Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2004-6-1
pubmed:abstractText
Lethal phenotypes of human prostate cancer are characterized by progression to androgen-independence and metastasis. For want of a clinically relevant animal model, mechanisms behind this progression remain unclear. Our study used an in vivo model of androgen-sensitive LNCaP human prostate cancer cell xenografts in male SCID mice to study the cellular and molecular biology of tumor progression. Primary tumors were established orthotopically, and the mice were then surgically castrated to withdraw androgens. Five generations of androgen-independent tumors were developed using castrated host mice. Tumor samples were used to determine expressions of cellular and molecular markers. Androgen-independent tumors had increased proliferation and decreased apoptosis compared to androgen-sensitive tumors, outcomes associated with elevated expression of p53, p21/waf1, bcl-2, bax and the bcl-2/bax ratio. Blood vessel growth in androgen-independent tumor was associated with increased expression of vascular endothelial growth factor. Overexpression of androgen receptor mRNA and reduced expression of androgen receptor protein in androgen-independent tumors suggest that the androgen receptor signaling pathway may play an important role in the progression of human prostate cancer to androgen-independence. The in vivo orthotopic LNCaP tumor model described in our study mimics the clinical course of human prostate cancer progression. As such, it can be used as a model for defining the molecular mechanisms of prostate cancer progression to androgen-independence and for evaluating the effect of preventive or therapeutic regimens for androgen-independent human prostate cancer.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-10029066, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-10200775, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-10460196, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-10476545, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-10547394, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-10797498, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-10881018, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-10910077, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-10948353, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-10960845, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-11176459, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-11325816, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-11717329, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-12242729, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-1289680, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-1458483, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-1708363, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-1712249, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-7512791, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-7541709, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-7609105, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-7671257, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-7692074, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-7723794, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-7795646, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-7913874, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-7971515, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-8169003, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-8604394, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-8623925, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-8808919, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-8824549, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-8826950, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-8883414, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-8971161, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-9000575, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-9108464, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-9724788, http://linkedlifedata.com/resource/pubmed/commentcorrection/15170660-9790948
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0020-7136
pubmed:author
pubmed:copyrightInfo
Copyright 2004 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
110
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
800-6
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Progression to androgen-independent LNCaP human prostate tumors: cellular and molecular alterations.
pubmed:affiliation
Nutrition/Metabolism Laboratory, Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Burlington-554B, Boston, MA 02215, USA. jrzhou@bidmc.harvard.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.