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1

Justice, M. J. "Mouse ENU Mutagenesis." Human Molecular Genetics 8, no. 10 (1999): 1955–63. http://dx.doi.org/10.1093/hmg/8.10.1955.

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2

Gunn, Teresa M. "Functional annotation and ENU." BMC Research Notes 5, no. 1 (2012): 580. http://dx.doi.org/10.1186/1756-0500-5-580.

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3

Wagner, S., J. Calzada-Wack, M. Rosemann, et al. "Charakterisierung von ENU-Mausmutanten." Der Pathologe 31, S2 (2010): 147–52. http://dx.doi.org/10.1007/s00292-010-1347-5.

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4

Adams, Mark D. "ENU mutagenesis for pharma." Drug Discovery Today 8, no. 5 (2003): 199–200. http://dx.doi.org/10.1016/s1359-6446(03)02621-7.

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5

Watanabe, Takao, Yoko Kashida, Makoto Ueda, et al. "Inhibition by Ethinylestradiol of N-Ethyl-N-Nitrosourea-Initiated Uterine Carcinogenesis in Transgenic Mice Carrying a Human Prototype C-Ha-ras Gene (rasH2 Mice)." Toxicologic Pathology 31, no. 5 (2003): 496–505. http://dx.doi.org/10.1080/01926230390226014.

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In order to demonstrate the tumor promoting effect of ethinylestradiol (EE) in our uterine carcinogenesis model, rasH2 or ICR mice given an intraperitoneal injection of 120 mg/kg body weight of N-ethyl- N-nitrosourea (ENU) or an intra-uterine injection of 50 mg/kg body weight of ENU, respectively, followed by 2.5 or 0 ppm EE in the diet for 24 weeks in experiment 1 and 6 weeks in experiment 2. In experiment 1, in ICR mice, the incidences of adenocarcinomas in the ENU alone and the ENU+EE groups were 0% and 37.5%, respectively, the difference being statistically significant. The incidences of a
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6

Beier, David R., and Bruce J. Herron. "Genetic Mapping and ENU Mutagenesis." Genetica 122, no. 1 (2004): 65–69. http://dx.doi.org/10.1007/s10709-004-1437-5.

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7

Stottmann, Rolf, and David Beier. "ENU Mutagenesis in the Mouse." Current Protocols in Mouse Biology 4, no. 2 (2014): 25–35. http://dx.doi.org/10.1002/9780470942390.mo140029.

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8

Solnica-Krezel, L., A. F. Schier, and W. Driever. "Efficient recovery of ENU-induced mutations from the zebrafish germline." Genetics 136, no. 4 (1994): 1401–20. http://dx.doi.org/10.1093/genetics/136.4.1401.

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Abstract We studied the efficiency with which two chemical mutagens, ethyl methanesulfonate (EMS) and N-ethyl-N-nitrosourea (ENU) can induce mutations at different stages of spermatogenesis in zebrafish (Brachydanio rerio). Both EMS and ENU induced mutations at high rates in post-meiotic germ cells, as indicated by the incidence of F1 progeny mosaic for the albino mutation. For pre-meiotic germ cells, however, only ENU was found to be an effective mutagen, as indicated by the frequencies of non-mosaic mutant progeny at four different pigmentation loci. Several mutagenic regimens that varied in
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9

Beier, David R. "ENU mutagenesis: a work in progress." Physiological Genomics 11, no. 3 (2002): 111–13. http://dx.doi.org/10.1152/physiolgenomics.00140.2002.

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10

Mohr, Manuela, Martina Klempt, Birgit Rathkolb, Martin Hrabé de Angelis, Eckhard Wolf, and Bernhard Aigner. "Hypercholesterolemia in ENU-induced mouse mutants." Journal of Lipid Research 45, no. 11 (2004): 2132–37. http://dx.doi.org/10.1194/jlr.m400236-jlr200.

