Relevant bibliographies by topics / RET Gene

Academic literature on the topic 'RET Gene'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "RET Gene"

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Chatterjee, Sumantra, Kameko M. Karasaki, Lauren E. Fries, Ashish Kapoor, and Aravinda Chakravarti. "A multi-enhancer RET regulatory code is disrupted in Hirschsprung disease." Genome Research 31, no. 12 (November 15, 2021): 2199–208. http://dx.doi.org/10.1101/gr.275667.121.

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The major genetic risk factors for Hirschsprung disease (HSCR) are three common polymorphisms within cis-regulatory elements (CREs) of the receptor tyrosine kinase gene RET, which reduce its expression during enteric nervous system (ENS) development. These risk variants attenuate binding of the transcription factors RARB, GATA2, and SOX10 to their cognate CREs, reduce RET gene expression, and dysregulate other ENS and HSCR genes in the RET–EDNRB gene regulatory network (GRN). Here, we use siRNA, ChIP, and CRISPR-Cas9 deletion analyses in the SK-N-SH cell line to ask how many additional HSCR-associated risk variants reside in RET CREs that affect its gene expression. We identify 22 HSCR-associated variants in candidate RET CREs, of which seven have differential allele-specific in vitro enhancer activity, and four of these seven affect RET gene expression; of these, two enhancers are bound by the transcription factor PAX3. We also show that deleting multiple variant-containing enhancers leads to synergistic effects on RET gene expression. These, coupled with our prior results, show that common sequence variants in at least 10 RET enhancers affect HSCR risk, seven with experimental evidence of affecting RET gene expression, extending the known RET–EDNRB GRN to reveal an extensive regulatory code modulating disease risk at a single gene.
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&NA;. "Germline mutation of RET gene." Advances in Anatomic Pathology 2, no. 3 (May 1995): 187. http://dx.doi.org/10.1097/00125480-199505000-00030.

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Gou, Qitao, Xiaochuan Gan, Longhao Li, Qiheng Gou, and Tao Zhang. "Precious Gene: The Application of RET-Altered Inhibitors." Molecules 27, no. 24 (December 13, 2022): 8839. http://dx.doi.org/10.3390/molecules27248839.

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The well-known proto-oncogene rearrangement during transfection (RET), also known as ret proto-oncogene Homo sapiens (human), is a rare gene that is involved in the physiological development of some organ systems and can activate various cancers, such as non-small cell lung cancer, thyroid cancer, and papillary thyroid cancer. In the past few years, cancers with RET alterations have been treated with multikinase inhibitors (MKIs). However, because of off-target effects, these MKIs have developed drug resistance and some unacceptable adverse effects. Therefore, these MKIs are limited in their clinical application. Thus, the novel highly potent and RET-specific inhibitors selpercatinib and pralsetinib have been accelerated for approval by the Food and Drug Administration (FDA), and clinical trials of TPX-0046 and zetletinib are underway. It is well tolerated and a potential therapeutic for RET-altered cancers. Thus, we will focus on current state-of-the-art therapeutics with these novel RET inhibitors and show their efficacy and safety in therapy.
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Schoffski, Patrick, Philippe Georges Aftimos, Christophe Massard, Antoine Italiano, Christiane Jungels, Karen Andreas, Mitchell Keegan, and Peter T. C. Ho. "A phase I study of BOS172738 in patients with advanced solid tumors with RET gene alterations including non-small cell lung cancer and medullary thyroid cancer." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): TPS3162. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.tps3162.

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TPS3162 Background: RET gene alterations (mutations and fusions) leading to constitutive kinase activity have been identified in various tumor types including non-small cell lung cancer (NSCLC), medullary thyroid (MTC), colon, breast and ovarian cancer. The current generation of multi-kinase inhibitors approved for treatment of such tumors, do not selectively target RET and exhibit significant off-target activity especially against vascular endothelial growth factor receptor 2 (VEGFR2), resulting in dose-limiting toxicities that prevent the full inhibition of RET in those tumors. Recently, early clinical data from a class of more selective RET inhibitors have shown promising results with a more favorable safety profile in patients with RET alterations. BOS172738 is a novel RET inhibitor with nanomolar potency against RET and approximately 300-fold selectivity against VEGFR2. This phase 1 study is assessing the safety and tolerability of BOS172738 in patients with advanced solid tumors with RET alterations. Methods: NCT03780517 is a phase 1, open label, multicenter, dose escalation trial to evaluate the safety, efficacy, pharmacokinetics, and pharmacodynamics of BOS172738, an orally dosed RET kinase inhibitor, in patients with advanced solid tumors with RET gene alterations. RET gene alteration status will be assessed locally but confirmed centrally. The study is comprised of 2 parts: in Part A (dose escalation), patients with advanced solid tumors with RET gene alterations will receive BOS172738 orally once daily in each 28-day cycle. Select patients in Part A are eligible for intrapatient dose escalation. On establishing the recommended phase 2 dose (RP2D), Part B (expansion) will enroll up to an additional 60 patients to 1 of 3 tumor type-specific cohorts. The 3 expansion cohorts will each consist of up to 20 advanced cancer patients with: 1) RET gene-fusion NSCLC; 2) RET gene-mutant MTC; and 3) other RET gene-altered advanced tumors or NSCLC/MTC with prior specific RET gene-targeted therapy. Patients in expansion cohorts will receive BOS172738 daily at the RP2D until disease progression or other discontinuation criteria have been met. The study is currently open to enrollment globally with the first patient entered in 01/2019. Clinical trial information: NCT03780517.
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Sijmons, R. H., R. M. W. Hofstra, F. A. Wijburg, T. P. Links, R. P. Zwierstra, A. Vermey, D. C. Aronson, et al. "Oncological implications of RET gene mutations in Hirschsprung’s disease." Gut 43, no. 4 (October 1, 1998): 542–47. http://dx.doi.org/10.1136/gut.43.4.542.

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Background—Germline mutations of the RET proto-oncogene identical to those found in the tumour predisposition syndrome multiple endocrine neoplasia type 2A (MEN2A), were detected in 2.5–5% of sporadic and familial cases of Hirschsprung’s disease. Some patients with Hirschsprung’s disease may therefore be exposed to a highly increased risk of tumours.Aims—To define clinical use of RET gene testing in Hirschsprung’s disease and related patient management from an oncological point of view.Methods—Sixty patients with Hirschsprung’s disease were screened for RET mutations. In three, MEN2A type RET mutations were detected. Case reports for these three patients are presented.Results and conclusions—Only 22 families or sporadic patients with Hirschsprung’s disease and MEN2A type RET mutations have been reported. Therefore, it is difficult to predict tumour risk for patients with familial or sporadic Hirschsprung’s disease, and their relatives, who carry these mutations. For these mutation carriers, periodic screening for tumours as in MEN2A is advised, but prophylactic thyroidectomy is offered hesitantly. RET gene testing in familial or sporadic Hirschsprung’s disease is not recommended at present outside a complete clinical research setting. In combined MEN2A/Hirschsprung’s disease families RET gene testing, tumour screening, and prophylactic thyroidectomy are indicated as in MEN2A.
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Ramone, Teresa, Chiara Mulè, Raffaele Ciampi, Valeria Bottici, Virginia Cappagli, Alessandro Prete, Antonio Matrone, et al. "RET Copy Number Alteration in Medullary Thyroid Cancer Is a Rare Event Correlated with RET Somatic Mutations and High Allelic Frequency." Genes 12, no. 1 (December 29, 2020): 35. http://dx.doi.org/10.3390/genes12010035.

