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1079 records – page 1 of 108.

The 3rd International Symposium on the Molecular Biology of Breast Cancer. Molde, Norway, 22-26 June 2005. Abstracts.

https://arctichealth.org/en/permalink/ahliterature16931
Source
Breast Cancer Res. 2005;7 Suppl 2:S1-62
Publication Type
Conference/Meeting Material
Article
Date
2005
Source
Breast Cancer Res. 2005;7 Suppl 2:S1-62
Date
2005
Language
English
Publication Type
Conference/Meeting Material
Article
Keywords
Animals
Breast Neoplasms - genetics
Humans
PubMed ID
15982407 View in PubMed
Less detail

3'-UTR poly(T/U) repeat of EWSR1 is altered in microsatellite unstable colorectal cancer with nearly perfect sensitivity.

https://arctichealth.org/en/permalink/ahliterature273744
Source
Fam Cancer. 2015 Sep;14(3):449-53
Publication Type
Article
Date
Sep-2015
Author
Johanna Kondelin
Sari Tuupanen
Alexandra E Gylfe
Mervi Aavikko
Laura Renkonen-Sinisalo
Heikki Järvinen
Jan Böhm
Jukka-Pekka Mecklin
Claus L Andersen
Pia Vahteristo
Esa Pitkänen
Lauri A Aaltonen
Source
Fam Cancer. 2015 Sep;14(3):449-53
Date
Sep-2015
Language
English
Publication Type
Article
Keywords
3' Untranslated Regions
Calmodulin-Binding Proteins - genetics
Colorectal Neoplasms - genetics
Denmark
Finland
Humans
Microsatellite Instability
Polyribonucleotides - genetics
RNA-Binding Proteins - genetics
Repetitive Sequences, Nucleic Acid
Abstract
Approximately 15% of colorectal cancers exhibit instability of short nucleotide repeat regions, microsatellites. These tumors display a unique clinicopathologic profile and the microsatellite instability status is increasingly used to guide clinical management as it is known to predict better prognosis as well as resistance to certain chemotherapeutics. A panel of five repeats determined by the National Cancer Institute, the Bethesda panel, is currently the standard for determining the microsatellite instability status in colorectal cancer. Recently, a quasimonomorphic mononucleotide repeat 16T/U at the 3' untranslated region of the Ewing sarcoma breakpoint region 1 gene was reported to show perfect sensitivity and specificity in detecting mismatch repair deficient colorectal, endometrial, and gastric cancers in two independent populations. To confirm this finding, we replicated the analysis in 213 microsatellite unstable colorectal cancers from two independent populations, 148 microsatellite stable colorectal cancers, and the respective normal samples by PCR and fragment analysis. The repeat showed nearly perfect sensitivity for microsatellite unstable colorectal cancer as it was altered in 212 of the 213 microsatellite unstable (99.5%) and none of the microsatellite stable colorectal tumors. This repeat thus represents the first potential single marker for detecting microsatellite instability.
PubMed ID
25930744 View in PubMed
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A 10-year follow-up of the National Cancer Act.

https://arctichealth.org/en/permalink/ahliterature26835
Source
Biomed Pharmacother. 1984;38(6):282-4
Publication Type
Article
Date
1984
Author
P. Reizenstein
J. Pontèn
Source
Biomed Pharmacother. 1984;38(6):282-4
Date
1984
Language
English
Publication Type
Article
Keywords
Humans
Legislation, Medical
Life Style
Neoplasms - genetics - immunology - prevention & control
Sweden
United States
Abstract
No decade has seen as great advances as the 1970's in the understanding of cancer and in treatment results. The discovery of the role of oncogens, of some viruses, carcinogenic chemicals, and life-style in carcinogenesis and the increased cure rates in childhood tumors, leukemias, lymphomas, and breast and testicular carcinomas are some examples. The National Cancer Act must be credited for these advances to an appreciable degree.
PubMed ID
6525429 View in PubMed
Less detail

17 beta-hydroxysteroid dehydrogenase gene expression in human breast cancer cells: regulation of expression by a progestin.

