ISPO

Published in Cancer Detection and Prevention 2000; 24(Supplement 1).

Profiling of differentially expressed genes in persistent gestational trophoblastic disease by complementary DNA expression array

PY Fong BSc 1, GSW Tsao PhD 2, HYS Ngan MD 3, PM Chiu BSc 1, ANY Cheung MD FRCPath 1

1,2,3 Departments of Pathology, Obstetrics and Gynecology, and Anatomy, University of Hong Kong, Hong Kong, China, pyfong@pathology.hku.hk

Hydatidiform moles (HM) is a form of gestational trophoblastic disease arising from abnormal trophoblasts. It has a substantial risk of developing persistent gestational trophoblastic disease (PTD) requiring chemotherapy. Some may even develop into choriocarcinoma. Except for the serial assays of serum and urine human chorionic gonadotrophin(hCG), there is no reliable predictor for the early detection of (PTD). Our previous studies on HM revealed association of apoptotic rates and telomerase activation with the development of (PTD). AIM: In this study, the profiling of differentially expressed genes from HM which subsequently developed PTD was compared with HM that later regressed spontaneously using human apoptosis array. METHOD: mRNA from persistent and regressive hydatidiform moles were reverse transcribed into cDNA. The cDNA was then hybridized to membranes with dotted arrays of human apoptotic cDNA including 205 genes related to apoptosis (CLONTECH's ATLASTM Human Apoptosis Array). RESULTS: Parallel analyses of the hybridized signals enabled identification of genes that were differentially expressed in HM that subsequently regressed and developed aggressive disease. Increased expression of several genes including p53-induced protein, mcl-1 and transforming protein rhoA H12, was found in the persistent mole. Several genes such as wee 1 Hu CDK-15, GRB2 isoform, c-myc blinding protein, insulin-like growth factor II and IGF-binding protein 3 were over-expressed in both tissues. CONCLUSION: This study confirmed the differential expression of certain apoptotic genes in HM that subsequently developed PTD. The roles of these genes in the pathogenesis and progression of HM will be further investigated in more clinical samples by reverse transcription- polymerase chain reaction and immunohistochemistry.

KEY WORDS: gestation trophoblastic disease, cDNA array, hydatidiform mole, apoptosis.

For more information, contact pyfong@pathology.hku.hk

Paper presented at the International Symposium on Impact of Biotechnology on Cancer Diagnostic & Prognostic Indicators; Geneva, Switzerland; October 28 - 31, 2000; in the section on metastasis & prevention.

http://www.cancerprev.org/Journal/Issues/24/101/113/3470