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Journal articles on the topic 'IT-ret'

Author: Grafiati

Published: 25 July 2024

Last updated: 31 July 2025

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1

Drilon, Alexander E., Dayong Zhai, Evan Rogers, et al. "The next-generation RET inhibitor TPX-0046 is active in drug-resistant and naïve RET-driven cancer models." Journal of Clinical Oncology 38, no. 15_suppl (2020): 3616. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.3616.

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3616 Background: RET fusions/mutations drive oncogenesis in lung and thyroid cancers, and several other malignancies. Selective RET inhibitors (selpercatinib/pralsetinib) are active in patients with these cancers; unfortunately, resistance often occurs. On-target resistance includes the acquisition of solvent front mutations (SFMs i.e. RET G810 substitutions). TPX-0046 is a structurally differentiated RET inhibitor that is potent against a range of RET fusions and mutations including SFMs. Methods: The rationally-designed, compact, macrocyclic RET/SRC inhibitor TPX-0046 was characterized in RE

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2

Ammer, Stefanie, Christian Lambertz, and Matthias Gauly. "Comparison of different measuring methods for body temperature in lactating cows under different climatic conditions." Journal of Dairy Research 83, no. 2 (2016): 165–72. http://dx.doi.org/10.1017/s0022029916000182.

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The aim of the research described here was to compare different methods of body temperature (BT) measurements in dairy cows. It was hypothesised that reticular temperature (RET) values reflect the physiological status of the animals in an equivalent way to rectal (RT) and vaginal (VT) measurements. RT, VT and RET temperatures of twelve lactating Holstein–Friesian cows were measured over five consecutive days in June and October 2013. While RT and VT were manually measured three times a day, RET was automatically recorded at 10 min intervals using a bolus in the reticulum. For comparison with R

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3

Hennige, Anita M., Reiner Lammers, Wolfgang Höppner, et al. "Inhibition of Ret Oncogene Activity by the Protein Tyrosine Phosphatase SHP1." Endocrinology 142, no. 10 (2001): 4441–47. http://dx.doi.org/10.1210/endo.142.10.8453.

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Abstract Germline mutations in the Ret protooncogene give rise to the inherited endocrine cancer syndromes MEN types 2A and 2B and familiar medullary thyroid carcinoma. Although it is well accepted that the constitutive active tyrosine kinase of Ret oncogenes ultimately leads to malignant transformation, it is not clear whether a decrease in the autophosphorylation of oncogenic Ret forms can affect the mitogenic and transforming activities of Ret. Potential modulators of the tyrosine kinase activity of Ret could be tyrosine phosphatases that are expressed in human thyroid tissue. Therefore, we

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4

Durick, Kyle, Gordon N. Gill, and Susan S. Taylor. "Shc and Enigma Are Both Required for Mitogenic Signaling by Ret/ptc2." Molecular and Cellular Biology 18, no. 4 (1998): 2298–308. http://dx.doi.org/10.1128/mcb.18.4.2298.

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ABSTRACT Ret/ptc2 is a constitutively active, oncogenic form of the c-Ret receptor tyrosine kinase. Like the other papillary thyroid carcinoma forms of Ret, Ret/ptc2 is activated through fusion of the Ret tyrosine kinase domain to the dimerization domain of another protein. Investigation of requirements for Ret/ptc2 mitogenic activity, using coexpression with dominant negative forms of Ras and Raf, indicated that these proteins are required for mitogenic signaling by Ret/ptc2. Because activation of Ras requires recruitment of Grb2 and SOS to the plasma membrane, the subcellular distribution of

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5

Carlomagno, Francesca, Teresa Guida, Suresh Anaganti, et al. "Identification of tyrosine 806 as a molecular determinant of RET kinase sensitivity to ZD6474." Endocrine-Related Cancer 16, no. 1 (2009): 233–41. http://dx.doi.org/10.1677/erc-08-0213.

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ZD6474 (vandetanib, Zactima, Astra Zeneca) is an anilinoquinazoline used to target the receptor tyrosine kinase RET in familial and sporadic thyroid carcinoma (IC50: 100 nM). The aim of this study was to identify molecular determinants of RET sensitivity to ZD6474. Here, we show that mutation of RET tyrosine 806 to cysteine (Y806C) induced RET kinase resistance to ZD6474 (IC50: 933 nM). Y806 maps close to the gate-keeper position at the RET kinase nucleotide-binding pocket. Although tyrosine 806 is a RET auto-phosphorylation site, its substitution to phenylalanine (Y806F) did not markedly affe

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6

Jones, Stanton L. "Rational-Emotive Therapy in Christian Perspective." Journal of Psychology and Theology 17, no. 2 (1989): 110–20. http://dx.doi.org/10.1177/009164718901700203.