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Copy number variations (CNV) of the RET gene have been described in 30% of Medullary Thyroid Cancer (MTC), but no information is available about their role in this tumor. This study was designed to clarify RET gene CNV prevalence and their potential role in MTC development. RET gene CNV were analyzed in 158 sporadic MTC cases using the ION Reporter Software (i.e., in silico analysis) while the multiplex ligation-dependent probe amplification assay (i.e., in vitro analysis) technique was performed in 78 MTC cases. We identified three categories of RET ploidy: 137 in 158 (86.7%) cases were diploid and 21 in 158 (13.3%) were aneuploid. Among the aneuploid cases, five out of 21 (23.8%) showed an allelic deletion while 16 out of 21 (76.2%) had an allelic amplification. The prevalence of amplified or deleted RET gene cases (aneuploid) was higher in RET positive tumors. Aneuploid cases also showed a higher allelic frequency of the RET driver mutation. The prevalence of patients with metastatic disease was higher in the group of aneuploid cases while the higher prevalence of disease-free patients was observed in diploid tumors. A statistically significant difference was found when comparing the ploidy status and mortality. RET gene CNVs are rare events in sporadic MTC and are associated with RET somatic mutation, suggesting that they could not be a driver mechanism of tumoral transformation per se. Finally, we found a positive correlation between RET gene CNV and a worse clinical outcome.
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Kim, Jeong-Oh, Jung-Young Shin, Min Young Kim, Kyoung Hwa Son, Chan-Kwon Jung, Tae-Jung Kim, Su Young Kim, et al. "Coexistence of rearranged during transfection (RET) variants and activating EGFR mutations with their molecular implications in lung adenocarcinomas." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): e20610-e20610. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e20610.

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e20610 Background: RET rearrangements have been identified in 1-2% of lung adenocarcinomas. The most common fusion is the KIF5B-RET, the function and roles of the RET fusion oncogene, and its downstream signaling molecules remain unclear. Methods: We constructed a tissue microarray (TMA) comprising 581 resected tumor tissues from lung adenocarcinoma patients and investigated them using FISH with RET break-apart and KIF5B-RET SY translocation probes. NanoString’s nCounter technology was used to assay RETtranscripts. We evaluated the protein expressions of RET and RET-related signaling molecules, including p-AKT and p-ERK, using TMA-based IHC staining. Results: Using FISH, we identified 51 cases (8.8%) of RET variants and 10 cases (1.7%) of KIF5B-RET fusion genes among the 581 cases. RET protein expression was lower in the group harboring KIF5B-RET fusion gene than that in the group harboring a wild type RET gene. We found the activating EGFR mutations in 11 (21.6%) cases of 51 RET variants. For the group with KIF5B-RET fusion gene, the expression of p-ERK was significantly lower in EGFR mutation subgroup with presence of RET protein compared to EGFR mutation subgroup with absence of RET protein. For the group with RET rearrangement, there were significant differences in the expression level of p-AKT (P = 0.028) and, p-ERK protein expression was remarkably increased, especially in cases with no RET protein expression. Conclusions: Taken together, the expression of p-ERK protein was meaningfully increased in the RET variants group regardless of RET protein expression. This result suggests that RET inhibitors combined with ERK inhibitors may be an effective treatment strategy for lung adenocarcinoma patients harboring the RET variants.
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Ciampi, Raffaele, Thomas J. Giordano, Kathryn Wikenheiser-Brokamp, Ronald J. Koenig, and Yuri E. Nikiforov. "HOOK3-RET: a novel type of RET/PTC rearrangement in papillary thyroid carcinoma." Endocrine-Related Cancer 14, no. 2 (June 2007): 445–52. http://dx.doi.org/10.1677/erc-07-0039.

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Chromosomal rearrangements of the RET proto-oncogene (RET/PTC) are the common feature of papillary thyroid carcinoma (PTC). In this study, we report the identification, cloning, and functional characterization of a novel type of RET/PTC rearrangement that results from the fusion of the 3′-portion of RET coding for the tyrosine kinase (TK) domain of the receptor to the 5′-portion of the Homo sapiens hook homolog 3 (HOOK3) gene. The novel fusion was identified in a case of PTC that revealed a gene expression signature characteristic of RET/PTC on DNA microarray analysis, but was negative for the most common types of RET rearrangement. A fusion product between exon 11 of HOOK3 and exon 12 of RET gene was identified by 5′RACE, and the presence of chimeric HOOK3-RET protein of 88 kDa was detected by western blot analysis with an anti-RET antibody. The protein is predicted to contain a portion of the coiled-coil domains of HOOK3 and the intact TK domain of RET. Expression of the HOOK3-RET cDNA in NIH3T3 cells resulted in the formation of transformed foci and in tumor formation after injection into nude mice, confirming the oncogenic nature of HOOK3-RET.
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Takahashi, M., and G. M. Cooper. "ret transforming gene encodes a fusion protein homologous to tyrosine kinases." Molecular and Cellular Biology 7, no. 4 (April 1987): 1378–85. http://dx.doi.org/10.1128/mcb.7.4.1378-1385.1987.

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The ret transforming gene was activated by recombination between two unlinked segments of human DNA, most likely during transfection of NIH 3T3 cells. To further define this transforming gene, we isolated and sequenced ret cDNA clones. The nucleotide sequence indicates that the active ret transforming gene encodes a fusion protein with a carboxy-terminal domain which is 40 to 50% homologous to members of the tyrosine kinase gene family. This tyrosine kinase domain is preceded by a hydrophobic sequence characteristic of a transmembrane domain. Transcription of the ret tyrosine kinase sequence was detected in the SK-N-SH neuroblastoma, HL-60 promyelocytic leukemia, and THP-1 monocytic leukemia cell lines, but not in 25 other human tumor cell lines surveyed. The ret tyrosine kinase may thus represent a cell surface receptor which is expressed in a restricted range of human cells.
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Takahashi, M., and G. M. Cooper. "ret transforming gene encodes a fusion protein homologous to tyrosine kinases." Molecular and Cellular Biology 7, no. 4 (April 1987): 1378–85. http://dx.doi.org/10.1128/mcb.7.4.1378.

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The ret transforming gene was activated by recombination between two unlinked segments of human DNA, most likely during transfection of NIH 3T3 cells. To further define this transforming gene, we isolated and sequenced ret cDNA clones. The nucleotide sequence indicates that the active ret transforming gene encodes a fusion protein with a carboxy-terminal domain which is 40 to 50% homologous to members of the tyrosine kinase gene family. This tyrosine kinase domain is preceded by a hydrophobic sequence characteristic of a transmembrane domain. Transcription of the ret tyrosine kinase sequence was detected in the SK-N-SH neuroblastoma, HL-60 promyelocytic leukemia, and THP-1 monocytic leukemia cell lines, but not in 25 other human tumor cell lines surveyed. The ret tyrosine kinase may thus represent a cell surface receptor which is expressed in a restricted range of human cells.
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Dissertations / Theses on the topic "RET Gene"

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Hofstra, Robert Martinus Wouter. "The RET gene and its associated diseases." [S.l. : [Groningen] : s.n.] ; [University Library Groningen] [Host], 1995. http://irs.ub.rug.nl/ppn/142201383.

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Carter, Melissa Terry. "Characterization of the mouse RET gene and a cross-species comparison of RET isoforms." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ63279.pdf.

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Lee, King-yiu. "The Ret gene in the enteric nervous system expression analysis and generation of ret deficient mice /." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B31449669.

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Lee, King-yiu, and 李景耀. "The Ret gene in the enteric nervous system: expression analysis and generation of ret deficient mice." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31449669.

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Guo, Kexiao. "DNA Secondary Structures in the Promoters of Human VEGF and RET Genes and Their Roles in Gene Transcriptional Regulation." Diss., The University of Arizona, 2008. http://hdl.handle.net/10150/195943.