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11

Mitchison, N. Avrion, and Bryan Clarke. "From ENU mutagenesis to population genetics." Mammalian Genome 19, no. 4 (2008): 221–25. http://dx.doi.org/10.1007/s00335-008-9104-2.

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12

Yates, Laura, Fiona McMurray, Youming Zhang, et al. "ENU mutagenesis as a tool for understanding lung development and disease." Biochemical Society Transactions 37, no. 4 (2009): 838–42. http://dx.doi.org/10.1042/bst0370838.

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ENU (N-ethyl-N-nitrosourea) is a chemical mutagen that randomly induces point mutations in DNA. Since the 1990s ENU has been successfully used as a means to obtain mouse mutants using both gene-driven (reverse genetics) and phenotype-driven (forward genetics) approaches. A high-efficiency ENU approach results in approx. 25 functional mutations per genome; most of these will result in hypomorphic alleles. Our group has recently begun using ENU mutagenesis as a tool for understanding lung development and disease. In collaboration with other groups at MRC Harwell, we have undertaken a screen for
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13

De Stasio, Elizabeth, Catherine Lephoto, Lynn Azuma, Charles Holst, Dinesh Stanislaus, and Jai Uttam. "Characterization of Revertants of unc-93(e1500) in Caenorhabditis elegans Induced by N-ethyl-N-nitrosourea." Genetics 147, no. 2 (1997): 597–608. http://dx.doi.org/10.1093/genetics/147.2.597.

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Phenotypic reversion of the rubber-band, muscle-defective phenotype conferred by unc-93(e1500) was used to determine the utility of N-ethyl-N-nitrosourea (ENU) as a mutagen for genetic research in Caenorhabditis elegans. In this system, ENU produces revertants at a frequency of 3 × 10–4, equivalent to that of the commonly used mutagen, EMS. The gene identity of 154 ENU-induced revertants shows that the distribution of alleles between three possible suppressor genes differs from that induced by EMS. A higher percentage of revertants are alleles of unc-93 and many fewer are alleles of sup-9 and
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14

Soewarto, Dian, Matthias Klaften, and Isabel Rubio-Aliaga. "Features and Strategies of ENU Mouse Mutagenesis." Current Pharmaceutical Biotechnology 10, no. 2 (2009): 198–213. http://dx.doi.org/10.2174/138920109787315079.

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15

Yu, Q. "ENU induced mutations causing congenital cardiovascular anomalies." Development 131, no. 24 (2004): 6211–23. http://dx.doi.org/10.1242/dev.01543.

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16

De Stasio, Elizabeth A., and Sara Dorman. "Optimization of ENU mutagenesis of Caenorhabditis elegans." Mutation Research/Genetic Toxicology and Environmental Mutagenesis 495, no. 1-2 (2001): 81–88. http://dx.doi.org/10.1016/s1383-5718(01)00198-x.

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17

Balling, Rudi. "ENU MUTAGENESIS: Analyzing Gene Function in Mice." Annual Review of Genomics and Human Genetics 2, no. 1 (2001): 463–92. http://dx.doi.org/10.1146/annurev.genom.2.1.463.

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18

Justice, Monica J., Don A. Carpenter, Jack Favor, et al. "Effects of ENU dosage on mouse strains." Mammalian Genome 11, no. 7 (2000): 484–88. http://dx.doi.org/10.1007/s003350010094.

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19

Imai, Yoshiyuki, Benjamin Feldman, Alexander F. Schier, and William S. Talbot. "Analysis of Chromosomal Rearrangements Induced by Postmeiotic Mutagenesis With Ethylnitrosourea in Zebrafish." Genetics 155, no. 1 (2000): 261–72. http://dx.doi.org/10.1093/genetics/155.1.261.

