchows Archiv : an international journal of pathology
[ISO-abbreviation]
Virchows Arch.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Mucins; 68238-35-7 / Keratins
72.
Midi A, Tecimer T, Bozkurt S, Ozkan N:
Differences in the structural features of atypical adenomatous hyperplasia and low-grade prostatic adenocarcinoma.
Indian J Urol
; 2008 Apr;24(2):169-77
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[Title]
Differences in the structural features of atypical
adenomatous
hyperplasia and low-grade prostatic
adenocarcinoma
.
AIM: Atypical
adenomatous
hyperplasia (AAH) is a small glandular proliferation that has histological similarities with Gleason grade 1 and 2 prostatic
adenocarcinoma
(PACG1,2).
Basal cell
-specific antikeratin was applied to these lesions.
We assumed that PACG1,2 lesions did have not
basal
cells
and we grouped the lesions as AAH and PACG1,2 based on this assumption.
RESULTS: We found differences between AAH and PACG1,2 lesions for some parameters including the number of glands, structures such as the main ductus and
basal
cells
.
We found similar properties in the two lesions for the following parameters: localization, multiplicity, diameter of the lesion, focus asymmetry, distance between glands, inflammatory
cells
in and out of the lesions, secretory
cell
shape on the luminal side, papillary projection towards the luminal side of gland, the shape of the outer gland, the infiltrative pattern of the gland, glandular pleomorphism, biggest gland diameter and median gland diameter.
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(PMID = 19468392.001).
[ISSN]
0970-1591
[Journal-full-title]
Indian journal of urology : IJU : journal of the Urological Society of India
[ISO-abbreviation]
Indian J Urol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
[Other-IDs]
NLM/ PMC2684265
[Keywords]
NOTNLM ; Adenosis / cancer / hyperplasia / low grade / proliferations / prostate / small glandular
73.
Sato T, Murakumo Y, Hagiwara S, Jijiwa M, Suzuki C, Yatabe Y, Takahashi M:
High-level expression of CD109 is frequently detected in lung squamous cell carcinomas.
Pathol Int
; 2007 Nov;57(11):719-24
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[Title]
High-level expression of CD109 is frequently detected in lung squamous
cell
carcinomas.
CD109 is a glycosylphosphatidylinositol (GPI)-anchored
cell
surface protein, which is a member of the alpha2-macroglobulin/C3, C4, C5 family of thioester-containing proteins.
It has been reported that CD109 is expressed in a subset of hematopoietic
cells
, endothelial
cells
and several kinds of human tumors.
Herein it is reported that the CD109 protein is preferentially expressed in lung squamous
cell
carcinomas compared with other types of lung carcinoma including
adenocarcinomas
, large
cell
carcinomas and small
cell
carcinomas.
Immunohistochemical staining of surgically resected lung specimens using an anti-CD109 antibody detected CD109 expression in
basal
cells
of bronchial and bronchiolar epithelia and myoepithelial
cells
of bronchial secretary glands, but not in bronchial and bronchiolar apical epithelial
cells
and alveolar epithelial
cells
.
Furthermore, the CD109 immunoreactivity was observed in squamous
cell
carcinomas at a high frequency compared with other types of lung carcinoma.
Although the detailed function of CD109 protein is unclear, these results suggest that CD109 expression may play a role in the development of lung squamous
cell
carcinoma.
[MeSH-major]
Antigens, CD / metabolism. Biomarkers, Tumor / analysis. Carcinoma, Squamous
Cell
/ metabolism. Lung Neoplasms / metabolism.
Neoplasm
Proteins / metabolism
[MeSH-minor]
Adenocarcinoma
/ metabolism.
Adenocarcinoma
/ pathology. Adult. Aged. Aged, 80 and over. Blotting, Western. Carcinoma, Large
Cell
/ metabolism. Carcinoma, Large
Cell
/ pathology. Carcinoma, Small
Cell
/ metabolism. Carcinoma, Small
Cell
/ pathology. Female. GPI-Linked Proteins. Gene Expression. Humans. Immunohistochemistry. Male. Middle Aged. RNA, Small Interfering
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(PMID = 17922683.001).
[ISSN]
1320-5463
[Journal-full-title]
Pathology international
[ISO-abbreviation]
Pathol. Int.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Australia
[Chemical-registry-number]
0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / CD109 protein, human; 0 / GPI-Linked Proteins; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering
74.
Yoshino M, Ishiwata T, Watanabe M, Matsunobu T, Komine O, Ono Y, Yamamoto T, Fujii T, Matsumoto K, Tokunaga A, Naito Z:
Expression and roles of keratinocyte growth factor and its receptor in esophageal cancer cells.
Int J Oncol
; 2007 Oct;31(4):721-8
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[Title]
Expression and roles of keratinocyte growth factor and its receptor in esophageal cancer
cells
.
The keratinocyte growth factor receptor (KGFR), also known as FGFR2 IIIb, is mainly localized in epithelial
cells
and is activated by the keratinocyte growth factor (KGF) that is predominantly synthesized by mesenchymal
cells
.
In noncancerous esophageal tissues, KGFR was localized in epithelial
cells
from the
basal
region of the epithelium to the lower one-third of the epithelium, and KGF was weakly localized in the
basal
to parabasal epithelial
cells
.
On the other hand, Ki-67 was localized in the parabasal
cells
.
In EC tissues, KGFR and KGF were expressed in cancer
cells
in 22 and 37 of 54 patients, respectively.
The coexpression of KGFR and KGF in cancer
cells
was detected in 14 of 54 (26%) patients.
Clinicopathologically, KGFR expression correlated with the well-differentiated
cell
type of EC (p<0.001), and KGF expression correlated with lymphatic invasion and lymph node metastasis (p=0.004 and 0.021, respectively).
The coexpression of KGFR and KGF in cancer
cells
correlated with the well-differentiated
cell
type of EC (p=0.001).
In human EC
cell
lines (TE-1, TE-8 and TE-11), KGFR mRNA was expressed but no KGF mRNA was detected.
The KGFR mRNA level was highest in TE-1
cells
, derived from well-differentiated SCC and lowest in TE-8
cells
.
KGFR was detected in the cancer
cell
lines by Western blot analysis.
Recombinant human KGF significantly stimulated the growth of TE-8 and -11
cells
, derived from moderately differentiated SCC, but had no effect on TE-1
cell
growth.
These results suggest that KGFR expression correlates with the differentiation of a normal esophageal epithelium and the well-differentiated
cell
type of EC.
