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Eun Hee Kim  (Kim EH) 8 Articles
Diabetes, Obesity and Metabolism
Prognostic Value of Triglyceride and Glucose Index for Incident Type 2 Diabetes beyond Metabolic Health and Obesity
Hwi Seung Kim, Jiwoo Lee, Yun Kyung Cho, Eun Hee Kim, Min Jung Lee, Hong-Kyu Kim, Joong-Yeol Park, Woo Je Lee, Chang Hee Jung
Endocrinol Metab. 2021;36(5):1042-1054.   Published online October 21, 2021
DOI: https://doi.org/10.3803/EnM.2021.1184
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AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
Metabolically healthy obese (MHO) phenotype is metabolically heterogeneous in terms of type 2 diabetes (T2D). Previously, the triglyceride and glucose (TyG) index has been considered for identifying metabolic health and future risk of T2D. This study aimed to evaluate the risk of incident T2D according to obesity status and metabolic health, categorized by four different criteria and the TyG index.
Methods
The study included 39,418 Koreans without T2D at baseline. The risk of T2D was evaluated based on four different definitions of metabolic health and obesity status and according to the baseline TyG index within each metabolic health and obesity group.
Results
During the median follow-up at 38.1 months, 726 individuals developed T2D. Compared with the metabolically healthy non-obese (MHNO) group with low TyG index, the MHO group with high TyG index showed increased risk of T2D in all four definitions of metabolic health with multivariate-adjusted hazard ratios of 2.57 (95% confidence interval [CI], 1.76 to 3.75), 3.72 (95% CI, 2.15 to 6.43), 4.13 (95% CI, 2.67 to 6.38), and 3.05 (95% CI, 2.24 to 4.15), when defined by Adult Treatment Panel III, Wildman, Karelis, and homeostasis model assessment (HOMA) criteria, respectively.
Conclusion
MHO subjects with high TyG index were at an increased risk of developing T2D compared with MHNO subjects, regardless of the definition of metabolic health. TyG index may serve as an additional factor for predicting the individual risk of incident T2D in MHO subjects.
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Thyroid
Accelerated Disease Progression after Discontinuation of Sorafenib in a Patient with Metastatic Papillary Thyroid Cancer
Kyung-Jin Yun, Woohyeon Kim, Eun Hee Kim, Min-Hee Kim, Dong-Jun Lim, Moo-Il Kang, Bong-Yun Cha
Endocrinol Metab. 2014;29(3):388-393.   Published online September 25, 2014
DOI: https://doi.org/10.3803/EnM.2014.29.3.388
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  • 24 Web of Science
  • 23 Crossref
AbstractAbstract PDFPubReader   

Distant metastases from papillary thyroid carcinoma (PTC) are rare and are associated with a poor prognosis. Here, we describe a patient with metastatic PTC who was treated with a tyrosine kinase inhibitor (TKI, sorafenib) for several months that was acutely exacerbated by discontinuation. A 43-year-old male was diagnosed with PTC in February 2004 and underwent total thyroidectomy followed by two courses of high-dose radioactive iodine (RAI) therapy. Despite two additional courses of high-dose RAI therapy, lung and muscle metastases were developed. Treatment with sorafenib was begun in September 2010. After 11 months treatment of sorafenib, newly developed metastatic lesions were found in mediastinal lymph nodes, liver, and bones. Considered as treatment failure, the administration of sorafenib was discontinued. Two weeks after sorafenib treatment was stopped, the disease progressed abruptly and caused death of the patient by respiratory failure. In our patient, PTC progressed rapidly after the cessation of sorafenib treatment. Patients with several other types of cancer have also experienced such rapid disease progression, termed "flare-ups." Physicians should be aware that flare-ups may occur in advanced PTC patients following the cessation of TKI therapy.

