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Baumhoer, D. ; Smida, J. ; Zillmer, S. ; Rosemann, M. ; Atkinson, M.J. ; Nelson, P.J.* ; Jundt, G.* ; von Luettichau, I.* ; Nathrath, M.

Strong expression of CXCL12 is associated with a favorable outcome in osteosarcoma.

Mod. Pathol. 25, 522-528 (2012)
Verlagsversion Volltext DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Hematogenous spread determines the outcome of osteosarcoma (OS) patients, but the pathogenesis of developing metastatic disease is still unclear. Chemokines are critical regulators of cell trafficking and adhesion, and have been reported to be aberrantly expressed and to correlate with an unfavorable prognosis and metastatic spread in several malignant tumors. The chemokine receptors CXCR4 and CXCR7 together with their common ligand CXCL12 form one of the most important chemokine axes in this context. To investigate a potential role of these chemokines in OSs, we analyzed their expression in a series of 223 well-characterized and pretherapeutic OS samples. Interestingly, we found the expression of CXCL12 and CXCR4 to correlate with a better long-term outcome and with a lower prevalence of metastases. These findings suggest a distinct role of CXCR4/CXCR7/CXCL12 signaling in the tumors of bone, as has also been previously described in acute leukemia. As many malignant tumors metastasize to bone, and tumor cells are thought to be directed to bone in response to CXCL12, OS cells expressing both CXCL12 and the corresponding receptors might be detained at their site of origin. The disruption of CXCR4/CXCR7/CXCL12 signaling could therefore be crucial in OSs for the migration of tumor cells from bone into circulation and for developing systemic disease.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter chemokines; CXCR4; CXCR7; CXCL12; metastases; osteosarcoma; prognosis; CHEMOKINE RECEPTOR; PROSTATE-CANCER; CXCR4; METASTASIS; SURVIVAL; CELLS; BONE; INHIBITION; PATHWAY; BLOOD
ISSN (print) / ISBN 0893-3952
e-ISSN 1530-0285
Zeitschrift Modern Pathology
Quellenangaben Band: 25, Heft: 4, Seiten: 522-528 Artikelnummer: , Supplement: ,
Verlag United States and Canadian Academy of Pathology ; Nature Publishing Group
Begutachtungsstatus