On the other hand, KGF may induce the growth of some EC
cells
in a paracrine manner and closely correlates with lymphatic invasion and lymph node metastasis.
[MeSH-minor]
Adenocarcinoma
/ metabolism.
Adenocarcinoma
/ pathology.
Adenocarcinoma
/ secondary. Adult. Aged. Aged, 80 and over. Blotting, Western. Carcinoma, Squamous
Cell
/ metabolism. Carcinoma, Squamous
Cell
/ pathology. Carcinoma, Squamous
Cell
/ secondary.
Cell
Differentiation. Epithelial
Cells
. Female. Humans. Ki-67 Antigen / metabolism. Lymphatic Metastasis. Male. Middle Aged.
Neoplasm
Staging. Prognosis. Survival Rate
Genetic Alliance.
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.
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consumer health - Esophageal Cancer
.
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The Lens.
Cited by Patents in
.
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(PMID = 17786302.001).
[ISSN]
1019-6439
[Journal-full-title]
International journal of oncology
[ISO-abbreviation]
Int. J. Oncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 126469-10-1 / Fibroblast Growth Factor 7; EC 2.7.1.- / keratinocyte growth factor receptor; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 2
75.
Uke M, Rekhi B, Ajit D, Jambhekar NA:
The use of p63 as an effective immunomarker in the diagnosis of pulmonary squamous cell carcinomas on de-stained bronchial lavage cytological smears.
Cytopathology
; 2010 Feb;21(1):56-63
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[Title]
The use of p63 as an effective immunomarker in the
diagnosis
of pulmonary squamous
cell
carcinomas on
de
-stained bronchial lavage cytological smears.
OBJECTIVES:
A diagnosis
in pulmonary onco-cytopathology primarily necessitates distinguishing small
cell
carcinoma (SCLC) from non-small
cell
carcinoma (NSCLC), which includes squamous
cell
carcinoma and
adenocarcinoma
.
Lately, p63 antibody has been used for distinguishing squamous
cell
carcinoma from SCLC and
adenocarcinoma
.
METHODS: A single Papanicolaou-stained conventional smear was
de
-stained and re-fixed with cold acetone and methanol for immunocytochemical staining with p63 antibody.
RESULTS: Out of 100 cases, 21 were cytologically diagnosed as squamous
cell
carcinoma.
Twenty of these showed 2+ or 3+ p63 positivity, whereas one, which was
adenocarcinoma
on histology, showed 1+ staining.
Of seven cases cytologically diagnosed as
adenocarcinoma
, six showed no p63 staining, whereas one, which was squamous
cell
carcinoma on histology, showed 1+ staining.
The former three were found to be SCLC on histology while the latter was squamous
cell
carcinoma.
The former eight were
adenocarcinoma
on histology and the latter two were squamous
cell
carcinoma.
The 10 cases that showed 1+ p63 staining were
adenocarcinomas
(n = 5), squamous
cell
carcinoma (n = 4) and NSCLC, not otherwise specified (n = 1).
Positive staining was seen in normal
basal
cells
, which acted as an internal control.
Overall sensitivity of p63 for squamous
cell
carcinoma was 100% and specificity was 90.4%.
CONCLUSIONS: p63 immunostaining on processed cytology smears can be used to help identify squamous
cell
carcinoma.
Its diffuse expression was specific for squamous
cell
carcinoma while focal staining was also seen in
adenocarcinoma
.
[MeSH-major]
Biomarkers, Tumor / metabolism. Carcinoma, Squamous
Cell
/ pathology. Lung Neoplasms / pathology. Trans-Activators / metabolism. Tumor Suppressor Proteins / metabolism
[MeSH-minor]
Adenocarcinoma
/
diagnosis
. Adult. Aged. Aged, 80 and over. Bronchoalveolar Lavage / methods. Bronchoalveolar Lavage Fluid / cytology. Carcinoma, Non-Small-
Cell
Lung /
diagnosis
.
Diagnosis
, Differential. Female. Humans. Male. Middle Aged. Transcription Factors
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(PMID = 19744186.001).
[ISSN]
1365-2303
[Journal-full-title]
Cytopathology : official journal of the British Society for Clinical Cytology
[ISO-abbreviation]
Cytopathology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
76.
Iczkowski KA, Montironi R:
Adenoid cystic/basal cell carcinoma of the prostate strongly expresses HER-2/neu.
J Clin Pathol
; 2006 Dec;59(12):1327-30
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[Title]
Adenoid cystic/
basal cell
carcinoma of the prostate strongly expresses HER-2/neu.
Adenoid cystic/
basal cell
carcinoma (ACBCC) is a rare
neoplasm
in the prostate.
Ten acinar
adenocarcinomas
of varying grades were also immunostained as controls.
Benign acini expressed HER-2/neu only in the
basal
layer.
The
finding
of strong, consistent HER-2/neu expression in ACBCC suggests that treatment with Herceptin (trastuzumab) may be effective in patients with this rare tumour.
[MeSH-major]
Carcinoma, Adenoid Cystic / metabolism. Carcinoma,
Basal Cell
/ metabolism. Mixed Tumor,
Malignant
/ metabolism. Prostatic Neoplasms / metabolism. Receptor, ErbB-2 / metabolism
[MeSH-minor]
Adult. Aged. Gene Expression. Humans. In Situ Hybridization. Male. Middle Aged. RNA, Messenger / genetics. RNA,
Neoplasm
/ genetics
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.
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.
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[Cites]
Cancer. 2002 May 15;94(10):2584-9
[
12173324.001
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[
15735163.001
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[Cites]
Am J Surg Pathol. 2003 Dec;27(12):1523-9
[
14657711.001
]
(PMID = 17142577.001).
[ISSN]
0021-9746
[Journal-full-title]
Journal of clinical pathology
[ISO-abbreviation]
J. Clin. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.1 / Receptor, ErbB-2
[Other-IDs]
NLM/ PMC1860524
77.
Zhang X:
Simultaneous exposure to dietary acrylamide and corn oil developed carcinogenesis through cell proliferation and inhibition of apoptosis by regulating p53-mediated mitochondria-dependent signaling pathway.
Toxicol Ind Health
; 2009 Mar;25(2):101-9
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[Title]
Simultaneous exposure to dietary acrylamide and corn oil developed carcinogenesis through
cell
proliferation and inhibition of apoptosis by regulating p53-mediated mitochondria-dependent signaling pathway.