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Rational-emotive therapy (RET), a common cognitive-behavioral approach to psychotherapy, is critiqued from a Christian perspective. Positively, RET is openly value-oriented, prizing of rationality, and balanced in its attempt to deal with the thoughts, behaviors, and feelings of the client from a rational perspective. Such an approach can be a helpful tool for the Christian therapist to use. Difficulties with RET thought from a Christian perspective include incompatibilities with values endorsed by RET, an overemphasis on rationality, problems with the understanding of rationality and emotion,

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7

Wang, Lei, Yu Zhang, Yu Gao, et al. "Prognostic and Predictive Values of Subcellular Localisation of RET in Renal Clear-Cell Carcinoma." Disease Markers 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/6870470.

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Metastatic renal cell carcinoma (RCC) presents a poor prognosis and an unpredictable course. To date, no validated biomarkers can predict the outcome of RCC. Ongoing efforts are conducted to identify the molecular markers of RCC progression, as well as the targets for novel therapeutic approaches. RET is a tyrosine kinase receptor which has been investigated as a possible target in other cancers because it is involved in oncogenic activation. To evaluate the predictive and prognostic functions of RET in ccRCC, a tissue microarray study was conducted on 273 ccRCC patients. Results showed that b

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8

Dawasaz, A. A., Ibrahim Alshahrani, Syed M. Yassin, et al. "Detection of Dental Caries’ and Dermatoglyphics’ Association with Relative Enamel Thickness Using CBCT Images in Saudi Subpopulation: A Novel Approach." BioMed Research International 2021 (July 26, 2021): 1–7. http://dx.doi.org/10.1155/2021/5550916.

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Background. Dental caries is the localized destruction of dental hard tissues (enamel and dentine). Decayed, Missing, and Filled Teeth (DMFT) index is the most commonly used dental caries index. Thickness of the outermost part of the tooth called the enamel is determined by the rate of deposition of enamel proteins. Relative enamel thickness (RET) gives a measure of enamel thickness with respect to dentine. Dental caries is influenced by a genetically determined factor called dermatoglyphics (DG). As the genes responsible for RET and DG lie on the same chromosome and develop during the same ti

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9

Zhang, Kai, Huajun Chen, Ye Wang, et al. "Clinical Characteristics and Molecular Patterns of RET-Rearranged Lung Cancer in Chinese Patients." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 27, no. 5 (2019): 575–82. http://dx.doi.org/10.3727/096504018x15344979253618.

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RET rearrangement has been proven as an oncogenic driver in patients with lung cancer. However, the prevalence, clinical characteristics, molecular features, and therapeutic options in RET-rearranged patients remain unclear, especially in Chinese lung cancer patients. We retrospectively collected 6,125 Chinese lung cancer patients who have been profiled using next-generation sequencing (NGS). The clinical demographics and molecular features of RET rearrangement-positive patients were analyzed. RET rearrangements were identified in 84 patients with a proportion of 1.4% in our cohort. The median

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10

Corsini, Raymond J. "Putting the “B” in ret: It had to be." Journal of Rational-Emotive and Cognitive-Behavior Therapy 13, no. 1 (1995): 5–7. http://dx.doi.org/10.1007/bf02354554.

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11

Ahn, Beung-chul, Viola W. Zhu, and Sun Min Lim. "The Next Target for NSCLC: Let It Be “RET”." Journal of Thoracic Oncology 15, no. 12 (2020): 1803–5. http://dx.doi.org/10.1016/j.jtho.2020.09.008.

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12

Sapio, Maria Rosaria, Anna Guerra, Vincenzo Marotta, et al. "High Growth Rate of Benign Thyroid Nodules Bearing RET/PTC Rearrangements." Journal of Clinical Endocrinology & Metabolism 96, no. 6 (2011): E916—E919. http://dx.doi.org/10.1210/jc.2010-1599.

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Context: Benign thyroid nodules display a broad range of behaviors from a stationary size to a progressive growth. The RET/PTC oncogene has been documented in a fraction of benign thyroid nodules, besides papillary thyroid carcinomas, and it might therefore influence their growth. Objective: The aim of the present work was to evaluate whether RET/PTC in benign thyroid nodules associates with a different nodular growth rate. Study Design: In this prospective multicentric study, 125 subjects with benign nodules were included. RET rearrangements were analyzed in cytology samples; clinical and ult

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13

Fusco, Alfredo, and Massimo Santoro. "20 years of RET/PTC in thyroid cancer: clinico-pathological correlations." Arquivos Brasileiros de Endocrinologia & Metabologia 51, no. 5 (2007): 731–35. http://dx.doi.org/10.1590/s0004-27302007000500010.

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The RET/PTC oncogene has been isolated almost twenty years ago. During these years, the research has given a final answer to several questions. In fact, it has been demonstrated that: a) RET/PTC is an early event in the process of thyroid carcinogenesis and has a critical role in the generation of the papillary carcinoma; b) RET/PTC activation is essentially restricted to the papillary histotype and to the Hürthle thyroid tumors; c) its incidence increases after exposure to radiations. However, some questions have not found a final answer yet: a) which is the real frequency of RET/PTC activati

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14

Pelicci, Giuliana, Flavia Troglio, Alessandra Bodini, et al. "The Neuron-Specific Rai (ShcC) Adaptor Protein Inhibits Apoptosis by Coupling Ret to the Phosphatidylinositol 3-Kinase/Akt Signaling Pathway." Molecular and Cellular Biology 22, no. 20 (2002): 7351–63. http://dx.doi.org/10.1128/mcb.22.20.7351-7363.2002.