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Abstract Mutations identified in zebrafish genetic screens allow the dissection of a wide array of problems in vertebrate biology. Most screens have examined mutations induced by treatment of spermatogonial (premeiotic) cells with the chemical mutagen N-ethyl-N-nitrosourea (ENU). Treatment of postmeiotic gametes with ENU induces specific-locus mutations at a higher rate than premeiotic regimens, suggesting that postmeiotic mutagenesis protocols could be useful in some screening strategies. Whereas there is extensive evidence that ENU induces point mutations in premeiotic cells, the range of mu
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20

Pachiyappan, Duraisamy, Yasmeen Ansari, Md Shabbir Alam, Prabha Thoudam, Kuppusamy Alagirisamy, and Palanisamy Manigandan. "Short and Long-Run Causal Effects of CO2 Emissions, Energy Use, GDP and Population Growth: Evidence from India Using the ARDL and VECM Approaches." Energies 14, no. 24 (2021): 8333. http://dx.doi.org/10.3390/en14248333.

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This paper investigates the nexus between CO2 emissions (CO2E), GDP, energy use (ENU), and population growth (PG) in India from 1980–2018 by comparing the “vector error correction” model (VECM) and “auto regressive distributed lag” (ARDL). We applied the unit root test, Johansen multi-variate cointegration, and performed a Variance decomposition analysis using the Cholesky approach. The VECM and ARDL-bound testing approaches to cointegration suggest a long-term equilibrium nexus between GDP, energy use, population growth and CO2E. The empirical outcomes show the existence of a long-term equili
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21

Aziza, Noor Laili, Noorkomala Sari, and Sofiya Irsalina. "Aktivitas Antagonistik Cendawan Endofit Asal Bunga Bawang Dayak (Eleutherine bulbosa (Mill.) Urb.) terhadap Fusarium sp. yang Menginfeksi Tanaman Cabai." Jurnal Fitopatologi Indonesia 17, no. 5 (2022): 210–15. http://dx.doi.org/10.14692/jfi.17.5.210-215.

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Penyakit layu yang disebabkan oleh Fusarium spp. merupakan penyakit penting dalam budi daya cabai. Salah satu cara potensial untuk mengendalikan penyakit tanaman ialah menggunakan agens hayati seperti cendawan endofit dari tanaman obat. Bawang dayak termasuk tanaman obat yang bersifat antibakteri, anticendawan, antiinflamasi, dan antioksidan. Penelitian bertujuan menentukan aktivitas antagonistik cendawan endofit yang berasal dari bunga bawang dayak terhadap cendawan patogen Fusarium spp. Sebanyak tujuh belas isolat cendawan endofit berhasil diperoleh dari bunga bawang dayak, yaitu isolat EnA,
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22

Nguyen, Nhung, Louise M. Judd, Anastasia Kalantzis, Belinda Whittle, Andrew S. Giraud, and Ian R. van Driel. "Random mutagenesis of the mouse genome: a strategy for discovering gene function and the molecular basis of disease." American Journal of Physiology-Gastrointestinal and Liver Physiology 300, no. 1 (2011): G1—G11. http://dx.doi.org/10.1152/ajpgi.00343.2010.

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Mutagenesis of mice with N-ethyl- N-nitrosourea (ENU) is a phenotype-driven approach to unravel gene function and discover new biological pathways. Phenotype-driven approaches have the advantage of making no assumptions about the function of genes and their products and have been successfully applied to the discovery of novel gene-phenotype relationships in many physiological systems. ENU mutagenesis of mice is used in many large-scale and more focused projects to generate and identify novel mouse models for the study of gene functions and human disease. This review examines the strategies and
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23

Lens, P. F., B. Altena, and R. Nusse. "Expression of c-sis and platelet-derived growth factor in in vitro-transformed glioma cells from rat brain tissue transplacentally treated with ethylnitrosourea." Molecular and Cellular Biology 6, no. 10 (1986): 3537–40. http://dx.doi.org/10.1128/mcb.6.10.3537-3540.1986.

