Research Papers:

The influence of PSA autoantibodies in prostate cancer patients: a prospective clinical study-II

Kosei Nakajima, Lance K. Heilbrun, Daryn Smith, Victor Hogan, Avraham Raz and Elisabeth Heath _

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Oncotarget. 2017; 8:17643-17650. https://doi.org/10.18632/oncotarget.12620

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Kosei Nakajima1,2,*, Lance K. Heilbrun1,3,*, Daryn Smith1,3, Victor Hogan1,2, Avraham Raz1,2 and Elisabeth Heath1

1 Department of Oncology, Karmanos Cancer Institute, School of Medicine, Wayne State University, Detroit, Michigan, USA

2 Department of Pathology, Karmanos Cancer Institute, School of Medicine, Wayne State University, Detroit, Michigan, USA

3 Biostatistics Core, Karmanos Cancer Institute, Wayne State University, Detroit, Michigan, USA

* Authors share equal credit

Correspondence to:

Elisabeth Heath, email:

Avraham Raz, email:

Keywords: PSA autoantibody, PSA test, false-results, prostate cancer, Galectin-3

Received: August 17, 2016 Accepted: October 07, 2016 Published: October 12, 2016


The U.S. Preventive Services Task Force (USPSTF) has recommended against PSA-based screening for prostate cancer due to potential possibilities of false-results. Since no alternative test is available to replace it, we have initiated a trial with the purpose of establishing whether Galectin-3 (Gal-3) serum level and/or the patients’ immune response to PSA and Gal-3 antigens could complement the PSA test as diagnostic tools for prostate cancer patients. A blind, prospective, single institution, pilot study was conducted. A total of 95 men were recruited and classified into 5 different groups: healthy controls (Group1), newly diagnosed patients (Group2), no recurrence after local therapy (Group3), rising PSA after local therapy (Group4), and metastatic patients (Group5). The primary endpoints were the levels of serum PSA, PSA autoantibodies (AAPSA), Gal-3, and Gal-3 autoantibodies (AAGal-3). Data were analyzed by Spearman’s rank correlation (rho) and least squares linear regression modeling. The expression levels of PSA, AAPSA, Gal-3, and AAGal-3 were determined in both healthy controls and prostate cancer patients. Negative correlations were observed between PSA and AAPSA levels among all 95 men combined (rho = -0.321, P = 0.0021; fitted slope -0.288, P = 0.0048), and in metastatic patients (rho = -0.472, P = 0.0413; fitted slope -1.145, P = 0.0061). We suggest an association between PSA and AAPSA, whereby the AAPSA may alter PSA levels. It provides a novel outlook for prostate cancer diagnosis, and should serve as a basis for an all-inclusive diagnostic trial centering on patients with metastasis.

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