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Archived Comments for: A novel combination of multiple primary carcinomas: Urinary bladder transitional cell carcinoma, prostate adenocarcinoma and small cell lung carcinoma- report of a case and review of the literature

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  1. Common Molecular Genetic Events In Multiple Primary Tumors

    Chakshu Gupta, Heartland Regional Medical Center, St. Joseph, Missouri

    10 August 2005

    I enjoyed reading the review on multiple synchronous and metachronous primary tumors by Koutsopoulos, et al.1 In their review they reference an article by Chun, et al, who found that rates of bladder cancers were 18 times higher in patient’s with prostate cancers and the rates of prostate cancer to 19 times higher in those with bladder cancers. In their review of 24 patients with both types of cancers, all had adenocarcinoma of the prostate and urothelial carcinoma of the urinary bladder. They also reviewed several other large series with similar findings. This interesting fact can be explained by examining the molecular genetics of both types of carcinomas. Deletions in tumor suppressor genes, including RB1 (13q14), TP53 (17p13), and PTEN (10q23), have been reported in both prostatic adenocarcinomas and urothelial carcinomas.2-6

    We recently encountered an elderly gentleman who underwent cystoprostatectomy for a bladder tumor. He was found to have a pure primary small-cell neuroendocrine carcinoma of the urinary bladder, as well as prostatic acinar adenocarcinoma (Gleason 3+2=5). To the best of my knowledge, these two synchronous tumors have not been reported together in one patient. Cheng, et al reported deletions in TP53 (17q13) in primary small-cell neuroendocrine bladder carcinomas, and suggested a common origin of both the neuroendocrine cells and native urothelial cells.7 This molecular genetic alteration is also present in prostate adenocarcinomas and thus may explain the presence of the two synchronous tumors in our patient.

    Chakshu Gupta, M.D.

    Heartland Regional Medical Center

    St. Joseph, Missouri

    References

    1. Anastasios V Koutsopoulos, Konstantina I Dambaki, George Datseris, Elpida Giannikaki, Marios Froudarakis, Efstathios Stathopoulos

    World Journal of Surgical Oncology 2005, 3:51 (26 July 2005)

    2. Chun CY. Coincidence of bladder and prostate cancer. J Urol 1997, 157:65-67

    3. Knowles MA. What we could do now: molecular pathology of bladder cancer. J Clin Pathol:Mol Pathol 2001, 54:215-221

    4. Schulz WA, Burchardt M, Cronauer MV. Molecular biology of prostate cancer. Mol Hum Repro 2003, 9(8):437-448

    5. Strohmeyer DM, Berger AP, Moore DH, Bartsch G, Klocker H, Carroll PR, et al. Genetic aberrations in prostate carcinoma detected by comparative genomic hybridization and microsatellite analysis: association with progression and angiogenesis. Prostate 2004, 59(1):43-58

    6. Visakorpi T. The molecular genetics of prostate cancer. Urol 2003, 62(5):3-10

    7. Cheng L, Jones TD, McCarthy RP, Eble JN, Wang M, MacLennan GT, et al. Molecular genetic evidence for a common clonal origin of urinary bladder small cell carcinoma and coexisting urothelial carcinoma. Am J Pathol 2005, 166(5):1533-1539

    Competing interests

    None

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