https://arctichealth.org/en/permalink/ahliterature24541
Source
Cancer Res. 1992 Jan 15;52(2):290-4
Publication Type
Article
Date
Jan-15-1992
Author
M. Poutanen
B. Moncharmont
R. Vihko
Author Affiliation
Department of Clinical Chemistry, University of Oulu, Finland.
Source
Cancer Res. 1992 Jan 15;52(2):290-4
Date
Jan-15-1992
Language
English
Publication Type
Article
Keywords
17-Hydroxysteroid Dehydrogenases - genetics - metabolism
Breast Neoplasms - enzymology - genetics
Gene Expression Regulation, Neoplastic - drug effects
Humans
Isoenzymes - genetics
Placenta - enzymology
Pregnenediones - pharmacology
Progesterone Congeners - pharmacology
RNA, Messenger - genetics
RNA, Neoplasm - genetics
Receptors, Estrogen - metabolism
Receptors, Progesterone - metabolism
Research Support, Non-U.S. Gov't
Tumor Cells, Cultured
Abstract
The expression of the 17 beta-hydroxysteroid dehydrogenase (17-HSD) gene in a series of human breast cancer cell lines was studied by Northern blot hybridization with a cDNA probe and by a time-resolved immunofluorometric assay using polyclonal antibodies against the enzyme protein. The 17-HSD enzyme protein concentration was measured in the 800 x g cell extract. A high concentration was measured in the BT-20 cell line, corresponding to one-fourth of the average concentration in placental tissue. Western blot analysis indicated that the antigen corresponded to a single Mr 35,000 band. In 2 other cell lines (MDA-MB-361 and T-47D), the 17-HSD protein concentration was much lower, but still measurable, whereas in the remaining 5 cell lines (HBL-100, MCF-7, MDA-MB-231, MDA-MB-468, and ZR-75-1) it was below the detection limit of the assay. Treatment of the cells for 5 days with the synthetic progestin, ORG2058, resulted in an increase of the 17-HSD protein concentration only in the T-47D cell line. By Northern blot analysis, a low level of 2.3-kilobase mRNA transcripts was detected in all 8 cell lines. In addition, a 1.3-kilobase 17-HSD mRNA was present in the samples from the 3 cell lines containing measurable amounts of 17-HSD protein in the cell extract, and the band intensities were proportional to the amount of protein measured with the immunofluorometric assay. Only in the T-47D cell line did progestin treatment correspond to an increased amount of the 17-HSD 1.3-kilobase mRNA. These results suggest that the 1.3-kilobase mRNA for 17-HSD is the form most closely associated with protein expression and is also the only form responding to the progestin induction of the 17-HSD gene.
PubMed ID
1728403 View in PubMed
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The 4154delA mutation carriers in the BRCA1 gene share a common ancestry.

https://arctichealth.org/en/permalink/ahliterature153810
Source
Fam Cancer. 2009;8(1):1-4
Publication Type
Article
Date
2009
Author
Silvija Ozolina
Olga Sinicka
Eriks Jankevics
Inna Inashkina
Jan Lubinski
Bohdan Gorski
Jacek Gronwald
Tatyana Nasedkina
Olga Fedorova
Ludmila Lyubchenko
Laima Tihomirova
Author Affiliation
Latvian Biomedical Research and Study Centre, Ratsupites str. 1, Riga, 1067, Latvia.
Source
Fam Cancer. 2009;8(1):1-4
Date
2009
Language
English
Publication Type
Article
Keywords
Breast Neoplasms - genetics
DNA Mutational Analysis
Female
Founder Effect
Genes, BRCA1
Genetic Predisposition to Disease
Haplotypes
Humans
Latvia
Male
Microsatellite Repeats
Mutation
Pedigree
Poland
Polymerase Chain Reaction
Polymorphism, Single Nucleotide
Polymorphism, Single-Stranded Conformational
Russia
Abstract
Uncertainty exists whether the 4154delA mutation of the BRCA1 gene detected in unrelated individuals from Latvia, Poland and Russia is a founder mutation with a common ancestral origin. To trace back this problem we analysed the mutation-associated haplotype of the BRCA1 intragenic SNPs as well as intragenic and nearby STR markers in mutation carriers from the aforementioned populations. The mutation-associated SNP alleles were found to be "T-A-A-A-A-G" for six intragenic SNPs of the BRCA1 gene (IVS8-58delT, 3232A/G, 3667A/G, IVS16-68A/G, IVS16-92A/G, IVS18+66G/A, respectively). The alleles 195, 154, 210 and 181 were found to be associated with the 4154delA mutation for STR markers D17S1325, D17S855, D17S1328 and D17S1320, correspondingly. Further analysis of markers in the 4154delA mutation carriers from all three populations allows us to assert that all analysed mutation carriers share a common ancestry.
PubMed ID
19067236 View in PubMed
Less detail

ABCC2 transporter gene polymorphisms, diet and risk of colorectal cancer: a Danish prospective cohort study.