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  • Resistance, rebound, and recurrence regrowth patterns in pediatric low-grade glioma treated by MAPK inhibition: A modified Delphi approach to build international consensus-based definitions—International Pediatric Low-Grade Glioma Coalition
    Patricia O’Hare, Tabitha Cooney, Peter de Blank, David H Gutmann, Mark Kieran, Till Milde, Jason Fangusaro, Michael Fisher, Shivaram Avula, Roger Packer, Kohei Fukuoka, Kshitij Mankad, Sabine Mueller, Angela J Waanders, Enrico Opocher, Eric Bouffet, Eric
    Neuro-Oncology.2024;[Epub]     CrossRef
  • Lenvatinib: an investigational agent for the treatment of differentiated thyroid cancer
    Silvia Martina Ferrari, Giusy Elia, Francesca Ragusa, Sabrina Rosaria Paparo, Valeria Mazzi, Mario Miccoli, Maria Rosaria Galdiero, Gilda Varricchi, Rudy Foddis, Giovanni Guglielmi, Claudio Spinelli, Concettina La Motta, Salvatore Benvenga, Alessandro Ant
    Expert Opinion on Investigational Drugs.2021; 30(9): 913.     CrossRef
  • Low Dose of Lenvatinib Treatment for Patients of Radioiodine-Refractory Differentiated Thyroid Carcinoma – A Real-World Experience
    He-Jiun Jiang, Yen-Hsiang Chang, Yen-Hao Chen, Che-Wei Wu, Pei-Wen Wang, Pi-Jung Hsiao
    Cancer Management and Research.2021; Volume 13: 7139.     CrossRef
  • Rapid disease progression after discontinuation of lenvatinib in thyroid cancer
    Haruhiko Yamazaki, Kiminori Sugino, Kenichi Matsuzu, Chie Masaki, Junko Akaishi, Kiyomi Hames, Chisato Tomoda, Akifumi Suzuki, Takashi Uruno, Keiko Ohkuwa, Wataru Kitagawa, Mitsuji Nagahama, Munetaka Masuda, Koichi Ito
    Medicine.2020; 99(11): e19408.     CrossRef
  • Lenvatinib for thyroid cancer treatment: discovery, pre-clinical development and clinical application
    Rosa Maria Paragliola, Andrea Corsello, Valeria Del Gatto, Giampaolo Papi, Alfredo Pontecorvi, Salvatore Maria Corsello
    Expert Opinion on Drug Discovery.2020; 15(1): 11.     CrossRef
  • Efficacy and Limitations of Lenvatinib Therapy for Radioiodine-Refractory Differentiated Thyroid Cancer: Real-World Experiences
    Chie Masaki, Kiminori Sugino, Naoko Saito, Junko Akaishi, Kiyomi Y. Hames, Chisato Tomoda, Akifumi Suzuki, Kenichi Matsuzu, Takashi Uruno, Keiko Ohkuwa, Wataru Kitagawa, Mitsuji Nagahama, Koichi Ito
    Thyroid.2020; 30(2): 214.     CrossRef
  • Papillary thyroid carcinoma with hyperthyroidism and multiple metastases
    Li-li Zhang, Bin Liu, Fang-fang Sun, Hong-yu Li, Shuang Li, Li-rong Zhao
    Medicine.2020; 99(30): e21346.     CrossRef
  • Missing Skeletal Muscle Metastases of Papillary Thyroid Carcinoma
    Leszek Herbowski
    Diagnostics.2020; 10(7): 457.     CrossRef
  • Reply to “Missing Skeletal Muscle Metastases of Papillary Thyroid Carcinoma”
    Liviu Hitu, Calin Cainap, Dragos Apostu, Katalin Gabora, Eduard-Alexandru Bonci, Marius Badan, Alexandru Mester, Andra Piciu
    Diagnostics.2020; 10(7): 458.     CrossRef
  • Hif-1α Inhibitors Could Successfully Inhibit the Progression of Differentiated Thyroid Cancer in Vitro
    Min-Hee Kim, Tae Hyeong Lee, Jin Soo Lee, Dong-Jun Lim, Peter Chang-Whan Lee
    Pharmaceuticals.2020; 13(9): 208.     CrossRef
  • Extended Real-World Observation of Patients Treated with Sorafenib for Radioactive Iodine-Refractory Differentiated Thyroid Carcinoma and Impact of Lenvatinib Salvage Treatment: A Korean Multicenter Study
    Hye-Seon Oh, Dong Yeob Shin, Mijin Kim, So Young Park, Tae Hyuk Kim, Bo Hyun Kim, Eui Young Kim, Won Bae Kim, Jae Hoon Chung, Young Kee Shong, Dong Jun Lim, Won Gu Kim
