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Gunnar Westin - One of the best experts on this subject based on the ideXlab platform.
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abstract 1982 tceb3c elongin a3 on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors
Cancer Research, 2013Co-Authors: Katarina Edfeldt, Peyman Björklund, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Gunnar WestinAbstract:Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC Small intestine neuroendocrine Tumors (SI-NETs) arise from the enterochromaffin cells and produce hormones which can cause the carcinoid syndrome. The incidence is increasing and the five-year survival rate is 60-80 %. Loss of one copy of chromosome 18 is a very frequent event in these Tumors, supporting the presence of a crucial Tumor Suppressor Gene. This study investigated whether TCEB3C, encoding Elongin A3, presents a putative Tumor Suppressor Gene in SI-NETs. This Gene is currently the only known imprinted Gene on chromosome 18, requiring only one Gene copy inactivation event to fulfill the Knudson hypothesis. Elongin A3 expression in SI-NETs (n=47) was heteroGeneous and negative in most cells. 5-Aza-2’-deoxycytidine induced expression of Elongin A3 in a carcinoid Tumor cell line and in Tumor derived primary cell cultures, but not in a control cell line. Also the General histone methyltransferase inhibitor 3-deazaneplanocin A induced TCEB3C expression in the carcinoid Tumor cell line, but not in control cells suggesting further that the TCEB3C Gene was epiGenetically suppressed in neuroendocrine Tumor cells. The TCEB3C Gene encompasses an CpG island and quantitative cytosine CpG methylation analysis will be presented. Furthermore, overexpression of Elongin A3 led to a decrease in clonogenic survival of carcinoid Tumor cells, but not of control cells strongly supporting a growth-regulatory role. These results support a putative Tumor Suppressor role of TCEB3C in neuroendocrine cells of the small intestine. Citation Format: Katarina Edfeldt, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Peyman Bjorklund, Gunnar Westin. TCEB3C (Elongin A3) on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1982. doi:10.1158/1538-7445.AM2013-1982
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Abstract 1982: TCEB3C (Elongin A3) on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors.
Molecular and Cellular Biology, 2013Co-Authors: Katarina Edfeldt, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Gunnar WestinAbstract:TCEB3C (Elongin A3) on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors.
Katarina Edfeldt - One of the best experts on this subject based on the ideXlab platform.
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abstract 1982 tceb3c elongin a3 on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors
Cancer Research, 2013Co-Authors: Katarina Edfeldt, Peyman Björklund, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Gunnar WestinAbstract:Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC Small intestine neuroendocrine Tumors (SI-NETs) arise from the enterochromaffin cells and produce hormones which can cause the carcinoid syndrome. The incidence is increasing and the five-year survival rate is 60-80 %. Loss of one copy of chromosome 18 is a very frequent event in these Tumors, supporting the presence of a crucial Tumor Suppressor Gene. This study investigated whether TCEB3C, encoding Elongin A3, presents a putative Tumor Suppressor Gene in SI-NETs. This Gene is currently the only known imprinted Gene on chromosome 18, requiring only one Gene copy inactivation event to fulfill the Knudson hypothesis. Elongin A3 expression in SI-NETs (n=47) was heteroGeneous and negative in most cells. 5-Aza-2’-deoxycytidine induced expression of Elongin A3 in a carcinoid Tumor cell line and in Tumor derived primary cell cultures, but not in a control cell line. Also the General histone methyltransferase inhibitor 3-deazaneplanocin A induced TCEB3C expression in the carcinoid Tumor cell line, but not in control cells suggesting further that the TCEB3C Gene was epiGenetically suppressed in neuroendocrine Tumor cells. The TCEB3C Gene encompasses an CpG island and quantitative cytosine CpG methylation analysis will be presented. Furthermore, overexpression of Elongin A3 led to a decrease in clonogenic survival of carcinoid Tumor cells, but not of control cells strongly supporting a growth-regulatory role. These results support a putative Tumor Suppressor role of TCEB3C in neuroendocrine cells of the small intestine. Citation Format: Katarina Edfeldt, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Peyman Bjorklund, Gunnar Westin. TCEB3C (Elongin A3) on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1982. doi:10.1158/1538-7445.AM2013-1982
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Abstract 1982: TCEB3C (Elongin A3) on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors.
Molecular and Cellular Biology, 2013Co-Authors: Katarina Edfeldt, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Gunnar WestinAbstract:TCEB3C (Elongin A3) on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors.
Andrew Arnold - One of the best experts on this subject based on the ideXlab platform.
