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8-Hydroxydeoxyguanosine: a new potential independent prognostic factor in breast cancer.

https://arctichealth.org/en/permalink/ahliterature97933
Source
Br J Cancer. 2010 Mar 16;102(6):1018-23
Publication Type
Article
Date
Mar-16-2010
Author
H. Sova
A. Jukkola-Vuorinen
U. Puistola
S. Kauppila
P. Karihtala
Author Affiliation
Department of Oncology and Radiotherapy, Oulu University Hospital, Finland. henrijuh@mail.student.oulu.fi
Source
Br J Cancer. 2010 Mar 16;102(6):1018-23
Date
Mar-16-2010
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Breast Neoplasms - diagnosis - metabolism - mortality - pathology
Carcinoma, Ductal, Breast - diagnosis - metabolism - mortality - pathology
Deoxyguanosine - analogs & derivatives - blood - metabolism
Female
Humans
Immunohistochemistry
Middle Aged
Neoplasm Staging
Prognosis
Survival Analysis
Tumor Markers, Biological - analysis - metabolism
Abstract
BACKGROUND: 8-Hydroxydeoxyguanosine (8-oxodG) is the commonly used marker of oxidative stress-derived DNA damage. 8-OxodG formation is regulated by local antioxidant capacity and DNA repair enzyme activity. Earlier studies have reported contradictory data on the function of 8-oxodG as a prognostic factor in different cancer types. METHODS: We assessed pre-operative serum 8-oxodG levels with an enzyme-linked immunosorbent assay in a well-defined series of 173 breast cancer patients. 8-OxodG expression in the nuclei of cancer cells from 150 of these patients was examined by immunohistochemistry. RESULTS: The serum 8-oxodG levels and immunohistochemical 8-oxodG expression were in concordance with each other (P
PubMed ID
20179711 View in PubMed
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Aberrant type I and type III collagen gene expression in human breast cancer in vivo.

https://arctichealth.org/en/permalink/ahliterature21082
Source
J Pathol. 1998 Nov;186(3):262-8
Publication Type
Article
Date
Nov-1998
Author
S. Kauppila
F. Stenbäck
J. Risteli
A. Jukkola
L. Risteli
Author Affiliation
Department of Medical Biochemistry, University of Oulu, Finland.
Source
J Pathol. 1998 Nov;186(3):262-8
Date
Nov-1998
Language
English
Publication Type
Article
Keywords
Breast - chemistry
Breast Neoplasms - metabolism - pathology
Carcinoma, Ductal, Breast - metabolism - pathology
Female
Fibroadenoma - metabolism - pathology
Humans
Immunohistochemistry
In Situ Hybridization
Mucins - genetics
Peptide Fragments - genetics
Procollagen - genetics
RNA, Messenger - analysis
Research Support, Non-U.S. Gov't
Tumor Markers, Biological - analysis
Abstract
Increased synthesis and degradation of extracellular matrix components are associated with breast cancer development. This study evaluated type I and type III procollagen mRNA expression and the corresponding protein synthesis and maturation, as well as the tissue distribution of these collagens, in benign breast lesions, infiltrating ductal carcinomas, and their metastases by in situ hybridization and immunohistochemistry. In the benign lesions, the type I and type III collagen bundles were regularly organized and the expression of the corresponding mRNA was weak, indicating a relatively slow collagen turnover. In the malignant tumours, increased expression of type I and type III procollagen mRNAs was observed in the fibroblastic cells of the stroma; the malignant epithelial cells did not participate. The staining of corresponding newly-synthesized pN-collagens showed aberrant bundles in the invasive front of the malignant tumours. Newly-synthesized type I and type III procollagens were occasionally observed in fibroblastic cells, particularly in grade 2 and grade 3 tumours. Metastases of breast carcinoma resembled poorly differentiated primary tumours with respect to their collagen synthesis and deposition. The increased synthesis of fibrillar type I and type III procollagens may serve as a pathway for tumour invasion. The enhanced synthesis is associated with the formation of aberrant collagen bundles, which may be more readily degradable and may thus facilitate breast tumour invasion.
