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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Migrant studies and studies examining the international variation of "latent" and clinical prostatic cancer imply that environmental factors play a prominent role in prostatic carcinogenesis. A strong familial tendency has been identified, but to what extent this is an effect of genetic factors has not been established. Hormones probably play an important role in the development of prostatic cancer, but it is not clear which hormones are critically involved, how they act and how they are influenced by genetic and environmental factors. The significance of sexual and occupational factors, benign prostatic hyperplasia and a history of vasectomy is also unclear. Overall, little is known about the factors responsible for the development of prostatic cancer and its progression to a clinically manifest form. Further understanding of the etiopathogenesis of prostate cancer could give rise to programmes for prevention and improve our ability to predict the behaviour of the individual tumour.
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PMID:[Risk factors of prostatic cancer]. 806 64

Because alcohol influences metabolism and serum levels of sex hormones and specifically increases metabolic clearance of testosterone, some role of alcohol consumption in the process of prostatic carcinogenesis is biologically plausible. The relationship between prostate cancer and total alcohol consumption was therefore investigated in a case-control study conducted in Northern Italy between 1985 and 1992 on 281 cases and 599 controls admitted to hospital for acute nonneoplastic diseases apparently unrelated to alcohol and tobacco consumption. No noteworthy relationship was found for major measures of alcohol intake: compared with teetotallers, the multivariate relative risks (RRs) of prostate cancer, after adjustment for age, study center, education, marital status, body mass index, and smoking status, were 1.3, 0.9, 1.2, and 1.1, respectively, for men drinking fewer than three, three to less than five, five to less than eight, or more than eight alcoholic beverages per day. None of the estimates was significant, nor was the trend in risk significant. Multivariate risks were also close to unity in the separate analysis of intake of wine (RR = 1.2 and 0.9 for < 5 and or = 5 drinks/day, respectively, compared with wine abstainers), beer (RR = 1.1 for beer drinkers compared with beer abstainers), and spirit (RR = 0.8 for spirit intake compared with beer abstainers). No relationship was observed with duration of use (< 40 and > or = 40 yrs, multivariate RRs = 1.1 and 1.3, respectively), and the alcohol-related risk estimates were similar for men < 70 and > or = 70 years of age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alcohol consumption and risk of prostate cancer. 818 20

DNA polymerase beta is a nuclear protein essential to DNA repair in mammalian cells. A high frequency of mutations in this gene has been reported in colorectal cancers. To clarify the tumorigenesis steps of human prostate cancers in the molecular basis, we examined the entire coding region of the human DNA polymerase beta gene in human prostate cancer tissues using polymerase chain reaction, single-strand conformational polymorphism analysis of RNA, and sequencing analysis. Consequently, we detected DNA polymerase beta gene mutations in 2 of 12 cases (17%). The first case is an A to G transition at nucleotide 893, resulting in a substitution of the amino acid from tyrosine to cysteine. In the second case, we found an A to G transition at nucleotide 305, a T deletion at nucleotide 569, and an A insertion into the 6 repeats of A from nucleotide 612 to 617. This T deletion shifted the subsequent reading frame and resulted in the premature termination at codon 163 instead of 336. The two cases were advanced grade and stage. Present results suggest that polymerase beta gene mutations, although they occurred at relatively low frequency, are involved in certain cases of human prostate carcinogenesis.
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PMID:DNA polymerase beta gene mutation in human prostate cancer. 818 60

While a general appreciation for the importance of chromosomes in the development of cancer has existed for decades, molecular genetic analyses have gained considerable attention in recent years through identification of proto-oncogenes and tumor suppressor genes. Several different chromosomal aberrations, alterations of proto-oncogenes and suppressor genes have been described in prostate cancer. Loss of genetic material has been found to occur most frequently on chromosomes 7, 8, 10 and 16. The existence of tumor suppressor genes relevant to prostate carcinogenesis is suspected in these chromosomal locations. Several investigators are currently trying to identify these genes. Altered expression of several different oncogenes has been reported in prostate cancer. Among these, the ras- and myc-families of oncogenes have been studied most intensively. Structural oncogene alterations have been detected infrequently, most of the changes appear to occur transcriptionally. Despite an abundance of clinical material, knowledge about genetic lesions in prostate cancer is still very limited and sometimes conflicting results have been reported. With recent methodologic improvements and a growing interest in correlating genetic alterations with clinical disease progression, definition of prostate carcinogenesis at the molecular level will advance rapidly in the near future.
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PMID:Basic research in prostate cancer: molecular biology. 819 25