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ABSTRACT Rai is a recently identified member of the family of Shc-like proteins, which are cytoplasmic signal transducers characterized by the unique PTB-CH1-SH2 modular organization. Rai expression is restricted to neuronal cells and regulates in vivo the number of postmitotic sympathetic neurons. We report here that Rai is not a common substrate of receptor tyrosine kinases under physiological conditions and that among the analyzed receptors (Ret, epidermal growth factor receptor, and TrkA) it is activated specifically by Ret. Overexpression of Rai in neuronal cell lines promoted survival by

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15

Santoro, M., W. T. Wong, P. Aroca, et al. "An epidermal growth factor receptor/ret chimera generates mitogenic and transforming signals: evidence for a ret-specific signaling pathway." Molecular and Cellular Biology 14, no. 1 (1994): 663–75. http://dx.doi.org/10.1128/mcb.14.1.663-675.1994.

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A chimeric expression vector which encoded for a molecule encompassing the extracellular domain of the epidermal growth factor (EGF) receptor (EGFR) and the intracellular domain of the ret kinase (EGFR/ret chimera) was generated. Upon ectopic expression in mammalian cells, the EGFR/ret chimera was correctly synthesized and transported to the cell surface, where it was shown capable of binding EGF and transducing an EGF-dependent signal intracellularly. Thus, the EGFR/ret chimera allows us to study the biological effects and biochemical activities of the ret kinase under controlled conditions o

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16

Santoro, M., W. T. Wong, P. Aroca, et al. "An epidermal growth factor receptor/ret chimera generates mitogenic and transforming signals: evidence for a ret-specific signaling pathway." Molecular and Cellular Biology 14, no. 1 (1994): 663–75. http://dx.doi.org/10.1128/mcb.14.1.663.

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A chimeric expression vector which encoded for a molecule encompassing the extracellular domain of the epidermal growth factor (EGF) receptor (EGFR) and the intracellular domain of the ret kinase (EGFR/ret chimera) was generated. Upon ectopic expression in mammalian cells, the EGFR/ret chimera was correctly synthesized and transported to the cell surface, where it was shown capable of binding EGF and transducing an EGF-dependent signal intracellularly. Thus, the EGFR/ret chimera allows us to study the biological effects and biochemical activities of the ret kinase under controlled conditions o

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17

Wu, Jie, and Vivek Subbiah. "RETooling the RET Inhibitor Pralsetinib for ESR1 Fusion–Positive Breast Cancer and Beyond." Cancer Research 83, no. 19 (2023): 3159–61. http://dx.doi.org/10.1158/0008-5472.can-23-1021.

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Abstract Transcriptionally active fusions of ESR1 (ESR1-TAF) and somatic mutations in the estrogen receptor alpha (ERα) ligand-binding domain (LBD) cause endocrine therapy resistance in breast cancer. In searching for therapeutic target kinase(s) in these breast cancers, Gou and colleagues identified FLT4, RET, JAK1, and IGF1R as the top upregulated kinases induced by ESR1-TAFs and ERα LBD mutants in breast cancer cells. Among them, inhibition of RET by pralsetinib suppressed ESR1-TAF–driven and ERα LBD mutant–driven cell proliferation and patient-derived xenograft growth. Pralsetinib is an in

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18

Vargiolu, Manuela, Daniela Fusco, Ivana Kurelac, et al. "The Tyrosine Kinase Receptor RET Interacts in Vivo with Aryl Hydrocarbon Receptor-Interacting Protein to Alter Survivin Availability." Journal of Clinical Endocrinology & Metabolism 94, no. 7 (2009): 2571–78. http://dx.doi.org/10.1210/jc.2008-1980.

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Context: RET is a tyrosine kinase transmembrane receptor expressed in two main alternative isoforms: RET9 and RET51. RET transduces a positive signal leading to survival, differentiation, or migration in the presence of its ligand glial cell line-derived neurotrophic factor, whereas in its absence a proapoptotic fragment that initiates a negative signaling for apoptosis is generated. The signal transduction mechanisms leading to apoptosis are still unclear. Objective: To shed light on the mechanisms of RET-induced apoptosis, we searched for novel interactors of RET51. Design: The “split ubiqui

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Chatterjee, Sumantra, Lauren E. Fries, Or Yaacov, Nan Hu, Hanna E. Berk-Rauch, and Aravinda Chakravarti. "RET enhancer haplotype-dependent remodeling of the human fetal gut development program." PLOS Genetics 19, no. 11 (2023): e1011030. http://dx.doi.org/10.1371/journal.pgen.1011030.