PubMed ID
10211114 View in PubMed
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Abnormal DNA content predicts the occurrence of carcinomas in non-dysplastic oral white patches.

https://arctichealth.org/en/permalink/ahliterature19552
Source
Oral Oncol. 2001 Oct;37(7):558-65
Publication Type
Article
Date
Oct-2001
Author
J. Sudbø
T. Ried
M. Bryne
W. Kildal
H. Danielsen
A. Reith
Author Affiliation
Division of Digital Pathology, Department of Pathology, The Norwegian Radium Hospital, University of Oslo, Montebello, Oslo 0310, Norway. jon.sudbo@rh.uio.no
Source
Oral Oncol. 2001 Oct;37(7):558-65
Date
Oct-2001
Language
English
Publication Type
Article
Keywords
Adult
Aged
Carcinoma, Squamous Cell - diagnosis - genetics
DNA, Neoplasm - analysis
Disease-Free Survival
Female
Follow-Up Studies
Humans
Image Cytometry - methods
Male
Middle Aged
Mouth Neoplasms - diagnosis - genetics
Ploidies
Precancerous Conditions - diagnosis - genetics
Prognosis
Research Support, Non-U.S. Gov't
Tumor Markers, Biological - analysis
Abstract
The majority of oral squamous cell carcinomas (OSCCs) are preceded by visible changes in the oral mucosa, most often white patches. Although the histological finding of dysplasia in oral white patches signals increased risk of developing OSCC, this may also occur in non-dysplastic lesions. However, no reliable markers exist to predict the occurrence of OSCC in these patients. From a total of 263 patients diagnosed with oral white patches, biopsies from 45 patients were selected on the criteria that the patients had lesions histologically proven to be non-dysplastic. The lesions were analyzed with respect to their DNA content. The clinical outcome of the patients was known from the Cancer Registry of Norway, and these data were compared to the DNA content of their lesions. Among the 45 patients, five cases (11%) later developed an OSCC. Four of the cases that subsequently developed an OSCC were among the five aneuploid (abnormal) cases (P=0.001). One aneuploid lesion did not develop a carcinoma during a follow-up time of 120 months. The fifth case that subsequently developed an OSCC was diploid (normal), and developed into an OSCC after an observation time of 73 months (P=0.001). In conclusion, aberrant DNA content reliably predicts the occurrence of OSCC in patients that otherwise would be regarded as at very low risk. Normal DNA content indicates low risk.
PubMed ID
11564576 View in PubMed
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Academic and nonacademic laboratories perform equally on CIQC immunohistochemistry proficiency testing.

https://arctichealth.org/en/permalink/ahliterature113089
Source
Am J Clin Pathol. 2013 Jul;140(1):55-60
Publication Type
Article
Date
Jul-2013
Author
Zhongchuan Will Chen
Heather Neufeld
Maria A Copete
John Garratt
C Blake Gilks
Emina E Torlakovic
Author Affiliation
Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada.
Source
Am J Clin Pathol. 2013 Jul;140(1):55-60
Date
Jul-2013
Language
English
Publication Type
Article
Keywords
Academic Medical Centers
Breast Neoplasms - diagnosis
Canada
Data Collection
Female
Hospitals, Rural
Hospitals, Urban
Humans
Immunohistochemistry - standards
Laboratories - standards
Laboratory Proficiency Testing - standards
Paraffin Embedding
Pathology - standards
Quality Assurance, Health Care
Reproducibility of Results
Tissue Array Analysis
Tumor Markers, Biological - analysis
Workload
Abstract
To test whether academic centers (ACs) are more successful than nonacademic centers (NACs) in immunohistochemistry (IHC) external quality assessment challenges in the Canadian Immunohistochemistry Quality Control (CIQC) program.
Results of 9 CIQC challenges for breast cancer marker (BM) and various non-breast cancer marker (NBM) tests were examined. Success rates were compared between AC/NAC laboratories and those located in small or large cities. Performance was also correlated with annual IHC case volumes.