Prostatic intraepithelial neoplasia (PIN) is regarded as the most important premalignant lesion of prostatic epithelium. The aim of this investigation was to find clues to formal pathogenesis of prostatic cancer. For this purpose DNA ploidy (determined by means of image cytometry [ICM] using 4-microns-thick Feulgen-stained paraffin sections) of PIN and invasive carcinoma was compared. Prostatic tissue of 72 patients (mean age, 67.5 years; 82 areas with carcinoma and 71 areas with PIN) was examined. In 44 cases PIN and carcinoma were coexistent in the same prostates, the PIN grade being high in 77% of these cases (P < .05). In higher-grade PIN and higher-grade carcinoma the c-values, 2.5c-exceeding-rate, and aneuploidy rate increased (P < .01). Carcinomas associated with diploid PIN (either low or high grade) showed diploidy and aneuploidy in an equal number of cases, whereas 70% of aneuploid PIN cases (all high grade) were associated with aneuploid invasive carcinomas (P < .01). Conversely, in 71% of the cases with aneuploid carcinoma the coexistent PIN (either low or high grade) was diploid. Our findings show that aneuploidy can be acquired at a preinvasive stage of carcinogenesis in the prostate and suggest that aneuploid high-grade PIN might be regarded as a precursor of some but not all aneuploid prostatic carcinomas. Image cytometry analysis seems to be a promising method for further subclassification of high-grade PIN lesions into groups with putatively lower or higher risk. However, further investigation is necessary to confirm the clinical importance of these results.
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PMID:Comparison of DNA ploidy in prostatic intraepithelial neoplasia and invasive carcinoma of the prostate: an image cytometric study. 820 Jun 45

The introduction of normal chromosomes into tumor cells by microcell fusion-mediated transfer is a powerful technique to identify putative tumor suppressor genes. We have used this approach to independently transfer human chromosomes 3 and 12 into a human prostate cancer cell line, DU 145. We showed that while the extra copy of chromosome 3 had no effect on the in vivo tumorigenicity of these cells, microcell hybrids containing an introduced portion of chromosome 12 (12pter-12q13) exhibited complete suppression of tumorigenicity in athymic nude mice. The presence of a dual selectable marker facilitated the selection for cells having segregated del(12)(q13). Loss of this fragment in three different clones led to reexpression of the malignant phenotype. These results demonstrate that one or more genes on human chromosome 12 function as tumor suppressors of prostate carcinogenesis.
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PMID:Suppression of tumorigenicity of human prostate cancer cells by introduction of human chromosome del(12)(q13). 820 20

Transgenic model systems provide tools for obtaining information that clarifies important relationships between genetic alterations and carcinogenesis. One such relationship is the induction of specific growth factor activities by dominantly acting oncogenes. Using a "transgenic organ" model referred to as mouse prostate reconstitution (MPR) under conditions where the ras and myc oncogenes were introduced using a recombinant retrovirus into both the mesenchymal and epithelial compartments of the urogenital sinus, poorly differentiated prostate cancer (PC) was produced with high frequency (> 90%) in inbred C57BL/6 mice. Time-course studies using northern blotting and immunohistochemical analysis showed that the transition from benign to malignant status invariably was associated with the induction of elevated transforming growth factor-beta 1 (TGF-beta 1) expression. Additional immunohistochemical analysis of TGF-beta 1 in human PC and benign prostatic hyperplasia (BPH) showed that positive extracellular staining was significantly more extensive in PC compared with BPH. This differential staining pattern was evident in focal areas of PC adjacent to BPH. These findings in both the MPR model system and human PC suggest that elevated TGF-beta 1 expression is involved in the progression to malignancy and that its pattern of expression may become a useful marker of PC. Additional studies using transgenic animal models will continue to provide important clinically useful information about PC in man.
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PMID:Transgenic models for the study of prostate cancer. 842 40