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Hirschsprung disease (HSCR) is associated with deficiency of the receptor tyrosine kinase RET, resulting in loss of cells of the enteric nervous system (ENS) during fetal gut development. The major contribution to HSCR risk is from common sequence variants in RET enhancers with additional risk from rare coding variants in many genes. Here, we demonstrate that these RET enhancer variants specifically alter the human fetal gut development program through significant decreases in gene expression of RET, members of the RET-EDNRB gene regulatory network (GRN), other HSCR genes, with an altered tran

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20

Ahmed, Attique, and Muhammad Naeem. "A Novel Framework for Selecting Elicitation Technique based on Attribute Mapping." International Journal of Engineering and Applied Computer Science 04, no. 02 (2022): 19–24. http://dx.doi.org/10.24032/ijeacs/0402/001.

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The software development process is completely based on the requirements of stakeholders. If the requirements of stakeholders are being integrated into the proposed system, then it can be assumed that the end product is going to be optimal and successful. To achieve a successful product, different Requirement Elicitation Techniques (RET) are being practiced. The selection of a suitable RET is based on the nature of the product being developed. So, a single RET doesn’t fit all products. In this paper, we differentiate all RETs from each other which makes it easier for an analyst to choose suita

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21

Luesma, M. J., I. Cantarero, J. M. Álvarez-Dotu, S. Santander, and C. Junquera. "New Insights into c-Ret Signalling Pathway in the Enteric Nervous System and Its Relationship with ALS." BioMed Research International 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/328348.

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The receptor tyrosine kinase Ret (c-Ret) transduces the glial cell line-derived neurotrophic factor (GDNF) signal, one of the neurotrophic factors related to the degeneration process or the regeneration activity of motor neurons in amyotrophic lateral sclerosis (ALS). The phosphorylation of several tyrosine residues of c-Ret seems to be altered in ALS. c-Ret is expressed in motor neurons and in the enteric nervous system (ENS) during the embryonic period. The characteristics of the ENS allow using it as model for central nervous system (CNS) study and being potentially useful for the research

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22

Rocco, Danilo, Luigi Sapio, Luigi Della Gravara, Silvio Naviglio, and Cesare Gridelli. "Treatment of Advanced Non-Small Cell Lung Cancer with RET Fusions: Reality and Hopes." International Journal of Molecular Sciences 24, no. 3 (2023): 2433. http://dx.doi.org/10.3390/ijms24032433.

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RET-selective tyrosine kinase inhibitors (TKIs) selpercatinib and pralsetinib have revolutionized the landscape of RET-positive (RET+) advanced non-small cell lung cancer (NSCLC) treatment thanks to their efficacy and safety profiles. This class of medications currently represents the standard of care for both naïve and patients that have not received selective RET-TKIs in the first-line setting. However, we presently lack a satisfactory understanding of resistance mechanism developing after selective RET-TKIs usage, as well as a specific treatment for patients progressing on selpercatinib or

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Rungngu, Susanti Lisupindan Palimbong, Audrey Wahani, and Max F. J. Mantik. "Reticulocyte hemoglobin equivalent for diagnosing iron deficiency anemia in children." Paediatrica Indonesiana 56, no. 2 (2016): 90. http://dx.doi.org/10.14238/pi56.2.2016.90-4.

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Background The prevalence of iron deficiency anemia (IDA) remains high in Indonesian children. When anemia is detected in a patient, the physician’s task is to identify the cause, address it, provide iron therapy, and prevent recurrence. However, prevention is best done by early detection. The reticulocyte hemoglobin equivalent (Ret-He) is a direct measurement of iron level in reticulocytes recently produced in the bone marrow. The Ret-He measurement may be an early indicator of iron deficiency, as it is sensitive at the initial stage of the condition.Objective To assess for a relationship bet

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Robb, Harold B. "Using RET to Reduce Psychological Dysfunction Associated with Supernatural Belief Systems." Journal of Cognitive Psychotherapy 7, no. 4 (1993): 281–89. http://dx.doi.org/10.1891/0889-8391.7.4.281.

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This paper provides a general approach to using Rational-Emotive Therapy with any person experiencing psychological dysfunction in relation to their supernatural belief system. It shows how the principles of RET are used when supernaturalism is: (1) used metaphorically, (2) conceptualized as origin, (3) in concert with RET and (4) in conflict with RET.

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Tang, Ming-Jer, Dane Worley, Michele Sanicola, and Gregory R. Dressler. "The RET–Glial Cell-derived Neurotrophic Factor (GDNF) Pathway Stimulates Migration and Chemoattraction of Epithelial Cells." Journal of Cell Biology 142, no. 5 (1998): 1337–45. http://dx.doi.org/10.1083/jcb.142.5.1337.

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Embryonic development requires cell migration in response to positional cues. Yet, how groups of cells recognize and translate positional information into morphogenetic movement remains poorly understood. In the developing kidney, the ureteric bud epithelium grows from the nephric duct towards a group of posterior intermediate mesodermal cells, the metanephric mesenchyme, and induces the formation of the adult kidney. The secreted protein GDNF and its receptor RET are required for ureteric bud outgrowth and subsequent branching. However, it is unclear whether the GDNF–RET pathway regulates cel

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Yusof, Nurasyikin. "The Paediatric Iron Deficiency Assessment with Reticulocyte Haemoglobin Equivalent (Ret-He) in Comparison with Biochemical Markers of Serum Ferritin and Transferrin Saturation." Medicine & Health 16, no. 2 (2021): 138–47. http://dx.doi.org/10.17576/mh.2021.1602.10.