There was no statistically significant difference in performance in any of the comparisons. However, overall performance on BM was significantly better (P
PubMed ID
23765534 View in PubMed
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Adenoma and tiny carcinoma in adenoma of the papilla of Vater--p53 and PCNA.

https://arctichealth.org/en/permalink/ahliterature20910
Source
Hepatogastroenterology. 1999 May-Jun;46(27):1959-62
Publication Type
Article
Author
T. Sato
K. Konishi
H. Kimura
K. Maeda
K. Yabushita
M. Tsuji
A. Miwa
Author Affiliation
Department of Surgery, Toyama Prefectural Central Hospital, Japan. YIB03163@niftyserve.or.jp
Source
Hepatogastroenterology. 1999 May-Jun;46(27):1959-62
Language
English
Publication Type
Article
Keywords
Adenocarcinoma - pathology - surgery
Adenoma - pathology - surgery
Adult
Aged
Ampulla of Vater - pathology - surgery
Cell Division - physiology
Cell Transformation, Neoplastic - pathology
Common Bile Duct Neoplasms - pathology - surgery
Humans
Male
Neoplasm Invasiveness
Neoplasms, Multiple Primary - pathology - surgery
Proliferating Cell Nuclear Antigen - analysis
Tumor Markers, Biological - analysis
Tumor Suppressor Protein p53 - analysis
Abstract
BACKGROUND/AIMS: Adenomas develop only rarely in the small bowel mucosa. We particularly tried to clarify the histologic change in atypia of ampullary adenomas which are not familial polyposis. METHODOLOGY: Four adenomas, 4 adenocarcinomas, and 4 normal mucosal regions of the ampulla of Vater were investigated in this study. All cases were characterized in paraffin sections for the presence of p53 protein using the anti-p53 monoclonal antibody (DO7, Dako Corp., Glostrup, Denmark) and proliferating cell nuclear antigen using the anti-PCNA antibody (PC 10, Dako A/S, Copenhagen, Denmark). To obtain the percentages (labeling index) of PCNA, a dual wavelength imaging microdensitometer (CAS 200, Elmhurst, IL) was used. RESULTS: Transition of adenoma into adenocarcinoma was recognized in 2 of 4 cases. Labeling index of PCNA was 12.2% in normal mucosa, 41.3% in adenomas, and 66.0% in adenocarcinoma, respectively. In 2 cases with carcinoma in adenoma, labeling index was higher in carcinomatous lesion than in adenomatous lesion. p53 Protein was positive in all cases of adenocarcinoma of the ampulla of Vater, and not in any case of normal mucosa or adenoma. CONCLUSIONS: The adenoma-carcinoma sequence was morphologically recognized especially in tiny carcinoma in adenoma of the papilla of Vater. Both p53 mutation and high proliferative activity play important roles for the histogenesis of invasive adenocarcinoma.
PubMed ID
10430377 View in PubMed
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Adjuvant capecitabine, docetaxel, cyclophosphamide, and epirubicin for early breast cancer: final analysis of the randomized FinXX trial.

