Patterns of TPD52 overexpression in multiple human solid tumor types analyzed by quantitative PCR

Tennstedt,Pierre; Bölch,Charlotte; Strobel,Gundula; Minner,Sarah; Burkhardt,Lia; Grob,Tobias; Masser,Sawinee; Sauter,Guido; Schlomm,Thorsten; Simon,Ronald

doi:10.3892/ijo.2013.2200

Patterns of TPD52 overexpression in multiple human solid tumor types analyzed by quantitative PCR

Authors:
- Pierre Tennstedt
- Charlotte Bölch
- Gundula Strobel
- Sarah Minner
- Lia Burkhardt
- Tobias Grob
- Sawinee Masser
- Guido Sauter
- Thorsten Schlomm
- Ronald Simon
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Affiliations: Martini-Clinic, Section for Translational Prostate Cancer Research, University Medical Center Hamburg-Eppendorf, Hamburg, Germany, Institute of Pathology, Section for Translational Prostate Cancer Research, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
Published online on: November 29, 2013 https://doi.org/10.3892/ijo.2013.2200
Pages: 609-615

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Abstract

Tumor protein D52 (TPD52) is located at chromosome 8q21, a region that is frequently gained or amplified in multiple human cancer types. TPD52 has been suggested as a potential target for new anticancer therapies. In order to analyze TPD52 expression in the most prevalent human cancer types, we employed quantitative PCR to measure TPD52 mRNA levels in formalin-fixed tissue samples from more than 900 cancer tissues obtained from 29 different human cancer types. TPD52 was expressed at varying levels in all tested normal tissues, including skin, lymph node, lung, oral mucosa, breast, endometrium, ovary, vulva, myometrium, liver, pancreas, stomach, kidney, prostate, testis, urinary bladder, thyroid gland, brain, muscle and fat tissue. TPD52 was upregulated in 18/29 (62%) tested cancer types. Strongest expression was found in non-seminoma (56-fold overexpression compared to corresponding normal tissue), seminoma (42-fold), ductal (28-fold) and lobular breast cancer (14-fold). In these tumor types, TPD52 upregulation was found in the vast majority (>80%) of tested samples. Downregulation was found in 11 (38%) tumor types, most strongly in papillary renal cell cancer (-8-fold), leiomyosarcoma (-6-fold), clear cell renal cell cancer (-5-fold), liposarcoma (-5-fold) and lung cancer (-4-fold). These results demonstrate that TPD52 is frequently and strongly upregulated in many human cancer types, which may represent candidate tumor types for potential anti-TPD52 therapies.

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