Colonic aberrant crypt foci (ACF) and tumors, including
adenomas
and carcinomas, were examined at 12, 24, 36, 48 week post ACR-exposure.
Colonic apoptosis and
cell
proliferation, expression of Wild type (wt) p53, Bcl-2, Bax and caspase-3, were detected at 48 week post ACR-exposure.
Apoptosis was decreased and
cell
proliferation was increased in colonic mucosa in ACR-treated rats on dietary corn oil compared to vehicle rats on
basal
diet (P < 0.05).
[MeSH-major]
Acrylamide / toxicity. Apoptosis / drug effects.
Cell
Proliferation / drug effects. Corn Oil / administration & dosage. Gene Expression Regulation, Neoplastic / drug effects. Precancerous Conditions / chemically induced. Tumor Suppressor Protein p53 / genetics
[MeSH-minor]
Adenocarcinoma
/ chemically induced.
Adenocarcinoma
/ pathology.
Adenoma
/ chemically induced.
Adenoma
/ pathology. Animals. Carcinogenicity Tests. Cocarcinogenesis. Colon / drug effects. Colon / pathology. Colonic Neoplasms / chemically induced. Colonic Neoplasms / pathology. Diet. Injections, Intraperitoneal. Intestinal Mucosa / drug effects. Intestinal Mucosa / pathology. Male. Mitochondria / drug effects. Mitochondria / metabolism. Rats. Rats, Sprague-Dawley. Signal Transduction / drug effects
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.
Hazardous Substances Data Bank.
Corn oil
.
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(PMID = 19458132.001).
[ISSN]
0748-2337
[Journal-full-title]
Toxicology and industrial health
[ISO-abbreviation]
Toxicol Ind Health
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Tumor Suppressor Protein p53; 20R035KLCI / Acrylamide; 8001-30-7 / Corn Oil
78.
Lisovsky M, Dresser K, Baker S, Fisher A, Woda B, Banner B, Lauwers GY:
Cell polarity protein Lgl2 is lost or aberrantly localized in gastric dysplasia and adenocarcinoma: an immunohistochemical study.
Mod Pathol
; 2009 Jul;22(7):977-84
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[Title]
Cell
polarity protein Lgl2 is lost or aberrantly localized in gastric dysplasia and
adenocarcinoma
: an immunohistochemical study.
The
diagnosis
of gastric epithelial dysplasia, a precursor lesion of gastric
adenocarcinoma
, is hindered by interobserver variability and by its resemblance to regenerative changes.
Loss of
cell
polarity, a histological feature of gastric epithelial dysplasia, may be difficult to ascertain, especially in the setting of inflammation or injury.
A biomarker of
cell
polarity could be useful in
diagnosis
of dysplasia, but has not been reported.
The Lethal giant larvae (lgl) gene controls apical-
basal
polarity of epithelial
cells
in Drosophila, and has properties of a tumor-suppressor gene.
The goal of our study was to test the hypothesis that Lgl2 protein expression and/or localization are disrupted in gastric epithelial dysplasia and
adenocarcinoma
.
Routinely processed pathology specimens including 94 benign mucosae of digestive organs, in addition to 36 reactive gastropathy, 57 gastric epithelial dysplasia, and 77 gastric
adenocarcinomas
, were immunostained for Lgl2 protein.
All but one case each of gastric epithelial dysplasia and
adenocarcinoma
showed either complete loss of anti-Lgl2 immunoreactivity or diffuse, mostly weak, cytoplasmic staining.
Complete loss of immunoreactivity was significantly more often observed in diffuse-type than in intestinal-type
adenocarcinomas
(79 vs 48%, respectively).
Our data suggest that Lgl2 expression is either aberrantly localized or lost in gastric epithelial dysplasia and
adenocarcinoma
, whereas it is maintained in reactive gastric mucosa.
We propose that Lgl2 may be a potential marker to rule out gastric epithelial dysplasia and
adenocarcinoma
in diagnostic specimens.
[MeSH-major]
Adenocarcinoma
/ metabolism. Biomarkers, Tumor / metabolism. Cytoskeletal Proteins / metabolism. Gastric Mucosa / metabolism. Precancerous Conditions / metabolism. Stomach Neoplasms / metabolism
[MeSH-minor]
Adenoma
/ metabolism.
Adenoma
/ pathology. Adolescent. Adult. Aged. Aged, 80 and over.
Cell
Polarity. Female. Fluorescent Antibody Technique, Direct. Humans. Immunoenzyme Techniques. Male. Middle Aged. Young Adult
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(PMID = 19407852.001).
[ISSN]
1530-0285
[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
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Cytoskeletal Proteins; 0 / Hugl-2 protein, human
79.
Hoffmann S, Wunderlich A, Lingelbach S, Musholt PB, Musholt TJ, von Wasielewski R, Zielke A:
Expression and secretion of endostatin in thyroid cancer.
Ann Surg Oncol
; 2008 Dec;15(12):3601-8
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The aim of this study was to evaluate endostatin expression in archival TC specimens and its secretion following stimulation with thyrotropin (TSH) and epidermal growth factor (EGF) in TC
cell
lines.
In vitro, six differentiated (FTC133, FTC236, HTC, HTC-TSHr, XTC, and TPC1) and three anaplastic (C643, Hth74, Kat4.0) TC
cell
lines were evaluated for
basal
as well as TSH (1-100 mU/ml) and EGF stimulated (1-100 ng/ml) endostatin.
In vitro,
basal
endostatin secretion varied between 33 +/- 5 pg/ml (FTC236) and 549 +/- 65 pg/ml (TPC1) and was doubled in FTC, when the "primary" (FTC133) was compared with the metastasis (FTC236).
Some
cell
lines showed TSH-induced (e.g., 60% in XTC) or EGF-induced (e.g., 120% in TPC1) upregulation of endostatin secretion, while others did not, despite documented receptor expression.
In vitro, endostatin secretion of some
cell
lines is regulated by TSH and EGF, however the individual differences deserve further functional studies.
[MeSH-major]
Adenocarcinoma
, Follicular / metabolism. Angiogenesis Inhibitors / metabolism. Carcinoma / metabolism. Carcinoma, Papillary / metabolism. Endostatins / metabolism. Thyroid Gland / metabolism. Thyroid Neoplasms / metabolism
[MeSH-minor]
Cell
Differentiation / drug effects. Enzyme-Linked Immunosorbent Assay. Epidermal Growth Factor / pharmacology. Humans. Immunoenzyme Techniques. Lymphatic Metastasis. Paraffin Embedding. Thyrotropin / pharmacology. Tumor
Cells
, Cultured
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.