    Thyroid.2019; 29(12): 1804.     CrossRef
  • Rapid pleural effusion after discontinuation of lenvatinib in a patient with pleural metastasis from thyroid cancer
    Taisuke Uchida, Hideki Yamaguchi, Kazuhiro Nagamine, Tadato Yonekawa, Eriko Nakamura, Nobuhiro Shibata, Fumiaki Kawano, Yujiro Asada, Masamitsu Nakazato
    Endocrinology, Diabetes & Metabolism Case Reports.2019;[Epub]     CrossRef
  • Thyroid Disorders in the Elderly
    Kevin Higgins
    Clinics in Geriatric Medicine.2018; 34(2): 259.     CrossRef
  • Treatment of refractory thyroid cancer
    Amandine Berdelou, Livia Lamartina, Michele Klain, Sophie Leboulleux, Martin Schlumberger, _ _
    Endocrine-Related Cancer.2018; 25(4): R209.     CrossRef
  • Clinical guidance for radioiodine refractory differentiated thyroid cancer
    Matti L. Gild, Duncan J. Topliss, Diana Learoyd, Francis Parnis, Jeanne Tie, Brett Hughes, John P. Walsh, Donald S.A. McLeod, Roderick J. Clifton‐Bligh, Bruce G. Robinson
    Clinical Endocrinology.2018; 88(4): 529.     CrossRef
  • Case for Stopping Targeted Therapy When Lung Cancer Progresses on Treatment in Hospice-Eligible Patients
    Thomas J. Smith, Nasser Hanna, David Johnson, Sherman Baker, William A. Biermann, Julie Brahmer, Peter M. Ellis, Giuseppe Giaccone, Paul J. Hesketh, Ishmael Jaiyesimi, Natasha B. Leighl, Gregory J. Riely, Joan H. Schiller, Bryan J. Schneider, Joan Tashbar
    Journal of Oncology Practice.2017; 13(12): 780.     CrossRef
  • Intermittent Dosing of Dabrafenib and Trametinib in Metastatic BRAFV600E Mutated Papillary Thyroid Cancer: Two Case Reports
    Paul S. White, Anita Pudusseri, Stephanie L. Lee, Omar Eton
    Thyroid.2017; 27(9): 1201.     CrossRef
  • Aggressive differentiated thyroid cancer with multiple metastases and NRAS and TERT promoter mutations: A case report
    Fabiana Pani, Elisabetta Macerola, Fulvio Basolo, Francesco Boi, Mario Scartozzi, Stefano Mariotti
    Oncology Letters.2017; 14(2): 2186.     CrossRef
  • Tumors Sharply Increased after Ceasing Pazopanib Therapy for a Patient with Advanced Uterine Leiomyosarcoma: Experience of Tumor Flare
    Terumi Tanigawa, Shintaro Morisaki, Hisanobu Fukuda, Shuichiro Yoshimura, Hisayoshi Nakajima, Kohei Kotera
    Case Reports in Obstetrics and Gynecology.2017; 2017: 1.     CrossRef
  • Initial Size of Metastatic Lesions Is Best Prognostic Factor in Patients with Metastatic Differentiated Thyroid Carcinoma Confined to the Lung
    Mijin Kim, Won Gu Kim, Suyeon Park, Hyemi Kwon, Min Ji Jeon, Jong Jin Lee, Jin-Sook Ryu, Tae Yong Kim, Young Kee Shong, Won Bae Kim
    Thyroid.2017; 27(1): 49.     CrossRef
  • Articles in 'Endocrinology and Metabolism' in 2014
    Won-Young Lee
    Endocrinology and Metabolism.2015; 30(1): 47.     CrossRef
  • Pharmacodynamic study of axitinib in patients with advanced malignancies assessed with 18F-3′deoxy-3′fluoro-l-thymidine positron emission tomography/computed tomography
    Justine Yang Bruce, Peter Colin Scully, Lakeesha L. Carmichael, Jens C. Eickhoff, Scott B. Perlman, Jill Marie Kolesar, Jennifer L. Heideman, Robert Jeraj, Glenn Liu
    Cancer Chemotherapy and Pharmacology.2015; 76(1): 187.     CrossRef
  • Optimal Differentiated Thyroid Cancer Management in the Elderly
    Donald S. A. McLeod, Kelly Carruthers, Dev A. S. Kevat
    Drugs & Aging.2015; 32(4): 283.     CrossRef
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A Case of Familial Multiple Endocrine Neoplasia Type 1 with a Novel Mutation in the MEN1 Gene.