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Unusual DNA secondary structures, especially G-quadruplexes and i-motifs, play important roles in gene transcriptional regulation and have been identified as novel drug targets. In this dissertation, I explored their formation in the human VEGF and RET promoters and their roles in gene transcriptional regulation. VEGF is a key regulator of angiogenesis and is up-regulated in many types of tumors. A poly-guanine/poly-cytosine (polyG/polyC) tract in its proximal promoter (-85 to -50 base pairs relative to the transcription starting site) is essential for both basal and inducible VEGF expression. I demonstrated that the guanine-rich (G-rich) and cytosine-rich (C-rich) strands in the VEGF proximal promoter are able to form G-quadruplex and i-motif structures, respectively. The major G-quadruplex formed by the VEGF G-rich sequence is an intramolecular parallel G-quadruplex containing three G-tetrads and a 1:4:1 arrangement of three double-chain-reversal loops (two single-base loops and one loop with four bases). The complementary C-rich sequence in the same region forms an intramolecular i-motif containing six semiprotonated cytosine-cytosine⁺ base pairs and a 2:3:2 loop configuration (two double-base loops and one loop with three bases). The Gquadruplexes formed by the native VEGF G-rich and its derivative sequences were also confirmed by NMR. In addition, various transcription factors including Sp1, hnRNP K, CNBP and nucleolin, which recognize different DNA structural elements including single-stranded, double-stranded or G-quadruplex/i-motif DNA in the VEGF proximal promoter, have been confirmed by EMSA, siRNA and chromatin immunoprecipitation (ChIP) assay, suggesting that the DNA in the VEGF proximal promoter region is capable of undergoing transitions between those three structures. Based on my studies, I have proposed a model to describe how various transcription factors recognize different DNA structures in the VEGF proximal promoter to regulate transcription. In the proximal promoter of another important oncogene RET, I demonstrated that the guanine-rich strand forms an intramolecular parallel G-quadruplex containing three G-tetrads and a 1:3:1 arrangement of three double-chain-reversal loops. The complementary cytosine-rich strand forms an i-motif structure containing six semiprotonated cytosine-cytosine⁺ base pairs and a 2:3:2 loop configuration. Moreover, G-quadruplex-interactive compounds TMPyP4 and telomestatin were shown to further stabilize the RET G-quadruplex structure.
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Santos, Marina Silva dos. "Genetic susceptibility to thyroid cancer: contributions of RET polymorphisms." Master's thesis, Universidade da Beira Interior, 2012. http://hdl.handle.net/10400.6/1199.

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Thyroid cancer is the most common malignancy of the endocrine system, represents more than 1% of all malignancies and has an estimated annual incidence of 212,000 cases worldwide. The term differentiated thyroid carcinoma (DTC) comprises the subtypes papillary thyroid carcinoma (PTC) and follicular thyroid carcinomas (FTC), these subtypes represent the two most common subtypes of thyroid cancer (approximately 80% and 10% respectively). Despite its incidence DTCs have a good prognosis with relatively few metastases and deaths associated. The polymorphisms (variants in DNA sequence among individuals that have a frequency of at least 1% in a population) of RET proto-oncogene have been studied in different populations for association with susceptibility to thyroid cancer, but with inconsistent findings mainly in DTC. To clarify the contribution of single locus or haplotypes (polymorphisms that are transmitted through generations as a unit) of RET polymorphisms to genetic susceptibility to DTC among Portuguese patients, we conducted a case–control study by analyzing four well-characterized RET polymorphisms (G691S, L769L, S836S and S904S). To achieve this aim, the RET polymorphisms were genotyped and haplotype frequencies were estimated in a population of 282 individuals with DTC and in a control population of 254 individuals. Allele, genotype and haplotype distributions were compared among cases and controls. Patient population was subdivided according to several clinical parameters and allele, genotype and haplotype distributions were compared among the subgroups. The single locus analysis showed an overrepresentation of the S836S polymorphism in patients when compared to controls. Also the heterozygous genotypes of the G691S/S904S polymorphisms were overrepresented in cases diagnosed after the age of 45 years and the heterozygous genotype of G691S polymorphism revealed an overrepresentation in patients with tumors larger then 10mm of diameter at diagnosis. The haplotype analysis showed an overrepresentation of GGTC haplotype in patients particularly in those diagnosed after the age of 45 years. In conclusion, our data suggest that the S836S polymorphism may be associated with increased risk of DTC. Also the heterozygous genotype of the G691S/S904S polymorphisms seems to be associated with age of onset of DTC and additionally the heterozygous genotype of G691S polymorphism appeared to be in association with tumor size. Finally, one haplotype appears to be associated with increased risk of DTC particularly in those developed in later age (after the age of 45 years). These findings need to be confirmed by larger studies in order re-evaluate the role of these variants in the susceptibility to DTC.
Thyroid cancer is the most common malignancy of the endocrine system, represents more than 1% of all malignancies and has an estimated annual incidence of 212,000 cases worldwide. The term differentiated thyroid carcinoma (DTC) comprises the subtypes papillary thyroid carcinoma (PTC) and follicular thyroid carcinomas (FTC), these subtypes represent the two most common subtypes of thyroid cancer (approximately 80% and 10% respectively). Despite its incidence DTCs have a good prognosis with relatively few metastases and deaths associated. The polymorphisms (variants in DNA sequence among individuals that have a frequency of at least 1% in a population) of RET proto-oncogene have been studied in different populations for association with susceptibility to thyroid cancer, but with inconsistent findings mainly in DTC. To clarify the contribution of single locus or haplotypes (polymorphisms that are transmitted through generations as a unit) of RET polymorphisms to genetic susceptibility to DTC among Portuguese patients, we conducted a case–control study by analyzing four well-characterized RET polymorphisms (G691S, L769L, S836S and S904S). To achieve this aim, the RET polymorphisms were genotyped and haplotype frequencies were estimated in a population of 282 individuals with DTC and in a control population of 254 individuals. Allele, genotype and haplotype distributions were compared among cases and controls. Patient population was subdivided according to several clinical parameters and allele, genotype and haplotype distributions were compared among the subgroups. The single locus analysis showed an overrepresentation of the S836S polymorphism in patients when compared to controls. Also the heterozygous genotypes of the G691S/S904S polymorphisms were overrepresented in cases diagnosed after the age of 45 years and the heterozygous genotype of G691S polymorphism revealed an overrepresentation in patients with tumors larger then 10mm of diameter at diagnosis. The haplotype analysis showed an overrepresentation of GGTC haplotype in patients particularly in those diagnosed after the age of 45 years. In conclusion, our data suggest that the S836S polymorphism may be associated with increased risk of DTC. Also the heterozygous genotype of the G691S/S904S polymorphisms seems to be associated with age of onset of DTC and additionally the heterozygous genotype of G691S polymorphism appeared to be in association with tumor size. Finally, one haplotype appears to be associated with increased risk of DTC particularly in those developed in later age (after the age of 45 years). These findings need to be confirmed by larger studies in order re-evaluate the role of these variants in the susceptibility to DTC.
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Le, Hir Hervé. "Etude de l'epissage alternatif des arn pre-messagers du gene ret et du gene de la tyrosine hydroxylase dans les pheochromocytomes." Paris 7, 1998. http://www.theses.fr/1998PA077089.

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J'ai etudie la regulation de l'epissage en relation avec le processus de tumorigenese, et choisi pour cela les pheochromocytomes (tumeurs de la medullo-surrenale). Ces tumeurs sont dans certains cas d'origine familiale, associees a des mutations activatrices du proto-oncogene ret. Ce gene code pour un recepteur a activite tyrosine-kinase agissant dans la voie de signalisation de ret avec le ligand gdnf et le co-recepteur gdnfr-. L'epissage alternatif de l'arn pre-messager ret conduit a la production de nombreux arnm codant pour dix isoformes du recepteur. Pour deux de celle-ci il a ete montre qu'elles possedent des activites transformantes differentes. J'ai mesure la quantite des arnm ret, gdnf et gdnfr- et montre que ces trois genes sont exprimes simultanement et que les genes ret et gdnf sont surexprimes dans la majorite des pheochromocytomes compare aux tissus sains. J'ai mesure l'abondance des divers arnm ret et montre que seuls les arnm codant pour deux isoformes de ret sont exprimes dans les tissus sains aussi bien que dans les tumeurs et ainsi que l'epissage alternatif du pre-messager ret n'est pas specifiquement altere dans les cellules tumorales. J'ai observe dans les pheochromocytomes la presence d'une nouvelle classe de transcrits contenant des introns non excises. En parallele du gene ret, j'ai etudie le patron d'epissage du gene de la tyrosine hydroxylase (th) dans ces tumeurs, dont le pre-messager est egalement sujet a un epissage alternatif. J'ai montre (i) que la moitie des introns ret et th sont retenus en quantite significative dans les arn cellulaires totaux et polyadenyles. (ii) peu ou pas de retention est detectee dans les tissus sains comme la medullo-surrenale et la substance noire. (iii) la majorite des introns sont retenus dans les memes molecules. Nous proposons que ce phenomene resulte d'une alteration generale de la machinerie d'epissage dans les pheochromocytomes.
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La, Perle Krista Marie DuBray. "Characterization of ret/PTC1 Transgenic-p53 knockout mice and sodium/iodide symporter gene transfer for Prostate Cancer /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486457871785739.