https://arctichealth.org/en/permalink/ahliterature126046
Source
Scand J Gastroenterol. 2012 May;47(5):572-4
Publication Type
Article
Date
May-2012

Aberrant expression of the human epidermal growth factor receptor 2 oncogene is not a common feature in osteosarcoma.

https://arctichealth.org/en/permalink/ahliterature101871
Source
Hum Pathol. 2011 Jun;42(6):859-66
Publication Type
Article
Date
Jun-2011
Author
Daniel Baumhoer
Jan Smida
Katja Specht
Karin Bink
Leticia Quintanilla-Martinez
Michael Rosemann
Heide Siggelkow
Walter B J Nathrath
Michael J Atkinson
Stefan Bielack
Gernot Jundt
Michaela Nathrath
Author Affiliation
Institute of Pathology, University Hospital Basel, 4031 Basel, Switzerland. dbaumhoer@mac.com
Source
Hum Pathol. 2011 Jun;42(6):859-66
Date
Jun-2011
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Bone Neoplasms - genetics - metabolism - pathology
Child
Child, Preschool
DNA, Neoplasm - analysis
Female
Gene Expression Regulation, Neoplastic - physiology
Humans
Immunohistochemistry
In Situ Hybridization, Fluorescence
Male
Middle Aged
Oligonucleotide Array Sequence Analysis
Osteosarcoma - genetics - metabolism - pathology
Polymorphism, Single Nucleotide
Prognosis
RNA, Messenger - metabolism
Receptor, erbB-2 - genetics - metabolism
Reverse Transcriptase Polymerase Chain Reaction
Tumor Markers, Biological - genetics - metabolism
Young Adult
Abstract
Human epidermal growth factor receptor 2 expression in osteosarcoma and its relationship to prognosis have been the subject of several conflicting reports, most of them relying on immunohistochemical studies. Because the urgent need of prognostic markers and effective new treatment options for osteosarcoma patients, we evaluated the role of human epidermal growth factor receptor 2 in 2 well-characterized sets of pretherapeutic osteosarcoma samples (46 paraffin-embedded and 46 fresh-frozen biopsy samples) using immunohistochemistry with 2 different antibodies [DAKO A0485 (Glostrup, Denmark) and Novocastra CB11 (Newcastle, UK)] as well as fluorescence in situ hybridization, real-time polymerase chain reaction, and SNP array analyses and correlated our findings with clinicopathological parameters. However, our study failed to detect unequivocal evidence of human epidermal growth factor receptor 2 gene amplification or overexpression of human epidermal growth factor receptor 2 messenger RNA or protein in any of the investigated tumors. Only in a small subset of samples, a moderate increase in messenger RNA levels (13.6%) or focal membranous immunoreactivity (8.7%; A0485) was detected but did not correlate with survival or response to chemotherapy. Cytoplasmic staining was identified more frequently (63%; CB11) but again did not show any association with clinicopathological parameters. In conclusion, our study does not support a role for human epidermal growth factor receptor 2 as a prognostic marker in osteosarcoma.
PubMed ID
21292304 View in PubMed
Less detail

Aberrant p53 protein expression in cervical intra-epithelial neoplasia.

https://arctichealth.org/en/permalink/ahliterature23877
Source
Histopathology. 1993 Nov;23(5):471-4
Publication Type
Article
Date
Nov-1993
Author
R. Pöllänen
Y. Soini
K. Vähäkangas
P. Pääkkö
V P Lehto
Author Affiliation
Department of Pathology, University of Oulu, Finland.
Source
Histopathology. 1993 Nov;23(5):471-4
Date
Nov-1993
Language
English
Publication Type
Article
Keywords
Cervical Intraepithelial Neoplasia - metabolism - microbiology
DNA, Viral - genetics - isolation & purification
Female
Gene Expression
Genes, p53
Humans
Mutation
Papillomavirus, Human - genetics - isolation & purification
Precancerous Conditions - genetics - metabolism - microbiology
Research Support, Non-U.S. Gov't
Tumor Suppressor Protein p53 - genetics - metabolism
Uterine Cervical Neoplasms - genetics - metabolism - microbiology
Abstract
We investigated aberrant p53 expression in 81 cases of cervical intra-epithelial neoplasias (CIN) using a polyclonal antibody CM-1. The presence of human papillomavirus (HPV) DNA was evaluated by in situ and dot blot hybridization. Significant (more than 1% of cells positive) p53 positivity was found in three cases (4%) of which only one contained HPV DNA. In an additional nine cases, occasional p53 staining was found in basal epithelial cells, frequently associated with epithelial hyperplasia and increased subepithelial inflammation. The results show that aberrant p53 expression is an infrequent finding in CIN lesions. It can be seen in lesions both with and without HPV infection. Most importantly, there was no p53 expression in most cases of HPV-negative CIN, suggesting that p53 inactivation is not an obligatory step in the development of cervical dysplasia. However, our findings do not exclude the possibility that p53 mutations can occur later in the course of cervical carcinogenesis.
PubMed ID
8314222 View in PubMed
Less detail

