M Nurhalim Shahib1, Djamhoer Martaadisoebrata, Hidenori Kato. 1. Department of Biochemistry, Faculty of Medicine, Padjadjaran University, Jl Raya Bandung-Sumedang Km 21, Jatinangor-Sumedang, 45363 Jawa Barat, Indonesia. nurhalim@biochem.fk.unpad.ac.id
Abstract
OBJECTIVE: To examine the expression of HASH2 in gestational trophoblastic disease (GTD). STUDY DESIGN: DNA and RNA were isolated from 54 cases of GTD comprising 27 complete hydatidiform moles (CMs), 12 invasive moles (IvMs), 1 placental site trophoblastic tumor (PSTT) and 14 choriocarcinomas (ChCas). Reverse transcriptase polymerase chain reaction and polymerase chain reaction were performed using 2 sets of primers. One pair was used to detect a 190-base pair (bp) segment of the coding region of HASH2 and the other a 68-bp segment of the 3'UTR of the gene that contains a SacII polymorphism. RESULTS: HASH2 was expressed in all normal placenta but not in any of the 27 CMs. In contrast, samples of IvM, PSTT and ChCa, the malignant forms of GTD, all expressed HASH2. Amplification of the 68-bp segment, in the 3'UTR, revealed a product in malignant disease that was larger than 68 bps and resistant to digestion with SacII. CONCLUSION: Negative expression of HASH2 in CM but positive expression in malignant tumors suggests the presence of a specific mechanism for inactivation of the HASH2 gene in CM and reactivation in IvM or ChCa. Based on our data, we speculate that the 3' end of the gene might play an important role in regulating transcription of HASH2.
OBJECTIVE: To examine the expression of HASH2 in gestational trophoblastic disease (GTD). STUDY DESIGN: DNA and RNA were isolated from 54 cases of GTD comprising 27 complete hydatidiform moles (CMs), 12 invasive moles (IvMs), 1 placental site trophoblastic tumor (PSTT) and 14 choriocarcinomas (ChCas). Reverse transcriptase polymerase chain reaction and polymerase chain reaction were performed using 2 sets of primers. One pair was used to detect a 190-base pair (bp) segment of the coding region of HASH2 and the other a 68-bp segment of the 3'UTR of the gene that contains a SacII polymorphism. RESULTS:HASH2 was expressed in all normal placenta but not in any of the 27 CMs. In contrast, samples of IvM, PSTT and ChCa, the malignant forms of GTD, all expressed HASH2. Amplification of the 68-bp segment, in the 3'UTR, revealed a product in malignant disease that was larger than 68 bps and resistant to digestion with SacII. CONCLUSION: Negative expression of HASH2 in CM but positive expression in malignant tumors suggests the presence of a specific mechanism for inactivation of the HASH2 gene in CM and reactivation in IvM or ChCa. Based on our data, we speculate that the 3' end of the gene might play an important role in regulating transcription of HASH2.