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Diagnosis of iron deficiency anaemia (IDA) is a challenge as the conventional methods often diagnose the disease at the later stage. Haemoglobin content of reticulocytes is useful to identify IDA at earlier stage. The objective of this study was to evaluate reticulocyte-haemoglobin equivalent (Ret-He) in diagnosing IDA in children and to compare it with other conventional methods. This prospective study was conducted on 120 paediatric patients aged 12 years and below, who attended Hospital Sultanah Aminah Johor Bahru, Malaysia with haemoglobin <12 g/dL. Ret-He and serum iron, ferritin and t

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Song, Xingju, Xu Yang, Taotao Zhang, Jing Liu, and Qun Liu. "A Novel Rhoptry Protein as Candidate Vaccine against Eimeria tenella Infection." Vaccines 8, no. 3 (2020): 452. http://dx.doi.org/10.3390/vaccines8030452.

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Eimeria tenella (E. tenella) is a highly pathogenic and prevalent species of Eimeria that infects chickens, and it causes a considerable disease burden worldwide. The secreted proteins and surface antigens of E. tenella at the sporozoite stage play an essential role in the host–parasite interaction, which involves attachment and invasion, and these interactions are considered vaccine candidates based on the strategy of cutting off the invasion pathway to interrupt infection. We selected two highly expressed surface antigens (SAGs; Et-SAG13 and Et-SAG) and two highly expressed secreted antigens

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Alqahtani, Tariq, Vishnu Kumarasamy, Sahar Saleh Alghamdi, et al. "Adefovir Dipivoxil as a Therapeutic Candidate for Medullary Thyroid Carcinoma: Targeting RET and STAT3 Proto-Oncogenes." Cancers 15, no. 7 (2023): 2163. http://dx.doi.org/10.3390/cancers15072163.

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Aberrant gene expression is often linked to the progression of various cancers, making the targeting of oncogene transcriptional activation a potential strategy to control tumor growth and development. The RET proto-oncogene’s gain-of-function mutation is a major cause of medullary thyroid carcinoma (MTC), which is part of multiple endocrine neoplasia type 2 (MEN2) syndrome. In this study, we used a cell-based bioluminescence reporter system driven by the RET promoter to screen for small molecules that potentially suppress the RET gene transcription. We identified adefovir dipivoxil as a trans

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Livia, Resvi, Fajar Wasilah, and Leni Lismayanti. "Comparison of Reticulocyte Hemoglobin Equivalent Levels between Low and Normal Birth Weight Newborns." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 29, no. 1 (2023): 64–68. http://dx.doi.org/10.24293/ijcpml.v29i1.1943.

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Low Birth Weight (LBW) newborns face a risk of iron deficiency. Iron deficiency hinders growth, and motoric, and cognitive development. Newborns with LBW sometimes suffer from inflammation, which affects the commonly used iron measurements. Reticulocyte hemoglobin equivalent (Ret-He) is considered a potential tool to measure iron profile because it measures functional iron, and it is not affected by inflammation. This study compared the Ret-He in LBW and normal birth weight newborns. This cross-sectional study was done retrospectively by observing and comparing the hematology data of newborns

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Zhu, Yongqiang, Jia Wang, and Minghong Shang. "Abstract LB330: FHND5071: a selective RET inhibitor with unique pharmacokinetic profile." Cancer Research 83, no. 8_Supplement (2023): LB330. http://dx.doi.org/10.1158/1538-7445.am2023-lb330.

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Abstract Background: Gene rearrangements (fusions) and mutations in RET have the potential to be oncogenic drivers and have been observed in a variety of tumors types. Selective RET inhibitors selpercatinib and pralsetinib have been approved for patients with RET-altered cancers. FHND5071 is a novel kinase inhibitor which specifically targets RET activated forms and has unique pharmacokinetic profile. Methods: The pharmacological profile of FHND5071 have been confirmed in in vitro and in vivo evaluations, including enzyme and cell-based assays, PK/PD study, and RET-dependent tumor models. Resu

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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 (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 c

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Bunker, Lisa D., Christina Nessler, and Julie L. Wambaugh. "Effect Size Benchmarks for Response Elaboration Training: A Meta-Analysis." American Journal of Speech-Language Pathology 28, no. 1S (2019): 247–58. http://dx.doi.org/10.1044/2018_ajslp-17-0152.