Min Jung Kim, Eun Hee Kim, Mi Seon Shin, Joo Hui Kim, Hee Kyung Na, Seong Joon Park, Sang Ah Lee, Eun Hee Koh, Woo Je Lee, Ki Ho Song, Joong Yeol Park, Ki Up Lee, Gu Hwan Kim, Han Wook Yoo, Min Seon Kim
Endocrinol Metab. 2011;26(2):171-176.   Published online June 1, 2011
DOI: https://doi.org/10.3803/EnM.2011.26.2.171
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  • 31 Download
  • 2 Crossref
AbstractAbstract PDF
Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by the occurrence of multiple tumors in the parathyroid gland, pancreatic islet, and pituitary gland. This condition is caused by mutations of MEN1, a tumor suppressor gene. Thus far, 565 different germline and somatic mutations of the MEN1 gene have been reported. Herein, we describe the case of a 23-year-old woman who suffered from a repetitive loss of consciousness. After workup, the patient was diagnosed with MEN1 with insulinoma, hyperparathyrodism due to parathyroid adenoma, and non-functioning pituitary microadenoma. She underwent a partial parathyroidectomy and distal pancreatectomy. Familial screening of MEN1 revealed that her brother had prolactinoma, hyperparathyroidism, pancreatic gastrinoma and non-functioning adrenal adenoma. Her father had hyperparathyroidism, pancreatic tumor, and adrenal adenoma. Upon genetic analysis of the MEN1 gene, a novel mutation in the MEN1 gene (exon 1, c.251del; p.Ser84LuefsX35) was detected in the patient, as well as her father and brother.

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  • Parathyroid disorder and concomitant thyroid cancer in patients with multiple endocrine neoplasia type 1
    Ying Wang, Sheng Cai, He Liu, Rui-Na Zhao, Xing-Jian Lai, Ke Lv, Yu-Xin Jiang, Jian-Chu Li
    Medicine.2021; 100(36): e27098.     CrossRef
  • Genetic and Epigenetic Analysis in Korean Patients with Multiple Endocrine Neoplasia Type 1
    Yoon Jung Chung, Sena Hwang, Jong Ju Jeong, Sun Yong Song, Se Hoon Kim, Yumie Rhee
    Endocrinology and Metabolism.2014; 29(3): 270.     CrossRef
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A Case of Painful Graves' Disease.
Ji Yun Jeong, Tae Yong Kim, Eun Hee Kim, Eui Young Kim, Sang Ah Lee, Ji Hye Yim, Kyung Min Kim, Won Bae Kim, Young Kee Shong
J Korean Endocr Soc. 2008;23(5):337-341.   Published online October 1, 2008
DOI: https://doi.org/10.3803/jkes.2008.23.5.337
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AbstractAbstract PDF
Graves' disease rarely presents as pain and tenderness of goiter, with only a few cases reported in the literature. We describe a case of painful Graves' disease presenting as 2 episodes of painful goiter.
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A Case of Carcinoma Showing Thymus-Like Differentiation (CASTLE) in the Thyroid.
