Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the United States, little has been done to compare the cancer risk of elderly subjects, aged 65 and older, with that of younger subjects. Although the elderly constitute only 12% of the population, they are diagnosed with more than 50% of the cancers. The study consisted of 7,783 Japanese-American men, born from 1900-1919 and examined from 1965-1968. During 154,000 person-years of follow-up, 1,478 incident cases of cancer were identified. The incidence rate of cancer was high among the elderly (142.7 per 10,000 person-years) compared with younger subjects (48.2 per 10,000 person-years), yielding a significant (p < 0.05) rate ratio of 3.0. Of the site-specific cancers, prostate cancer showed the highest rate ratio of 7.0, followed by oral, stomach, lung, and colon cancer. In addition, the five-year age-specific rates for stomach and colon cancer rose directly with age. A similar pattern was also observed for lung and prostate cancer in men before age 80, but the rates declined thereafter. The findings from this study suggest that the reduction in risk for cancers of the prostate, oral cavity, stomach, lung, and colon must be viewed as a major goal for improving the public health in the elderly population.
Asia Pac J Public Health
PMID:Cancer in the elderly: a prospective study among Hawaiian Japanese men. 134 46

Antiandrogens are compounds able to block the effect of androgens directly on their target cells by inhibiting their binding to the androgen receptor (AR). Two chemical classes of antiandrogens are presently on the market or in clinical trials: steroids (cyproterone, megestrol acetates), and nonsteroids (flutamide, nilutamide). Steroid antiandrogens interact not only with AR but also with progestin and glucocorticoid receptors and thus give rise to progestin and glucocorticoid effects. By contrast, nonsteroid antiandrogens interact only with AR and are thus devoid of other hormonal or antihormonal activities. Nilutamide does not need to be transformed into an active metabolite, unlike flutamide, and interacts with dog, rat, and human prostate AR in vitro. Its kinetics lead to a prolonged interaction with AR in vivo after administration to rats. In prostate cancer treatment, it is necessary to combine an antiandrogen to surgical or chemical (estrogens, LH-RH agonists) castration to obtain a complete suppression of androgens. The antiandrogen will block specifically, at the target site, the trophic effect of adrenal androgens left intact by castration, and the secretion of which can only be suppressed by treatments (adrenalectomy, aminoglutethimide, ketoconazole) that also suppress corticoid synthesis. We have shown that nilutamide counteracts the trophic effect, on the prostate of castrated rats, of adrenal androgens administered continuously (minipumps) at circulating levels similar to those recorded in castrated men. Nilutamide will also impede the flare-up effect of the testosterone increase induced by LH-RH agonists at the beginning of treatment. We have shown in the rat treated with buserelin that the increase in prostate weight observed during the initial days of treatment by the LH-RH agonist can be inhibited by a combined treatment with nilutamide. This combined treatment "nilutamide plus castration" has been tested in an experimental androgen-dependent cancer model, the Shionogi tumor. The administration of nilutamide to mice, castrated twenty-four hours before the inoculation of tumor cells, delayed the appearance of tumors and reduced their number. Finally, the absence of androgen effect and the antiandrogen activity of the product were also demonstrated in human tumor cells in culture (T-47 D cells) transfected with the MMTV androgen-dependent promoter coupled with the CAT reporter gene.
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PMID:Pharmacology of antiandrogens and value of combining androgen suppression with antiandrogen therapy. 199 2

Three new potential biomarkers--PAC, PMA, and the 7E11-C5 glycoprotein--have been identified. All three have unique features that could augment current diagnostic and therapeutic modalities. Some of the important characteristics of these potential markers are summarized in Table 1. Further studies will be required to determine if any of them will provide clinical information beyond that provided by PSA and if they will have a significant impact on the management of patients with prostate cancer. The MAb 7E11-C5 (CYT-356), now in clinical trials, promises to offer new strategies for radioimmunodetection and radioimmunotherapy of prostate cancer.
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PMID:Biomolecular and clinical characteristics of PSA and other candidate prostate tumor markers. 750 67

One of the most frequent genetic abnormalities in prostate cancer is loss of the complete or part of the short arm of chromosome 8, indicating the localization of one or more tumor suppressor genes on this chromosomal arm. Using allelotyping, a frequently deleted region in prostate cancer in a genetic interval of approximately 17 cM between sequence tagged sites D8S87 and D8S133 at chromosome arm 8p12-21 was previously detected. A detailed physical map of this region is now available. Using known and novel polymorphic and nonpolymorphic sequence tagged sites in this interval, a search for homozygous deletions in DNAs from 14 prostate cancer-derived cell lines and xenografts was carried out. In DNA from xenograft PC133, the presence of a small homozygously deleted region of 730-1,320 kb was unambiguously established. At one site, the deletion disrupts the Werner syndrome gene. Data from allelotyping were confirmed and extended by fluorescence in situ hybridization analysis of PC133 chromosome spreads using centromere, YAC, and PAC chromosome 8 probes.
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PMID:Identification of a homozygous deletion at 8p12-21 in a human prostate cancer xenograft. 988 78