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Purpose With a number of single-case experimental design studies reporting the effects of treatment for response (and modified response) elaboration training (RET/M-RET), it is important to consolidate data over multiple participants to allow comparison within/between individuals and across similar treatments. The purpose of this study was to conduct a meta-analysis of single-case experimental design studies of RET/M-RET and to determine effect size (ES) benchmarks to allow comparison to “group” data. Method Database and bibliographical searches identified 20 investigations of RET/M-RET. Nine

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Khatri, Ujjwol, Neetu Dayal, Xueqing Hu, et al. "Abstract 3851: Targeting RET solvent-front mutants with an alkynyl nicotinamide-based inhibitor." Cancer Research 83, no. 7_Supplement (2023): 3851. http://dx.doi.org/10.1158/1538-7445.am2023-3851.

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Abstract Selpercatinib (LOXO-292, LY3527723) and pralsetinib (BLU-667) are first-in-class RET-targeted cancer therapy drugs. However, secondary RET mutations that confer selpercatinib/pralsetinib resistance have been identified, necessitating development of next-generation RET Tyrosine kinase inhibitors (TKIs). While the G810C/R/S/V mutations located at the RET kinase solvent-front site were detected in selpercatinib-treated patients, it was unclear whether all of these and other potential G810 mutants are resistant to selpercatinib and pralsetinib. We profiled selpercatinib and pralsetinib on

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Sijmons, R. H., R. M. W. Hofstra, F. A. Wijburg, et al. "Oncological implications of RET gene mutations in Hirschsprung’s disease." Gut 43, no. 4 (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

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Sahakian, Nicolas, Frédéric Castinetti, and Pauline Romanet. "Molecular Basis and Natural History of Medullary Thyroid Cancer: It is (Almost) All in the RET." Cancers 15, no. 19 (2023): 4865. http://dx.doi.org/10.3390/cancers15194865.

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Medullary thyroid cancer (MTC) is a rare disease, which can be either sporadic (roughly 75% of cases) or genetically determined (multiple endocrine neoplasia type 2, due to REarranged during Transfection RET germline mutations, 25% of cases). Interestingly, RET pathogenic variants (mainly M918T) have also been reported in aggressive forms of sporadic MTC, suggesting the importance of RET signalling pathways in the pathogenesis of MTC. The initial theory of RET codon-related MTC aggressiveness has been recently questioned by studies suggesting that this would only define the age at disease onse

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Peng, Hai Xin, and Rui Kang. "Stimulate and Eliminate Electronic Product Design Defects By Reliability Enhancement Testing." Advanced Materials Research 663 (February 2013): 621–25. http://dx.doi.org/10.4028/www.scientific.net/amr.663.621.

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This paper first introduces the test profile of Reliability Enhancement Testing(RET) then completed in the past three years, a large number of the implementation results of the RET test were statistically analyzed, given the distribution of the design defect, the last two design defects excitation and elimination process were be detailed explanation, and demonstrated it is exceptionally effective that the RET test inspire and eliminate electronic product design defects.

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Di Cristofaro, J., V. Vasko, V. Savchenko, et al. "ret/PTC1 and ret/PTC3 in thyroid tumors from Chernobyl liquidators: comparison with sporadic tumors from Ukrainian and French patients." Endocrine-Related Cancer 12, no. 1 (2005): 173–83. http://dx.doi.org/10.1677/erc.1.00884.

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Like children exposed to Chernobyl fallout, the workers who cleaned up after the accident, also known as liquidators, have exhibited an increased incidence of thyroid cancer. A high prevalence of ret/PTC3 rearrangement has been found in pediatric post-Chernobyl thyroid tumors, but this feature has not been investigated in liquidator thyroid tumors. In this study we analyzed the prevalence of ret/PTC1 and ret/PTC3 in thyroid tumors from 21 liquidators, 31 nonirradiated adult Ukrainian patients, and 34 nonirradiated adult French patients. ret rearrangements in carcinomas were found in 83.3% of l

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Bhujbal, Swapnil P., Seketoulie Keretsu, and Seung Joo Cho. "Molecular Modelling Studies on Pyrazole Derivatives for the Design of Potent Rearranged during Transfection Kinase Inhibitors." Molecules 26, no. 3 (2021): 691. http://dx.doi.org/10.3390/molecules26030691.

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RET (rearranged during transfection) kinase, one of the receptor tyrosine kinases, plays a crucial role in the development of the human nervous system. It is also involved in various cell signaling networks responsible for the normal cell division, growth, migration, and survival. Previously reported clinical studies revealed that deregulation or aberrant activation of RET signaling can cause several types of human cancer. For example, medullary thyroid carcinoma (MTC) and multiple endocrine neoplasia (MEN2A, MEN2B) occur due to sporadic mutation or germline RET mutation. A number of RET kinas

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Sung, Bongsuk, and Woo-Yong Song. "Are Political Factors More Relevant Than Economic Factors in Firm-Level Renewable Energy Technology Export? Evidence from Path Analysis." Sustainability 13, no. 16 (2021): 8788. http://dx.doi.org/10.3390/su13168788.