Absence of p53 mutations in benign and pre-malignant male genital lesions with over-expressed p53 protein.

https://arctichealth.org/en/permalink/ahliterature21534
Source
Int J Cancer. 1998 Aug 31;77(5):674-8
Publication Type
Article
Date
Aug-31-1998
Author
K. Castrén
K. Vähäkangas
E. Heikkinen
A. Ranki
Author Affiliation
Department of Pharmacology and Toxicology, University of Oulu, Finland.
Source
Int J Cancer. 1998 Aug 31;77(5):674-8
Date
Aug-31-1998
Language
English
Publication Type
Article
Keywords
Biopsy
Bowen's Disease - genetics - pathology
Carcinoma in Situ - genetics - pathology
Carcinoma, Squamous Cell - genetics - pathology
Condylomata Acuminata - genetics - pathology
Exons
Female
Genes, p53
Genital Diseases, Male - genetics - pathology - surgery
Genital Neoplasms, Male - genetics - pathology - surgery
Humans
Male
Mutation
Papillomavirus, Human - isolation & purification
Precancerous Conditions - genetics - pathology - surgery
Research Support, Non-U.S. Gov't
Skin Neoplasms - genetics - pathology
Tumor Suppressor Protein p53 - biosynthesis
Uterine Cervical Neoplasms - genetics
Vulvar Neoplasms - pathology
Abstract
Mutations of the tumor-suppressor gene p53 are common in epithelial tumors. Clonal mutations of p53 have been found in cervical and vulvar carcinomas negative for human papillomavirus (HPV), though at least in cervical cancer HPV infection and p53 mutations are not mutually exclusive. We have previously shown that about 40% of male genital warts and bowenoid papulosis lesions exhibit immunohistochemically detectable aberrant p53 protein, irrespective of the presence of HPV DNA. We studied p53 mutations in exons 4-8 with SSCP and sequencing in 13 male patients with 1 to 3 therapy-resistant genital warts or intra-epithelial neoplasias each and in 4 patients with penile squamous cell carcinoma. Thus, 13 genital warts, 6 bowenoid papulosis, 1 Queyrat's erythroplasia and 1 carcinoma in situ were studied. p53 protein was detected immunohistochemically, and HPV status was analyzed with DNA in situ hybridization and amplification of HPV-specific DNA. There was no correlation between p53 protein expression and HPV status. No mutations in exons 5-8 of the p53 gene were found in any of the lesions, and furthermore, no exon 4 mutations were found in lesions positive in p53 immunohistochemistry. In conclusion, overexpression of p53 does not indicate a p53 mutation in male genital warts, pre-malignant lesions or malignant squamous cell carcinomas. Our study thus suggests that p53 mutations are not important, or at least not early, events in male genital carcinogenesis.
PubMed ID
9688297 View in PubMed
Less detail

Absence of the common Insulin-like growth factor-1 19-repeat allele is associated with early age at breast cancer diagnosis in multiparous women.

https://arctichealth.org/en/permalink/ahliterature78723
Source
Br J Cancer. 2007 Mar 12;96(5):712-7
Publication Type
Article
Date
Mar-12-2007
Author
Bågeman E.
Ingvar C.
Rose C.
Jernström H.
Author Affiliation
Department of Oncology, Clinical Sciences, Lund University, SE-221 85 Lund, Sweden.
Source
Br J Cancer. 2007 Mar 12;96(5):712-7
Date
Mar-12-2007
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Aged
Aged, 80 and over
Alleles
Breast Neoplasms - genetics
Female
Genetic Predisposition to Disease
Genotype
Humans
Insulin-Like Growth Factor I - genetics
Middle Aged
Parity
Polymerase Chain Reaction
Pregnancy
Abstract
Multiparity decreases the risk of breast cancer in white women, whereas it is a risk factor in black women
PubMed ID
17311016 View in PubMed
Less detail

1079 records – page 1 of 108.