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(PMID = 18818971.001).
[ISSN]
1534-4681
[Journal-full-title]
Annals of surgical oncology
[ISO-abbreviation]
Ann. Surg. Oncol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Angiogenesis Inhibitors; 0 / Endostatins; 62229-50-9 / Epidermal Growth Factor; 9002-71-5 / Thyrotropin
80.
Segawa N, Tsuji M, Nishida T, Takahara K, Azuma H, Katsuoka Y:
Basal cell carcinoma of the prostate: report of a case and review of the published reports.
Int J Urol
; 2008 Jun;15(6):557-9
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[Title]
Basal cell
carcinoma of the prostate: report of a case and review of the published reports.
Prostatic
basal cell
carcinoma (BCC), a distinctive variant of
adenocarcinoma
, is rare.
[MeSH-major]
Carcinoma,
Basal Cell
. Prostatic Neoplasms
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.
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(PMID = 18489650.001).
[ISSN]
1442-2042
[Journal-full-title]
International journal of urology : official journal of the Japanese Urological Association
[ISO-abbreviation]
Int. J. Urol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Australia
[Number-of-references]
10
81.
Sadok A, Bourgarel-Rey V, Gattacceca F, Penel C, Lehmann M, Kovacic H:
Nox1-dependent superoxide production controls colon adenocarcinoma cell migration.
Biochim Biophys Acta
; 2008 Jan;1783(1):23-33
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[Title]
Nox1-dependent superoxide production controls colon
adenocarcinoma cell
migration.
Recently, new homologues of the catalytic subunit of NADPH oxidase have been discovered in non-phagocytic
cells
.
Using Nox1 siRNA, we show that Nox1-dependent superoxide production affects the migration of HT29-D4 colonic
adenocarcinoma
cells
on collagen-I.
An addition of arachidonic acid stimulated Nox1-dependent superoxide production and HT29-D4
cell
migration.
Inhibition of 12-lipoxygenase decreased
basal
and arachidonic acid induced Nox1-dependent superoxide production and
cell
migration.
Protein kinase C delta inhibition by rottlerin (and also GO6983) prevented Nox1-dependent superoxide production and inhibited
cell
migration, while other protein kinase C inhibitors were ineffective.
We conclude that Nox1 activation by arachidonic acid metabolism occurs through 12-lipoxygenase and protein kinase C delta, and controls
cell
migration by affecting integrin alpha 2 subunit turn-over.
[MeSH-major]
Adenocarcinoma
/ metabolism.
Adenocarcinoma
/ pathology.
Cell
Movement. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. NADPH Oxidase / metabolism. Superoxides / metabolism
[MeSH-minor]
Arachidonate 12-Lipoxygenase / metabolism. Arachidonic Acids / pharmacology.
Cell
Membrane / metabolism. HT29
Cells
. Humans. Integrin alpha2beta1 / metabolism. Protein Kinase C-delta / metabolism
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
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(PMID = 18023288.001).
[ISSN]
0006-3002
[Journal-full-title]
Biochimica et biophysica acta
[ISO-abbreviation]
Biochim. Biophys. Acta
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Arachidonic Acids; 0 / Integrin alpha2beta1; 11062-77-4 / Superoxides; EC 1.13.11.31 / Arachidonate 12-Lipoxygenase; EC 1.6.3.- / NOX1 protein, human; EC 1.6.3.1 / NADPH Oxidase; EC 2.7.11.13 / Protein Kinase C-delta
82.
Andreadis D, Nomikos A, Epivatianos A, Poulopoulos A, Barbatis C:
Basaloid squamous cell carcinoma versus basal cell adenocarcinoma of the oral cavity.
Pathology
; 2005 Dec;37(6):560-3
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[Title]
Basaloid squamous
cell
carcinoma versus
basal cell adenocarcinoma
of the oral cavity.
[MeSH-major]
Carcinoma, Basosquamous / pathology. Carcinoma, Squamous
Cell
/ pathology. Oropharyngeal Neoplasms / pathology. Salivary Gland Neoplasms / pathology. Salivary Glands, Minor / pathology
[MeSH-minor]
Biomarkers, Tumor / analysis.
Diagnosis
, Differential. Humans. Immunohistochemistry
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.
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(PMID = 16373238.001).
[ISSN]
0031-3025
[Journal-full-title]
Pathology
[ISO-abbreviation]
Pathology
[Language]
eng
[Publication-type]
Letter
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor
83.
National Toxicology Program:
Toxicology and carcinogenesis studies of divinylbenzene-HP (Cas No. 1321-74-0) in F344/N rats and B6C3F1 mice (inhalation studies).
Natl Toxicol Program Tech Rep Ser
; 2006 Nov;(534):1-290
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Incidences of degeneration of the olfactory epithelium in 200 and 400 ppm rats and
basal cell
hyperplasia of the olfactory epithelium in rats exposed to 100 ppm or greater were significantly increased.
Following combined analysis of single and step-section data, the incidences of renal tubule
adenoma
and
adenoma
or carcinoma (combined) were marginally higher in 200 and 400 ppm males, and the incidence of renal tubule hyperplasia was significantly increased in 400 ppm males.
The incidences of
malignant
glial
cell
tumors (
malignant
astrocytoma and oligodendroglioma) in the brain were slightly increased in 100 and 200 ppm males, and the incidence in the 200 ppm group exceeded the historical range for chamber controls.
The incidences of alveolar/bronchiolar
adenoma
and alveolar/bronchiolar
adenoma
or carcinoma (combined) in 100 ppm males were greater than chamber control incidences, but the incidences of
adenoma
or carcinoma (combined) were within the historical control range.
The incidences of alveolar/bronchiolar
adenoma
and alveolar/bronchiolar
adenoma
or carcinoma (combined) in all exposed groups of females were generally greater than those of the chamber controls; the incidences were at the upper end or exceeded the historical control ranges.
There was equivocal evidence of carcinogenic activity of divinylbenzene-HP in female B6C3F1 mice based on the incidences of alveolar/bronchiolar
adenoma
or carcinoma (combined) in the lung.
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(PMID = 17342197.001).
