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Int J Clin Exp Pathol 2010;3(8):743-754
Original Article
Differential expression of type 2 3α/type 5 17β-hydroxysteroid dehydrogenase (AKR1C3)
in tumors of the central nervous system
Aubrey L. Park, Hsueh-Kung Lin, Qing Yang, Chor Wing Sing, Michael Fan, Timothy B. Mapstone, Naina L. Gross, Mary K. Gumerlock, Michael
D. Martin, Craig Rabb, Kar-Ming Fung
College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Department of Urology, University of
Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Oklahoma City Department of Veterans Affairs Medical Center, Oklahoma
City, OK 73104, USA; Molecular Biotechnology Program, Chinese University of Hong Kong, Hong Kong, China; Department of Chemistry &
Chemical Biology, Rutgers University, Piscataway, NJ, 08854, USA; Department of Neurosurgery, University of Oklahoma Health Sciences
Center, Oklahoma City, OK 73104, USA; Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104,
USA.
Received September 11, 2010; accepted September , 2010; available online September, 2010
Abstract: Human aldo-keto reductase (AKR) 1C3, type 2 3α-hydroxysteroid dehydrogenase (HSC)/ type 5 17β-HSD, is known to be involved in
steroids, prostaglandins, and lipid aldehydes metabolism. The expression of AKR1C3 has been demonstrated in hormone-dependent normal
tissues such as breast, endometrium, prostate, and testis; and de-regulated AKR1C3 expression has been shown in breast carcinoma,
endometrial hyperplasia, endometrial carcinoma, and prostate carcinoma. AKR1C3 expression has also been demonstrated in hormone-
independent normal tissues (renal tubules and urothelium) and neoplastic tissues (renal cell carcinoma, Wilm's tumor, and urothelial cell
carcinoma). Extensive expression of AKR1C3 in normal and neoplastic as well as hormone-dependent and hormone-independent tissues
indicates that AKR1C3 may have functions beyond steroid hormone metabolism. In this report, we describe a widespread expression of
AKR1C3 in glial neoplasms and meningiomas, with limited expression in medulloblastoma and no expression in Schwannoma. These
tumors, except meningioma, are not classically considered to be sex hormone-dependent or related brain tumors. The current results
corroborate our earlier observations that AKR1C3 is expressed in both sex hormone-dependent and hormone-independent malignancies.
Similar to AKR1C3 distribution in Wilm’s tumor, we also demonstrate that expression of AKR1C3 is reduced in tumors with embryonic
phenotypes. (IJCEP1009003).
Keywords: AKR1C3, astrocytoma, ependymoma, glioblastoma, medulloblastoma, meningioma, oligodendroglioma, schwannoma
Full text PDF
Address all correspondence to:
Kar-Ming Fung, MD, PhD
Department of Pathology
University of Oklahoma Health Sciences Center
BMSB. 451, 940 Stanton Young Blvd.
Oklahoma City, OK 73104
PHONE: (405) 271-5653
FAX: (405) 271-2524
E-mail: karming-fung@ouhsc.edu
Original Article
Differential expression of type 2 3α/type 5 17β-hydroxysteroid dehydrogenase (AKR1C3)
in tumors of the central nervous system
Aubrey L. Park, Hsueh-Kung Lin, Qing Yang, Chor Wing Sing, Michael Fan, Timothy B. Mapstone, Naina L. Gross, Mary K. Gumerlock, Michael
D. Martin, Craig Rabb, Kar-Ming Fung
College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Department of Urology, University of
Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA; Oklahoma City Department of Veterans Affairs Medical Center, Oklahoma
City, OK 73104, USA; Molecular Biotechnology Program, Chinese University of Hong Kong, Hong Kong, China; Department of Chemistry &
Chemical Biology, Rutgers University, Piscataway, NJ, 08854, USA; Department of Neurosurgery, University of Oklahoma Health Sciences
Center, Oklahoma City, OK 73104, USA; Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104,
USA.
Received September 11, 2010; accepted September , 2010; available online September, 2010
Abstract: Human aldo-keto reductase (AKR) 1C3, type 2 3α-hydroxysteroid dehydrogenase (HSC)/ type 5 17β-HSD, is known to be involved in
steroids, prostaglandins, and lipid aldehydes metabolism. The expression of AKR1C3 has been demonstrated in hormone-dependent normal
tissues such as breast, endometrium, prostate, and testis; and de-regulated AKR1C3 expression has been shown in breast carcinoma,
endometrial hyperplasia, endometrial carcinoma, and prostate carcinoma. AKR1C3 expression has also been demonstrated in hormone-
independent normal tissues (renal tubules and urothelium) and neoplastic tissues (renal cell carcinoma, Wilm's tumor, and urothelial cell
carcinoma). Extensive expression of AKR1C3 in normal and neoplastic as well as hormone-dependent and hormone-independent tissues
indicates that AKR1C3 may have functions beyond steroid hormone metabolism. In this report, we describe a widespread expression of
AKR1C3 in glial neoplasms and meningiomas, with limited expression in medulloblastoma and no expression in Schwannoma. These
tumors, except meningioma, are not classically considered to be sex hormone-dependent or related brain tumors. The current results
corroborate our earlier observations that AKR1C3 is expressed in both sex hormone-dependent and hormone-independent malignancies.
Similar to AKR1C3 distribution in Wilm’s tumor, we also demonstrate that expression of AKR1C3 is reduced in tumors with embryonic
phenotypes. (IJCEP1009003).
Keywords: AKR1C3, astrocytoma, ependymoma, glioblastoma, medulloblastoma, meningioma, oligodendroglioma, schwannoma
Full text PDF
Address all correspondence to:
Kar-Ming Fung, MD, PhD
Department of Pathology
University of Oklahoma Health Sciences Center
BMSB. 451, 940 Stanton Young Blvd.
Oklahoma City, OK 73104
PHONE: (405) 271-5653
FAX: (405) 271-2524
E-mail: karming-fung@ouhsc.edu
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