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Long-term culturing of brain cells from neonatal BD-IX rats after transplacental treatment with N-ethyl-N-nitrosourea (ENU) results in malignantly transformed cells after a lag period of about 250 days. During culturing, the brain cells undergo a sequence of morphological changes. We examined oncogene expression in cultured cells from ENU-treated animals and found that transformed glioma cells differ from premalignant glial cells by containing high levels of c-sis transcripts. We also report that the transformed cells synthesize functional platelet-derived growth factor. Because glial cells ha
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24

Lens, P. F., B. Altena, and R. Nusse. "Expression of c-sis and platelet-derived growth factor in in vitro-transformed glioma cells from rat brain tissue transplacentally treated with ethylnitrosourea." Molecular and Cellular Biology 6, no. 10 (1986): 3537–40. http://dx.doi.org/10.1128/mcb.6.10.3537.

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Long-term culturing of brain cells from neonatal BD-IX rats after transplacental treatment with N-ethyl-N-nitrosourea (ENU) results in malignantly transformed cells after a lag period of about 250 days. During culturing, the brain cells undergo a sequence of morphological changes. We examined oncogene expression in cultured cells from ENU-treated animals and found that transformed glioma cells differ from premalignant glial cells by containing high levels of c-sis transcripts. We also report that the transformed cells synthesize functional platelet-derived growth factor. Because glial cells ha
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25

Hardisty, R. E., P. Mburu, and S. D. M. Brown. "Enu Mutagenesis and the Search for Deafness Genes." British Journal of Audiology 33, no. 5 (1999): 279–83. http://dx.doi.org/10.3109/03005369909090110.

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26

Oliver, P. L., and K. E. Davies. "New insights into behaviour using mouse ENU mutagenesis." Human Molecular Genetics 21, R1 (2012): R72—R81. http://dx.doi.org/10.1093/hmg/dds318.

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27

MEIDL, EVA. "BETWEEN LANGUAGES: JAKOV LIND’S NOVELTRAVELS TO THE ENU." Journal of the Australasian Universities Language and Literature Association 93, no. 1 (2000): 51–66. http://dx.doi.org/10.1179/aulla.2000.005.

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28

Alexa, Kristen, Seong-Kyu Choe, Nicolas Hirsch, et al. "ENU screen for mutations in zebrafish pancreas development." Developmental Biology 331, no. 2 (2009): 492. http://dx.doi.org/10.1016/j.ydbio.2009.05.397.

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29

Nelms, Keats A., and Christopher C. Goodnow. "Genome-Wide ENU Mutagenesis to Reveal Immune Regulators." Immunity 15, no. 3 (2001): 409–18. http://dx.doi.org/10.1016/s1074-7613(01)00199-6.

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30

Cook, Matthew C., Carola G. Vinuesa, and Christopher C. Goodnow. "ENU-mutagenesis: insight into immune function and pathology." Current Opinion in Immunology 18, no. 5 (2006): 627–33. http://dx.doi.org/10.1016/j.coi.2006.07.011.

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31

Sakuraba, Yoshiyuki, Hideki Sezutsu, K. Ryo Takahasi, et al. "Molecular characterization of ENU mouse mutagenesis and archives." Biochemical and Biophysical Research Communications 336, no. 2 (2005): 609–16. http://dx.doi.org/10.1016/j.bbrc.2005.08.134.

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32

Jang, Taichang, N. Scott Litofsky, Thomas W. Smith, Alonzo H. Ross, and Lawrence D. Recht. "Aberrant nestin expression during ethylnitrosourea-(ENU)-induced neurocarcinogenesis." Neurobiology of Disease 15, no. 3 (2004): 544–52. http://dx.doi.org/10.1016/j.nbd.2003.11.016.

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33

Brown, S. D. M., C. T. Esapa, I. Barbaric, et al. "Genetic models of bone disease using ENU mutagenesis." Bone 44 (May 2009): S19. http://dx.doi.org/10.1016/j.bone.2009.01.041.

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34

Achour, Bachir, and Mahmoud Debabeche. "Ressaut contrôléar seuil dans un canal profilé enU." Journal of Hydraulic Research 41, no. 1 (2003): 97–103. http://dx.doi.org/10.1080/00221680309499933.

