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Pathophysiologie der Skelettmetastasierung urologischer Karzinome

Pathophysiology of bone metastases in urologic carcinomas

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Zusammenfassung

Das Skelettsystem ist häufig der Metastasierungsort urologischer Karzinome. Ossäre Metastasen werden in osteoneutral, osteolytisch, osteoblastisch und gemischtförmig unterschieden. Osteolytisch wirkende Metastasen führen über Aktivierung der Osteoklasten zur Knochenresorption, wohingegen osteoblastische Metastasen durch parakrine Sekretion Osteoblasten aktivieren und so die Osteoneogenese fördern. Neben dem lokalen osteoblastischen Effekt kommt es zu einem sekundären systemischen Knochenabbau. Als supportive Therapie hat sich der Einsatz von Bisphosphonaten etabliert. Neue, z. T. noch experimentelle Ansätze bestehen in der gezielten Intervention in die Pathophysiologie der Knochenmetastasierung und der Radioimmuntherapie.

Abstract

The skeletal system is the most frequent metastatic site of hematogenous spread of urologic carcinomas. Osseus metastases are classified as osteoneutral, osteolytic, osteoblastic and combinations thereof. Osteolytic metastases lead to bone resorption by activating osteoclasts, while osteoblastic metastases stimulate osteoblasts by paracrine mechanisms. The local osteoblastic effect is associated with secondary systemic bone resorption. The use of bisphosphonates is now an established supportive therapy and newer treatment strategies including targeted intervention in the pathophysiology of bone metastases and radioimmunotherapy are being applied or will be coming soon.

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Literatur

  1. Berruti A, Dogliotti L, Tucci M et al. (2001) Metabolic bone disease induced by prostatic cancer: rationale for the use of bisphosphonates. J Urol 166: 2023–2031

    Article  PubMed  CAS  Google Scholar 

  2. Brouwers AH, Buijs WC, Mulders PF et al. (2005) Radioimmunotherapy with [131I]cG250 in patients with metastasized renal cell cancer: dosimetric analysis and immunologic response. Clin Cancer Res 11: 7178–7186

    Article  Google Scholar 

  3. Desai B, Rogers M, Chellaiah MA (2007) Mechanisms of osteopontin and CD44 as metastatic principles in prostate cancer cells. Mol Cancer 6: 18

    Article  PubMed  Google Scholar 

  4. Dorfman HD, Czerniak B (1998) Metastatic Tumors in Bone. In: Dorfman HD, Czerniak B (eds) Bone Tumors. Mosby, St. Louis Baltimore Boston Carlsbad Chicago Minneapolis New York Philadelphia Portland London Milan Sydney Tokio Toronto, pp 1009–1040

  5. Guise TA, Mundy GR (1998) Cancer and Bone. Endocr Rev 19: 18–54

    Article  PubMed  CAS  Google Scholar 

  6. Inoue K, Karashima T, Fukata S et al. (2005) Effect of combination therapy with a novel bisphosphonate, minodronate (YM529), and Docetaxel on a model of bone metastasis by human transitional cell carcinoma. Clin Cancer Res 11: 6669–6677

    Article  PubMed  CAS  Google Scholar 

  7. Jundt G (2004) Skelettmetastasen. In: Böcker W, Denk H, Heitz PU (Hrsg) Pathologie 3. Aufl. Urban & Fischer, München Jena, S 1057

  8. Koeneman KS, Yeung F, Chung LW (1999) Osteomimetic properties of prostate cancer cells: a hypothesis supporting the predilection of prostate cancer metastasis and growth in the bone environment. Prostate 39: 246–261

    Article  PubMed  CAS  Google Scholar 

  9. Lipton A (2004) Pathophysiology of bone metastases: How this knowledge may lead to therapeutic intervention. J Support Oncol 2: 205–220

    PubMed  Google Scholar 

  10. Lipton A, Colombo-Berra A, Bukowski RM et al. (2004) Skeletal complications in patients with bone metastasis from renal cell carcinoma and therapeutic benefits of zoledronic acid. Clin Cancer Res 10: 6397–6403

    Article  Google Scholar 

  11. Saad F, Lipton A (2005) Zoledronic acid is effective in preventing and delaying skeletal events in patients with bone metastases secondary to genitourinary cancers. BJU Int 96: 964–969

    Article  PubMed  CAS  Google Scholar 

  12. Vessella C, Corey E (2006) Targeting factors involved in bone remodeling as treatment strategies in prostate cancer bone metastasis. Clin Cancer Res (Suppl 20) 12: 6285–6290

    Article  Google Scholar 

  13. Wallmeroth A, Wagner U, Moch H et al. (1999) Patterns of metastasis in muscle-invasive bladder cancer. Urol Int 62:69–75

    Article  PubMed  CAS  Google Scholar 

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Authors and Affiliations

  1. Institut für Pathologie, Universitätsklinikum Ulm, Albert-Einstein-Allee 11, 89081, Ulm, Deutschland

    G. Sauer, T.F.E. Barth &  P. Möller

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  1. G. Sauer
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  2. T.F.E. Barth
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  3. P. Möller
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Correspondence to P. Möller.

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Sauer, G., Barth, T. & Möller, P. Pathophysiologie der Skelettmetastasierung urologischer Karzinome. Urologe 46, 888–890 (2007). https://doi.org/10.1007/s00120-007-1519-y

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  • DOI: https://doi.org/10.1007/s00120-007-1519-y

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