Nuklearmedizin 1989; 28(05): 193-200
DOI: 10.1055/s-0038-1629491
Orticle Articles
Schattauer GmbH

Die Anämie bei malignen Tumorerkrankungen

I. Tumorbedingte Verluste von Transferrin und ihre Abhängigkeit von Tumorgröße und Malignitätsgrad am Modell der RatteAnemia in Malignant DiseaseI. Tumor-Related Transferrin Loss and its Dependence on Tumor Size and Degree of Malignancy in the Rat
E. Aulbert
1   Ev. Waldkrankenhaus Spandau, Berlin, BRD
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Publikationsverlauf

Eingegangen: 05. Dezember 1988

in revidierter Form: 23. Juni 1989

Publikationsdatum:
05. Februar 2018 (online)

Cellular uptake of 67Ga-labelled transferrin by the tumor tissue was studied in rats with tumors of different malignancy and different tumor mass using the slowly growing Morris hepatoma 5123C, the moderately growing Novikoff hepatoma and the very fast and aggressive Yoshida hepatoma AH130. The cellular accumulation of 67Ga-transferrin was found to correlate with the proliferation activity of the tumor. The 67Ga-transferrin concentration in the very fast growing Yoshida hepatoma was 4.8 times higher than the concentration in the slowly growing Morris hepatoma. The uptake of 67Ga-transferrin by the tumors resulted in a faster disappearance of circulating 67Ga-transferrin from the blood. The rate of disappearance correlated with the proliferation activity and the spread of the tumors. Using tumors of identical size the elimination of 67Ga-transferrin from the blood was much faster in the rats with Yoshida hepatoma than in those with the slowly growing Morris hepatoma. On the other hand, using tumors of different tumor size it could be demonstrated that the rate of disappearance of 67Ga-transferrin from the blood correlated directly with tumor mass. It is concluded that cellular incorporation of transferrin within the tumor cells results in a loss of circulating transferrin, which correlates with tumor mass and proliferation of tumor. This mechanism is supposed to be the cause for the hypotransferrinemia seen in patients with malignant tumors.

Zusammenfassung

Es wird am Modell des langsam wachsenden Morris-Hepatoms 5123C, des mäßig schnell wachsenden Novikoff-Hepatoms und des sehr schnell und aggressiv wachsenden Yoshida- Hepatoms AH130 die Aufnahme von 67Ga-markiertem Transferrin in das Tumorgewebe untersucht. Es zeigt sich dabei mit zunehmender Proliferationsaktivität der Tumoren eine ansteigende 67Ga-Transferrinaufnahme proGramm Tumorfeuchtgewicht. Diese Aufnahme von 67Ga-Transferrin ins Tumorgewebe geht mit einem Verlust von zirkulierendem 67Ga- Transferrin aus dem Blut einher. Die Elimination von zirkulierendem 67Ga- Transferrin hängt einerseits von der Tumormasse, andererseits von der Proliferationsrate der Tumoren ab. So zeigte sich bei gleicher Tumorgröße der verschiedenen Tumormodelle, daß die Elimination von 67Ga-Transferrin aus dem Blut bei Tieren mit dem sehr schnell wachsenden Yoshida-Hepatom sehr viel schneller erfolgte als bei dem weniger schnell wachsenden Novikoff-Hepatom und dem langsam wachsenden Morris-Hepatom. Andererseits zeigte sich bei histologisch gleichem Tumortyp mit zunehmender Tumorgröße eine zunehmend schnelle Elimination von 67Ga- Transferrin aus dem Blut. Aus diesen Befunden wird geschlossen, daß die zelluläre Anreicherung von Transferrin im Tumorgewebe und, damit verbunden, die Verluste von Transferrin aus dem zirkulierenden Blut die Ursache für die bei malignen Tumorerkrankungen bekannte Hypotransferrinämie darstellt.

 
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