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Marsee, Derek K. "Exploration of novel therapies for thyroid cancer adenoviral gene therapy and 17-allylamino-17-demethoxygeldanamycin /." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1087497053.

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Thesis (Ph. D.)--Ohio State University, 2004.
Title from first page of PDF file. Document formatted into pages; contains xv, 118 p.; also includes graphics (some col.) Includes bibliographical references (p. 106-118). Available online via OhioLINK's ETD Center
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Pasini, Andrea. "Bases biologiques des néoplasies endocriniennes multiples de type 2 et de la maladie de Hirschsprung : étude des conséquences fonctionnelles des mutations du gène RET." Lyon 1, 1997. http://www.theses.fr/1997LYO1T249.

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Books on the topic "RET Gene"

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Red genes, blue genes: Exposing political irrationality. Brooklyn, N.Y: Autonomedia, 2009.

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Aydın, Gülşah Sinem. Kira sözleşmesinin genel hükümlere göre sona ermesi, (TBK m. 327-333). Şişli, İstanbul: XII Levha, 2013.

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Li, Jack Jun. Cloning and characterization of the rat bone sialoprotein (BSP) gene promoter. [Toronto: University of Toronto, Faculty of Dentistry], 1998.

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Costigan, Michael. Basement membrane gene expression in the normal and streptozotocin diabetic rat. Manchester: Universityof Manchester, 1996.

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Mondo, John Paul Di. Isolation and sequencing of the rat endothelin-A receptor (ETA) gene. Ottawa: National Library of Canada, 1996.

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Fox, Diane. Red or Blue. [Place of publication not identified]: Orchard, 2013.

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1965-, Wang Dengfeng, ed. Ji yin yu ren xing: Genes and human nature. Beijing Shi: Beijing da xue chu ban she, 2009.

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Ren lei ji jin de quan li yan jiu. Beijing Shi: Fa lü chu ban she, 2009.

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Tsatsos, Jim. Nicotine regulates opioid peptide and dopamine receptor gene expression in the rat brain and pituitary. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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Harding, Helen Louise. The regulation of PEPCK gene expression by insulin and epidermal growth factor in rat hepatocytes. Manchester: University of Manchester, 1995.

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Book chapters on the topic "RET Gene"

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Stine, Zachary E., and Andrew S. McCallion. "The Contributions of RET Noncoding Variation to Hirschsprung Disease." In Gene Regulatory Sequences and Human Disease, 169–94. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-1683-8_9.

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Uchino, Shinya, Daishu Miura, and Takahiro Okamoto. "CQ26. What Is the Usefulness of RET Gene Mutation Analysis for Medullary Carcinoma?" In Treatment of Thyroid Tumor, 159–62. Tokyo: Springer Japan, 2012. http://dx.doi.org/10.1007/978-4-431-54049-6_37.

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Catelain, Cyril, Emma Pailler, Marianne Oulhen, Vincent Faugeroux, Anne-Laure Pommier, and Françoise Farace. "Detection of Gene Rearrangements in Circulating Tumor Cells: Examples of ALK-, ROS1-, RET-Rearrangements in Non-Small-Cell Lung Cancer and ERG-Rearrangements in Prostate Cancer." In Advances in Experimental Medicine and Biology, 169–79. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55947-6_9.

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Szpirer, C., J. Szpirer, M. Q. Islam, and G. Levan. "The Rat Gene Map." In Genetics of Immunological Diseases, 33–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-50059-6_5.

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Gupta, G. S. "Regenerating (Reg) Gene Family." In Animal Lectins: Form, Function and Clinical Applications, 847–80. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-1065-2_39.

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Berchtold, M. W. "The Rat Parvalbumin Gene." In Proceedings in Life Sciences, 40–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73042-9_3.

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Raff, Martin C. "Glial Cell Lineages and Differentiation in the Rat Optic Nerve." In Coordinated Regulation of Gene Expression, 205–8. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2245-0_19.

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Jump, Donald B. "Thyroid Hormone Regulation of Rat Liver S14 Gene Expression." In Gene Regulation by Steroid Hormones IV, 144–62. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3666-5_9.

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Ritzer, Ivo. "Black Power, White Noise, Red Heat: Synthesen kritischer Medienästhetik." In Genre und Race, 161–86. Wiesbaden: Springer Fachmedien Wiesbaden, 2021. http://dx.doi.org/10.1007/978-3-658-32187-1_9.

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Janssen, Yvonne M. W., Joanne P. Marsh, Paul J. A. Borm, Piyawan Surinrut, Kaaren Haldeman, and Brooke T. Mossman. "Asbestos Mediated Gene Expression in Rat Lung." In Mechanisms in Fibre Carcinogenesis, 359–65. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-1363-2_29.

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Conference papers on the topic "RET Gene"

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Shin, Jung-Young, Min-Young Kim, Kyoung-Hwa Son, Jeong-Oh Kim, and Jin-Hyoung Kang. "Abstract 2710: Tumorigenic activity of a novel KIF5B-RET fusion gene." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2710.

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Kohno, Takashi, Hitoshi Ichikawa, Koji Tsuta, Tatsuji Mizukami, Yoko Shimada, Mamoru Kato, Hiromi Sakamoto, et al. "Abstract 1214: RET fusion gene: translation to the therapy of lung adenocarcinoma." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1214.

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Kim, Min-Young, Jung-Young Shin, Jeong-Oh Kim, Kyoung-Hwa Son, and Jin Hyoung Kang. "Abstract 1687: KIF5B-RET fusion gene may induce EMT via the regulation of two transcription factors, FOXA2 and STAT5A." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1687.

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Sun, Daekyu, and Yoon-Joo Shin. "Abstract 745: Role of G-quadruplex structures in the human RET promoter region in the regulation of this gene." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-745.

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Rand, Casey M., Erin E. West, Min Yu, Debra E. Weese-Mayer, and Lawrence Jennings. "Multiplex Ligation-Dependent Probe Amplification To Detect Deletions And Duplications In The Ret Gene In Sudden Infant Death Syndrome Cases." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3707.

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Huber, P., J. Dalmon, M. Laurent, G. Courtois, D. Thevenon, and G. Marguerie. "CHARACTERIZATION OFTHE 5’FLANKING REGION FOR THE HUMAN FIBRINOGEN β GENE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642889.

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Fibrinogen is coded by three separate genes located in a 50kb region of chromosome 4 and organized in a α - β - γ orientation with an inversion of the gene 3- A human genomic library was constructed using the EMBL4 phage and screened with cDNA probes coding for human fibrinogen Aα, Bβ and γ chains. Clones, covering the fibrinogen locus,were identified, and their organization was analyzed by means of hybridization and restriction mapping. Among these clones one recombinant phage containing the β gene and large 5’ and 3’ -flanking sequences was isolated.To identify the regulatory sequences Dpstream from the human β gene, a 1.5 kb fragment of the immediate 5’-flanking region was sequenced. The SI mapping experiments revealed three transcription initiation sites. PotentialTATA and CAAT sequences were identified upstream the initiation start points at the positions -21 and -58 from the first initiation start point.Comparison of this sequence with that previously reported for the same region upstream from the human γ gene revealed no significant homology which suggests that the potential promoting sequences of these genes are different. In contrast, comparison of the 5’flanking regions of human and rat β genes showed more than 80% homology for 142 bp upstream from the gene. This highly conserved region is a potential candidate for a regulatory sequence of the human β gene.To verify this activity, a β fibrinogen minigene was constructed by deletion of the internal part of the normal gene and including 3.4kb of the 5’flanking region and 1.4kb of the 3’flanking region. The minigene was transfected into HepG2, a human hepatoma cell line, to show whether the 5’flanking region of the human fibrinogen gene contains DNA sequences sufficient for efficient transcription in HepG2. Constructions of several parts of the sequenced 5’flanking region of the human β gene with the gene of the chloramphenical acetyl transferase have been also transfected in the HepG2 cells to determine the specificity of the gene expression and to localize the sequences controlling the transcription of the gene.
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Pannekoek, H., M. Linders, J. Keijer, H. Veerman, H. Van Heerikhuizen, and D. J. Loskutoff. "THE STRUCTURE OF THE HUMAN ENDOTHELIAL PLASMINOGEN ACTIVATOR INHIBITOR (PAI-1) GENE: NON-RANDOM POSITIONING OF INTRONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644767.

