We have located links that may give you full text access.
Journal Article
Research Support, Non-U.S. Gov't
Altered imprinting, promoter usage, and expression of insulin-like growth factor-II gene in gestational trophoblastic diseases.
Gynecologic Oncology 2003 March
OBJECTIVE: We aimed to understand the involvement of imprinted genes in the pathogenesis of gestational trophoblastic diseases (GTD) such as hydatidiform mole (H-mole) and gestational trophoblastic tumors (GTT).
METHODS: An allelic-typing assay was performed using a PCR-RFLP-based method for identification of heterozygous informative cases. The usage of insulin-like growth factor-II (IGF2) promoters was examined by RT-PCR using promoter-specific primers. The mRNA expression of IGF2 and H19 was quantified using a densitometer.
RESULTS: The imprinting of IGF2 and H19 was maintained in all normal placenta tissues (n = 15) but relaxed in GTD (n = 47). Loss of imprinting (LOI) of IGF2 was in the order of GTT (57%) > complete H-mole (43%) > partial H-mole (25%). Similarly, LOI of H19 was in the order of GTT (40%) > complete H-mole (18%) > partial H-mole (0%). Promoter usage pattern of IGF2 changed with gestation stage of normal placentae and GTD. In normal placentae, the usage of promoter P1 was higher than that of P4 in the first trimester but lowered in the full term. H-mole and GTT predominantly used promoter P1 with relative silencing of promoter P4. Although normal early placenta and various GTD tissues showed the similar usage of IGF2 promoter P1, GTT tissues revealed the higher expression levels of IGF2 but a down-regulation of H19 relative to the normal early placentae.
CONCLUSIONS: These results suggest that LOI, deregulation of IGF2 promoters, and the altered expression levels of IGF2 and H19 genes might be associated with the progression of GTD.
METHODS: An allelic-typing assay was performed using a PCR-RFLP-based method for identification of heterozygous informative cases. The usage of insulin-like growth factor-II (IGF2) promoters was examined by RT-PCR using promoter-specific primers. The mRNA expression of IGF2 and H19 was quantified using a densitometer.
RESULTS: The imprinting of IGF2 and H19 was maintained in all normal placenta tissues (n = 15) but relaxed in GTD (n = 47). Loss of imprinting (LOI) of IGF2 was in the order of GTT (57%) > complete H-mole (43%) > partial H-mole (25%). Similarly, LOI of H19 was in the order of GTT (40%) > complete H-mole (18%) > partial H-mole (0%). Promoter usage pattern of IGF2 changed with gestation stage of normal placentae and GTD. In normal placentae, the usage of promoter P1 was higher than that of P4 in the first trimester but lowered in the full term. H-mole and GTT predominantly used promoter P1 with relative silencing of promoter P4. Although normal early placenta and various GTD tissues showed the similar usage of IGF2 promoter P1, GTT tissues revealed the higher expression levels of IGF2 but a down-regulation of H19 relative to the normal early placentae.
CONCLUSIONS: These results suggest that LOI, deregulation of IGF2 promoters, and the altered expression levels of IGF2 and H19 genes might be associated with the progression of GTD.
Full text links
Related Resources
Trending Papers
Challenges in Septic Shock: From New Hemodynamics to Blood Purification Therapies.Journal of Personalized Medicine 2024 Februrary 4
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection.International Journal of Molecular Sciences 2024 April 4
The 'Ten Commandments' for the 2023 European Society of Cardiology guidelines for the management of endocarditis.European Heart Journal 2024 April 18
A Guide to the Use of Vasopressors and Inotropes for Patients in Shock.Journal of Intensive Care Medicine 2024 April 14
Diagnosis and Management of Cardiac Sarcoidosis: A Scientific Statement From the American Heart Association.Circulation 2024 April 19
Essential thrombocythaemia: A contemporary approach with new drugs on the horizon.British Journal of Haematology 2024 April 9
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app