PROSTATE CANCER

Overview:

Screening for prostate carcinoma:

  • Screening for prostate carcinoma: Unlike breast cancer screening, which has been shown to reduce mortality, prostate cancer screening has not yet been evaluated and there are several reasons why it may be less effective. Many men with prostate cancer never experience any ill effects because some tumours are slow growing and not aggressive. The most sensitive screening tests for prostate cancer are based on levels of prostate specific antigen (PSA). However, the PSA test and follow up biopsies cannot predict reliably whether a man has a cancer that will progress to cause ill health or death. This article concludes that evidence from randomised controlled trials of prostate cancer screening using PSA (or similar tests) and treatment are needed before consideration is given to funding prostate screening - http://www.york.ac.uk/inst/crd/pdf/em22.pdf
  • Detection of Subclinical Cancers by Prostate-specific Antigen Screening in Asymptomatic Men from High-Risk Prostate Cancer Families: This study suggests that prostate cancer development in genetically predisposed individuals is preceded by a subclinical period when PSA detection is possible and thus serum PSA screening may be particularly useful in men with a family history of early-onset prostate cancer - http://clincancerres.aacrjournals.org/cgi/content/abstract/5/6/1275?ijkey=7d63a298871f3a77486ab4153f7ce14edc562fdb&keytype2=tf_ipsecsha

Genetics of Carcinoma Prostate:

  • Molecular Genetics and Epidemiology of Prostate Carcinoma: This commentary has reviewed a series of genetic and phenotypic alterations that are potentially involved in prostate carcinogenesis. Using this information one might ultimately be able to construct a risk profile based on a combination of several genetic and phenotypic alterations. With such a risk profile, it might be possible to discriminate men whose disease will remain clinically controlled from those who will develop life-threatening PCa. Moreover, one might ultimately be able to design therapeutic approaches other than empirically based - http://edrv.endojournals.org/cgi/content/full/20/1/22
  • Combined Analysis of Hereditary Prostate Cancer Linkage to 1q24-25: Results from 772 Hereditary Prostate Cancer Families from the International Consortium for Prostate Cancer Genetics: The present study describes a combined analysis for six markers in the 1q24-25 region in 772 families affected by hereditary prostate cancer and ascertained by the members of the International Consortium for Prostate Cancer Genetics (ICPCG) from North America, Australia, Finland, Norway, Sweden, and the United Kingdom. The results of this study support the finding of a prostate cancer–susceptibility gene linked to 1q24-25, albeit in a defined subset of prostate cancer families. It suggests that although HPC1 accounts for only small proportion of all families affected by hereditary prostate cancer, it appears to play a more prominent role in the subset of families with several members affected at an early age and with male-to-male disease transmission - http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=10712209
  • Genetic and chromosomal alterations in prostatic intraepithelial neoplasia and carcinoma detected by fluorescence in situ hybridization: Fluorescence in situ hybridization (FISH) is a useful technique to determine genetic relationships between cancer and its precursors. Prostatic intraepithelial neoplasia PIN and prostatic carcinoma foci have a similar proportion of genetic alterations, suggesting that PIN is often a precursor of prostatic carcinoma. Genes on chromosomes 7, 8, 10, 16 and 18 may play an important role in both initiation and progression of prostatic carcinoma - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10325509&dopt=Abstract
  • Molecular genetics of prostate cancer: Much research has been dedicated to identifying prognostic markers that distinguish indolent versus aggressive forms of prostate cancer. In contrast, significantly less research has been devoted to understanding the molecular mechanisms that underlie normal prostate growth and development or cancer initiation and progression. In this review, the authors have addressed recent progress toward the central objectives of understanding parameters of normal versus abnormal prostatic development and of elucidating a molecular pathway for prostate cancer progression. Moreover, its being tried to focus on key regulatory molecules that have been implicated by analysis of patterns of allelic loss in human prostate cancers and/or by reverse genetic approaches in the mouse - http://www.genesdev.org/cgi/content/full/14/19/2410
  • Genetics of Prostate Cancer - National Cancer Institute: There are marked differences in international prostate cancer incidence and mortality. These differences may be due to genetic, environmental, and social influences (such as access to health care), which affect the development and progression of the disease. A genetic contribution to prostate cancer risk has been documented, but knowledge of the molecular genetics of prostate cancer is still limited. Malignant transformation of prostate epithelial cells, and progression of prostate carcinoma are likely to result from a complex series of initial and promotional events under both genetic and environmental influences - http://jncicancerspectrum.oxfordjournals.org/cgi/pdq/jncipdq;CDR00002
  • Risk of prostate cancer and family history of cancer: a population-based study in China: This study evaluated prostate cancer risk and family history of cancers using data from a case−control study in China. The results of this study did not confirm the familial tendency toward prostate cancer but other cancers prevalent in China appeared to be aggregate, particularly oesophageal cancer. Larger studies are needed to confirm these findings, and to clarify the genetic and lifestyle factors that may be involved - http://www.nature.com/pcan/journal/v8/n1/full/4500775a.html
  • Major Susceptibility Locus for Prostate Cancer on Chromosome 1 Suggested by a Genome-Wide Search: A genome-wide scan performed in 66 high-risk prostate cancer families has provided evidence of linkage to the long arm of chromosome 1 (1q24-25). Analysis of an additional set of 25 North American and Swedish families with markers in this region resulted in significant evidence of linkage in the combined set of 91 families. The data provide strong evidence of a major prostate cancer susceptibility locus on chromosome 1 - http://www.sciencemag.org/cgi/content/full/274/5291/1371?ijkey=10915d506c45a6ac9adc3a493192512b8def71a1
  • Evidence for a prostate cancer susceptibility locus on the X chromosome: This study presents evidence for the location of a prostate cancer susceptibility gene, which by heterogeneity estimates accounts for approximately 16% of hereditary prostate cancer (HPC) cases. This HPC locus resides on the X chromosome (Xq27-28), a finding consistent with results of previous population-based studies suggesting an X-linked mode of HPC inheritance. Genetic mapping of the locus represents an important initial step in the identification of an X-linked gene implicated in the aetiology of HPC - http://www.nature.com/ng/journal/v20/n2/full/ng1098_175.html