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35

Salinger, A. P., and M. J. Justice. "Mouse Mutagenesis Using N-Ethyl-N-Nitrosourea (ENU)." Cold Spring Harbor Protocols 2008, no. 5 (2008): pdb.prot4985. http://dx.doi.org/10.1101/pdb.prot4985.

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36

Giordana, M. T., A. Migheli, F. Villare, and D. Schiffer. "RADIAL GLIA IN RATS TREATED TRANSPLACENTALLY BY ENU." Journal of Neuropathology and Experimental Neurology 49, no. 3 (1990): 273. http://dx.doi.org/10.1097/00005072-199005000-00043.

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37

Jackson, I., B. Starbuck, L. McKie, et al. "Eye diseases identified in the ENU-Ageing Screen." Acta Ophthalmologica 93 (September 23, 2015): n/a. http://dx.doi.org/10.1111/j.1755-3768.2015.0162.

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38

Crozat, Karine, Philippe Georgel, Sophie Rutschmann, et al. "Analysis of the MCMV resistome by ENU mutagenesis." Mammalian Genome 17, no. 5 (2006): 398–406. http://dx.doi.org/10.1007/s00335-005-0164-2.

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39

Cook, Melloni N., Jonathan P. Dunning, Ronald G. Wiley, et al. "Neurobehavioral mutants identified in an ENU-mutagenesis project." Mammalian Genome 18, no. 8 (2007): 559–72. http://dx.doi.org/10.1007/s00335-007-9035-3.

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40

Soewarto, Dian, Christiane Fella, Andreas Teubner, et al. "The large-scale Munich ENU-mouse-mutagenesis screen." Mammalian Genome 11, no. 7 (2000): 507–10. http://dx.doi.org/10.1007/s003350010097.

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41

Sotelo, Julio, Guadalupe Palencia, Norma Rosas, and Rodolfo Perez. "Effect of chronic stress on ENU-induced tumors." Biological Psychiatry 26, no. 7 (1989): 690–94. http://dx.doi.org/10.1016/0006-3223(89)90103-0.

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42

Hoyos-Manchado, Rafael, Sergio Villa-Consuegra, Modesto Berraquero, Juan Jiménez, and Víctor A. Tallada. "Mutational Analysis of N-Ethyl-N-Nitrosourea (ENU) in the Fission Yeast Schizosaccharomyces pombe." G3: Genes|Genomes|Genetics 10, no. 3 (2020): 917–23. http://dx.doi.org/10.1534/g3.119.400936.

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Forward genetics in model organisms has boosted our knowledge of the genetic bases of development, aging, and human diseases. In this experimental pipeline, it is crucial to start by inducing a large number of random mutations in the genome of the model organism to search for phenotypes of interest. Many chemical mutagens are used to this end because most of them display particular reactivity properties and act differently over DNA. Here we report the use of N-ethyl-N-nitrosourea (ENU) as a mutagen in the fission yeast Schizosaccharomyces pombe. As opposed to many other alkylating agents, ENU
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43

Pastink, A., C. Vreeken, M. J. Nivard, L. L. Searles, and E. W. Vogel. "Sequence analysis of N-ethyl-N-nitrosourea-induced vermilion mutations in Drosophila melanogaster." Genetics 123, no. 1 (1989): 123–29. http://dx.doi.org/10.1093/genetics/123.1.123.

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Abstract The mutational specificity of N-ethyl-N-nitrosourea (ENU) was determined in Drosophila melanogaster using the vermilion locus as a target gene. 25 mutants (16 F1 and 9 F2 mutants) were cloned and sequenced. Only base-pair changes were observed; three of the mutants represented double base substitutions. Transition mutations were the most prominent sequence change: 61% were GC----AT and 18% AT----GC substitutions. Both sequence changes can be explained by the miscoding properties of the modified guanine and thymine bases. A strong bias of neighboring bases on the occurrence of the GC--
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44

Funk, Ryan K., Taylor J. Maxwell, Masayo Izumi, et al. "Quantitative trait loci associated with susceptibility to therapy-related acute murine promyelocytic leukemia in hCG-PML/RARA transgenic mice." Blood 112, no. 4 (2008): 1434–42. http://dx.doi.org/10.1182/blood-2008-01-132084.

