Relevant bibliographies by topics / Zfhx1a

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  2. Dissertations / Theses
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Academic literature on the topic 'Zfhx1a'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Zfhx1a"

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Liu, Yongqing, Mary E. Costantino, Diego Montoya-Durango, Yujiro Higashi, Douglas S. Darling, and Douglas C. Dean. "The zinc finger transcription factor ZFHX1A is linked to cell proliferation by Rb–E2F1." Biochemical Journal 408, no. 1 (October 29, 2007): 79–85. http://dx.doi.org/10.1042/bj20070344.

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ZFHX1A is expressed in proliferating cells in the developing embryo, and in the present study we provide evidence that its expression is confined to proliferating cells through dependence on the Rb (retinoblastoma protein) family/E2F cell cycle pathway. Mutation of the Rb or E2F1 genes lead to induction of ZFHX1A mRNA, implying that the Rb–E2F1 repressor complex is important for repression of ZFHX1A. This repression is associated with recruitment of an E2F–Rb–histone deacetylase repressor complex to the promoter. A dominant-negative form of E2F1 inhibited ZFHX1A expression in p16INK4a(−) cells where Rb is constitutively hyperphosphorylated and inactive, suggesting that E2F can contribute to ZFHX1A transactivation in the absence of functional Rb. ZFHX1A is an E-box-binding transcription factor whose binding sites overlap with those bound by Snail1 and 2, and ZFHX1B/SIP1 (leading to at least partially overlapping function; for example, each of the proteins can repress E-cadherin expression). We found that expression of Snail1 and ZFHX1B/SIP1 is also regulated by E2Fs, but in contrast with ZFHX1A this regulation is Rb-family-independent. Snail2 expression was unaffected by either E2F or the Rb family. We propose that the differential effects of the Rb family/E2F pathway on expression of these E-box-binding proteins are important in maintaining their distinct patterns (and thus distinct functions) during embryogenesis.
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신정오, 정한성, 복진웅, and 이종민. "Expression patterns of Zfhx1a and Zfhx1b during mouse craniofacial development." Korean Journal of Oral Anatomy 39, no. 1 (December 2018): 1–8. http://dx.doi.org/10.35607/kjoa.39.1.201812.001.

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Kowase, Takanori, Heidi E. Walsh, Douglas S. Darling, and Margaret A. Shupnik. "Estrogen Enhances Gonadotropin-Releasing Hormone-Stimulated Transcription of the Luteinizing Hormone Subunit Promoters via Altered Expression of Stimulatory and Suppressive Transcription Factors." Endocrinology 148, no. 12 (December 1, 2007): 6083–91. http://dx.doi.org/10.1210/en.2007-0407.

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Transcription of the LH subunit genes is stimulated by GnRH and may be modulated physiologically by steroids such as 17β-estradiol (E). We found that E treatment amplified GnRH stimulation of the rat LHβ and α-subunit promoters, and expression of the endogenous mRNA, in LβT2 gonadotrope cells 2- to 5-fold above GnRH alone. We examined gene expression in LβT2 cells after E and/or GnRH treatment, and found that E suppressed expression of transcription factor Zfhx1a, and enhanced GnRH stimulation of Egr-1 mRNA and protein. E effects were abolished in the presence of antiestrogen. Egr-1 is critical for LHβ expression; however, the role of Zfhx1a, which binds to E-box sequences, was untested. We found E-box motifs in both the rat LHβ (−381, −182, and −15 bp) and α-subunit (−292, −64, −58 bp) promoters. Zfhx1a overexpression suppressed basal and GnRH-stimulated activity of both promoters. Mutation of the α-subunit promoter E boxes at either −64 or −58 bp eliminated Zfhx1a suppression, whereas mutation of the −292 bp E box had no effect. Gel shift assays demonstrated that Zfhx1a bound to the −64 and −58, but not −292, bp E-box DNA. Similarly, mutation of LHβ promoter E boxes at either −381 or −182, but not −15, bp reduced Zfhx1a suppression, correlating with binding of Zfhx1a. The −381 bp LHβ E box overlaps with an Sp1 binding site in the distal GnRH-stimulatory region, and increased Sp1 expression overcame Zfhx1a suppression. Thus, one mechanism by which E may enhance GnRH-stimulated LH subunit promoter activity is through regulation of both activators and suppressors of transcription.
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Tylzanowski, Przemko, Dirk De Valck, Vera Maes, Jenny Peeters, and Frank P. Luyten. "Zfhx1a and Zfhx1b mRNAs have non-overlapping expression domains during chick and mouse midgestation limb development." Gene Expression Patterns 3, no. 1 (March 2003): 39–42. http://dx.doi.org/10.1016/s1567-133x(02)00092-3.