The beclin 1 (BECN1) gene encodes a 60-kDa coiled-coil protein that interacts with the prototypic apoptosis inhibitor Bcl-2. Previous studies indicate that beclin 1 maps to a region approximately 150 kb centromeric to BRCA1 on chromosome 17q21 that is commonly deleted in breast, ovarian, and prostate cancer. The complete cDNA sequence of beclin 1 encodes a 2098-bp transcript, with a 120-bp 5' UTR, 1353-bp coding region, and 625-bp 3' UTR. Hybridization screening of a human genomic PAC library identified PAC 452O8, which contains the complete beclin 1 gene. Determination of the exon-intron structure of beclin 1 reveals 12 exons, ranging from 61 to 794 bp, which extend over 12 kb of the human genome. FISH analysis of human breast carcinoma cell lines using PAC 452O8 as probe identified allelic beclin 1 deletions in 9 of 22 cell lines. Sequencing of genomic DNA from 10 of these cell lines revealed no mutations in coding regions or splice junctions. Additionally, Northern blot analysis of 11 cell lines did not identify any abnormalities in beclin 1 transcripts. These results indicate that human breast carcinoma cell lines frequently contain allelic deletions of beclin 1, but not beclin 1 coding mutations.
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PMID:Cloning and genomic organization of beclin 1, a candidate tumor suppressor gene on chromosome 17q21. 1039

A genomic interval of approximately 1-1.5 Mb centered at the MSR marker on 8p22 has emerged as a possible site for a tumor suppressor gene, based on high rates of allele loss and the presence of a homozygous deletion found in metastatic prostate cancer. The objective of this study was to prepare a bacterial contig of this interval, integrate the contig with radiation hybrid (RH) databases, and use these resources to identify transcription units that might represent the candidate tumor suppressor genes. Here we present a complete bacterial contig across the interval, which was assembled using 22 published and 17 newly originated STSs. The physical map provides twofold or greater coverage over much of the interval, including 17 BACs, 15 P1s, 2 cosmids, and 1 PAC clone. The position of the selected markers across the interval in relation to the other markers on the larger chromosomal scale was confirmed by RH mapping using the Stanford G3 RH panel. Transcribed units within the deletion region were identified by exon amplification, searching of the Human Transcript Map, placement of unmapped expressed sequence tags (ESTs) from the Radiation Hybrid Database (RHdb), and from other published sources, resulting in the isolation of six unique expressed sequences. The transcript map of the deletion interval now includes two known genes (MSR and N33) and six novel ESTs.
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PMID:High-resolution physical map and transcript identification of a prostate cancer deletion interval on 8p22. 1067 82

We conducted a review of previous cohort studies on the association between a history of diabetes mellitus (DM) and the occurrence of cancer. We limited the papers to those concerning cohort studies on 9 cancer sites, i.e. the kidney, liver, biliary tract, pancreas, colon or rectum, prostate, breast, endometrium, and ovary, in addition to all cancers. With regard to kidney, liver, biliary tract, pancreatic, colorectal, breast, and endometrial cancers, the risk of cancer development has been consistently reported to be positively associated with DM by two or more cohort studies. In contrast, DM was shown to relate negatively to the risk of prostate cancer by two cohort studies. However, there were no cohort studies which showed an either significantly positive or negative association of DM with ovarian cancer. Elevated levels of insulin or IGFs among DM patients have been proposed as a causal mechanism of increased risk for most of the reviewed cancers. In addition, increased estrogen levels in DM patients have been suggested to explain the casual mechanism of increased risk for kidney, breast and endometrial cancers, and decreased risk for prostate cancer. On the other hand, the possibility of detection bias has been suggested in the association of DM with the risk of most of these cancers. Obesity and heavy consumption of alcohol have been indicated as confounding factors in the relationship of DM to the risk for some of them. Thus, further studies are necessary for firm conclusions regarding the association of DM with cancer risk.
Asian Pac J Cancer Prev 2000
PMID:A Review of Cohort Studies on the Association Between History of Diabetes Mellitus and Occurrence of Cancer. 1271 99