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The endothelium plays a crucial role in the regulation of the fibrinolytic process, since it synthesizes and secretes tissue-type plasminogen activator (t-PA) as well as the fast-acting plasminogen activator inhibitor (PAI-1). Molecular cloning of full-length PAI-1 cDNA, employing a human endothelial cDNA expression library, and a subsequent determination of the complete nucleotide sequence, allowed a prediction of the amino-acid sequence of the PAI-1 glycoprotein. It was observed that the amino-acid sequence is significantly homologous to those of members of the serine protease inhibitor ("Serpin") family, e.g. αl-antitrypsin and antithrombin III. Serpins are regulators of various processes, such as coagulation, inflammatory reactions, complement activation and share a common functional principle and a similar structure, indicative for a common primordial gene. The intron-exon arrangement of Serpin genes may provide a record for the structure of a primordial gene. A comparison of the location of introns among members of the Serpin family reveals that some introns are indeed present at identical or almost identical positions, however in many other cases there is no correspondence between the intron positions among different Serpin genes.Obviously, more data on the chromosomal gene structure of members of this family are required to formulate a scheme for the evolutionary creation of the Serpins. To that end, we have established the number and the precise location of the introns in the PAI-1 gene and have compared these data with those reported on other Serpin genes. For that purpose a human genomic cosmid DNA library of about 340.000 independent colonies was screened with radiolabelled full-length PAI-1 cDNA as probe. Two clones were found which contain the entire PAI-1 gene. Restriction site mapping, electron microscopic inspection of heteroduplexes and nucleotide sequence analysis demonstrate that the PAI-1 gene comprises about 12.2kilo basepairs and consists of nine exons and eight introns. Intron-exon boundaries are all in accord with the "GT-AG" rule, including a cryptic acceptor splice site found in intron 7. Furthermore, it is observed that intron 3 of the PAI-1 gene occupies an identical position as intron E of chicken ovalbumin and intron E of the ovalbumin-related gene Y. The location of the other seven introns is unrelated to the known location of introns in the genes encoding the Serpins, rat angiotensin, chicken ovalbumin (and gene Y), human antithrombin III and human al-antitrypsin. The 3' untranslated region of the PAI-1 gene is devoid of introns, indicating that the two mRNA species detected in cultured endothelial cells which share an identical 5' untranslated segment and codogenic region, but differ in the length of the 3' untranslated region, arise by alternative polyadenylation. An extrapolation of the position of the introns to the amino-acid sequence of PAI-1, and adaption of the view that the subdomain structure of the Serpins is analogous, shows that the introns of PAI-1 are non-randomly distributed. Except for intron 7, the position of the other seven introns corresponds with randon-coil regions of the protein or with the borders of β-sheets and a-helices. Extrapolation of the position of introns in the genes of other Serpins to their respective amino-acid sequences and subdomain structures also reveals a preference for random-coil regions and borders of subdomains. These observations are reminiscent of an evolutionary model, called "intron sliding", that accounts for variations in surface loops of the same protein in different species by aberrant splicing (Craik et al., Science 220 (1983) 1125). The preferential presence of introns in gene segments, encoding these variable regions, and absence in regions determining the general folding of these proteins would explain conservation of the structure during the evolution of those genes.
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Fowlkes, P. M., P. K. Lund, M. Blake, and J. Snouwaert. "THE REGULATION OF FIBRINOGEN PRODUCTION INVOLVES AT LEAST ONE OTHER HEPATOCYTE GENE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644317.

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It is currently thought that glucocorticosteriods have a direct effect on the transcription of the alpha, beta and gamma fibrinogen genes. However, our studies indicate that while corticosteriods play a role in fibrinogen production, this role is not due to transcriptional activation via glucocorticosteriod receptors. In initial experiments, we compared the levels of fibrinogen mRNA in hepatocytes isolated from hypophysectomized rats to those from control animals. The levels of mRNA in hypophysectomized rats, which produce little ACTH or corticosteriods, were significantly higher than the levels in control animals. Albumin mRNA levels were unaffected by hypophysectomy. These results are in opposition to those which we had anticipated. Based on previously published data, we had thought that physiologic deprivation of corticosteriods would lead to decreased levels of fibrinogen. We propose that these results are related to the negative feedback that corticosteroids have on Hepatocyte Stimulating Factor (HSF) production through a tightly controlled feedback circuit. To investigate the role of corticosteriods in fibrinogen gene regulation, we have conducted experiments with primary hepatocytes in culture and rat FAZA cells (continuous hepatoma cell line). There is a 4 to 5 fold increase in fibrinogen production when these cells are treated with HSF but no change when these cells are treated with dexamethasone alone. However, there is a marked additional increase in the production of fibrinogen with the combination of dexamethasone and HSF. Data gathered through kinetic analysis of this synergistic interaction suggest that the maximum response to HSF requires another gene product whose production is responsive to dexamethasone. Detailed analysis of the rate of transcription of thegamma fibrinogen gene, its processing and mRNA turnover suggests a specific role for this gene product in regulating fibrinogen synthesis. Characterization of this gene product will lead to greater understanding of the regulation of the Acute Phase Reactants.
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MacPherson, Kevin Alexander, Meghan M. Joly, Brittany Allen-Petersen, Carl Pelz, Mary C. Thoma, Kristof Torkenczy, Andrew Adey, Daniel Liefwalker, Patrick J. Worth, and Rosalie C. Sears. "Abstract 2480: RE1-silencing transcription factor (REST) controls neuroendocrine gene programs in pancreatic ductal adenocarcinoma." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2480.

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Rodrigues, Antonio Rony da S. P., and Edinalda Maria Cavalcante. "ESTUDO GENÉTICO DO CÂNCER DE TIREOIDE – UMA REVISÃO." In I SIMPÓSIO MARANHENSE DE GENÉTICA E GENÔMICA EM SAÚDE. Doity - Plataforma de Eventos, 2022. http://dx.doi.org/10.55664/simaggens2022.005.

