Accelerated growth rates of recurrent hepatocellular carcinoma after liver transplantation

The growth rates of recurrent hepatocellular carcinoma (HCC) after orthotopic liver transplantation (OLTX) were estimated by calculating the tumor doubling time (TDT) in 20 patients. The mean TDT, calculated by multiple measurement of tumor size, was 44.3 ± 11.3 days (mean ± standard error) in 12 pa...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Cancer 1991-11, Vol.68 (10), p.2095-2100
Hauptverfasser: Yokoyama, Itsuo, Carr, Brian, Saitsu, Hideki, Iwatsuki, Shunzaburo, Starzl, Thomas E.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:The growth rates of recurrent hepatocellular carcinoma (HCC) after orthotopic liver transplantation (OLTX) were estimated by calculating the tumor doubling time (TDT) in 20 patients. The mean TDT, calculated by multiple measurement of tumor size, was 44.3 ± 11.3 days (mean ± standard error) in 12 patients with pulmonary metastasis (range, 10 to 161 days) and 37.6 ± 8.9 days (range, 7 to 65 days) in 5 patients with liver allograft recurrence. The TDT as estimated by serum alpha‐fetoprotein (AFP) levels in 6 patients was 37.3 ± 10.0 days (range, 12 to 84 days). The mean TDT obtained from 5 control subjects with HCC who were treated with liver resection (without immunosuppression) was 273.8 ± 79.1 days (range, 82 to 560 days). The disease‐free period and survival time after OLTX both correlated well with the TDT (r = 0.546 and r = 0.701, respectively). The patients with fibrolamellar HCC had a greater TDT and a longer survival time than those with nonfibrolamellar HCC. Despite a wide range of TDT in patients who received transplants, their recurrent HCC tumors grew significantly faster than those of patients with the same disease who did not receive transplants. The factors involved in this accelerated growth rate may include the use of immunosuppressive drugs and the consequent suppression of host immunity against the growth of micrometastasis. Cancer 68:2095–2100.
ISSN:0008-543X
1097-0142
DOI:10.1002/1097-0142(19911115)68:10<2095::AID-CNCR2820681002>3.0.CO;2-Y