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Elevated Oestrogen Receptor Splice Variant ER??5 Expression in Tumour-adjacent Hormone-responsive Tissue

Siân E. Taylor, Imran I. Patel, Paras B. Singh, Caroline M. Nicholson, Helen F. Stringfellow, R. K. Gopala Krishna, Shyam S. Matanhelia, Pierre L. Martin-Hirsch and Francis L. Martin
Additional contact information
Siân E. Taylor: Centre for Biophotonics, Lancaster Environment Centre, Lancaster University, Bailrigg, Lancaster LA1 4YQ, UK
Imran I. Patel: Centre for Biophotonics, Lancaster Environment Centre, Lancaster University, Bailrigg, Lancaster LA1 4YQ, UK
Paras B. Singh: Centre for Biophotonics, Lancaster Environment Centre, Lancaster University, Bailrigg, Lancaster LA1 4YQ, UK
Caroline M. Nicholson: Lancashire Teaching Hospitals NHS Trust, Sharoe Green Lane, Fulwood, Preston PR2 9HT, UK
Helen F. Stringfellow: Lancashire Teaching Hospitals NHS Trust, Sharoe Green Lane, Fulwood, Preston PR2 9HT, UK
R. K. Gopala Krishna: Wockhardt Hospitals & Kidney Institute, 111A, Rash Behari Avenue, Kolkata 700029, India
Shyam S. Matanhelia: Lancashire Teaching Hospitals NHS Trust, Sharoe Green Lane, Fulwood, Preston PR2 9HT, UK
Pierre L. Martin-Hirsch: Centre for Biophotonics, Lancaster Environment Centre, Lancaster University, Bailrigg, Lancaster LA1 4YQ, UK
Francis L. Martin: Centre for Biophotonics, Lancaster Environment Centre, Lancaster University, Bailrigg, Lancaster LA1 4YQ, UK

IJERPH, 2010, vol. 7, issue 11, 1-19

Abstract: Susceptibility to prostate or endometrial cancer is linked with obesity, a state of oestrogen excess. Oestrogen receptor (ER) splice variants may be responsible for the tissue-level of ER activity. Such micro-environmental regulation may modulate cancer initiation and/or progression mechanisms. Real-time reverse transcriptase (RT) polymerase chain reaction (PCR) was used to quantitatively assess the levels of four ER splice variants ( ER ? ? 3 , ER ? ? 5 , ER ?2 and ER ? 5 ), plus the full-length parent isoforms ER ? and ER ? 1 , in high-risk [tumour-adjacent prostate ( n = 10) or endometrial cancer ( n = 9)] vs . low-risk [benign prostate ( n = 12) or endometrium ( n = 9)], as well as a comparison of UK ( n = 12) vs . Indian ( n = 15) benign prostate. All three tissue groups expressed the ER splice variants at similar levels, apart from ER ? ? 5 . This splice variant was markedly raised in all of the tumour-adjacent prostate samples compared to benign tissues. Immunofluorescence analysis for ER ? 2 in prostate tissue demonstrated that such splice variants are present in comparable, if not greater, amounts as the parent full-length isoform. This small pilot study demonstrates the ubiquitous nature of ER splice variants in these tissue sites and suggests that ER ? ? 5 may be involved in progression of prostate adenocarcinoma.

Keywords: endometrial cancer; oestrogen receptor; prostate cancer; real-time RT PCR; splice variant (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2010
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