Eun Hee Kim, Ji Yun Jeong, Eui Young Kim, Sang Ah Lee, Kyung Min Kim, Ji Hye Yim, Won Gu Kim, Tae Yong Kim, Sun A Kim, Gyungyup Gong, Young Kee Shong, Won Bae Kim
J Korean Endocr Soc. 2008;23(4):272-276.   Published online August 1, 2008
DOI: https://doi.org/10.3803/jkes.2008.23.4.272
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  • 2 Crossref
AbstractAbstract PDF
Carcinoma Showing Thymus-Like Differentiation (CASTLE) is a very rare malignant neoplasm of the thyroid, and this resembles lymphoepithelioma or squamous cell carcinoma of the thymus. It originates from ectopic thymic tissue or remnants of the branchial pouches. We recently experienced a case of CASTLE in the thyroid gland of a 61-year-old woman. She presented with an asymptomatic mass in the right thyroid gland and she was diagnosed with 'poorly differentiated carcinoma' of the thyroid by fine needle aspiration cytology (FNAC). Total thyroidectomy was performed for both diagnostic and therapeutic purposes. Histologic examination of the resected tumor showed that the tumor was lobulated with expanding fibrous bands, and it was infiltrated by lymphocytes and plasma cells. The tumor cells had oval, large vesicular nuclei and prominent nucleoli, and the immunohistochemical staining was positive for CD5 and bcl-2, so the patient was diagnosed with thyroid CASTLE. We report here on a case of CASTLE in the thyroid gland treated by surgery and external neck radiation therapy.

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  • Intrathyroidal thymic carcinoma exhibiting neuroendocrine differentiation: Case report with cytomorphology, immunocytochemistry, and review of the literature focusing on cytology
    Wen‐hao Ren, Kun Dong, Xiao‐zheng Huang, Yan‐li Zhu
    Diagnostic Cytopathology.2019; 47(11): 1197.     CrossRef
  • Cytologic Findings of Thyroid Carcinoma Showing Thymus-like Differentiation: A Case Report
    Sunhee Chang, Mee Joo, Hanseong Kim
    Korean Journal of Pathology.2012; 46(3): 302.     CrossRef
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A Case of Diffuse Hemorrhage into the Thyroid Gland after Fine Needle Aspiration, and This was Treated by Arterial Embolization.
Eui Young Kim, Jung Min Kim, Eun Hee Kim, Ji Yun Jeong, Sang Ah Lee, Ji Young Choi, Ji Hye Yim, Pil Hyung Lee, Tae Yong Kim, Young Kee Shong, Won Bae Kim
J Korean Endocr Soc. 2008;23(3):199-203.   Published online June 1, 2008
DOI: https://doi.org/10.3803/jkes.2008.23.3.199
  • 2,071 View
  • 29 Download
  • 2 Crossref
AbstractAbstract PDF
Although hematoma formation after fine needle aspiration cytology fine needle aspiration cytology (FNAC) is a most common complication and most of these hematomas are self-limiting with minimal pain, a massive intra-thyroidal hemorrhage that produces acute airway obstruction had rarely been reported on.

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  • Characteristics Evaluation of Hobun Pigments according to Shell Types and Calcination
    Ju Hyun Park, Sun Myung Lee, Myoung Nam Kim, Jin Young Hong
    Economic and Environmental Geology.2023; 56(6): 899.     CrossRef
  • Endovascular treatment of massive hemorrhage arising from inferior thyroid artery after fine needle aspiration of thyroid: a case report
    Ho Sig Jang, Yook Kim
    BMC Surgery.2021;[Epub]     CrossRef
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Changes in Somatostatin Receptor mRNA Levels by G Protein Mutation in GH3 Cells Which Show Responsiveness to Growth Hormone-Releasing Hormone.