[ISSN]
0888-8051
[Journal-full-title]
National Toxicology Program technical report series
[ISO-abbreviation]
Natl Toxicol Program Tech Rep Ser
[Language]
eng
[Publication-type]
Journal Article; Technical Report
[Publication-country]
United States
[Chemical-registry-number]
0 / Vinyl Compounds; IZ715T4SBU / divinyl benzene
84.
Kohno H, Suzuki R, Yasui Y, Miyamoto S, Wakabayashi K, Tanaka T:
Ursodeoxycholic acid versus sulfasalazine in colitis-related colon carcinogenesis in mice.
Clin Cancer Res
; 2007 Apr 15;13(8):2519-25
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They are then maintained on a
basal
diet mixed with UDCA (0.016%, 0.08%, or 0.4%) or sulfasalazine (0.05%) for 17 weeks.
The immunohistochemical expression of the proliferating
cell
nuclear antigen labeling index in colonic epithelial malignancies was also assessed.
RESULTS: Feeding the mice with UDCA at all doses significantly inhibited the multiplicity of colonic
adenocarcinoma
.
The treatment also significantly lowered the proliferating
cell
nuclear antigen labeling index in the colonic malignancies.
Sulfasalazine caused a nonsignificant reduction in the incidence and multiplicity of colonic
neoplasia
and did not affect these mRNA expression.
[MeSH-minor]
Animals. Anticarcinogenic Agents. Azoxymethane / toxicity. Cyclooxygenase 2 / genetics.
Disease
Models, Animal. Male. Mice. Mice, Inbred ICR. RNA, Messenger / genetics
Hazardous Substances Data Bank.
SULFASALAZINE
.
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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(PMID = 17438113.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Anticarcinogenic Agents; 0 / RNA, Messenger; 3XC8GUZ6CB / Sulfasalazine; 724L30Y2QR / Ursodeoxycholic Acid; EC 1.14.99.1 / Cyclooxygenase 2; MO0N1J0SEN / Azoxymethane
85.
Adley BP, Yang XJ:
Application of alpha-methylacyl coenzyme A racemase immunohistochemistry in the diagnosis of prostate cancer: a review.
Anal Quant Cytol Histol
; 2006 Feb;28(1):1-13
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[Title]
Application of alpha-methylacyl coenzyme A racemase immunohistochemistry in the
diagnosis
of prostate cancer: a review.
Alpha-methylacyl coenzyme A racemase (AMACR) is a recently discovered enzyme protein that has been shown to be increased at both the mRNA and protein levels in prostatic
adenocarcinoma
as compared with normal prostatic tissues.
Since its discovery, AMACR has gained wide acceptance for use in the
diagnosis
of prostatic
adenocarcinoma
in conjunction with morphology and immunohistochemical staining for
basal cell
markers.
This review focuses on AMACR expression in prostate cancer and its
morphologic
variants, high grade prostatic intraepithelial
neoplasia
, adenosis and benign conditions of the prostate.
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(PMID = 16566275.001).
[ISSN]
0884-6812
[Journal-full-title]
Analytical and quantitative cytology and histology
[ISO-abbreviation]
Anal. Quant. Cytol. Histol.
[Language]
ENG
[Publication-type]
Evaluation Studies; Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
[Number-of-references]
63
86.
Holcomb B, Yip-Schneider MT, Matos JM, Dixon J, Kennard J, Mahomed J, Shanmugam R, Sebolt-Leopold J, Schmidt CM:
Pancreatic cancer cell genetics and signaling response to treatment correlate with efficacy of gemcitabine-based molecular targeting strategies.
J Gastrointest Surg
; 2008 Feb;12(2):288-96
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[Title]
Pancreatic cancer
cell
genetics and signaling response to treatment correlate with efficacy of gemcitabine-based molecular targeting strategies.
We hypothesize that pancreatic cancer
cell
genetics and signaling response to treatment correlate with efficacy of gemcitabine-based molecular targeting strategies.
MATERIALS AND METHODS: PANC-1, PaCa-2, and BxPC-3
cells
were treated with curcumin, LY294002, or PD325901 alone or in combination with gemcitabine.
Proliferation was measured by
cell
counts and enzyme activity by Western blot and electrophoretic mobility shift assay.
All
cells
decreased NF-kappaB activity with curcumin(24 h) except PaCa-2, MEK activity with PD325901(24 h), and PI3Kinase with LY294002(3 h).
However, PI3K rebounded to(PaCa-2) or above (Panc-1,BxPC-3)
basal
in LY294002-treated
cells
(24 h).
LY294002 + gemcitabine was nearly synergistic in PaCa-2
cells
, which showed a lower induction of PI3Kinase activity with LY294002.
CONCLUSIONS: These results demonstrate differences in treatment efficacy, which correlate with the
cell
's signaling response to treatment.
[MeSH-major]
Adenocarcinoma
/ drug therapy.
Adenocarcinoma
/ genetics. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents / administration & dosage. Chromones / administration & dosage. Curcumin / administration & dosage. Deoxycytidine / analogs & derivatives. Enzyme Inhibitors / administration & dosage. Morpholines / administration & dosage. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / genetics
[MeSH-minor]
Blotting, Western.
Cell
Proliferation / drug effects. Dose-Response Relationship, Drug. Drug Synergism. Drug Therapy, Combination. Electrophoretic Mobility Shift Assay. Humans. MAP Kinase Signaling System / drug effects. NF-kappa B / drug effects. NF-kappa B / physiology. Proto-Oncogene Proteins c-akt / drug effects. Proto-Oncogene Proteins c-akt / physiology. Tumor
Cells
, Cultured
Genetic Alliance.
consumer health - Pancreatic cancer
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MedlinePlus Health Information.
consumer health - Pancreatic Cancer
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
CURCUMIN
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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[ISSN]
1091-255X
[Journal-full-title]
Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
[ISO-abbreviation]
J. Gastrointest. Surg.
[Language]
eng
[Publication-type]
Journal Article; 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 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / NF-kappa B; 0W860991D6 / Deoxycytidine; 31M2U1DVID / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; B76N6SBZ8R / gemcitabine; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; IT942ZTH98 / Curcumin
87.
Stewart J, Fleshner N, Cole H, Sweet J:
Comparison of annexin II, p63 and alpha-methylacyl-CoA racemase immunoreactivity in prostatic tissue: a tissue microarray study.
J Clin Pathol
; 2007 Jul;60(7):773-80
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BACKGROUND: Current ancillary markers for
diagnosis
in prostate biopsies include p63 and alpha-methylacyl-CoA racemase (AMACR).
