Hereditary Prostate Cancer

Damber, Jan‐Erik

doi:10.1080/00365599950510012-1

Cited by 6 publications

(4 citation statements)

References 38 publications

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“…Presently, several candidate chromosomal loci potentially linked to familial prostate cancer have not borne up to detailed scrutiny (Damber, 1999;Ostrander and Stanford, 2000;Witte et al, 2000;Ahman et al, 2001;Elo and Visakorpi, 2001). An X-chromosome linked locus is one of several being actively pursued (Monroe et al, 1995;Karayi et al, 2000;Hemminki et al, 2001;Peters et al, 2001).…”

Section: Methodologies To Identify Candidate Metastasis and Progressimentioning

confidence: 99%

Molecular markers and determinants of prostate cancer metastasis

Gopalkrishnan

Kang

Fisher

2001

Journal Cellular Physiology

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Although intensely studied, the molecular and biochemical determinants of prostate cancer development and progression remain ill-de®ned. Moreover, current markers and methodologies cannot distinguish between a tumor that will remain indolent and not impinge on patient survival, versus a tumor with aggressive traits culminating in metastatic spread and death. Once prostate cancer is con®rmed the most signi®cant threat to a patient's survival and quality of life involves tumor metastasis. Radical surgery notwithstanding, prostate cancer accounts for 10% of all cancer-related deaths primarily arising through development of metastasis. Metastasis markers demonstrating an acceptable level of reliability are an obvious necessity if disproportionate and costly treatment is to be avoided and a reasonably accurate determination of clinical prognosis and measure of successful response to treatment is to be made. Therapeutic strategies that speci®cally inhibit metastatic spread are not presently possible and may not become available in the immediate future. This is because, while localized tumorigenesis has been relatively amenable to detection, analysis and treatment, metastasis remains a relatively unde®ned, complex and underexplored area of prostate cancer research. New ®ndings in the ®eld such subclasses of genes called metastasis suppressors and cancer progression suppressors, have opened up exciting avenues of investigation. We review current methodological approaches, model experimental systems and genes presently known or having potential involvement in human prostate cancer metastasis.

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Section: Methodologies To Identify Candidate Metastasis and Progressimentioning

confidence: 99%

Molecular markers and determinants of prostate cancer metastasis

Gopalkrishnan

Kang

Fisher

2001

Journal Cellular Physiology

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“…For these reasons, DRNAi can be used to screen the functional significance of human novel genes with no known function as identified by the Human Genome Project. For example, recent studies suggested that prostate cancer may be associated with loci in chromosome 1 (1q24-25) and X-chromosome (Xq27-28) [23]; a systemic silencing of the function of genes in 1q24-25 and Xq27-28 as identified by the Human Genome Project can be performed by D-RNAi which may result in the function of genes of interest. Furthermore, because the knockout of an important gene is usually lethal to transgenic mice, the D-RNAi may provide an alternative tool for gene function research in animals other than transgenic mice both locally or systematically.…”

Section: The In Vivo Silencing Effects Of D-rnaimentioning

confidence: 99%

D-RNAi (Messenger RNA-antisense DNA Interference) as a Novel Defense System Against Cancer and Viral Infections.

Lin¹,

Ying²

2001

CCDT

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D-RNAi (Messenger RNA-antisense DNA interference), a novel posttranscriptional phenomenon of silencing gene expression by transfection of mRNA-aDNA hybrids, was originally observed in the effects of bcl-2 on phorbol ester-induced apoptosis in human prostate cancer LNCaP cells. This phenomenon was also demonstrated in chicken embryos and a human CD4 + T cell line, H9. The in vivo transduction of β-catenin DRNAi was shown to knock out more than 99% endogenous β-catenin gene expression, while the in cell transfection of HIV-1 D-RNAi homolog rejected viral gene replication completely. D-RNAi was found to have long-term gene knockout effects resulting from a posttranscriptional gene silencing mechanism that may involve the homologous recombination between intracellular mRNA and the mRNA components of a D-RNAi construct. These findings provide a potential intracellular defense system against cancer and viral infections.

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“…The cytochrome P450 1B1 protein is a monooxygenase catalyzing 4-hydroxylation of 17b-estradiol into 4-OH catechol estrogen, which can be converted into either 4-catecholestrogen semiquinone or 4-catecholestrogen quinone. These reactive metabolites bind purines in DNA, which results in the formation of abasic sites and prostate carcinogenesis (Shimada et al, 1996;Tang et al, 1996;Hasler et al, 1999;McLellan et al, 2000;Spink et al, 2000;Guntupalli et al, 2007) To date, six polymorphisms of the CYP1B1 gene have been described, of which four result in amino acid substitutions (at codon 48C-T, 119G-T, 432C-G, and 453A-G) (Damber, 1999;Aklillu et al, 2002;Saintot et al, 2004). The variant A119S causes hyperactivation of the CYP1B1 gene.…”

Section: Introductionmentioning

confidence: 99%

Frequency of CYP1B1 homozygous genotype 355T/T in prostate cancer families from Poland

Schab

Janiszewska²,

Jarzemski³

et al. 2010

European Journal of Cancer Prevention

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A group of 98 families were analyzed for CYP1B1 gene 355T/T homozygous genotype frequency because of prostate cancer history. Molecular investigations were performed using the restriction fragment length polymorphism-PCR method. 355T/T genotype was detected in 14 of the 98 prostate cancer patients (14.3%). Among them, it was found in one man (7.1%) from a family suspected of hereditary prostate cancer (his age at prostate cancer diagnosis was 57 years) and in 13 men (92.9%) originating from families that did not strictly fulfill hereditary prostate cancer criteria (the median age at prostate cancer diagnosis was 60.1 years). Among 14 355T/T genotype-positive families, in 10 (71.4%) other types of cancers, for example, breast, uterus, stomach, colon, ovary, lung, larynx, bladder, pancreas and melanoma other than prostate cancer, were present, and in four (28.6%) only one cancer type, that is, prostate cancer, occurred. In the Polish population, the CYP1B1 355T/T genotype seems to be associated with prostate cancer; the frequency of this genotype was 5.9% higher in prostate cancer patients than in the general population (8.4%). However, it is not associated with prostate cancer family history.

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Hereditary Prostate Cancer

Cited by 6 publications

References 38 publications

Molecular markers and determinants of prostate cancer metastasis

Molecular markers and determinants of prostate cancer metastasis

D-RNAi (Messenger RNA-antisense DNA Interference) as a Novel Defense System Against Cancer and Viral Infections.

Frequency of CYP1B1 homozygous genotype 355T/T in prostate cancer families from Poland

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