https://arctichealth.org/en/permalink/ahliterature129460
Source
J Clin Oncol. 2012 Jan 1;30(1):11-8
Publication Type
Article
Date
Jan-1-2012
Author
Heikki Joensuu
Pirkko-Liisa Kellokumpu-Lehtinen
Riikka Huovinen
Arja Jukkola-Vuorinen
Minna Tanner
Riitta Kokko
Johan Ahlgren
Päivi Auvinen
Outi Paija
Leena Helle
Kenneth Villman
Paul Nyandoto
Greger Nilsson
Marjo Pajunen
Raija Asola
Paula Poikonen
Mika Leinonen
Vesa Kataja
Petri Bono
Henrik Lindman
Author Affiliation
Department of Oncology, Helsinki University Central Hospital, Haartmaninkatu 4, PO Box 180, FIN-00029 Helsinki, Finland. heikki.joensuu@hus.fi
Source
J Clin Oncol. 2012 Jan 1;30(1):11-8
Date
Jan-1-2012
Language
English
Publication Type
Article
Keywords
Adult
Aged
Antimetabolites, Antineoplastic - administration & dosage
Antineoplastic Combined Chemotherapy Protocols - therapeutic use
Breast Neoplasms - chemistry - drug therapy - mortality - pathology - surgery
Carcinoma, Ductal, Breast - drug therapy - pathology
Carcinoma, Lobular - drug therapy - pathology
Chemotherapy, Adjuvant
Cyclophosphamide - administration & dosage
Deoxycytidine - administration & dosage - analogs & derivatives
Disease-Free Survival
Drug Administration Schedule
Epirubicin - administration & dosage
Female
Finland
Fluorouracil - administration & dosage - analogs & derivatives
Follow-Up Studies
Humans
Lymphatic Metastasis
Mastectomy - methods
Middle Aged
Neoplasm Grading
Neoplasm Staging
Prospective Studies
Survival Analysis
Taxoids - administration & dosage
Treatment Outcome
Tumor Markers, Biological - analysis
Abstract
Capecitabine is an active agent in the treatment of breast cancer. It is not known whether integration of capecitabine into an adjuvant regimen that contains a taxane, an anthracycline, and cyclophosphamide improves outcome in early breast cancer.
Women with axillary node-positive or high-risk node-negative breast cancer were randomly assigned to receive either three cycles of docetaxel and capecitabine (TX) followed by three cycles of cyclophosphamide, epirubicin, and capecitabine (CEX; n = 753) or three cycles of docetaxel (T) followed by three cycles of cyclophosphamide, epirubicin, and fluorouracil (CEF; n = 747). The primary end point was recurrence-free survival (RFS).
During a median follow-up time of 59 months, 214 RFS events occurred (local or distant recurrences or deaths; TX/CEX, n = 96; T/CEF, n = 118). RFS was not significantly different between the groups (hazard ratio [HR], 0.79; 95% CI, 0.60 to 1.04; P = .087; 5-year RFS, 86.6% for TX/CEX v 84.1% for T/CEF). Fifty-six patients assigned to TX/CEX died during the follow-up compared with 75 of patients assigned to T/CEF (HR, 0.73; 95% CI, 0.52 to 1.04; P = .080). In exploratory analyses, TX/CEX improved breast cancer-specific survival (HR, 0.64; 95% CI, 0.44 to 0.95; P = .027) and RFS in women with triple-negative disease and in women who had more than three metastatic axillary lymph nodes at the time of diagnosis. We detected little severe late toxicity.
Integration of capecitabine into a regimen that contains docetaxel, epirubicin, and cyclophosphamide did not improve RFS significantly compared with a similar regimen without capecitabine.
Notes
Comment In: J Clin Oncol. 2012 Jan 1;30(1):1-222105825
PubMed ID
22105826 View in PubMed
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Advanced glycation end products, soluble receptor for advanced glycation end products, and risk of colorectal cancer.

https://arctichealth.org/en/permalink/ahliterature134920
Source
Cancer Epidemiol Biomarkers Prev. 2011 Jul;20(7):1430-8
Publication Type
Article
Date
Jul-2011
Author
Li Jiao
Philip R Taylor
Stephanie J Weinstein
Barry I Graubard
Jarmo Virtamo
Demetrius Albanes
Rachael Z Stolzenberg-Solomon
Author Affiliation
Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland, USA. jiao@bcm.edu
Source
Cancer Epidemiol Biomarkers Prev. 2011 Jul;20(7):1430-8
Date
Jul-2011
Language
English
Publication Type
Article
Keywords
Aged
Blood glucose
Case-Control Studies
Cohort Studies
Colorectal Neoplasms - blood - epidemiology
Enzyme-Linked Immunosorbent Assay
Finland
Glycosylation End Products, Advanced - blood
Humans
Insulin - blood
Male
Middle Aged
Proportional Hazards Models
Receptors, Immunologic - blood
Risk factors
Smoking
Tumor Markers, Biological - analysis - blood
Abstract
Advanced glycation end products (AGE) accumulate in human tissue proteins during aging, particularly under hyperglycemia conditions. AGEs induce oxidative stress and inflammation via the receptor for AGEs (RAGE) and soluble RAGE (sRAGE) can neutralize the effects mediated by RAGE-ligand engagement.