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INTRODUÇÃO: O câncer de tireoide é um dos agravos mais comuns ao sistema endócrino, com o maior aumento anual de incidência em diferentes países, principalmente devido à melhoria das tecnologias de diagnóstico, sendo mais proeminente em regiões com acesso aos cuidados de saúde amplamente disponíveis. Alguns eventos moleculares são descritos tanto na carciogênese da tireoide quanto na evolução do tumor glandular. Dados do Atlas do câncer no Genoma Humano dividiu os carcinomas papilíferos de tireoide nas categorias BRAF e RAS, com base nos resultados do exoma do sequenciamento de DNA, RNA e perfil proteômico, e padrões de metilação. OBJETIVOS: Observar nos estudos da literatura os marcadores genéticos relacionados ao câncer de tireóide. MÉTODOS MÉTODOS: Para alcançar os objetivos propostos neste estudo, o método eleito foi a Revisão Integrativa que inclui a análise de pesquisas relevantes que dão suporte para a tomada de decisão, permitindo a incorporação desses achados na prática clínica. A partir de então, foi feita uma busca, ocorrida entre fevereiro e março de 2022, em 5 bases de dados: LILACS (Literatura Latino-Americana e do Caribe em Ciências da Saúde) e SciELO (Scientific Electronic Library Online), PubMed (Central: PMC- National Library of Medicine National Institutes of Health), ScienceDirect e IBECS (Índice Bibliográfico Espanhol em Ciências da Saúde). A pesquisa por artigos foi feita através dos termos em língua inglesa: “thyroid cancer”, “risk markers” e “thyroid cancer genetics” junto ao operador booleano AND. Os resultados obtidos foram comparados, estabelecendo-se concordância quanto a formulação da amostra final. Os achados foram apresentados a partir do método de “nuvem de palavras”, utilizando o software wordle. Nuvem de palavras é uma forma de facilitar a demonstração de quais são as palavras mais frequentes quando pesquisado por determinado assunto ou tema. RESULTADOS E DISCUSSÃO: Na etapa de seleção subsequente os artigos foram lidos na íntegra onde 213 artigos foram excluídos por não se apresentarem dentro do objeto estudo, e incluídos 14 trabalhos na versão final da revisão. A análise proteica demostrou projeção da estrutura molecular e homologia proteica dos seguintes marcadores moleculares de câncer de tireoide: proto-oncogene receptor tirosina quinase (RET); proto-oncogene do receptor de tirosina quinase neurotrófico 1 (NTRK1); homólogo de fosfatase tensina (PTEN); gene da proteína tumoral p53 (TP53); fosfoinositida 3-quinase/treonina proteína quinase (PI3K/AKT); catenina beta 1 (CTNNB1); gama de receptor ativado por proliferador de peroxissoma de caixa pareada 8 (PAX8-PPARG); oncogene viral de sarcoma de rato (RAS); proto-oncogene B-raf, serina/treonina quinase (BRAF); e receptor do hormônio estimulante da tireóide (TSHR). Experimentos utilizando o tipo de array identificaram três genes diferencialmente expressos, cuja expressão foi analisada por RT-PCR em 10 amostras de cada tipo de tecido. Dois deles foram capazes de diferenciar carcinomas papilíferos de tecido normal e bócio com 89% de precisão para o tumor maligno e 80% para os tecidos não malignos. Conclusão: Após a análise dos resultados desta RI, foi possível observar alguns marcadores de risco para câncer de tireóide. Desse modo, o presente trabalho contribui para o aprofundamento e desenvolvimento de novas reflexões dos estudos sobre marcadores genéticos canceriginos
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Reports on the topic "RET Gene"

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Reisch, Bruce, Avichai Perl, Julie Kikkert, Ruth Ben-Arie, and Rachel Gollop. Use of Anti-Fungal Gene Synergisms for Improved Foliar and Fruit Disease Tolerance in Transgenic Grapes. United States Department of Agriculture, August 2002. http://dx.doi.org/10.32747/2002.7575292.bard.

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Original objectives . 1. Test anti-fungal gene products for activity against Uncinula necator, Aspergillus niger, Rhizopus stolonifer and Botrytis cinerea. 2. For Agrobacterium transformation, design appropriate vectors with gene combinations. 3. Use biolistic bombardment and Agrobacterium for transformation of important cultivars. 4. Characterize gene expression in transformants, as well as level of powdery mildew and Botrytis resistance in foliage of transformed plants. Background The production of new grape cultivars by conventional breeding is a complex and time-consuming process. Transferring individual traits via single genes into elite cultivars was proposed as a viable strategy, especially for vegetatively propagated crops such as grapevines. The availability of effective genetic transformation procedures, the existence of genes able to reduce pathogen stress, and improved in vitro culture methods for grapes, were combined to serve the objective of this proposal. Effective deployment of resistance genes would reduce production costs and increase crop quality, and several such genes and combinations were used in this project. Progress The efficacy of two-way combinations of Trichoderma endochitinase (CHIT42), synthetic peptide ESF12 and resveratrol upon the control of growth of Botrytis cinerea and Penicillium digitatum were evaluated in vitro. All pairwise interactions were additive but not synergistic. Per objective 2, suitable vectors with important gene combinations for Agrobacterium transformation were designed. In addition, multiple gene co-transformation by particle bombardment was also tested successfully. In New York, transformation work focused on cultivars Chardonnay and Merlot, while the technology in Israel was extended to 41B, R. 110, Prime, Italia, Gamay, Chardonnay and Velika. Transgenic plant production is summarized in the appendix. Among plants developed in Israel, endochitinase expression was assayed via the MuchT assay using material just 1-5 days after co-cultivation. Plants of cv. Sugraone carrying the gene coding for ESF12, a short anti-fungal lytic peptide under the control of the double 358 promoter, were produced. Leaf extracts of two plants showed inhibition zones that developed within 48 h indicating the inhibitory effect of the leaf extracts on the six species of bacteria. X fastidiosa, the causal organism of Pierce's disease, was very sensitive to leaf extracts from ESF12 transformed plants. Further work is needed to verify the agricultural utility of ESF12 transformants. In New York, some transformants were resistant to powdery mildew and Botrytis fruit rot. Major conclusions, solutions, achievements and implications The following scientific achievements resulted from this cooperative BARD project: 1. Development and improvement of embryogenesis and tissue culture manipulation in grape, while extending these procedures to several agriculturally important cultivars both in Israel and USA. 2. Development and improvement of novel transformation procedures while developing transformation techniques for grape and other recalcitrant species. 3. Production of transgenic grapevines, characterization of transformed vines while studying the expression patterns of a marker gene under the control of different promoter as the 35S CaMV in different part of the plants including flowers and fruits. 4. Expression of anti-fungal genes in grape: establishment of transgenic plants and evaluation of gene expression. Development of techniques to insert multiple genes. 5. Isolation of novel grape specific promoter to control the expression of future antimicrobial genes. It is of great importance to report that significant progress was made in not only the development of transgenic grapevines, but also in the evaluation of their potential for increased resistance to disease as compared with the non engineered cultivar. In several cases, increased disease resistance was observed. More research and development is still needed before a product can be commercialized, yet our project lays a framework for further investigations.
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Shani, Moshe, and C. P. Emerson. Genetic Manipulation of the Adipose Tissue via Transgenesis. United States Department of Agriculture, April 1995. http://dx.doi.org/10.32747/1995.7604929.bard.

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The long term goal of this study was to reduce caloric and fat content of beef and other red meats by means of genetic modification of the animal such that fat would not be accumulated. This was attempted by introducing into the germ line myogenic regulatory genes that would convert fat tissue to skeletal muscle. We first determined the consequences of ectopic expression of the myogenic regulatory gene MyoD1. It was found that deregulation of MyoD1 did not result in ectopic skeletal muscle formation but rather led to embryonic lethalities, probably due to its role in the control of the cell cycle. This indicated that MyoD1 should be placed under stringent control to allow survival. Embryonic lethalities were also observed when the regulatory elements of the adipose-specific gene adipsin directed the expression of MyoD1 or myogenin cDNAs, suggesting that these sequences are probably not strong enough to confer tissue specificity. To determine the specificity of the control elements of another fat specific gene (adipocyte protein 2-aP2), we fused them to the bacterial b-galactosidase reporter gene and established stable transgenic strains. The expression of the reporter gene in none of the strains was adipose specific. Each strain displayed a unique pattern of expression in various cell lineages. Most exciting results were obtained in a transgenic strain in which cells migrating from the ventro-lateral edge of the dermomyotome of developing somites to populate the limb buds with myoblasts were specifically stained for lacZ. Since the control sequences of the adipsin or aP2 genes did not confer fat specificity in transgenic mice we have taken both molecular and genetic approaches as an initial effort to identify genes important in the conversion of a multipotential cell such as C3H10T1/2 cell to adipoblast. Several novel adipocyte cell lines have been established that differ in the expression of transcription factors of the C/EBP family known to be markers for adipocyte differentiation. These studies revealed that one of the genetic programming changes which occur during 10T1/2 conversion from multipotential cell to a committed adipoblast is the ability to linduce C/EBPa gene expression. It is expected that further analysis of this gene would identify elements which regulate this lineage-specific expression. Such elements might be good candidates in future attempts to convert adipoblasts to skeletal muscle cells in vivo.
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Ficht, Thomas, Gary Splitter, Menachem Banai, and Menachem Davidson. Characterization of B. Melinensis REV 1 Attenuated Mutants. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7580667.bard.