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Renewable energy technology (RET) firms are key economic entities in the export of RET-related products and components, in which RET firms’ exports are affected largely by policy and market. Nonetheless, the effects of policy and market factors on RET firm-level export have never received attention from researchers. This study aims to fill the gap by taking a political economy approach to establish a structural equation model to analyze the path of political-economic factor-firms’ market orientation-based export. This study reveals that RET firms’ market-orientation-based export enhancement de

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Lin, Hao, Yujie Liu, Ruitao Zhou, et al. "Noncanonical RET fusions in Chinese patients with non-small cell lung cancer from DNA-based next-generation sequencing." Journal of Clinical Oncology 42, no. 16_suppl (2024): e20000-e20000. http://dx.doi.org/10.1200/jco.2024.42.16_suppl.e20000.

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e20000 Background: The FDA has approved selpercatinib and pralsetinib for the treatment of metastatic RET fusion-positive non-small cell lung cancer in adult patients. Although the overall response rate is high and the response is durable, the outcomes may vary due to different fusion types of the same driver gene. Methods: We retrospectively collected and analyzed 14062 samples (tumour tissue or plasma) from Chinese lung cancer patients who underwent tissue-based or ctDNA-based next-generation sequencing (NGS) assays at HaploX Genomic Sequencing Center from May 18, 2020, to January 11, 2024.

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Imtiaz, Isma, Ayesha Younas, Ayisha Imran, Abuzar Siddique, Nauman Aslam Malik, and Akhtar Sohail Chughtai. "SIGNIFICANCE OF MEASURING RETICULOCYTE HEMOGLOBIN (RET-HE) IN CHRONIC KIDNEY DISEASE PATIENTS." Pakistan Journal of Pathology 34, no. 2 (2023): 37–41. http://dx.doi.org/10.55629/pakjpathol.v34i2.748.

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Objective: To determine the significance of measuring reticulocyte hemoglobin (Ret-He) in chronic kidney disease patients. Material and Methods: It was a cross sectional study conducted at Chughtai Healthcare from March 2021 to March 2022. Approval was obtained from the ethical and research committee of the institute. 102 patients, both males and females, between the ages of 10-75 years, diagnosed cases of CKD were included in the study. Informed consent was taken from all the patients. Blood specimens were collected in EDTA vials and serum separating vials and tested for serum iron, serum fer

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Kotani, Takaya, Junya Takegaki, Ryo Takagi, Koichi Nakazato, and Naokata Ishii. "Consecutive bouts of electrical stimulation-induced contractions alter ribosome biogenesis in rat skeletal muscle." Journal of Applied Physiology 126, no. 6 (2019): 1673–80. http://dx.doi.org/10.1152/japplphysiol.00665.2018.

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Ribosome biogenesis has been implicated in resistance exercise training (RET)-induced skeletal muscle hypertrophy. However, it is unclear how increasing bouts of RET affects ribosome content and biogenesis. This was investigated in the present study using simulated RET where rat skeletal muscle is subjected to increasing bouts of electrical stimulation. Sprague-Dawley rats were randomly assigned to the following seven groups: sedentary for 5 days (SED) or 6 wk (SED_6w), resistance-exercise trained with 1 bout (1B), 2 bouts (2B), 3 bouts (3B), 6 bouts (6B), and 18 bouts (18B). RET was simulated

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Stanescu, Laura-Semonia, Adina Ghemigian, Mihai-Lucian Ciobica, et al. "Thyroid Malignancy and Cutaneous Lichen Amyloidosis: Key Points Amid RET Pathogenic Variants in Medullary Thyroid Cancer/Multiple Endocrine Neoplasia Type 2 (MEN2)." International Journal of Molecular Sciences 25, no. 18 (2024): 9765. http://dx.doi.org/10.3390/ijms25189765.

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We aimed to provide an updated narrative review with respect to the RET pathogenic variants and their implications at the clinical and molecular level in the diagnosis of medullary thyroid cancer (MTC)/multiple endocrine neoplasia (MEN) type 2, particularly with respect to the presence of cutaneous lichen amyloidosis (CLA). We searched English-language, in extenso original articles with no timeline nor study design restriction that were published on PubMed. A traditional interplay stands for CLA and MTC in MEN2 (not MEN3) confirmation. While the connection has been reported for more than three

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Borrello, Maria Grazia, Antonella Aiello, Bernard Peissel, et al. "Functional characterization of the MTC-associated germline RET-K666E mutation: evidence of oncogenic potential enhanced by the G691S polymorphism." Endocrine-Related Cancer 18, no. 4 (2011): 519–27. http://dx.doi.org/10.1530/erc-10-0306.

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Activating mutations of RET, a gene encoding two isoforms of a tyrosine kinase receptor physiologically expressed in several neural crest-derived cell lineages, are associated with the inherited forms of medullary thyroid carcinoma (MTC). The identification and characterization of novel RET mutations involved in MTC is valuable, as RET gene testing plays a crucial role in the management of these patients. In an MTC patient, we have identified a germline c.1996A>G transition in heterozygosis leading to K666E substitution. In addition, the conservative S904S (c.2712C>G) and the non-conserv

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Garcia-Rendueles, Angela R., Miguel Chenlo, Fernando Oroz-Gonjar, et al. "RET signalling provides tumorigenic mechanism and tissue specificity for AIP-related somatotrophinomas." Oncogene 40, no. 45 (2021): 6354–68. http://dx.doi.org/10.1038/s41388-021-02009-8.