Epidemiology of Prostate Cancer:

  • The complex genetic epidemiology of prostate cancer:  The search for prostate cancer susceptibility genes by linkage studies offered early hope that finding genes would be as ‘easy’ as finding genes for breast cancer and colon cancer susceptibilities. However, this hope has been dampened by the difficulty of replicating promising regions of linkage. This review provides updates on recent developments, and a broad view of the disparate findings from different linkage studies. Up to now, a total of 10 genome-wide linkage scans for prostate cancer susceptibility have been completed, and are reviewed - http://hmg.oxfordjournals.org/cgi/content/full/13/suppl_1/R103
  • A Genetic Epidemiological Study of Hereditary Prostate Cancer (HPC) in Finland: Frequent HPCX Linkage in Families with Late-onset Disease: Several predisposition loci for hereditary prostate cancer (HPC) have been suggested, including HPC1 at 1q24-q25 (OMIM #601518) and HPCX at Xq27-q28 (OMIM #300147). Genetically homogeneous populations, such as that of Finland, and distinct subsets of families may help to minimize the genetic heterogeneity that complicates the genetic dissection of complex traits. Here, the role of the HPC1 and HPCX loci in a series of Finnish prostate cancer families was studied, especially in subgroups of families defined by age, number of affected cases, and the mode of disease transmission. This study suggests that the HPCX-linked prostate cancer families represent a distinct subgroup characterized by NMM transmission of disease and late age of diagnosis - http://clincancerres.aacrjournals.org/cgi/content/full/6/12/4810
  • Epidemiology of Prostate Cancer: It is estimated that 29,900 men in the US will die secondary to prostate cancer in 2004. Incidence of prostate cancer is highest in the US, Canada, and Scandinavia, and lowest in China and Asian countries. This variation could be due to different genetic predisposition, differences in diet, variation in quality of healthcare, and deficiencies in cancer registration; or it could be due to the multiple factors previously mentioned - http://www.touchbriefings.com/pdf/1322/Crawford.pdf
  • Prostate cancer epidemiology: With newly available molecular tools, a new generation of large-scale multidisciplinary population based studies is beginning to investigate gene-gene and gene-environment interactions. Results of these studies may lead to better detection, treatment, and, ultimately, prevention of prostate cancer -http://dceg.cancer.gov/pdfs/hsing1113882006.pdf