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Abstract Therapy-related acute myelogenous leukemia (t-AML) is an important late adverse effect of alkylator chemotherapy. Susceptibility to t-AML has a genetic component, yet specific genetic variants that influence susceptibility are poorly understood. We analyzed an F2 intercross (n = 282 mice) between mouse strains resistant or susceptible to t-AML induced by the alkylator ethyl-N-nitrosourea (ENU) to identify genes that regulate t-AML susceptibility. Each mouse carried the hCG-PML/RARA transgene, a well-characterized initiator of myeloid leukemia. In the absence of ENU treatment, transgen
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45

Imgruet, Molly K., Ningfei An, Saira Khan, et al. "Deficiency of CUX1, Encoded on 7q, Blocks the Normal HSC DNA Damage Response and Drives Highly Penetrant Therapy-Related Myeloid Neoplasms in Mice." Blood 134, Supplement_1 (2019): 641. http://dx.doi.org/10.1182/blood-2019-130717.

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An unintended late-effect of the use of chemotherapy and/or irradiation in cancer treatment is the development of therapy-related myeloid neoplasms (t-MN). T-MN are associated with high-risk cytogenetic abnormalities and a poor prognosis of less than one year survival. The most common cytogenetic change in t-MN is the loss of chromosome 7 (-7) or the long arm, del(7q), occurring in almost half of patients and associated with alkylating agent exposure. Del(7q), or inactivating mutations of the CUX1 transcription factor encoded on 7q, have been reported to exist prior to exposure to genotoxic th
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46

Alfonso Pierola, Ana, Matteo Marchesini, Koichi Takahashi, et al. "The Role of Chip-Related DNA Damage Response Dysfunction in Therapy-Related Myeloid Neoplasms." Blood 128, no. 22 (2016): 958. http://dx.doi.org/10.1182/blood.v128.22.958.958.

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Abstract Although clonal hematopoiesis of indeterminate potential (CHIP) has been identified as a risk factor for the development of therapy-related myeloid neoplasms (t-MNs), the cellular and molecular mechanisms underlying the adverse effects of chemotherapy on the hematopoietic stem cell (HSC) compartment in patients with CHIP are currently unknown. Understanding these processes is a critical step to clarifying the interaction between CHIP, chemotherapy, and t-MN pathogenesis and identifying earlier therapeutic intervention opportunities in patients who are at high risk of developing these
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47

Crozat, Karine, and Philippe Georgel. "Identification of Mouse Cytomegalovirus Resistance Loci by ENU Mutagenesis." Viruses 1, no. 3 (2009): 460–83. http://dx.doi.org/10.3390/v1030460.

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48

Arnold, Carrie N., Michael J. Barnes, Michael Berger, et al. "ENU-induced phenovariance in mice: inferences from 587 mutations." BMC Research Notes 5, no. 1 (2012): 577. http://dx.doi.org/10.1186/1756-0500-5-577.

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49

Takeshima, Fuminao, Keisuke Iwasaki, Isao Shimokawa, Takayoshi Ikeda, and Takeshi Matsuo. "Immunohistochemical Localization of Gangliosides in ENU-induced Rat Glioma." Pathology International 42, no. 8 (2008): 558–65. http://dx.doi.org/10.1111/j.1440-1827.1992.tb03105.x.

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50

Shoji, Hirotaka, Keiko Toyama, Yoshihiro Takamiya, Shigeharu Wakana, Yoichi Gondo, and Tsuyoshi Miyakawa. "Comprehensive behavioral analysis of ENU-induced Disc1 mutant mice." Neuroscience Research 71 (September 2011): e299-e300. http://dx.doi.org/10.1016/j.neures.2011.07.1306.

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