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analysis of cyp27b1 encoding 25 hydroxyvitamin d 1α hydroxylase as a candidate Tumor Suppressor Gene in primary and severe secondary tertiary hyperparathyroidism
Journal of Bone and Mineral Research, 2009Co-Authors: Kelly Lauter, Andrew ArnoldAbstract:CYP27B1, encoding 25-hydroxyvitamin D-1α-hydroxylase, converts 25-hydroxyvitamin D to its active form, 1,25-dihydroxyvitamin D, and is expressed primarily in the kidney but also in nontraditional sites including the parathyroid glands. Whereas the role of locally produced 1,25-dihydroxyvitamin D is not yet clear, it is possible that it contributes importantly to vitamin D–mediated inhibition of parathyroid cell growth, so CYP27B1 can be considered a candidate parathyroid Tumor Suppressor Gene in that its acquired inactivation in a parathyroid cell could confer a Tumorigenic growth advantage. Expression of CYP27B1 has also been reported to be altered in parathyroid neoplasms. Because detection of inactivating mutations is the central criterion for validating a candidate Tumor Suppressor, we directly sequenced the coding region and all splice sites of CYP27B1 in 31 sporadic parathyroid adenomas and 31 parathyroid Tumors from patients with refractory secondary/tertiary hyperparathyroidism. No nonsense, frameshift, or other inactivating mutations were found, and there was no sign of homozygous deletion. Our findings indicate that CYP27B1 does not commonly serve as a classical Tumor Suppressor Gene in the development of sporadic parathyroid adenomas or of refractory secondary/tertiary hyperparathyroidism.
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mutational analysis of cdkn1b a candidate Tumor Suppressor Gene in refractory secondary tertiary hyperparathyroidism
Kidney International, 2008Co-Authors: Kelly Lauter, Andrew ArnoldAbstract:Most patients with refractory secondary/tertiary hyperparathyroidism have monoclonal parathyroid Tumors. Inactivating mutations of CDKN1B, encoding the p27 cyclin-dependent kinase inhibitor, were reported to cause hyperparathyroidism in a multiple endocrine neoplasia type 1-like syndrome. Further, there was decreased expression of CDKN1B in parathyroid Tumors of patients with chronic kidney disease. We sequenced the entire coding region and splice sites of CDKN1B in 50 parathyroid Tumors from 35 patients to see if inactivating mutations could cause monoclonal TumoriGenesis in refractory secondary/tertiary hyperparathyroidism. No frameshift, nonsense, or other clearly inactivating mutations were found, nor was there evidence of homozygous deletion or loss of heterozygosity. The absence of clonal inactivating mutations suggests that CDKN1B is not a classical Tumor-Suppressor Gene in secondary/tertiary parathyroid Tumors.
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mutational analysis of the vitamin d receptor does not support its candidacy as a Tumor Suppressor Gene in parathyroid adenomas
The Journal of Clinical Endocrinology and Metabolism, 2006Co-Authors: Elizabeth Hanna Samander, Andrew ArnoldAbstract:Context: The vitamin D receptor Gene (VDR) is a compelling candidate Tumor Suppressor Gene for parathyroid adenomas based on existing evidence of the vitamin D system’s antiproliferative actions in parathyroid and other tissues, its reported inhibition of PTH Gene transcription, and the decreased expression of VDR mRNA and VDR protein observed in parathyroid adenomas. Objective: Because demonstration of intragenic mutations is required to establish the authenticity and primary role in pathoGenesis for any candidate Tumor Suppressor Gene, we examined the VDR Gene in parathyroid adenomas for the presence of such mutations and other loss-of-function abnormalities. Methods and Results: Genomic DNA samples from 37 sporadic parathyroid adenomas and matched normal control DNA from the same individuals were subjected to direct sequencing of the entire VDR coding region and all intron-exon boundaries. No VDR coding region or junctional mutations were identified. The Tumors were also analyzed for loss of heterozygo...
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loss of the retinoblastoma Tumor Suppressor Gene in parathyroid carcinoma
The New England Journal of Medicine, 1994Co-Authors: Vincent L Cryns, Ann D Thor, Hong Ji Xu, Shi Xue Hu, Margaret E Wierman, Austin L Vickery, William F Benedict, Andrew ArnoldAbstract:Background The origin and molecular pathoGenesis of parathyroid carcinoma are unknown. This life-threatening cause of primary hyperparathyroidism cannot be reliably distinguished from its benign counterpart on the basis of histopathological features alone. Because the PRAD1, or cyclin D1, Gene, a cell-cycle regulator, has been implicated in a subgroup of benign parathyroid Tumors, we examined the possibility that another cell-cycle regulator with possible functional links to PRAD1, the retinoblastoma Tumor-Suppressor Gene (RB), might be involved in the molecular pathoGenesis of parathyroid carcinoma. Methods Parathyroid carcinomas from 9 patients and adenomas from 21 were studied for evidence of Tumor-specific loss of RB Gene DNA (allelic loss) by analysis of four DNA polymorphisms and for evidence of altered expression of RB protein by immunohistochemical staining. Results All of 11 specimens from 5 patients with parathyroid carcinoma and informative DNA patterns and 1 of 19 specimens from 19 patients wi...