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Manavella, Pablo A., Gonzalo Roqueiro, Douglas S. Darling, and Ana M. Cabanillas. "The ZFHX1A gene is differentially autoregulated by its isoforms." Biochemical and Biophysical Research Communications 360, no. 3 (August 2007): 621–26. http://dx.doi.org/10.1016/j.bbrc.2007.06.088.

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Gordon, M. S. "Hypoxia-Inducible Factor-1-Dependent Repression of E-cadherin in von Hippel-Lindau Tumor Suppressor—Null Renal Cell Carcinoma Mediated by TCF3, ZFHX1A, and ZFHX1B." Yearbook of Oncology 2007 (January 2007): 109–10. http://dx.doi.org/10.1016/s1040-1741(08)70352-x.

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Tylzanowski, Przemko, Dirk De Valck, Vera Maes, Jenny Peeters, and Frank P. Luyten. "Erratum to ‘Zfhx1a and Zfhx1b mRNAs have non-overlapping expression domains during chick and mouse midgestation limb development’ [Gene Expression Patterns 3 (2003) 39–42]." Gene Expression Patterns 3, no. 3 (June 2003): 383. http://dx.doi.org/10.1016/s1567-133x(03)00052-8.

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Krishnamachary, Balaji, David Zagzag, Hideko Nagasawa, Karin Rainey, Hiroaki Okuyama, Jin H. Baek, and Gregg L. Semenza. "Hypoxia-Inducible Factor-1-Dependent Repression of E-cadherin in von Hippel-Lindau Tumor Suppressor–Null Renal Cell Carcinoma Mediated by TCF3, ZFHX1A, and ZFHX1B." Cancer Research 66, no. 5 (March 1, 2006): 2725–31. http://dx.doi.org/10.1158/0008-5472.can-05-3719.

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Jin, Jiu-Zhen, Qun Li, Yujiro Higashi, Douglas S. Darling, and Jixiang Ding. "Analysis of Zfhx1a mutant mice reveals palatal shelf contact-independent medial edge epithelial differentiation during palate fusion." Cell and Tissue Research 333, no. 1 (May 10, 2008): 29–38. http://dx.doi.org/10.1007/s00441-008-0612-x.

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Anose, Bynthia M., and Michel M. Sanders. "Androgen Receptor Regulates Transcription of the ZEB1 Transcription Factor." International Journal of Endocrinology 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/903918.

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The zinc finger E-box binding protein 1 (ZEB1) transcription factor belongs to a two-member family of zinc-finger homeodomain proteins involved in physiological and pathological events mostly relating to cell migration and epithelial to mesenchymal transitions (EMTs). ZEB1 (also known as δEF1, zfhx1a, TCF8, and Zfhep) plays a key role in regulating such diverse processes as T-cell development, skeletal patterning, reproduction, and cancer cell metastasis. However, the factors that regulate its expression and consequently the signaling pathways in which ZEB1 participates are poorly defined. Because it is induced by estrogen and progesterone and is high in prostate cancer, we investigated whethertcf8, which encodes ZEB1, is regulated by androgen. Data herein demonstrate thattcf8is induced by dihydrotestosterone (DHT) in the human PC-3/AR prostate cancer cell line and that this induction is mediated by two androgen response elements (AREs). These results demonstrate that ZEB1 is an intermediary in androgen signaling pathways.
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Dissertations / Theses on the topic "Zfhx1a"