We examined the association between N(e)-(carboxymethyl)lysine (CML), a prominent AGE, and sRAGE and colorectal cancer risk in a prospective case-cohort study nested within a cancer prevention trial among 29,133 Finnish male smokers. Among study subjects who were alive without cancer 5 years after baseline (1985-1988), we identified 483 incident colorectal cancer cases and randomly sampled 485 subcohort participants as the comparison group with the follow-up to April 2006. Baseline serum levels of CML-AGE, sRAGE, glucose and insulin were determined. Weighted Cox proportional hazard regression models were used to calculate relative risks (RR) and 95% CI.
Comparing highest with lowest quintile of sRAGE, the RR for incident colorectal cancer was 0.65 (95% CI, 0.39-1.07; P(trend) = 0.03), adjusting for age, years of smoking, body mass index, and CML-AGE. Further adjustment for serum glucose strengthened the association (RR = 0.52; 95% CI, 0.30-0.89; P(trend) = 0.009). Highest quintile of CML-AGE was not associated with an increased risk of colorectal cancer (multivariate RR = 1.20; 95% CI, 0.64-2.26).
Higher prediagnostic levels of serum sRAGE were associated with lower risk of colorectal cancer in male smokers.
This is the first epidemiologic study to implicate the receptor for AGEs in colorectal cancer development.
Notes
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PubMed ID
21527578 View in PubMed
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[Angiogenesis: prognostic marker in prostatic cancer]

https://arctichealth.org/en/permalink/ahliterature20936
Source
Ugeskr Laeger. 1999 Jun 21;161(25):3832-6
Publication Type
Article
Date
Jun-21-1999
Author
M. Borre
I B Offersen
B. Nerstrøm
J. Overgaard
Author Affiliation
Arhus Universitetshospital, Kraeftens Bekaempelse, afdeling for eksperimentel klinisk onkologi.
Source
Ugeskr Laeger. 1999 Jun 21;161(25):3832-6
Date
Jun-21-1999
Language
Danish
Publication Type
Article
Keywords
Antigens
Denmark - epidemiology
English Abstract
Factor VIII - immunology
Humans
Male
Microcirculation - immunology
Neovascularization, Pathologic - immunology
Prognosis
Prostatic Neoplasms - blood supply - immunology - mortality
Tumor Markers, Biological - analysis
Abstract
Angiogenesis, the formation of new blood vessels, has been suggested to provide important prognostic information in prostate cancer. The aim of this study was to investigate, whether microvessel density (MVD) at diagnosis was correlated with disease-specific survival in a non-curative treated population of prostate cancer patients. MVD was immunohistochemically (factor VIII-related antigen) quantified in archival tumours obtained at diagnosis in 221 prostate cancer patients. The maximal MVD was quantified inside a 0.25 mm2 area of the tumour and the median MVD was 43 (range 16-151). MVD was statistically significantly correlated with clinicopathological characteristics and disease-specific survival. A multivariate analysis demonstrated that MVD was a significant predictor of disease-specific survival in the entire cancer population, as well as in the clinically localized cancer population. These findings suggest that quantitation of angiogenesis reflects the spontaneous clinical outcome of prostate cancer.
PubMed ID
10412301 View in PubMed
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An immunohistochemical analysis of mdr-1 and bcl-2 expressions in neuroblastoma.

https://arctichealth.org/en/permalink/ahliterature214141
Source
Pathol Res Pract. 1995 Oct;191(10):1010-5
Publication Type
Article
Date
Oct-1995
Author
C J Kim
Y A Lee
H S Ahn
C K Yun
C W Kim
J G Chi
Author Affiliation
Department of Pathology, Seoul National University College of Medicine, Korea.