Staining was evaluated in benign and atrophic glands, high-grade prostatic intraepithelial
neoplasia
(HGPIN), and prostatic
adenocarcinoma
.
RESULTS: Diffuse cytoplasmic expression of ANXII correlated with p63 reactivity in
basal
cells
.
CONCLUSIONS: Immunohistochemical staining for ANXII is a consistent and reliable marker of prostatic
neoplasia
.
[MeSH-major]
Adenocarcinoma
/ metabolism. Annexin A2 / metabolism. Biomarkers, Tumor / metabolism. Prostatic Neoplasms / metabolism
[MeSH-minor]
Adult. Aged. DNA-Binding Proteins / metabolism. Humans. Immunoenzyme Techniques. Male. Middle Aged.
Neoplasm
Proteins / metabolism. Organ Size. Prostate / pathology. Prostatectomy. Prostatic Intraepithelial
Neoplasia
/
diagnosis
. Prostatic Intraepithelial
Neoplasia
/ metabolism. Prostatic Intraepithelial
Neoplasia
/ pathology. Prostatic Intraepithelial
Neoplasia
/ surgery. Racemases and Epimerases / metabolism. Trans-Activators / metabolism. Transcription Factors. Tumor Suppressor Proteins / metabolism
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[ISSN]
0021-9746
[Journal-full-title]
Journal of clinical pathology
[ISO-abbreviation]
J. Clin. Pathol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Annexin A2; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
[Other-IDs]
NLM/ PMC1995785
88.
Domingo-Domenech J, Mellado B, Ferrer B, Truan D, Codony-Servat J, Sauleda S, Alcover J, Campo E, Gascon P, Rovira A, Ross JS, Fernández PL, Albanell J:
Activation of nuclear factor-kappaB in human prostate carcinogenesis and association to biochemical relapse.
Br J Cancer
; 2005 Nov 28;93(11):1285-94
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Nuclear factor (NF)-kappaB/p65 regulates the transcription of a wide variety of genes involved in
cell
survival, invasion and metastasis.
We characterised by immunohistochemistry the expression of NF-kappaB/p65 protein in six histologically normal prostate, 13 high-grade prostatic intraepithelial
neoplasia
(PIN) and 86 prostate
adenocarcinoma
specimens.
Nuclear localisation of NF-kappaB was only seen in scattered
basal
cells
in normal prostate glands.
In prostate
adenocarcinomas
, cytoplasmic NF-kappaB was detected in 57 (66.3%) specimens, and nuclear NF-kappaB (activated) in 47 (54.7%).
[MeSH-major]
Adenocarcinoma
/ pathology.
Cell
Transformation, Neoplastic. NF-kappa B / biosynthesis. Prostatic Intraepithelial
Neoplasia
/ pathology. Prostatic Neoplasms / pathology
[MeSH-minor]
Aged. Biomarkers, Tumor / analysis.
Cell
Nucleus. Cytoplasm / chemistry. Gene Expression Profiling. Humans. Immunohistochemistry. Male. Middle Aged. Multivariate Analysis.
Neoplasm
Recurrence, Local. Prognosis. Prostate-Specific Antigen. Risk Factors. Transcription Factor RelA / analysis. Transcription Factor RelA / biosynthesis. Transcription Factor RelA / pharmacokinetics
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[ISSN]
0007-0920
[Journal-full-title]
British journal of cancer
[ISO-abbreviation]
Br. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / NF-kappa B; 0 / Transcription Factor RelA; EC 3.4.21.77 / Prostate-Specific Antigen
[Other-IDs]
NLM/ PMC2361509
89.
Casas A, Battah S, Di Venosa G, Dobbin P, Rodriguez L, Fukuda H, Batlle A, MacRobert AJ:
Sustained and efficient porphyrin generation in vivo using dendrimer conjugates of 5-ALA for photodynamic therapy.
J Control Release
; 2009 Apr 17;135(2):136-43
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In vivo, the porphyrin kinetics from ALA exhibited an early peak between 3 and 4 h in most tissues, whereas the dendrimer induced sustained porphyrin production for over 24 h and
basal
values were not reached until 48 h after administration.
[MeSH-minor]
Adenocarcinoma
/ drug therapy. Animals.
Cell
Line, Tumor.
Cell
Survival / drug effects. Coloring Agents / metabolism. Dose-Response Relationship, Drug. Injections, Subcutaneous. Male. Mammary Neoplasms, Experimental / drug therapy. Mice. Mice, Inbred BALB C. Molecular Structure. Molecular Weight. Protoporphyrins / biosynthesis. Structure-Activity Relationship. Tetrazolium Salts / metabolism. Thiazoles / metabolism. Time Factors. Xenograft Model Antitumor Assays
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(PMID = 19168101.001).
[ISSN]
1873-4995
[Journal-full-title]
Journal of controlled release : official journal of the Controlled Release Society
[ISO-abbreviation]
J Control Release
[Language]
eng
[Grant]
United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/D011329/1; United Kingdom / Wellcome Trust / / 067062/Z/029/Z; United Kingdom / Biotechnology and Biological Sciences Research Council / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Coloring Agents; 0 / Dendrimers; 0 / Photosensitizing Agents; 0 / Porphyrins; 0 / Protoporphyrins; 0 / Tetrazolium Salts; 0 / Thiazoles; 88755TAZ87 / Aminolevulinic Acid; C2K325S808 / protoporphyrin IX; EUY85H477I / thiazolyl blue
90.
Ou-Yang RJ, Hui P, Yang XJ, Zynger DL:
Expression of glypican 3 in placental site trophoblastic tumor.
Diagn Pathol
; 2010;5:64
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BACKGROUND: Glypican-3 (GPC3) is a membrane-bound heparan sulfate proteoglycan that functions in embryonic
cell
growth and differentiation and is highly expressed in the placenta.
The purpose of this study was to investigate the immunohistochemical expression of GPC3 in placental site trophoblastic tumor (PSTT), a very rare gestational trophoblastic
neoplasm
which may be morphologically confused with non-trophoblastic tumors, and to assess its possible utility as a diagnostic marker.
METHODS: Fifteen cases of PSTT, as well as samples from placental site nodule (PSN) (n = 2), leiomyosarcoma (n = 1), leiomyoma (n = 1), invasive cervical squamous
cell
carcinoma (n = 7) and endometrial
adenocarcinoma
(n = 11) were examined.