Eun Hee Kim, Sook Jin Sohn, Min A Lee, Sang Hee Seo, Sung Hee Ju, Dahm Lee, Hyun Ju Chung, Jee Chang Jung, Seung Joon Park
J Korean Endocr Soc. 2005;20(4):323-333.   Published online August 1, 2005
DOI: https://doi.org/10.3803/jkes.2005.20.4.323
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AbstractAbstract PDF
BACKGROUND
S: GH3 cells lack growth hormone(GH)-releasing hormone(GHRH) receptors. In this study, GH3 cells permanently transfected with human GHRH receptor cDNA(GH3-GHRHR cells), were established in order to examine the effects of GHRH and G protein mutation(gsp oncogene) on the levels of somatostatin receptor mRNA. METHODS: GH3 cells were permanently transfected with a plasmid expressing human GHRH receptor cDNA. The GHRH receptor mRNA was detected by RT-PCR. The responsiveness to GHRH was evaluated using a GHRH binding assay, Western blot analysis, Northern blot analysis, and measurements of the intracellular cAMP levels and GH release. Cells were transiently transfected with the gsp oncogene, and then treated with GHRH or octreotide for 4h. The sst1 and sst2 mRNA levels were measured using real-time RT-PCR analyses. RESULTS: GHRH receptor mRNA was detected in the GH3 cells permanently transfected with human GHRH receptor cDNA. The GHRH binding assay showed that GHRH was bound to the GH3-GHRHR cells. The GHRH treatment increased the intracellular cAMP levels, GH release, GH mRNA levels, and MAPK activity, as well as the levels of sst1 and sst2 mRNA. Transient expression of the gsp oncogene for 48h increased the cAMP, GH release, and levels of sst1 and sst2 mRNA. In the gsp-transfected GH3-GHRHR cells, GHRH stimulation resulted in decreases in the magnitude of the increase in the levels of sst1 and sst2 mRNA compared to those transfected with a control vector. Octreotide treatment did not alter the levels of sst1 and sst2 mRNA in either the control or gsp-transfected cells. CONCLUSION: These results suggest that GH3 cells permanently transfected with the GHRH receptor are useful in the in vitro studies on the actions of GHRH. The gsp oncogene was shown to increases the levels of sst1 and sst2 mRNA in GH3 cells, but these findings are unlikely to be the major mechanism by which gsp-positive pituitary tumors show a greater response to somatostatin. The discrepancy between the in vivo and these in vitro results should be examined further.
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Gene Expression of the Somatostatin Receptors, Gi2 alpha and Pit-1 alpha in GH3 Cells Permanently Transfected with a Mutant Gs alpha Gene.
Cheol young Park, In myung Yang, Eun hee Kim, Sook jin Sohn, Mee sook Ryu, Jeong taek Woo, Sung woon Kim, Jin woo Kim, Young seol Kim, Young kil Choi, Seung joon Park
J Korean Endocr Soc. 2002;17(2):170-182.   Published online April 1, 2002
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AbstractAbstract PDF
BACKGROUND
Cyclic AMP stimulates the expression of the somatostatin (SRIF) receptor (sst1-5) and human growth hormone (GH)-secreting pituitary tumors with the gsp oncogene which increases intracellular cAMP levels, and shows a good inhibitory response of the GH to SRIF. Taken together, we hypothesized that the gsp oncogene may increase the SRIF receptor expression or and factors related to the postreceptor signal transduction of the SRIF, in order to enhance its responsiveness to SRIF. To test this hypothesis, we investigated if the gsp oncogene could increase the sst1, sst2, Gi2 alpha, and pit-1 alpha gene expression in GH3 cells. METHODS: GH3 cells were permanently transfected with the plasmid expressing Gs alpha gene, where the arginine of codon 201 was replaced with histidine. Intracellular cAMP levels and GH concentrations were measured by radioimmunoassays. Gene expressions of the sst1, sst2, Gi2 alpha, and pit-1 alpha were determined by RT-PCR. RESULTS: Intracellular cAMP levels and medium GH release were increased by 1.7 and 2.7-fold in GH3 cells expressing the gsp oncogene, respectively. In GH3 cells expressing the gsp oncogene, the sst1 mRNA levels were decreased, whereas those of the sst2, Gi2 alpha and pit-1 alpha mRNA were increased. A 4-h forskolin (10 M) stimulation remarkably increased the sst1 and sst2 mRNA levels in GH3 cells expressing wild and mutant Gs alpha . However, forskolin did not affect the Gi2 alpha and pit-1 alpha mRNA levels. In contrast, SRIF (1 M, 2 h) decreased the sst2 mRNA levels only in GH3 cells expressing the gsp oncogene. CONCLUSION: These results suggest that higher expressions of sst2, Gi2 alpha, and pit-1 alpha, induced by the gsp oncogene may be a mechanism by which gsp-positive pituitary tumors show a greater response to SRIF. The discrepancy between these and in vivo results should be explored further.
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