Source
Pathol Res Pract. 1995 Oct;191(10):1010-5
Date
Oct-1995
Language
English
Publication Type
Article
Keywords
Adolescent
Antibodies, Monoclonal - diagnostic use
Cell Membrane - chemistry
Cell Nucleus - chemistry
Child
Child, Preschool
Female
Gene Expression
Humans
Immunohistochemistry
Infant
Male
Neoplasm Staging
Neuroblastoma - chemistry - pathology
P-Glycoprotein - analysis
Proto-Oncogene Proteins c-bcl-2 - analysis
Retrospective Studies
Tumor Markers, Biological - analysis
Abstract
Among the differentiation-related changes in neuroblastoma are expressions of mdr-1 and bcl-2, which may be potentially related to the resistance to anticancer chemotherapy. In the present study, the authors performed an immunohistochemical analysis of mdr-1 and bcl-2 expressions in 30 neuroblastomas using monoclonal anti-P-glycoprotein(mdr-1 product) antibody and monoclonal anti-bcl-2 antibody to investigate the significance of their expression. The overall incidence of mdr-1 and bcl-2 expressions were 53.3% (16/30) and 93.3% (28/30), respectively. The expressions of mdr-1 and bcl-2 didn't seem to be related to the status of preoperative chemotherapy or stage of disease. The expression of mdr-1 was closely related to the differentiation of tumor cells (p
PubMed ID
8838369 View in PubMed
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An increase in the number of adhesion proteins with altered expression is associated with an increased risk of cancer death for colon carcinoma patients.

https://arctichealth.org/en/permalink/ahliterature174420
Source
Int J Colorectal Dis. 2006 Apr;21(3):231-7
Publication Type
Article
Date
Apr-2006
Author
Johan Bondi
Geir Bukholm
Jahn M Nesland
Arne Bakka
Ida R K Bukholm
Author Affiliation
Department of Surgery, Akershus University Hospital, 1474, Nordbyhagen, Norway.
Source
Int J Colorectal Dis. 2006 Apr;21(3):231-7
Date
Apr-2006
Language
English
Publication Type
Article
Keywords
Adenocarcinoma - mortality - pathology
Adult
Aged
Aged, 80 and over
Cadherins - analysis
Catenins - analysis
Colonic Neoplasms - mortality - pathology
Female
Humans
Male
Middle Aged
Norway
Survival Analysis
Tumor Markers, Biological - analysis
Abstract
Reduced expression of components of the cell-cell adhesive cadherin-catenin complex has been related to the invasive phenotype in many malignancies, but the prognostic value of altered expression of its separate components varies in colon cancer. Our objective was evaluation of the cadherin-catenin complex, considered as a functional unit, in colon carcinomas and its relationship to patient outcome.
Tumours from 206 patients operated for colon adenocarcinoma were analysed using immunohistochemistry of E-cadherin, alpha, beta, and gamma-catenins, and p120ctn. The sum of proteins with altered membranous expression was calculated as an overall adhesion score (ranging from 0 to 5) for each patient. The results were correlated with patient outcome.
Of the tumours included in the analysis 0.5% had score 0, 4.9% had score 1, 13.6% had score 2, 31.6% had score 3, 33.0% had score 4, and 16.5% tumours had score 5. None of the proteins examined had individual, independent prognostic value. However, an increase in the number of proteins in the cadherin-catenin complex with altered expression was associated with an increased risk of cancer death (univariate P=0.002; multivariate P=0.007, HR 1.48, 95% CI 1.11-1.96).
An increase in the number of adhesion proteins with altered expression in the primary tumour is associated with increasingly impaired prognosis for patients operated for colon carcinoma. The results reveal that the entire cadherin-catenin complex should be evaluated when assessing its prognostic value in the disease.
PubMed ID
15937692 View in PubMed
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199 records – page 1 of 20.