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-160C/A polymorphism in the E-cadherin gene promoter and risk of hereditary, familial and sporadic prostate cancer.

https://arctichealth.org/en/permalink/ahliterature17926
Source
Int J Cancer. 2004 Apr 10;109(3):348-52
Publication Type
Article
Date
Apr-10-2004
Author
Jonsson B-A
Adami H-O
Hägglund M
Bergh A
Göransson I
Stattin P
Wiklund F
Grönberg H
Author Affiliation
Department of Medical Biosciences, Pathology, Umeå University, Umeå, Sweden.
Source
Int J Cancer. 2004 Apr 10;109(3):348-52
Date
Apr-10-2004
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Cadherins - genetics
Case-Control Studies
Comparative Study
Gene Frequency
Genetic Predisposition to Disease
Genotype
Humans
Male
Middle Aged
Polymorphism, Single Nucleotide
Promoter Regions (Genetics)
Prostate
Prostatic Neoplasms - epidemiology - genetics
Research Support, Non-U.S. Gov't
Risk factors
Sweden - epidemiology
Abstract
The E-cadherin (CDH1) gene has been associated with prostate carcinogenesis. The C/A polymorphism--160 base pairs relative to the transcription start site has been shown to decrease gene transcription. We analyzed the association between this polymorphism and the risk of sporadic, familial (2 close relatives) and hereditary (3 or more close relatives) prostate cancer. We combined data from 3 population-based epidemiologic studies in Sweden encompassing altogether 1,036 prostate cancer cases and 669 controls that were genotyped for the short nucleotide polymorphism. Odds ratios with 95% confidence intervals were estimated through unconditional logistic regression. We found no significant association between the A-allele and sporadic (OR = 1.0; 95% CI = 0.8-1.2) or familial (OR = 1.4; 95% CI = 0.9-2.2) prostate cancer. In contrast, risk of hereditary cancer was increased among heterozygote CA carriers (OR = 1.7; 95% CI = 1.0-2.7) and particularly among homozygote AA carriers (OR = 2.6; 95% CI = 1.4-4.9). Our data indicate that the -160 single nucleotide polymorphism in CDH1 is a low-penetrant prostate cancer susceptibility gene that might explain a proportion of familial and notably hereditary prostate cancer.
PubMed ID
14961571 View in PubMed
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Association between the presence of bacterial 16S RNA in prostate specimens taken during transurethral resection of prostate and subsequent risk of prostate cancer (Sweden).

https://arctichealth.org/en/permalink/ahliterature80484
Source
Cancer Causes Control. 2006 Nov;17(9):1127-33
Publication Type
Article
Date
Nov-2006
Author
Alexeyev O.
Bergh J.
Marklund I.
Thellenberg-Karlsson C.
Wiklund F.
Grönberg H.
Bergh A.
Elgh F.
Author Affiliation
Department of Medical Biosciences/Pathology, Umeå University, S-90185, Umeå, Sweden. oleg.alexeyev@medbio.umu.se
Source
Cancer Causes Control. 2006 Nov;17(9):1127-33
Date
Nov-2006
Language
English
Publication Type
Article
Keywords
Aged
Case-Control Studies
DNA, Bacterial - isolation & purification
Disease Progression
Follow-Up Studies
Gram-Negative Bacterial Infections - complications - epidemiology - microbiology
Gram-Positive Bacterial Infections - complications - epidemiology - microbiology
Humans
Logistic Models
Male
Polymerase Chain Reaction
Propionibacterium acnes - isolation & purification
Prostatic Hyperplasia - microbiology - surgery
Prostatic Neoplasms - epidemiology - microbiology - surgery
RNA, Bacterial - isolation & purification
RNA, Ribosomal, 16S - isolation & purification
Risk factors
Sensitivity and specificity
Sequence Analysis, RNA
Severity of Illness Index
Specimen Handling
Sweden - epidemiology
Transurethral Resection of Prostate
Treatment Outcome
Abstract
OBJECTIVE: To study bacterial 16S RNA in archival prostate samples from 352 patients with benign prostate hyperplasia (BPH) and evaluate whether the presence of bacterial DNA was different in those who later developed prostate cancer (n = 171) and in the matched controls that did not progress to cancer (n = 181). METHODS: 16S DNA PCR followed by cloning and sequencing the positive samples. RESULTS: In 96/352 (27%) of the prostate tissue specimens 16S RNA were detected. Sequence analysis revealed Propionibacterium acnes as the predominant microorganism (23% of 16S RNA positive patients). The second most frequent isolate-Escherichia coli was found in 12 (12%) patients. The other isolates included Pseudomonas sp. (3 patients), Actinomyces sp. (2), Streptococcus mutans (1), Corynebacterium sp. (2), Nocardioides sp. (1), Rhodococcus sp. (1) Veillonella sp. (2). In P. acnes positive samples 62% exhibited severe histological inflammation versus 50% in the bacteria-negative group (p = 0.602). The presence of P. acnes in the prostate was associated with prostate cancer development (OR 2.17, 95% CI 0.77-6.95). CONCLUSIONS: This study has revealed P. acnes as the most common bacteria in the prostate in BPH. Further studies are needed to clarify its role in contributing to the development of prostatic inflammation and prostate cancer.
PubMed ID
17006718 View in PubMed
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Two Swedish founder MSH6 mutations, one nonsense and one missense, conferring high cumulative risk of Lynch syndrome.

https://arctichealth.org/en/permalink/ahliterature83110
Source
Clin Genet. 2005 Dec;68(6):533-41
Publication Type
Article
Date
Dec-2005
Author
Cederquist K.
Emanuelsson M.
Wiklund F.
Golovleva I.
Palmqvist R.
Grönberg H.
Author Affiliation
Medical and Clinical Genetics, Department of Medical Biosciences, Umea University, Sweden. kristina.cederquist@medbio.umu.se
Source
Clin Genet. 2005 Dec;68(6):533-41
Date
Dec-2005
Language
English
Publication Type
Article
Keywords
Codon, Nonsense - genetics
Colorectal Neoplasms, Hereditary Nonpolyposis - epidemiology - genetics - pathology
DNA Mutational Analysis
DNA-Binding Proteins - genetics
Female
Genetic Predisposition to Disease
Humans
Immunohistochemistry
Male
Microsatellite Repeats - genetics
Mutation, Missense - genetics
Pedigree
Risk factors
Sex Factors
Sweden - epidemiology
Abstract
Lynch syndrome, or hereditary non-polyposis colorectal cancer (HNPCC), is a cancer susceptibility syndrome caused by germline mutations in mismatch-repair genes, predominantly MLH1, MSH2 and MSH6. A majority of the mutations reported are truncating, but for MSH6, missense mutations constitute over one third. Few have been proven pathogenic in functional studies or shown to segregate in families. In this study, we show segregation of the putative pathogenic MSH6 missense mutation c.1346T>C p.Leu449Pro with microsatellite instability-high Lynch syndrome-related tumours lacking MSH6 expression in a large 17th century pedigree. Another large family with the MSH6 nonsense c.2931C>G, p.Tyr977X mutation is similar in tumour spectra, age of onset and cumulative risk. These MSH6 families, despite their late age of onset, have a high lifetime risk of all Lynch syndrome-related cancers, significantly higher in women (89% by age 80) than in men (69%). The gender differences are in part explained by high endometrial (70%) and ovarian (33%) cancer risks added upon the high colorectal cancer risk (60%). The several occurrences of breast cancer are not due to the MSH6 mutations. These findings are of great importance for counselling, management and surveillance of families with MSH6 mutations.
PubMed ID
16283884 View in PubMed
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