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AbstractIt is unclear how loss-of-function germline mutations in the widely-expressed co-chaperone AIP, result in young-onset growth hormone secreting pituitary tumours. The RET receptor, uniquely co-expressed in somatotrophs with PIT1, induces apoptosis when unliganded, while RET supports cell survival when it is bound to its ligand. We demonstrate that at the plasma membrane, AIP is required to form a complex with monomeric-intracellular-RET, caspase-3 and PKCδ resulting in PIT1/CDKN2A-ARF/p53-apoptosis pathway activation. AIP-deficiency blocks RET/caspase-3/PKCδ activation preventing PIT1 a

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Loura, Luís M. S., Rodrigo F. M. de Almeida, and Manuel Prieto. "Methodologies and formalisms of resonance energy transfer in biophysics. Application to membrane model systems." International Journal of Photoenergy 5, no. 4 (2003): 223–31. http://dx.doi.org/10.1155/s1110662x03000369.

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The formalisms of resonance energy transfer (RET) to a distribution of acceptors are reviewed for several geometries relevant to membranes (planar, bilayer, multilayer) and random probe distribution. Models for nonrandom probe distribution (mean concentration model, phase separation model) are presented. Selected examples of quantitative applications of RET to these systems are described. It is illustrated how information about domain size, partition coefficients, phase composition, phase separation kinetics and bilayer aggregation can be obtained from time-resolved RET data.

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Muhibullah, Nouman Shafique, Navneet Kaur, et al. "Efficacy and safety of selpercatinib in advanced RET-altered thyroid cancers: A meta-analysis and systematic review." Journal of Clinical Oncology 42, no. 16_suppl (2024): e18073-e18073. http://dx.doi.org/10.1200/jco.2024.42.16_suppl.e18073.

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e18073 Background: Selpercatinib is a highly selective RET inhibitor that is used for the treatment of RET-mutant medullary thyroid cancers, but its efficacy and safety is not fully understood. Our objective is to summarize available literature on the safety and efficacy profile of Selpercatinib. Methods: A search was conducted on PubMed, Embase and Cochrane from foundation to 31st January 2024. Patients aged above 18 with Advanced RET-Altered Medullary Thyroid Cancers who received Selpercatinib were identified. Data abstraction was done based on objective response rate, complete response rate

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Prazeres, Hugo, Joana Torres, Fernando Rodrigues, et al. "How to Treat a Signal? Current Basis for RET-Genotype-Oriented Choice of Kinase Inhibitors for the Treatment of Medullary Thyroid Cancer." Journal of Thyroid Research 2011 (2011): 1–10. http://dx.doi.org/10.4061/2011/678357.

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The significance ofRETin thyroid cancer comes from solid evidence that, when inherited, anRETactivating mutation primes C-cells to transform into medullary carcinomas. Moreover, environmental exposure to radiation also induces rearranged transforming RET “isoforms” that are found in papillary thyroid cancer. TheRETgene codes for a tyrosine kinase receptor that targets a diverse set of intracellular signaling pathways. The nature ofRETpoint mutations predicts differences in the mechanisms by which the receptor becomes activated and correlates with different forms of clinical presentation, age o

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Cetta, Francesco, Gennaro Chiappetta, Rosa Marina Melillo, et al. "The ret/ptc1 Oncogene Is Activated in Familial Adenomatous Polyposis-Associated Thyroid Papillary Carcinomas1." Journal of Clinical Endocrinology & Metabolism 83, no. 3 (1998): 1003–6. http://dx.doi.org/10.1210/jcem.83.3.4614.

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Familial adenomatous polyposis (FAP) is caused by germ-line mutations of the apc gene, and it is associated with an increased risk of developing papillary thyroid carcinomas. We have previously reported that a significant fraction of sporadic human papillary thyroid carcinomas is characterized by gene rearrangements affecting the ret protooncogene. These rearrangements generate chimeric transforming oncogenes designated ret/ptc. By a combined immunohistochemical and RT-PCR approach, we analyzed, for ret/ptc oncogene activation, papillary thyroid carcinomas occurred in two FAP kindreds, both sh

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Ibáñez, Carlos F., Gustavo Paratcha та Fernanda Ledda. "RET-independent signaling by GDNF ligands and GFRα receptors". Cell and Tissue Research 382, № 1 (2020): 71–82. http://dx.doi.org/10.1007/s00441-020-03261-2.

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Abstract The discovery in the late 1990s of the partnership between the RET receptor tyrosine kinase and the GFRα family of GPI-anchored co-receptors as mediators of the effects of GDNF family ligands galvanized the field of neurotrophic factors, firmly establishing a new molecular framework besides the ubiquitous neurotrophins. Soon after, however, it was realized that many neurons and brain areas expressed GFRα receptors without expressing RET. These observations led to the formulation of two new concepts in GDNF family signaling, namely, the non-cell-autonomous functions of GFRα molecules,

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