Statistics:

Measures:

Clinical:

  • American Urological Association Urinary Symptom Index: This index asks eight questions that take just a couple of minutes to answer. Outside the United States, this questionnaire is called the International Prostate Symptom Score (IPSS). This questionnaire is designed to help determine the severity of urinary symptoms - http://www.mayoclinic.com/health/prostate-symptoms/MC00046_D1
  • Online Enlarged Prostate Health Assessment: This online assessment helps a person determine that whether at all he has symptoms suggestive of enlarged prostate and if so, should he report to the doctor or not -  http://www.realage.com/health_guides/bph/introduction.asp?memberId=&cbr=

Imaging Studies:

  • National Kidney and Urological Diseases Information Clearinghouse (NKUDIC) - Medical Tests for Prostate Problems - http://kidney.niddk.nih.gov/kudiseases/pubs/medtestprostate/
  • Carcinoma prostate - radiology: In this article a comprehensive account of carcinoma prostate with particular emphasis on the radiological investigations done in the diagnostic work-up of a carcinoma prostate case - http://www.emedicine.com/radio/topic574.htm
  • Transrectal ultrasonography (TRUS) for evaluation of various benign and malignant prostatic lesions and their histopathological correlation: Various methods are available for sonographic evaluation of prostate but transrectal ultrasonography (TRUS) has received increasing attention recently because of its potential for early detection of prostate cancer. It provides greater detail of zonal anatomy of prostate and echo pattern of the gland and its various lesion. The objective of this study was to study the transrectal ultrasonographic findings in benign and malignant prostatic lesions with respect to its site, echopattern, capsular status, local invasion and their histopathological correlation. The study concluded that the characterization of the zonal involvement of the gland, echopattern, capsular status and adjacent organ invasion was much better by TRUS as compared to transabdominal sonography - http://www.ijri.org/articles/ARCHIVES/2004-14-2/gastro_Imaging-155.htm
  • High-intensity focused ultrasound for prostate cancer - NICE guidance: Current evidence on the safety and efficacy of high-intensity focused ultrasound (HIFU), as measured by reduction in prostate-specific antigen (PSA) levels and biopsy findings, appears adequate to support the use of this procedure for the treatment of prostate cancer provided that the normal arrangements are in place for consent, audit and clinical governance - http://www.nice.org.uk/pdf/ip/IPG118guidance.pdf
  • American College of Radiology - Ultrasound of the Prostate: http://www.radiologyinfo.org/content/us-prostate.htm

Lab Tests:

Tumour Markers:

Prostatic Biopsy:

  • Repeat prostate biopsy: who, how and when - a review: In this review article, the authors have evaluated the current knowledge on repeat prostate biopsies, focusing on when to perform them and in which patients, how many samples to take, where to direct the biopsies and what morbidity should be expected - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12160578&dopt=Abstract
  • Gleason score: A Gleason score is given to prostate cancer based upon its microscopic appearance.
  • Combination of prostate-specific antigen, clinical stage, and Gleason score to predict pathological stage of localized prostate cancer. A multi-institutional update: The objective of this study was to combine the clinical data from 3 academic institutions that serve as centres of excellence for the surgical treatment of clinically localized prostate cancer and develop a multi-institutional model combining serum prostate-specific antigen (PSA) level, clinical stage, and Gleason score to predict pathological stage for men with clinically localized prostate cancer. The study concluded that the nomograms given in this study will enable patients and physicians to make more informed treatment decisions based on the probability of a pathological stage, as well as risk tolerance and the values they place on various potential outcomes - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9145716&dopt=Abstract

 Questionnaire:


Document Provenance and History

Document Author: Dr. Fazal Danish

Document Created: 30th March 2006

Document Edits:

 


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