Immunoreactivity was semi-quantitatively evaluated as negative (0, < 5% of
cells
stained), focally positive (1+, 5-10% of
cells
stained), positive (2+, 11-50% of
cells
stained) or diffusely positive (3+, > 50% of
cells
stained).
Staining intensity for each
subtype
was graded from 0 to 3 and a mean intensity was calculated.
Stronger, predominately cytoplasmic staining was seen in larger multi- and mononucleated
cells
with smaller mononucleate
cells
showing weak muddy cytoplasmic staining.
Both PSN cases were positive (1+, 50%; 2+, 50%) and two of nine invasive cervical squamous
cell
carcinomas showed staining (0, 57%; 1+, 29%; 2+, 14%), predominately in a
basal
distribution.
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(PMID = 20868507.001).
[ISSN]
1746-1596
[Journal-full-title]
Diagnostic pathology
[ISO-abbreviation]
Diagn Pathol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / GPC3 protein, human; 0 / Glypicans
[Other-IDs]
NLM/ PMC2954974
91.
Leite KR, Srougi M, Sanudo A, Dall'oglio MF, Nesrallah A, Antunes AA, Cury J, Camara-Lopes LH:
The use of immunohistochemistry for diagnosis of prostate cancer.
Int Braz J Urol
; 2010 Sep-Oct;36(5):583-90
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[Title]
The use of immunohistochemistry for
diagnosis
of prostate cancer.
The use of antibodies to mark
basal
cells
is currently a common practice, in order to avoid rebiopsies.
There has been no reported study that has reviewed characteristics of radical prostatectomies (RPs) when immunohistochemistry (IHC) was necessary for definitive
diagnosis
.
The results of surgical specimens of 27 patients treated by RP after the
diagnosis
of prostate cancer (PC) was made using IHC (Group 1) were compared with 1040 patients where IHC was not necessary (Group 2).
In Group 1, two (7.4%)
adenocarcinomas
were insignificant versus 29 (2.9%) for Group 2.
CONCLUSION: The use of IHC did not lead to
diagnosis
of insignificant tumors as illustrated by absence of differences in pathological stage or positive surgical margins in men submitted to RP.
[MeSH-major]
Adenocarcinoma
/ pathology. Prostate / pathology. Prostatic Neoplasms / pathology
[MeSH-minor]
Aged. Aged, 80 and over. Biopsy.
Cell
Proliferation. Humans. Immunohistochemistry / methods. Male. Middle Aged
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(PMID = 21044375.001).
[ISSN]
1677-6119
[Journal-full-title]
International braz j urol : official journal of the Brazilian Society of Urology
[ISO-abbreviation]
Int Braz J Urol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Brazil
92.
Morichetti D, Mazzucchelli R, Stramazzotti D, Santinelli A, Lopez-Beltran A, Scarpelli M, Bono AV, Cheng L, Montironi R:
Immunohistochemical expression of somatostatin receptor subtypes in prostate tissue from cystoprostatectomies with incidental prostate cancer.
BJU Int
; 2010 Oct;106(7):1072-80
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MATERIALS AND METHODS: The five SSTRs (SSTR1-5) were evaluated in 'normal-looking' epithelium (NEp), high-grade prostatic intraepithelial
neoplasia
(HGPIN) and pT2a Gleason score 6
adenocarcinoma
in 20 CyP specimens with incidental prostate cancer and 20 radical prostatectomy (RP) specimens with clinically detected prostate cancer.
RESULTS: For cytoplasm expression, the mean percentage of positive secretory
cells
with strong cytoplasmic staining increased from NEp to HGPIN and prostate cancer, being slightly lower in the CyP than in the RP specimens.
Both in the CyP and RP specimens SSTR4 was found in the highest percentage of
cells
.
There was membrane staining in the secretory
cells
for SSTR3 and SSTR4.
There was nuclear staining in the secretory
cells
for SSTR4 and SSTR5.
For SSTR1 and SSTR3 the mean proportions of positive
basal
cells
were higher than for the other three subtypes, and greater in NEp than in HGPIN.
There were positive smooth muscle and endothelial
cells
for all five SSTR subtypes, the highest proportions being SSTR1 and the lowest SSTR5.
[MeSH-major]
Prostatic Intraepithelial
Neoplasia
/ pathology. Prostatic Neoplasms / pathology. Receptors, Somatostatin / metabolism
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[Copyright]
© 2010 THE AUTHORS. JOURNAL COMPILATION © 2010 BJU INTERNATIONAL.
(PMID = 20201837.001).
[ISSN]
1464-410X
[Journal-full-title]
BJU international
[ISO-abbreviation]
BJU Int.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Receptors, Somatostatin
93.
Went PT, Sauter G, Oberholzer M, Bubendorf L:
Abundant expression of AMACR in many distinct tumour types.
Pathology
; 2006 Oct;38(5):426-32
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AIMS: Alpha-methylacyl-CoA racemase (AMACR), a mitochondrial and peroxisomal enzyme, is a valuable tool to confirm the
diagnosis
of prostate cancer, especially if combined with
basal cell
markers.
RESULTS: Microarray analysis revealed that tumours with prominent AMACR expression included
adenocarcinomas
of the prostate (72%), hepatocellular carcinomas (77%), papillary renal
cell
carcinomas (70%), and colorectal
adenocarcinomas
(71%).
AMACR expression was equally frequent in colorectal
adenomas
and carcinomas.
In the thyroid, AMACR expression was found in 42% of the follicular carcinomas but in only 16% of follicular
adenomas
.
However, a more detailed analysis on a thyroid tissue microarray did not confirm a significant difference of AMACR expression in follicular
adenoma
and carcinomas.
CONCLUSION: Taken together, the results indicate that AMACR is expressed in a wide variety of
adenocarcinomas
, and its diagnostic utility is restricted to specific areas.
[MeSH-major]
Adenocarcinoma
/ metabolism. Biomarkers, Tumor / metabolism. Neoplasms / metabolism. Racemases and Epimerases / metabolism
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(PMID = 17008281.001).
[ISSN]
0031-3025
[Journal-full-title]
Pathology
[ISO-abbreviation]
Pathology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
94.
Wang GF, Lai MD, Yang RR, Chen PH, Su YY, Lv BJ, Sun LP, Huang Q, Chen SZ:
Histological types and significance of bronchial epithelial dysplasia.
