Linkage analysis of prostate cancer susceptibility: confirmation of linkage at 8p22–23

Wiklund, Fredrik; Jonsson, Bengt‐Gunnar; Göransson, Ingela; Bergh, Anders; Grönberg, Henrik

doi:10.1007/s00439-003-0916-6

Cited by 40 publications

(8 citation statements)

References 26 publications

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“…However other than a replication by the group describing the initial results on chromosome 20, none of these peaks coincided precisely with any of the previously reported linkage peaks. The most promising were the results on chromosome 19 by Wiklund et al (24) which is close to the peak on chromosome 19 originally reported by reported by Hsieh et al (27).…”

Section: Loci Mapped To Datesupporting

confidence: 75%

Prostate Cancer Susceptibility Loci: Finding the Genes

Ostrander

Johannesson²

2008

Hormonal Carcinogenesis V

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Studies to date suggest that PC is a genetically very heterogeneous disease. High-risk families, in which multiple men are affected likely, reflect the contributions of a number of genes, some that are rare and highly penetrant, while others are more common and weakly penetrant. In this review, we have discussed only the first type of loci, and found that the identification of such genomic regions is a formidable problem. Replication between seemingly similar data sets is weak, likely reflecting the older age of onset associated with the disease, the inability to collect affected individuals from more than two generations in a family, and the variation seen in disease presentation, in addition to the underlying locus heterogeneity. Indeed, the definition of PC is ever changing, as diagnostic criteria and tools for pinpointing early lesions improve. Are we making progress? Clearly the answer is yes. The ability to divide large data sets into homogenous subset of families likely to share common genetic under-pinnings has improved power to identify loci and reproducibility between loci is now more common. Indeed, several groups report linkage to loci on chromosomes 1, 17, 19, and 22. Key to our continued success is our ever increasing ability to understand the disease. Identifying the subset of men who are likely to get clinically significant disease is the goal of genetic studies like these, and identifying the underlying loci is the key for developing diagnostics. The willingness of the community to work together has been an important factor in the successes the community has enjoyed to date, and will likely be as important as we move forward to untangle the genetics of this complex and common disorder.

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Section: Loci Mapped To Datesupporting

confidence: 75%

Prostate Cancer Susceptibility Loci: Finding the Genes

Ostrander

Johannesson²

2008

Hormonal Carcinogenesis V

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“…Bostwick et al detected loss of 8p21–12 in 37% of PIN foci and in 46% of cancer foci. In a recent study, 7 potentially important mutations in the macrophage scavenger receptor 1 gene (MSR1), located at 8p22, were observed in families affected with prostate cancer, and an indication of cosegregation between these mutations and prostate cancer was reported 1297. These findings suggest that more than 1 tumor suppressor gene may be located on 8p, and inactivation of these tumor suppressor genes may be important for the initiation of prostate cancer.…”

Section: 0 Goalsmentioning

confidence: 97%

Human prostate cancer risk factors

Bostwick

Burke

Djakiew

et al. 2004

Cancer

510

359

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“…In addition to its linkage to hereditary CaP, the macrophage receptor scavenger 1 ( MSR1 ) gene is located at a locus (8p22) that is often deleted in prostate tumors [ 118 , 119 ]. MSR1 mutations have been associated with CaP risk in both hereditary and sporadic CaP among Caucasian and AA men [ 98 ].…”

Section: Germline Mutations Associated With Hereditary Prostate Camentioning

confidence: 99%

Prostate Cancer Genomics: Recent Advances and the Prevailing Underrepresentation from Racial and Ethnic Minorities

Tan

Petrovics

Srivastava

2018

IJMS

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Prostate cancer (CaP) is the most commonly diagnosed non-cutaneous cancer and the second leading cause of male cancer deaths in the United States. Among African American (AA) men, CaP is the most prevalent malignancy, with disproportionately higher incidence and mortality rates. Even after discounting the influence of socioeconomic factors, the effect of molecular and genetic factors on racial disparity of CaP is evident. Earlier studies on the molecular basis for CaP disparity have focused on the influence of heritable mutations and single-nucleotide polymorphisms (SNPs). Most CaP susceptibility alleles identified based on genome-wide association studies (GWAS) were common, low-penetrance variants. Germline CaP-associated mutations that are highly penetrant, such as those found in HOXB13 and BRCA2, are usually rare. More recently, genomic studies enabled by Next-Gen Sequencing (NGS) technologies have focused on the identification of somatic mutations that contribute to CaP tumorigenesis. These studies confirmed the high prevalence of ERG gene fusions and PTEN deletions among Caucasian Americans and identified novel somatic alterations in SPOP and FOXA1 genes in early stages of CaP. Individuals with African ancestry and other minorities are often underrepresented in these large-scale genomic studies, which are performed primarily using tumors from men of European ancestry. The insufficient number of specimens from AA men and other minority populations, together with the heterogeneity in the molecular etiology of CaP across populations, challenge the generalizability of findings from these projects. Efforts to close this gap by sequencing larger numbers of tumor specimens from more diverse populations, although still at an early stage, have discovered distinct genomic alterations. These research findings can have a direct impact on the diagnosis of CaP, the stratification of patients for treatment, and can help to address the disparity in incidence and mortality of CaP. This review examines the progress of understanding in CaP genetics and genomics and highlight the need to increase the representation from minority populations.

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Linkage analysis of prostate cancer susceptibility: confirmation of linkage at 8p22–23

Cited by 40 publications

References 26 publications

Prostate Cancer Susceptibility Loci: Finding the Genes

Prostate Cancer Susceptibility Loci: Finding the Genes

Human prostate cancer risk factors

Prostate Cancer Genomics: Recent Advances and the Prevailing Underrepresentation from Racial and Ethnic Minorities

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