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Brucella Mutagenesis (TAMU) The working hypothesis for this study was that survival of Brucella vaccines was directly related to their persistence in the host. This premise is based on previously published work detailing the survival of the currently employed vaccine strains S19 and Rev 1. The approach employed signature-tagged mutagenesis to construct mutants interrupted in individual genes, and the mouse model to identify mutants with attenuated virulence/survival. Intracellular survival in macrophages is the key to both reproductive disease in ruminants and reticuloendothelial disease observed in most other species. Therefore, the mouse model permitted selection of mutants of reduced intracellular survival that would limit their ability to cause reproductive disease in ruminants. Several classes of mutants were expected. Colonization/invasion requires gene products that enhance host-agent interaction or increase resistance to antibacterial activity in macrophages. The establishment of chronic infection requires gene products necessary for intracellular bacterial growth. Maintenance of chronic infection requires gene products that sustain a low-level metabolism during periods characterized little or no growth (1, 2). Of these mutants, the latter group was of greatest interest with regard to our originally stated premise. However, the results obtained do not necessarily support a simplistic model of vaccine efficacy, i.e., long-survival of vaccine strains provides better immunity. Our conclusion can only be that optimal vaccines will only be developed with a thorough understanding of host agent interaction, and will be preferable to the use of fortuitous isolates of unknown genetic background. Each mutant could be distinguished from among a group of mutants by PCR amplification of the signature tag (5). This approach permitted infection of mice with pools of different mutants (including the parental wild-type as a control) and identified 40 mutants with apparently defective survival characteristics that were tentatively assigned to three distinct classes or groups. Group I (n=13) contained organisms that exhibited reduced survival at two weeks post-infection. Organisms in this group were recovered at normal levels by eight weeks and were not studied further, since they may persist in the host. Group II (n=11) contained organisms that were reduced by 2 weeks post infection and remained at reduced levels at eight weeks post-infection. Group III (n=16) contained mutants that were normal at two weeks, but recovered at reduced levels at eight weeks. A subset of these mutants (n= 15) was confirmed to be attenuated in mixed infections (1:1) with the parental wild-type. One of these mutants was eliminated from consideration due to a reduced growth rate in vitro that may account for its apparent growth defect in the mouse model. Although the original plan involved construction of the mutant bank in B. melitensis Rev 1 the low transformability of this strain, prevented accumulation of the necessary number of mutants. In addition, the probability that Rev 1 already carries one genetic defect increases the likelihood that a second defect will severely compromise the survival of this organism. Once key genes have been identified, it is relatively easy to prepare the appropriate genetic constructs (knockouts) lacking these genes in B. melitensis Rev 1 or any other genetic background. The construction of "designer" vaccines is expected to improve immune protection resulting from minor sequence variation corresponding to geographically distinct isolates or to design vaccines for use in specific hosts. A.2 Mouse Model of Brucella Infection (UWISC) Interferon regulatory factor-1-deficient (IRF-1-/- mice have diverse immunodeficient phenotypes that are necessary for conferring proper immune protection to intracellular bacterial infection, such as a 90% reduction of CD8+ T cells, functionally impaired NK cells, as well as a deficiency in iNOS and IL-12p40 induction. Interestingly, IRF-1-/- mice infected with diverse Brucella abortus strains reacted differently in a death and survival manner depending on the dose of injection and the level of virulence. Notably, 50% of IRF-1-/- mice intraperitoneally infected with a sublethal dose in C57BL/6 mice, i.e., 5 x 105 CFU of virulent S2308 or the attenuated vaccine S19, died at 10 and 20 days post-infection, respectively. Interestingly, the same dose of RB51, an attenuated new vaccine strain, did not induce the death of IRF-1-/- mice for the 4 weeks of infection. IRF-1-/- mice infected with four more other genetically manipulated S2308 mutants at 5 x 105 CFU also reacted in a death or survival manner depending on the level of virulence. Splenic CFU from C57BL/6 mice infected with 5 x 105 CFU of S2308, S19, or RB51, as well as four different S2308 mutants supports the finding that reduced virulence correlates with survival Of IRF-1-/- mice. Therefore, these results suggest that IRF-1 regulation of multi-gene transcription plays a crucial role in controlling B. abortus infection, and IRF-1 mice could be used as an animal model to determine the degree of B. abortus virulence by examining death or survival. A3 Diagnostic Tests for Detection of B. melitensis Rev 1 (Kimron) In this project we developed an effective PCR tool that can distinguish between Rev1 field isolates and B. melitensis virulent field strains. This has allowed, for the first time, to monitor epidemiological outbreaks of Rev1 infection in vaccinated flocks and to clearly demonstrate horizontal transfer of the strain from vaccinated ewes to unvaccinated ones. Moreover, two human isolates were characterized as Rev1 isolates implying the risk of use of improperly controlled lots of the vaccine in the national campaign. Since atypical B. melitensis biotype 1 strains have been characterized in Israel, the PCR technique has unequivocally demonstrated that strain Rev1 has not diverted into a virulent mutant. In addition, we could demonstrate that very likely a new prototype biotype 1 strain has evolved in the Middle East compared to the classical strain 16M. All the Israeli field strains have been shown to differ from strain 16M in the PstI digestion profile of the omp2a gene sequence suggesting that the local strains were possibly developed as a separate branch of B. melitensis. Should this be confirmed these data suggest that the Rev1 vaccine may not be an optimal vaccine strain for the Israeli flocks as it shares the same omp2 PstI digestion profile as strain 16M.
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Dubcovsky, Jorge, Tzion Fahima, and Ann Blechl. Positional cloning of a gene responsible for high grain protein content in tetraploid wheat. United States Department of Agriculture, September 2003. http://dx.doi.org/10.32747/2003.7695875.bard.

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High Grain Protein Content (GPC) is a desirable trait in breadmaking and pasta wheat varieties because of its positive effects on quality and nutritional value. However, selection for GPC is limited by our poor understanding of the genes involved in the accumulation of protein in the grain. The long-term goal of this project is to provide a better understanding of the genes controlling GPC in wheat. The specific objectives of this project were: a) to develop a high-density genetic map of the GPC gene in tetraploid wheat, b) to construct a T. turgidum Bacterial Artificial Chromosome (BAC) library, c) to construct a physical map of the GPC gene and identify a candidate for the GPC gene. A gene with a large effect on GPC was detected in Triticum turgidum var. dicoccoides and was previously mapped in the short arm of chromosome 6B. To define better the position of the Gpc-B1 locus we developed homozygous recombinant lines with recombination events within the QTL region. Except for the 30-cM region of the QTL these RSLs were isogenic for the rest of the genome minimizing the genetic variability. To minimize the environmental variability the RSLs were characterized using 10 replications in field experiments organized in a Randomized Complete Block Design, which were repeated three times. Using this strategy, we were able to map this QTL as a single Mendelian locus (Gpc-B1) on a 2.6-cM region flanked by RFLP markers Xcdo365 and Xucw67. All three experiments showed that the lines carrying the DIC allele had an average absolute increase in GPC of 14 g/kg. Using the RFLP flanking markers, we established the microcolinearity between a 2.l-cM region including the Gpc-B1 gene in wheat chromosome 6BS and a 350-kb region on rice chromosome 2. Rice genes from this region were used to screen the Triticeae EST collection, and these ESTs were used to saturate the Gpc-B1 region with molecular markers. With these new markers we were able to map the Gpc-B1 locus within a 0.3-cM region flanked by PCR markers Xucw83 and Xucw71. These flanking markers defined a 36-kb colinear region with rice, including one gene that is a potential candidate for the Gpc-B1 gene. To develop a physical map of the Gpc-B1 region in wheat we first constructed a BAC library of tetraploid wheat, from RSL#65 including the high Gpc-B1 allele. We generated half- million clones with an average size of l3l-kb (5.1 X genome equivalents for each of the two genomes). This coverage provides a 99.4% probability of recovering any gene from durum wheat. We used the Gpc-BI flanking markers to screen this BAC library and then completed the physical map by chromosome walking. The physical map included two overlapping BACs covering a region of approximately 250-kb, including two flanking markers and the Gpc-B1 gene. Efforts are underway to sequence these two BACs to determine if additional wheat genes are present in this region. Weare also developing new RSLs to further dissect this region. We developed PCR markers for flanking loci Xucw79andXucw71 to facilitate the introgression of this gene in commercial varieties by marker assisted selection (httQ://maswheat.ucdavis.edu/ orotocols/HGPC/index.hlm). Using these markers we introgressed the Gpc-B1 gene in numerous pasta and common wheat breeding lines.
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5

Gould, Michael, and V. A. Ford. Mapping Mammary Carcinoma Suppressor Genes in the Laboratory Rat. Fort Belvoir, VA: Defense Technical Information Center, June 1995. http://dx.doi.org/10.21236/ada298730.