Eva Tiensuu Janson - One of the best experts on this subject based on the ideXlab platform.
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abstract 1982 tceb3c elongin a3 on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors
Cancer Research, 2013Co-Authors: Katarina Edfeldt, Peyman Björklund, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Gunnar WestinAbstract:Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC Small intestine neuroendocrine Tumors (SI-NETs) arise from the enterochromaffin cells and produce hormones which can cause the carcinoid syndrome. The incidence is increasing and the five-year survival rate is 60-80 %. Loss of one copy of chromosome 18 is a very frequent event in these Tumors, supporting the presence of a crucial Tumor Suppressor Gene. This study investigated whether TCEB3C, encoding Elongin A3, presents a putative Tumor Suppressor Gene in SI-NETs. This Gene is currently the only known imprinted Gene on chromosome 18, requiring only one Gene copy inactivation event to fulfill the Knudson hypothesis. Elongin A3 expression in SI-NETs (n=47) was heteroGeneous and negative in most cells. 5-Aza-2’-deoxycytidine induced expression of Elongin A3 in a carcinoid Tumor cell line and in Tumor derived primary cell cultures, but not in a control cell line. Also the General histone methyltransferase inhibitor 3-deazaneplanocin A induced TCEB3C expression in the carcinoid Tumor cell line, but not in control cells suggesting further that the TCEB3C Gene was epiGenetically suppressed in neuroendocrine Tumor cells. The TCEB3C Gene encompasses an CpG island and quantitative cytosine CpG methylation analysis will be presented. Furthermore, overexpression of Elongin A3 led to a decrease in clonogenic survival of carcinoid Tumor cells, but not of control cells strongly supporting a growth-regulatory role. These results support a putative Tumor Suppressor role of TCEB3C in neuroendocrine cells of the small intestine. Citation Format: Katarina Edfeldt, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Peyman Bjorklund, Gunnar Westin. TCEB3C (Elongin A3) on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1982. doi:10.1158/1538-7445.AM2013-1982
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Abstract 1982: TCEB3C (Elongin A3) on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors.
Molecular and Cellular Biology, 2013Co-Authors: Katarina Edfeldt, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Gunnar WestinAbstract:TCEB3C (Elongin A3) on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors.
Tanvver Ahmad - One of the best experts on this subject based on the ideXlab platform.
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abstract 1982 tceb3c elongin a3 on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors
Cancer Research, 2013Co-Authors: Katarina Edfeldt, Peyman Björklund, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Gunnar WestinAbstract:Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC Small intestine neuroendocrine Tumors (SI-NETs) arise from the enterochromaffin cells and produce hormones which can cause the carcinoid syndrome. The incidence is increasing and the five-year survival rate is 60-80 %. Loss of one copy of chromosome 18 is a very frequent event in these Tumors, supporting the presence of a crucial Tumor Suppressor Gene. This study investigated whether TCEB3C, encoding Elongin A3, presents a putative Tumor Suppressor Gene in SI-NETs. This Gene is currently the only known imprinted Gene on chromosome 18, requiring only one Gene copy inactivation event to fulfill the Knudson hypothesis. Elongin A3 expression in SI-NETs (n=47) was heteroGeneous and negative in most cells. 5-Aza-2’-deoxycytidine induced expression of Elongin A3 in a carcinoid Tumor cell line and in Tumor derived primary cell cultures, but not in a control cell line. Also the General histone methyltransferase inhibitor 3-deazaneplanocin A induced TCEB3C expression in the carcinoid Tumor cell line, but not in control cells suggesting further that the TCEB3C Gene was epiGenetically suppressed in neuroendocrine Tumor cells. The TCEB3C Gene encompasses an CpG island and quantitative cytosine CpG methylation analysis will be presented. Furthermore, overexpression of Elongin A3 led to a decrease in clonogenic survival of carcinoid Tumor cells, but not of control cells strongly supporting a growth-regulatory role. These results support a putative Tumor Suppressor role of TCEB3C in neuroendocrine cells of the small intestine. Citation Format: Katarina Edfeldt, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Peyman Bjorklund, Gunnar Westin. TCEB3C (Elongin A3) on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1982. doi:10.1158/1538-7445.AM2013-1982
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Abstract 1982: TCEB3C (Elongin A3) on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors.
Molecular and Cellular Biology, 2013Co-Authors: Katarina Edfeldt, Tanvver Ahmad, Goran Akerstrom, Eva Tiensuu Janson, Per Hellman, Peter Stalberg, Gunnar WestinAbstract:TCEB3C (Elongin A3) on chromosome 18 presents a putative Tumor Suppressor Gene of small intestine neuroendocrine Tumors.