1. In the present study, we describe the expression of the neuropeptides vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) as well as their receptors in PC-3 cells, a human prostate cancer cell line. In addition, we have investigated their role in apoptosis induced by serum starvation. 2. By RT-PCR and immunocytochemistry assays, we have demonstrated the production of VIP and PACAP in PC-3 cells. 3. We have demonstrated by RT-PCR and binding assays the expression of common PACAP/VIP (VPAC(1) and VPAC(2)) receptors, but not PACAP-specific (PAC(1)) receptors. The pharmacological profile of [(125)I]-VIP binding assays was as follows: VPAC(1) antagonist=VPAC(1) agonist>VIP>VPAC(2) agonist (IC(50)=1.2, 1.5, 2.3 and 30 nM, respectively). In addition, both receptor subtypes are functional since VIP, PACAP-27 or VPAC(1) and VPAC(2) agonists all increased the intracellular levels of cAMP. 4. The expression of both peptides and their receptors is similar in serum-cultured and serum-deprived PC-3 cells. The treatment of serum-deprived PC-3 cells with exogenous VIP or PACAP-27 increases cell number and viability in a dose-dependent manner, as demonstrated by cellular counting and MTT assays. The increased cell survival is exerted through the VPAC(1) receptor, since a VPAC(1), but not VPAC(2), receptor agonist, mimics the effects and a VPAC(1) receptor antagonist blocks it. Moreover, VIP and PACAP-27 inhibit genomic DNA fragmentation in PC-3 cells triggered by serum starvation, and increase the immunoreactivity of the antiapoptotic protein bcl-2. 5. Our results suggest that VIP and PACAP are autocrine/paracrine factors that protect PC-3 cells from apoptosis through VPAC1 receptors.
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PMID:VIP and PACAP are autocrine factors that protect the androgen-independent prostate cancer cell line PC-3 from apoptosis induced by serum withdrawal. 1283 80

The life-stage approach, which views the behaviours and exposures of an individual from the preconceptual situation of the parent through pregnancy, infancy, childhood and adolescence, and into the advancing years through adulthood, is the basis of analysis of strategies to improve long-term health. Among the behaviours of note is the dietary selection pattern, conditioning our exposure to nutrients and dietary constituents that influences growth, nutriture, cognitive and physical performance, and disease resistance and susceptibility. The African Diaspora created a population displaced from Africa to the Western Hemisphere as part of the African slave trade from the 16th to 18th centuries. It continues to manifest distinct dietary and lifestyle practices in the context of a health experience that is different both from the population in their African countries of origin and from the other ethnicities in their countries of displacement and current residence. Afro-Americans are more susceptible to a series of diseases and conditions including low birth weight, violence, and HIV/AIDS, as well as the non-communicable diseases: obesity, diabetes mellitus, cardiovascular disease, hypertension, stroke, renal failure, breast cancer, prostate cancer and lead poisoning. The differential nature of dietary practices are conditioned at times by the poverty and marginalisation of the populace, resulting in either disadvantageous or beneficial outcomes relative to others' eating habits. Serious consideration must be given to the possibility that ethnic difference give rise to different requirements and tolerances for essential nutrients and distinct protective or adverse responses to foods and dietary substances. The major challenges to health improvement for the African Diaspora is coming to grips with the policy and programmatic nuances of differential treatment and the effecting the behavioural changes that would be needed in a population skeptical of the motives of media and of the power elites of their societies.
Asia Pac J Clin Nutr 2003
PMID:Diet and long-term health: an African Diaspora perspective. 1450 96

In recent years medical ethics has become an undisputed part of medical studies. Many people believe that modern advances in medical technology - such as the development of dialysis machines, respirators, magnetic resonance imaging and genetic testing and types of cancer screenings - have created bioethical dilemmas that confront physicians in the 21st century. Debates over research and screening ethics have until recently revolved around two related questions: the voluntary, informed consent of subjects, and the appropriate relationship between risk and benefit to subjects. Every patient has a right to full and accurate information about his or her medical condition. This legal principle arose primarily through court decisions concerning informed consent, but over time physicians recognized that most patients prefer to learn the truth about their condition and use the information well. To screen is to search for disease in the absence of symptoms or, in other words, to attempt to find disease in someone not thought to have a disease. Examples of screening include routine mammography to detect breast cancer, routine pap smears to detect cervical cancer, and routine Prostate Specific Antigen (PSA) testing to detect prostate cancer. Ethical principles to be followed in cancer screening programmes are intended mainly to minimize unnecessary harm for the participating individuals. Numerous ethical questions can be raised about the practice of screening for disease. Here, we examine four leading cancer killers worldwide and we review the screening of protocols of these cancer types and their possible ethics.
Asian Pac J Cancer Prev
PMID:Ethical issues for cancer screening. 1472 98


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