For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
15
views
59
references
 Top references
cited by
2
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      358
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The molecular basis for ethnic variation and histological subtype differences in prostate cancer

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Prostate cancer is a common malignancy among men in Western countries. Recently the morbidity and mortality of prostate cancer increase dramatically in several oriental countries including China. Rapidly evolving technology in molecular biology such as high-throughput sequencing and integrative analysis of genomic and transcriptomic landscapes have enabled the identification of key oncogenic events for prostate cancer initiation, progression and resistance to hormonal therapy. These surging data of prostate cancer genome also provide insights on ethnic variation and the differences in histological subtype of this disease. In this review, differences in the incidence of prostate cancer and the prevalence of main genetic alterations between Asian and Western populations are discussed. We also review the recent findings on the mechanisms underlying neuroendocrine differentiation of prostate cancer and the development of small cell neuroendocrine carcinoma after androgen deprivation therapy.

          Related collections

          Most cited references59

          • Record: found
          • Abstract: found
          • Article: not found

          Chemokine signaling via the CXCR2 receptor reinforces senescence.

          Juan C. Acosta, Ana O'Loghlen, Ana Banito … (2008)
          Cells enter senescence, a state of stable proliferative arrest, in response to a variety of cellular stresses, including telomere erosion, DNA damage, and oncogenic signaling, which acts as a barrier against malignant transformation in vivo. To identify genes controlling senescence, we conducted an unbiased screen for small hairpin RNAs that extend the life span of primary human fibroblasts. Here, we report that knocking down the chemokine receptor CXCR2 (IL8RB) alleviates both replicative and oncogene-induced senescence (OIS) and diminishes the DNA-damage response. Conversely, ectopic expression of CXCR2 results in premature senescence via a p53-dependent mechanism. Cells undergoing OIS secrete multiple CXCR2-binding chemokines in a program that is regulated by the NF-kappaB and C/EBPbeta transcription factors and coordinately induce CXCR2 expression. CXCR2 upregulation is also observed in preneoplastic lesions in vivo. These results suggest that senescent cells activate a self-amplifying secretory network in which CXCR2-binding chemokines reinforce growth arrest.
          Article 0 comments Cited 621 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Prostate-specific deletion of the murine Pten tumor suppressor gene leads to metastatic prostate cancer.

            Shunyou Wang, Jing Gao, Qunying Lei … (2003)
            The murine Pten prostate cancer model described in this study recapitulates the disease progression seen in humans: initiation of prostate cancer with prostatic intraepithelial neoplasia (PIN), followed by progression to invasive adenocarcinoma, and subsequent metastasis with defined kinetics. Furthermore, while Pten null prostate cancers regress after androgen ablation, they are capable of proliferating in the absence of androgen. Global assessment of molecular changes caused by homozygous Pten deletion identified key genes known to be relevant to human prostate cancer, including those "signature" genes associated with human cancer metastasis. This murine prostate cancer model provides a unique tool for both exploring the molecular mechanism underlying prostate cancer and for development of new targeted therapies.
            Article 0 comments Cited 258 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Germline mutations in HOXB13 and prostate-cancer risk.

              Charles Ewing, Anna Ray, Ethan Lange … (2012)
              Family history is a significant risk factor for prostate cancer, although the molecular basis for this association is poorly understood. Linkage studies have implicated chromosome 17q21-22 as a possible location of a prostate-cancer susceptibility gene. We screened more than 200 genes in the 17q21-22 region by sequencing germline DNA from 94 unrelated patients with prostate cancer from families selected for linkage to the candidate region. We tested family members, additional case subjects, and control subjects to characterize the frequency of the identified mutations. Probands from four families were discovered to have a rare but recurrent mutation (G84E) in HOXB13 (rs138213197), a homeobox transcription factor gene that is important in prostate development. All 18 men with prostate cancer and available DNA in these four families carried the mutation. The carrier rate of the G84E mutation was increased by a factor of approximately 20 in 5083 unrelated subjects of European descent who had prostate cancer, with the mutation found in 72 subjects (1.4%), as compared with 1 in 1401 control subjects (0.1%) (P=8.5x10(-7)). The mutation was significantly more common in men with early-onset, familial prostate cancer (3.1%) than in those with late-onset, nonfamilial prostate cancer (0.6%) (P=2.0x10(-6)). The novel HOXB13 G84E variant is associated with a significantly increased risk of hereditary prostate cancer. Although the variant accounts for a small fraction of all prostate cancers, this finding has implications for prostate-cancer risk assessment and may provide new mechanistic insights into this common cancer. (Funded by the National Institutes of Health and others.).
              Article 0 comments Cited 215 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-journal-id): 101529880
                Journal ID (pubmed-jr-id): 37609
                Journal ID (nlm-ta): Sci China Life Sci
                Journal ID (iso-abbrev): Sci China Life Sci
                Title: Science China. Life sciences
                ISSN (Print): 1674-7305
                ISSN (Electronic): 1869-1889
                Publication date Nihms-submitted: 30 May 2014
                Publication date (Electronic): 13 July 2013
                Publication date (Print): September 2013
                Publication date PMC-release: 02 July 2014
                Volume: 56
                Issue: 9
                Pages: 780-787
                Affiliations
                [1 ]Howard Hughes Medical Institute, University of California, Los Angeles, CA 90095, USA
                [2 ]Departments of Molecular and Medical Pharmacology, University of California, Los Angeles, CA 90095, USA
                [3 ]Pathology and Laboratory Medicine, University of California, Los Angeles, CA 90095, USA
                [4 ]Urology, University of California, Los Angeles, CA 90095, USA
                [5 ]Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
                [6 ]Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, CA 90095, USA
                Author notes
                [* ]Corresponding author. ( jiaotihuang@ 123456mednet.ucla.edu )
                Article
                Manuscript ID: NIHMS594444
                DOI: 10.1007/s11427-013-4522-0
                PMC ID: 4078990
                PubMed ID: 23852643
                SO-VID: b9aa063c-5003-4e4d-b0d2-d3ad4cc3ac2c
                Copyright © © The Author(s) 2013.
                License:

                This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.

                History
                Categories
                Subject: Article

                Keywords: prostate cancer,castration resistance,neuroendocrine differentiation,small cell neuroendocrine carcinoma
                Data availability:
                Keywords: prostate cancer, castration resistance, neuroendocrine differentiation, small cell neuroendocrine carcinoma

                Comments

                Comment on this article

                scite_

                Similar content358

                See all similar

                Cited by2

                See all cited by

                Most referenced authors1,384

                See all reference authors