Physical activity potentially encourages a healthy lifestyle and it could have a more direct preventive effect on certain forms of carcinogenesis (for instance, by speeding gastrointestinal transit, or by moderating sex hormone levels). However, there are also potential negative effects, particularly an excessive exposure to ultraviolet light in certain water sports. The many types of neoplasm and the equally varied sources of physical activity militate against finding any simple relationship between the risk of malignancy and the individual's physical activity history. Nevertheless, evidence that physical activity protects against certain forms of cancer can be deduced from studies of experimental animals, former athletes, people employed in active occupations, and those with an active recreational lifestyle. Many occupational surveys and a number of studies of recreational activity show an association between sedentary living and a risk of colon cancer, both in men and in women. Moreover, an application of Bradford Hill's criteria gives some support to the causal nature of the association. More limited data suggest that a history of active leisure is associated with a reduced risk of all-cause cancer and in women of breast and reproductive system cancers. The last observation must still be reconciled with an apparent increase in the risk of prostatic cancer in active men. Since moderate exercise elevates mood and helps to conserve lean tissue, it may finally be a helpful component of treatment after a neoplasm has been diagnosed.
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PMID:Exercise in the prevention and treatment of cancer. An update. 846 Feb 89

Hormones play a major role in the aetiology of several of the commonest cancers worldwide, including cancers of the endometrium, breast and ovary in women and cancer of the prostate in men. It is likely that the main mechanisms by which hormones affect cancer risk are by controlling the rate of cell division, the differentiation of cells and the number of susceptible cells. Hormones have very marked effects on cell division in the endometrium; oestrogens stimulate mitosis whereas progestins oppose this effect. The risk for endometrial cancer increases with late menopause, oestrogen replacement therapy and obesity, and decreases with parity and oral contraceptive use; thus risk increases in proportion to the duration of exposure to oestrogens unopposed by progestins, probably because unopposed oestrogens stimulate endometrial cell division. The effects of hormones on breast epithelial cell division in non-pregnant women are much less clear-cut than their effects on the endometrium, but both oestrogens and progestins appear to stimulate mitosis. Breast cancer risk increases with early menarche, late menopause and oestrogen replacement therapy, probably due to increased exposure of the breasts to oestrogen and/or progesterone. Early first pregnancy and multiparity reduce the risk for breast cancer, probably due to the hormonally-induced differentiation of breast cells and the corresponding reduction in the number of susceptible cells. Hormones do not have marked direct effects on the epithelial cells covering the ovaries, but hormones stimulate ovulation which is followed by cell division during repair of the epithelium. Risk for ovarian cancer increases with late menopause and decreases with parity and oral contraceptive use, suggesting that the lifetime number of ovulations may be a determinant of risk. For all three of these cancers risk changes within a few years of changes in exposure to sex hormones and some of the changes in risk persist for many years, indicating that hormones can affect both early and late stages of carcinogenesis. Understanding of the role of sex hormones in the aetiology of prostate cancer and of some rarer cancers is less complete.
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PMID:Hormones and cancer in humans. 853 37

Despite the clinical relevance of prostate cancer, few aspects regarding the molecular alterations involved in the process of prostate carcinogenesis are clearly understood. Cytogenetic and molecular genetic studies have identified specific abnormalities in prostate tumors, mainly on chromosomes 8, 10 and 16. On the basis of these findings, we designed a study to further characterize the altered regions on chromosome 10, using 15 microsatellite markers on a population composed of 20 paired normal and primary non-metastatic prostatic-tumor samples. Overall, 65% (13/20) of the cases analyzed showed molecular alterations, mainly rearrangements and deletions. The locus presenting the highest rate of abnormalities was D1OS221, which maps to 10q23-q24. Another region with frequent alterations was 10q21, at the DIOS109 locus. There was no statistical association between microsatellite abnormalities and Gleason grade or tumor stage in the prostate cancer cases studied. These results suggest that microsatellite alterations on the long arm of chromosome 10 are non-random events occurring in prostate cancer and that they may play a role in the process of tumorigenesis in these neoplasms.
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PMID:Microsatellite instability and deletion analysis of chromosome 10 in human prostate cancer. 860 77


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