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Letters |
1
Co-operative Research Centre, for Diagnostic Technologies, and,
2
Centre for Molecular Biotechnology, School of Life Sciences, Queensland University of Technology, GPO Box 2434, Brisbane 4001, Queensland, Australia
Departments of
3
Chemical Pathology, and,
4
Urology, Princess Alexandra Hospital, Woolloongabba 4102, Queensland, Australia
5
Department of Pathology, and, Laboratory Medicine, Mount Sinai Hospital, Toronto, Ontario, M5G 1X5 Canada
a Address correspondence to this author at: Center for Molecular Biotechnology, School of Life Sciences, Queensland University of Technology, GPO Box 2434, Brisbane 4001, Queensland, Australia. Fax 61-7-38641534; e-mail
j.clements{at}qut.edu.au.
To the Editor:
Immunoreactive prostate-specific antigen (PSA) has been detected in the sera of female and male renal cell carcinoma (RCC) patients in several studies (1)(2)(3). These measurements were attributed to the tumor because PSA reverted to undetectable concentrations after nephrectomy. However, attempts to definitively ascribe this increase to PSA were not successful either by immunohistochemistry with PSA monoclonal antibodies (1)(2) or by amplification of PSA by reverse transcription-PCR (RT-PCR) (3), suggesting cross-reaction with a PSA-like protein. Prostaglandin D synthase (PGDS) in amniotic fluid has been found to cross-react with a PSA polyclonal antibody, but not with PSA monoclonal antibodies (4). PGDS is present in the kidney (5) and is increased in the serum of patients with renal failure (6)(7). Because the Chiron PSA immunoassay (ACS:180) used in our original study (3) utilizes a polyclonal antibody, albeit immunopurified, we investigated whether PGDS could be responsible for the increased concentrations of PSA detected in RCC patients.
RNA was extracted from six female and six male tumor samples and from
nondiseased kidney tissue adjacent to the tumor. A 573-bp
fragment of PGDS was amplified by RT-PCR. Southern blot hybridization
and DNA sequencing of the PCR product confirmed the presence of PGDS.
PGDS was expressed in both the nondiseased kidney samples adjacent to
the tumor and in most tumor samples, but was not up-regulated in the
tumor (Fig. 1
).
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Serum from the six female RCC patients was also assayed for PSA, using the ACS:180 assay and the ultrasensitive PSA immunofluorometric assay developed by Yu and Diamandis (8), and for PGDS, using the immunoassay developed by Melegos et al. (9). The results for these six patients, respectively, were as follows: PSA (ACS:180), 0.89, 0.54, 0.39, 0.27, 0.26, and 0.15 µg/L (concentrations in healthy females were undetectable at <0.04 µg/L); PSA (Yu assay), undetectable; PGDS, 798, 281, 294, 480, 366, and 705 mg/L. There was no correlation between the serum samples that exhibited the highest PSA concentrations and those with higher PGDS. In fact, the PGDS concentrations, although variable, were all within the reference interval. Of interest was the inability of the monoclonal-based Yu assay to detect PSA.
From these preliminary data, it appears that PGDS expression is not increased in RCC and that PGDS is unlikely to be the source of the cross-reacting antigen detected previously in the serum of women with RCC. In keeping with these findings, we have determined that PGDS does not cross-react with several commercially available PSA antibodies and assay systems (data not shown). Although PSA could not be detected here with a more specific and sensitive PSA assay, PSA expression was detected recently in some RCC cell lines (10) and a cDNA library (11). These findings are yet to be extrapolated to human tissue. Other potential PSA-related antigens are currently being examined as candidates for the cross-reacting protein.
References
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