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Ohayon, David-Robert. "Caractérisation d'une nouvelle fonction anti-apoptotique des facteurs de transcription Zfh1 dans le système nerveux périphérique par une approche Evo-Dévo." Montpellier 2, 2008. http://www.theses.fr/2008MON20204.

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Les membres de la famille des gènes zfh1 codent pour des régulateurs transcriptionnels atypiques, constitués de deux domaines à doigts-de-zinc et d'un homéodomaine. Une grande partie de mon travail de thèse a porté sur l'étude du rôle de la protéine zfh1 dans le système nerveux pe��riphérique de drosophile. Ceci a permis de révéler une nouvelle fonction anti-apoptotique pour ce facteur de transcription dans un type particulier de cellules gliales périphériques, au moins en partie grâce à sa capacité d'interférer avec un programme apoptotique dépendant de la voie de signalisation JNK. Une seconde partie de mon travail s'est porté sur l'étude d'une éventuelle conservation de cette fonction dans le système nerveux périphérique des Vertébrés chez lesquels on trouve 2 orthologues: Zfhx1a et Zfhx1b. Ceux-ci présentent des patrons d'expression qui se superposent largement dans le système nerveux en développement. Nous avons tiré profit de l'existence d'une forme dominante-négative -antagonisant la fonction des deux protéines- pour initier des analyses fonctionnelles aussi bien in vitro (par transfection de neurones sensoriels en culture) qu'in vivo (en générant un modèle transgénique où la forme dominante-négative s'exprime de manière conditionnelle). Les premiers résultats obtenus sur les neurones sensoriels du ganglion rachidien dorsal suggèrent que cette fonction anti-apoptotique a été conservée au cours de l'évolution
Zfh1 family members encode atypical transcriptional regulators containing two zinc-finger domains associated with a homeodomain-like motif. One part of my work has been focused on the role of zfh1 in the drosophila peripheral nervous system. This allowed us to reveal a new anti-apoptotic function for this transcription factor in a specific peripheral glial cell population, at least in part through its capacity to interfere with an apoptotic program involving the JNK signaling pathway. A second part of my work consisted in studying the putative conservation of this function in the peripheral nervous system in Vertebrates, where two orthologues have been described: Zfhx1a and Zfhx1b. The expression pattern of these two proteins largely overlaps during the development of the nervous system. We took advantage of the characterization of a dominant-negative form -antagonizing the two molecules- to initiate functional analysis both in vitro (by transfecting cultured sensory neurons) as well as in vivo (by generating an animal model in which the dominant-negative form is conditionally expressed). Our preliminary results on sensory neurons of the dorsal root ganglia suggest that this anti- apoptotic function has been conserved throughout evolution
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Vincent, Céline. "Syndrome de Mowat-Wilson : à propos d'un cas." Paris 13, 2004. http://www.theses.fr/2004PA130013.

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Miquelajáuregui, Graf Amaya [Verfasser], Victor [Akademischer Betreuer] Tarabykin, Walter [Akademischer Betreuer] Stühmer, Herbert [Akademischer Betreuer] Jäckle, and Nils [Akademischer Betreuer] Brose. "Role of Smad-interacting Protein 1 (Sip1/Zfhx1b) in the development of the cerebral cortex / Amaya Miquelajáuregui Graf. Gutachter: Walter Stühmer ; Herbert Jäckle ; Nils Brose. Betreuer: Victor Tarabykin." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2006. http://d-nb.info/1046135104/34.

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Puretskaia, Olga. "Signalling in the Somatic Stem Cell Niche of the Drosophila Testis." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-221172.

