Replication linkage study for prostate cancer susceptibility genes

Suarez, Brian K.; Lin, Jennifer; Witte, John S.; Conti, David V.; Resnick, Martin I.; Klein, Eric A.; Burmester, James K.; Vaske, D. A.; Banerjee, Tarit K.; Catàlona, William J.

doi:10.1002/1097-0045(20001001)45:2<106::aid-pros4>3.0.co;2-h

Cited by 33 publications

(13 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…45 However, independent analysis of families collected at Marshfield Clinic did support 16q as the location of a gene in familial prostate cancer (unpublished data). In contrast, other whole genome scans of affected patients did not provide evidence of a gene on 16q.…”

Section: Discussionmentioning

confidence: 95%

Genetics of Prostate Cancer

Zhang

Salzman²,

Reding³

et al. 2003

Clinical Medicine & Research

View full text Add to dashboard Cite

Prostate cancer is the most frequently diagnosed visceral cancer of men, responsible for approximately 40,000 deaths in adult males per year. To identify the genetic causes of prostate cancer, we performed a whole genome scan of affected sib pairs, using DNA markers spaced evenly across the human genome. We demonstrated that regions on chromosomes 1,4,5,7,8,11,16 and 19 might harbor genes that predispose individuals to prostate cancer and may affect tumor growth rate and tumor aggressiveness. Here we present DNA sequence analysis of KIAA 0872 and 17-β hydroxysteroid dehydrogenase that are located on chromosome 16 within the mapped region, and we demonstrate that neither of these genes carries mutations in the protein coding region or their splice junction sites. These results suggest that these genes are less likely to be associated with the cause of familial prostate cancer. INTRODUCTIONProstate cancer is the second leading cause of cancer mortality for men in the U.S. with a rate of 26 deaths per 100,000. 1 Although prostate cancer is potentially curable in its early stages, treatment of advanced hormone-refractory prostate cancer is ineffective, making early detection and treatment of disease a necessity. 2 Unfortunately, approximately 30% of men with prostate cancer have tumor that has spread beyond the prostate gland at the time of diagnosis. Despite the impressive response of metastases to androgen hormone deprivation, the survival rate is dismal, with greater than 90% of these patients dying from their cancer. 3 Screening tests for prostate cancer include digital rectal examination, transrectal ultrasonography, and measurement of prostate-specific antigen. However, these tests often do not detect the tumors before they have spread. The development of additional tests for earlier identification of prostate tumors will be extremely important. 4,5

show abstract

Section: Discussionmentioning

confidence: 95%

Genetics of Prostate Cancer

Zhang

Salzman²,

Reding³

et al. 2003

Clinical Medicine & Research

View full text Add to dashboard Cite

show abstract

“…Several different deletion mutations have been detected in one of the Magmas alleles in prostate adenocarcinoma samples (Short and Jubinsky, unpublished data). While linkage analysis suggests that the entire arm of 16p could be involved in an increased susceptibility (Suarez et al 2000), there are no reports describing chromosomal translocations involving 16p13.3 in prostate cancer.…”

Section: Discussionmentioning

confidence: 99%

Magmas expression in neoplastic human prostate

et al. 2005

View full text Add to dashboard Cite

Magmas, is a 13-kDa mitochondrial protein which is ubiquitously expressed in eukaryotic cells. It was identified as a granulocyte-macrophage-colony stimulating factor (GM-CSF) inducible gene in hematopoietic cells and has a key role in the transport of mitochondrial proteins in yeast. Because GM-CSF receptor levels are elevated in prostate cancer, Magmas expression was examined in normal and neoplastic tissue. Magmas protein levels were barely detectable in non-neoplastic prostate glands. Increased amounts were observed in some samples of intraepithelial neoplasia. Approximately one half of the adenocarcinoma samples examined had weak Magmas expression, while the remainder had intermediate to high levels. The increased Magmas observed in malignant tissue was a result of higher protein expression and not from changes in mitochondrial content. Interestingly, in some patients, the normal prostate tissue had more Magmas message than the malignant portion. The results indicated that Magmas expression in prostate cancer is heterogeneous and independent of clinical stage and Gleason score. Further studies are needed to determine if Magmas expression has prognostic significance in prostate cancer.

show abstract

“…Because genetic heterogeneity not only reduces power, but can also result in failure to replicate reported linkages, 23 analysis was limited to the forty-two families reporting Caucasian ancestry.…”

Section: Methodsmentioning

confidence: 99%

Linkage analysis of chromosome 4 in families with familial pancreatic cancer

Klein

Andrade

Hruban

et al. 2007

Cancer Biology & Therapy

View full text Add to dashboard Cite

Background: Approximately 10% of pancreatic ductal adenocarcinomas have a familial basis. While a small portion of this familial clustering can be explained by inherited mutations in known genes (BRCA2, p16/CDKN2A, PRSS1, and STK11), the genetic basis for the majority of this familial clustering remains unknown. In addition, a pancreatic cancer susceptibility locus has been reported to be linked to chromosome 4q32-34 in a single family having a high penetrance of early-onset pancreatic ductal adenocarcinoma and pancreatic insufficiency. The goal of this study is to determine if linkage to chromosome 4q exists in our series of well-characterized families with idiopathic familial pancreatic cancer enrolled in the Pancreatic Cancer Genetic Epidemiology Consortium (PACGENE).Methods: Parametric and nonparametric linkage analyses were performed using 21 microsatellite markers on chromosome 4 on affected individuals with pancreatic cancer from 42 familial pancreatic cancer kindreds.Results: Markov Chain Monte Carlo parametric and nonparametric linkage analyses using SIMWALK2 as well as nonparametric linkage analysis using MERLIN did not provide strong evidence of linkage in this region (LOD < 1.0). Only one family provided a multipoint LOD score of >0.5 adjacent to the reported region.Conclusions: Our results do not support linkage to the 4q32-34 region in the majority of our familial pancreatic cancer kindreds. However, because multiple pancreatic cancer susceptibility genes are likely to exist, it is possible that a subset of the families in this study may be linked to this region.

show abstract

Replication linkage study for prostate cancer susceptibility genes

Cited by 33 publications

References 24 publications

Genetics of Prostate Cancer

Genetics of Prostate Cancer

Magmas expression in neoplastic human prostate

Linkage analysis of chromosome 4 in families with familial pancreatic cancer

Contact Info

Product

Resources

About