Mod Pathol
; 2006 Mar;19(3):429-37
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Squamous dysplasia and atypical
adenomatous
hyperplasia have been identified and classified as preinvasive lesions of squamous
cell
carcinoma and peripheral pulmonary
adenocarcinoma
, respectively.
By examining 114 resection lung specimens, we concluded that there are four histological patterns of bronchial epithelial dysplasia based on morphological features (
basal cell
dysplasia, columnar
cell
dysplasia, bronchial epithelial dysplasia with transitional differentiation, and squamous dysplasia).
Basal cell
dysplasia was focally positive for cytokeratin (CK) 17 and 10/13; columnar
cell
dysplasia was generally positive for CK7, 8, and 18; bronchial epithelial dysplasia with transitional differentiation had a heterogeneous immunoprofile, while squamous dysplasia was positive for CK10/13 and focally positive for CK17.
(1) bronchial epithelium can develop various patterns of dysplasia with abnormal/ambiguous
cell
differentiation and abnormal expressions of p53 and Ki-67.
[MeSH-minor]
Adult. Aged. Bronchial Neoplasms / metabolism. Bronchial Neoplasms / pathology. Carcinoma, Bronchogenic / metabolism. Carcinoma, Bronchogenic / pathology.
Cell
Differentiation. Epithelial
Cells
/ chemistry. Epithelial
Cells
/ pathology. Female. Humans. Immunohistochemistry. Keratins / analysis. Ki-67 Antigen / analysis. Male. Middle Aged. Respiratory Mucosa / chemistry. Respiratory Mucosa / pathology. Tumor Suppressor Protein p53 / analysis
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(PMID = 16415791.001).
[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
[Publication-country]
United States
[Chemical-registry-number]
0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; 68238-35-7 / Keratins
95.
Muqit MM, Roberts F:
In regards to Conill et al.: Brachytherapy with 192Ir as treatment of carcinoma of the tarsal structure of the eyelid (Int J Radiat Oncol Bio Phys 2004;59:1326-1329).
Int J Radiat Oncol Biol Phys
; 2006 Jul 1;65(3):959
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[MeSH-minor]
Adenocarcinoma
/ pathology.
Adenocarcinoma
/ radiotherapy. Carcinoma,
Basal Cell
/ pathology. Carcinoma,
Basal Cell
/ radiotherapy. Carcinoma, Squamous
Cell
/ pathology. Carcinoma, Squamous
Cell
/ radiotherapy. Humans. Iridium Radioisotopes / therapeutic use
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[CommentOn]
Int J Radiat Oncol Biol Phys. 2004 Aug 1;59(5):1326-9
[
15275716.001
]
(PMID = 16751086.001).
[ISSN]
0360-3016
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
eng
[Publication-type]
Comment; Letter
[Publication-country]
United States
[Chemical-registry-number]
0 / Iridium Radioisotopes
96.
Kantrow SM, Ivan D, Williams MD, Prieto VG, Lazar AJ:
Metastasizing adenocarcinoma and multiple neoplastic proliferations arising in a nevus sebaceus.
Am J Dermatopathol
; 2007 Oct;29(5):462-6
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[Title]
Metastasizing
adenocarcinoma
and multiple neoplastic proliferations arising in a nevus sebaceus.
Many neoplasms have been reported to arise in association with nevus sebaceus, most commonly trichoblastoma/
basal cell
carcinoma and syringocystadenoma papilliferum.
We report a case of a 66-year-old woman with an
adenocarcinoma
as well as multiple neoplastic proliferations arising in a long standing nevus sebaceus on the scalp, with subsequent occipital neck metastatic
disease
.
Most of the lesion was composed of an
adenocarcinoma
with areas showing ductal differentiation with decapitation secretion, well-formed papillae and focal cribriform structures.
Other portions demonstrated a high-grade
neoplasm
with prominent nuclear atypia and a solid pattern of growth resembling high-grade breast carcinoma.
Anti-epithelial membrane antigen strongly labeled tumor
cells
and highlighted ductal structures.
Less than 1% of
cells
expressed progesterone or estrogen receptors.
Her2/neu reactivity was focally present, showing 1+ membranous reactivity in 10% of
cells
.
Anti-p63 labeled basaloid
cells
surrounding the tumor lobules.
This report illustrates an extraordinary case of adnexal
neoplasia
displaying various lines of differentiation arising in association with nevus sebaceus.
[MeSH-major]
Adenocarcinoma
/ secondary. Head and Neck Neoplasms / secondary. Nevus / pathology. Skin Neoplasms / pathology
[MeSH-minor]
Aged.
Cell
Proliferation. Female. Humans. Membrane Proteins / metabolism. Mucin-1 / metabolism. Receptor, ErbB-2 / metabolism
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.
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.
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.
MedlinePlus Health Information.
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.
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(PMID = 17890915.001).
[ISSN]
0193-1091
[Journal-full-title]
The American Journal of dermatopathology
[ISO-abbreviation]
Am J Dermatopathol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / CKAP4 protein, human; 0 / Membrane Proteins; 0 / Mucin-1; EC 2.7.10.1 / Receptor, ErbB-2
97.
Gerdes MJ, Yuspa SH:
The contribution of epidermal stem cells to skin cancer.
Stem Cell Rev
; 2005;1(3):225-31
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[Title]
The contribution of epidermal stem
cells
to skin cancer.
Tumors arising from the skin are of multiple phenotypes, with differing degrees of
malignant
potential.
In mouse models of skin carcinogenesis, tumors of squamous phenotype are the most common; however, human
disease
indicates that multiple phenotypes may arise from a common pool of stem
cells
that are then influenced by epigenetic factors.
The use of transgenic and knockout gene technologies with mice is unraveling some of the specific genes regulating fate determination in stem
cells
other than squamous lineage, including
basal cell
carcinoma and sebaceous
adenomas
.
The following review examines the evidence for the stem
cell
origin of epidermal tumors and the contribution of some specific gene families toward stem
cell
fate decisions during epidermal tumor progression.
[MeSH-major]
Adenocarcinoma
, Sebaceous / genetics. Carcinoma,
Basal Cell
/ genetics. Epidermis. Epigenesis, Genetic. Neoplastic Stem
Cells
. Skin Neoplasms / genetics
[MeSH-minor]
Animals.
Disease
Models, Animal. Gene Expression Regulation, Neoplastic / genetics. Humans. Mice. Mice, Knockout
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Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
The Lens.
Cited by Patents in
.
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[Cites]
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12221288.001
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[Cites]
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[