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Stem cell niches are specialized signalling microenvironments that allow maintenance of the stem cells. According to the traditional model of the stem cell niche, the niche signalling input is integrated by a cell towards a binary decision between stemness and differentiation. I have studied the regulation of somatic cyst stem cell (CyCS) proliferation in the testicular stem cell niche of Drosophila melanogaster by performing the DamID screen for targets of the transcriptional regulator Zfh1, a shared target of Jak/STAT and Hedgehog niche signalling. I have found that Zfh1 binds to the regulatory regions of kibra and salvador, tumour suppressors of the Hippo/Yorkie pathway, and downregulates them, restricting Yorkie activity to the Zfh1 positive CySCs. Clonal inactivation of the Hippo pathway is sufficient for CySC proliferation, but does not affect their differentiation ability. I therefore proposed a different stem cell niche model, whereby the niche signalling directly “micromanage” stem cell behavior, not involving the cell fate decision making.
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Edwards, Jessica K. "Investigating the roles of zinc finger homeobox 3 in circadian rhythms." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:1444375c-b7de-425a-a2ed-53b715833737.

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Dang, Thi Hoang Lan. "The Role of Zfhx1b in Mouse Neural Stem Cell Development." Thesis, 2012. http://hdl.handle.net/1807/32692.

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Construction of the vertebrate nervous system begins with the decision of a group of ectoderm cells to take on a neural fate. Studies using Xenopus ectodermal explants, or with mouse ectoderm cells or embryonic stem (ES) cells, demonstrated that this process of neural determination occurred by default – the ectoderm cells became neural after the removal of inhibitory signals. Whether ectoderm or ES cells directly differentiate into bona fide neural stem cells is not clear. One model suggests that there is an intermediate stage where “primitive” neural stem cells (pNSC) emerge harbouring properties of both ES cells and neural stem cells. The goal of my research was to address this question by evaluating the role of growth factor signaling pathways and their impact on the function of the zinc-finger homeobox transcription factor, Zfhx1b, during mouse neural stem cell development. I tested whether FGF and Wnt signaling pathways could regulate Zfhx1b expression to control early neural stem cell development. Inhibition of FGF signaling at a time when the ectoderm is acquiring a neural fate resulted in the accumulation of too many pNSCs, at the expense of the definitive neural stem cells. Interestingly, over-expression of Zfhx1b was sufficient to rescue the transition from a pNSC to definitive NSC. These data suggested that definitive NSC fate specification in the mouse ectoderm was facilitated by FGF activation of Zfhx1b, whereas canonical Wnt signaling repressed Zfhx1b expression. Next I sought to determine whether Zfhx1b was similarly required during neural lineage development in ES cells. FGF and Wnt signaling modulated expression of Zfhx1b in ES cell cultures in manner resembling my observations from similar experiments using mouse ectoderm. Knockdown of Zfhx1b in ES cells using siRNA did not affect the initial transition of ES cells to pNSC fate, but did limit the ability of these neural cells to further develop into definitive NSCs. Thus, my findings using ES cells were congruent with evidence from mouse embryos and supported a model whereby intercellular signaling induced Zfhx1b, required for the development of definitive NSCs, subsequent to an initial neural specification event that was independent of this pathway.
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Miquelajauregui, Amaya. "Role of Smad-interacting Protein 1 (Sip1/Zfhx1b) in the development of the cerebral cortex." Doctoral thesis, 2006. http://hdl.handle.net/11858/00-1735-0000-0006-B5EC-C.

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Tai-HongKuo and 郭泰宏. "Identify enhancers of the transcription factor Zfh1-downstream target genes." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/3gd2f6.

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Chia-WeiKao and 高嘉偉. "Identify downstream target genes of the transcription factor Zfh1 during Drosophila mesoderm development." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/cxgum2.

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Puretskaia, Olga. "Signalling in the Somatic Stem Cell Niche of the Drosophila Testis." Doctoral thesis, 2016. https://tud.qucosa.de/id/qucosa%3A30216.