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6

Sengupta-Gopalan, Champa, Shmuel Galili, and Rachel Amir. Improving Methionine Content in Transgenic Forage Legumes. United States Department of Agriculture, February 2001. http://dx.doi.org/10.32747/2001.7580671.bard.

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Leguminous forage crops are high in proteins but deficient in S- amino acids. It has been shown that both wool quality and milk production can be limited by the post-ruminal supply of sulfur-containing amino acids. Efforts to use conventional plant breeding and cell selection techniques to increase the S-amino acid content of alfalfa have met with little success. With the objective to increase the S-amino acid content of forage legumes, the goal of this project was to co- express the methionine rich zein genes from corn along with a gene for a key enzyme in methionine biosynthesis, aspartate kinase(AK). The zeins are seed storage proteins from corn and are groupec into four distinct classes based on their amino acid sequence homologies. The b-zein (15kd) and the 6zein (10kD and 18kD) have proportionately high levels of methionine (10%, 22% and 28%, respectively). Initial studies from our lab had shown that while the 15kD zein accumulated to high levels in vegetative tissues of transgenic tobacco the l0kD zein did not. However, co-expression of the 10kD zein with the 15kD zein genes in tobacco showed stabilization of the 10kD zein and the co-localization of the 10kD and 15kD zein proteins in unique ER derived protein bodies. AK is the key enzyme for producing carbon skeletons for all amino acids of the aspartate family including methionine. It is, however, regulated by end-product feedback inhibition. The specific objectives of this proposal were: i. to co-express the 15kD zein with the 10/18kD zein genes in alfalfa in order to enhance the level of accumulation of the 10/18kD zein; ii. to increase methionine pools by expressing a feedback insensitive AK gene in transformants co-expressing the 15kD and 10/18kD zein genes. The Israeli partners were successful in expressing the AK gene in alfalfa which resulted in an increase in free and bound threonine but not in methionine (Galili et al., 2000). Since our target was to increase methionine pools, we changed our second objective to replace the AK gene with the gene for cystathionine gamma synthase (CGS) in the co-expression studies. The first methionine specific reaction is catalyzed by CGS. An additional objective was to develop a transformation system for Berseem clover, and to introduce the appropriate gene constructs into it with the goal of improving their methionine content. Genes for the 15kD zein along with the genes for either the 10kD or 18kD zein have been introduced into the same alfalfa plant both by sexual crosses and by re-transformation. Analysis of these zein co-expressors have shown that both the IOkD and 18kD zein levels go up 5 to 10 fold when co-expressed with the 15kD zein (Bagga et al., MS in preparation). Incubation of the leaves of transgenic alfalfa co-expressing the 15kD and 10kD zein genes, in the rumen of cows have shown that the zein proteins are stable in the rumen. To increase the level of zein accumulation in transgenic alfalfa different promoters have been used to drive the zein genes in alfalfa and we have concluded that the CaMV 35S promoter is superior to the other strong leaf -specific promoters. By feeding callus tissue of alfalfa plants co-expressing the 15kD and 10kD zein genes with methionine and its precursors, we have shown that the zein levels could be significantly enhanced by increasing the methionine pools. We have now introduced the CGS gene (from Arabidopsis; kindly provided to us by Dr. Leustek), into the 15kD zein transformants and experiments are in progress to check if the expression of the CGS gene indeed increases the level of zein accumulation in alfalfa. We were not successful in developing a transformation protocol for Berseem clover.
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7

Breiman, Adina, Jan Dvorak, Abraham Korol, and Eduard Akhunov. Population Genomics and Association Mapping of Disease Resistance Genes in Israeli Populations of Wild Relatives of Wheat, Triticum dicoccoides and Aegilops speltoides. United States Department of Agriculture, December 2011. http://dx.doi.org/10.32747/2011.7697121.bard.

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Wheat is the most widely grown crop on earth, together with rice it is second to maize in total global tonnage. One of the emerging threats to wheat is stripe (yellow) rust, especially in North Africa, West and Central Asia and North America. The most efficient way to control plant diseases is to introduce disease resistant genes. However, the pathogens can overcome rapidly the effectiveness of these genes when they are wildly used. Therefore, there is a constant need to find new resistance genes to replace the non-effective genes. The resistance gene pool in the cultivated wheat is depleted and there is a need to find new genes in the wild relative of wheat. Wild emmer (Triticum dicoccoides) the progenitor of the cultivated wheat can serve as valuable gene pool for breeding for disease resistance. Transferring of novel genes into elite cultivars is highly facilitated by the availability of information of their chromosomal location. Therefore, our goals in this study was to find stripe rust resistant and susceptible genotypes in Israeli T. dicoccoides population, genotype them using state of the art genotyping methods and to find association between genetic markers and stripe rust resistance. We have screened 129 accessions from our collection of wild emmer wheat for resistance to three isolates of stripe rust. About 30% of the accessions were resistant to one or more isolates, 50% susceptible, and the rest displayed intermediate response. The accessions were genotyped with Illumina'sInfinium assay which consists of 9K single nucleotide polymorphism (SNP) markers. About 13% (1179) of the SNPs were polymorphic in the wild emmer population. Cluster analysis based on SNP diversity has shown that there are two main groups in the wild population. A big cluster probably belongs to the Horanum ssp. and a small cluster of the Judaicum ssp. In order to avoid population structure bias, the Judaicum spp. was removed from the association analysis. In the remaining group of genotypes, linkage disequilibrium (LD) measured along the chromosomes decayed rapidly within one centimorgan. This is the first time when such analysis is conducted on a genome wide level in wild emmer. Such a rapid decay in LD level, quite unexpected for a selfer, was not observed in cultivated wheat collection. It indicates that wild emmer populations are highly suitable for association studies yielding a better resolution than association studies in cultivated wheat or genetic mapping in bi-parental populations. Significant association was found between an SNP marker located in the distal region of chromosome arm 1BL and resistance to one of the isolates. This region is not known in the literature to bear a stripe rust resistance gene. Therefore, there may be a new stripe rust resistance gene in this locus. With the current fast increase of wheat genome sequence data, genome wide association analysis becomes a feasible task and efficient strategy for searching novel genes in wild emmer wheat. In this study, we have shown that the wild emmer gene pool is a valuable source for new stripe rust resistance genes that can protect the cultivated wheat.
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8

Maria Akopyan, Maria Akopyan. It's Not Easy Being Green: The Color of Gene Diversity in Red-eyed Treefrogs. Experiment, January 2015. http://dx.doi.org/10.18258/4416.

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9

Ceremuga, Thomas E. Effects of Herbal Supplements on PTSD-Induced Changes in Rat Behavior & Brain Gene Expression. Fort Belvoir, VA: Defense Technical Information Center, June 2014. http://dx.doi.org/10.21236/ada608252.

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10

Zhang, Jing. Platelet-Derived Growth Factor-BB Stimulates Fibronectin Gene Expression in Fibroblasts Isolated from Rat Thoracic Aorta. Fort Belvoir, VA: Defense Technical Information Center, May 1994. http://dx.doi.org/10.21236/ad1011392.

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