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Insulin receptor expression by human prostate cancers
The Prostate, 2009-01, Vol.69 (1), p.33-40
Cox, Michael E.
Gleave, Martin E.
Zakikhani, Mahvash
Bell, Robert H.
Piura, Esther
Vickers, Elaine
Cunningham, Matthew
Larsson, Ola
Fazli, Ladan
Pollak, Michael
2009
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Cox, Michael E.
Gleave, Martin E.
Zakikhani, Mahvash
Bell, Robert H.
Piura, Esther
Vickers, Elaine
Cunningham, Matthew
Larsson, Ola
Fazli, Ladan
Pollak, Michael
Titel
Insulin receptor expression by human prostate cancers
Ist Teil von
The Prostate, 2009-01, Vol.69 (1), p.33-40
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2009
Quelle
MEDLINE
Beschreibungen/Notizen
BACKGROUND Although recent laboratory and population studies suggest that prostate cancer may be responsive to insulin, there is a gap in knowledge concerning the expression of insulin receptors on benign or malignant prostate tissue. METHODS We immunostained 644 cores on tissue microarrays prepared from 29 prostate tissue samples without malignancies, 78 Gleason grade 3 cancers, 21 Gleason grade 4 cancers and 33 Gleason grade 5 cancers with antibodies against the insulin‐like growth factor I receptor and the insulin receptor. RESULTS We observed immunoreactivity with both antibodies, which implies the presence of hybrid receptors as well as IGF‐I receptors and insulin receptors. Insulin receptor staining intensity was significantly (P < 0.001) higher on malignant than benign prostate epithelial cells. Analysis of information from public gene expression databases confirmed that co‐expression of insulin receptor mRNA and IGF‐I receptor mRNA is common in prostate cancer specimens. RT‐PCR methods provided evidence for the presence of mRNA for both IR‐A and IR‐B insulin receptor isoforms. CONCLUSION These observations document the presence of insulin receptors on primary human prostate cancers. The findings are relevant not only to ongoing clinical trials of drug candidates that target IGF‐I and/or insulin receptors, but also to the hypothesis that obesity‐associated hyperinsulinemia mediates the adverse effect of obesity on prostate cancer prognosis. Prostate 69: 33–40, 2009. © 2008 Wiley–Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0270-4137, 1097-0045
eISSN: 1097-0045
DOI: 10.1002/pros.20852
Titel-ID: cdi_swepub_primary_oai_prod_swepub_kib_ki_se_118091997
Format
–
Schlagworte
Antibody Specificity
,
Biological and medical sciences
,
Cell Line, Tumor
,
Gene Expression Regulation, Neoplastic
,
Gleason grade
,
Gynecology. Andrology. Obstetrics
,
Humans
,
Hyperinsulinism - metabolism
,
Hyperinsulinism - pathology
,
Hyperinsulinism - physiopathology
,
Immunohistochemistry
,
insulin receptor
,
insulin-like growth factor receptor
,
Liver Neoplasms
,
Male
,
Male genital diseases
,
Medical sciences
,
Medicin och hälsovetenskap
,
metabolic syndrome
,
Metabolic Syndrome - metabolism
,
Metabolic Syndrome - pathology
,
Metabolic Syndrome - physiopathology
,
Nephrology. Urinary tract diseases
,
obesity
,
Obesity - metabolism
,
Obesity - pathology
,
Obesity - physiopathology
,
Oligonucleotide Array Sequence Analysis
,
prostate cancer
,
Prostatic Neoplasms - metabolism
,
Prostatic Neoplasms - pathology
,
Prostatic Neoplasms - physiopathology
,
Receptor, IGF Type 1 - genetics
,
Receptor, IGF Type 1 - immunology
,
Receptor, IGF Type 1 - metabolism
,
Receptor, Insulin - genetics
,
Receptor, Insulin - immunology
,
Receptor, Insulin - metabolism
,
RNA, Messenger - metabolism
,
Signal Transduction - physiology
,
Tumors
,
Tumors of the urinary system
,
Urinary tract. Prostate gland
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