Hormonal therapy for hepatocellular carcinoma.
Hepatocellular carcinoma is not only the leading cause of male cancer death in Taiwan, but also one of the most common cancers in the world. The survival of hepatocellular carcinoma patients is very low, mainly due to the lack of effective treatments. Radiation and chemotherapies in general are not satisfactory: surgery itself is the most effective treatment for hepatocellular carcinoma but only on small resectable tumors. The overall prognosis is still poor. Previously, we have found that the level of glucocorticoid receptor and its mRNA in hepatocellular carcinoma was significantly higher than that of the adjacent liver tissue. This correlated well with the elevated serum alpha-fetoprotein levels in patients with hepatocellular carcinoma. Recently, a female hormone, progesterone, has been found to inhibit the expression of alpha-fetoprotein in hepatoma cells. In addition, progesterone has been used to treat a few hepatocellular carcinoma patients with promising responses. These results together with our hypothesis that the expression of alpha-fetoprotein is regulated by glucocorticoid receptor complex in proliferating hepatocellular carcinoma cells lead to the conclusion that steroid hormones and/or their antagonists may interfere with the function of glucocorticoid receptors in tumors, consequently regulate tumor growth. The potential of hormonal therapy for treatment of hepatocellular carcinoma is worthy of further investigation.
Lui
W Y
WY
Department of General Surgery, Veterans General Hospital-Taipei, Taiwan, Republic of China.
P'eng
F K
FK
Liu
T Y
TY
Chi
C W
CW
D006528:Carcinoma, Hepatocellular / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D008113:Liver Neoplasms / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D011374:Progesterone / Q000627:therapeutic use*; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D000509:alpha-Fetoproteins / Q000378:metabolism
D005938:Glucocorticoids; D011965:Receptors, Glucocorticoid; D000509:alpha-Fetoproteins; D011374:Progesterone