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Stem cell niches are specialized signalling microenvironments that allow maintenance of the stem cells. According to the traditional model of the stem cell niche, the niche signalling input is integrated by a cell towards a binary decision between stemness and differentiation. I have studied the regulation of somatic cyst stem cell (CyCS) proliferation in the testicular stem cell niche of Drosophila melanogaster by performing the DamID screen for targets of the transcriptional regulator Zfh1, a shared target of Jak/STAT and Hedgehog niche signalling. I have found that Zfh1 binds to the regulatory regions of kibra and salvador, tumour suppressors of the Hippo/Yorkie pathway, and downregulates them, restricting Yorkie activity to the Zfh1 positive CySCs. Clonal inactivation of the Hippo pathway is sufficient for CySC proliferation, but does not affect their differentiation ability. I therefore proposed a different stem cell niche model, whereby the niche signalling directly “micromanage” stem cell behavior, not involving the cell fate decision making.
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Book chapters on the topic "Zfhx1a"

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"ZFHX1A." In Encyclopedia of Signaling Molecules, 6039. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_104202.

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"ZFHX1B Gene." In Encyclopedia of Metalloproteins, 2345. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_101341.

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"Danio rerio: Zeb2b, sip1b, zfhx1b." In Encyclopedia of Signaling Molecules, 1313. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_100953.

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"Mus musculus: Zeb2, Zfx1b, Zfhx1b." In Encyclopedia of Signaling Molecules, 3270. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_102437.

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"Homo sapiens: SIP1, SIP-1, SMADIP1, ZFHX1B." In Encyclopedia of Signaling Molecules, 2421. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_105205.

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Conference papers on the topic "Zfhx1a"

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Hanley, A., E. Ronzier, W. Hucker, H. Jameson, S. Clauss, M. Barraza, E. Abraham, L. Xiao, D. Milan, and P. Ellinor. "56 Role of ZFHX3 in atrial fibrillation." In Irish Cardiac Society Annual Scientific Meeting & AGM, Thursday October 4th – Saturday October 6th 2018, Galway Bay Hotel, Galway, Ireland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-ics.56.

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S., Akshayaa, Vidhya R., Hima Vyshnavi A.M., and Krishnan Namboori P.K. "Exploring Pain Insensitivity Inducing Gene ZFHX2 by using Deep Convolutional Neural Network." In 2019 3rd International Conference on Computing Methodologies and Communication (ICCMC). IEEE, 2019. http://dx.doi.org/10.1109/iccmc.2019.8819666.

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Casalino-Matsuda, M., F. Chen, F. Gonzalez, H. Matsuda, P. T. Ruhoff, G. J. Beitel, and P. H. S. Sporn. "Zfhx3 Mediates Hypercapnia-Induced Changes in Global Gene Transcription in Murine Alveolar Macrophages." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6500.

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Oyama, Y., S. Shigeta, K. Tsuji, H. Tokunaga, M. Shimada, and N. Yaegashi. "220 Functional analysis of ZFHX4 as a novel therapeutic target in ovarian cancer." In IGCS 2020 Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2020. http://dx.doi.org/10.1136/ijgc-2020-igcs.188.

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Oyama, Yoshiko, Shogo Shigeta, Keita Tsuji, Hideki Tokunaga, Muneaki Shimada, and Nobuo Yaegashi. "Abstract 1285: Functional analysis of ZFHX4 as a novel therapeutic target in ovarian cancer." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1285.

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Walker, Christopher J., Mario A. Miranda, Matthew O'Hern, Kevin Coombes, Ralf Bundschuh, David G. Mutch, and Paul J. Goodfellow. "Abstract 5300: Loss of function of two closely linked tumor suppressors contributes to biologic aggressiveness in endometrial cancers: Co-mutation of CTCF and ZFHX3." 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.am2015-5300.

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