{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T16:04:46Z","timestamp":1789142686261,"version":"build-2803163510"},"reference-count":40,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2013,11,13]],"date-time":"2013-11-13T00:00:00Z","timestamp":1384300800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European J of Haematology"],"published-print":{"date-parts":[[2014,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Chronic myeloid leukemia (<jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content>) is one of the most frequent hematological neoplasia worldwide. The abnormal accumulation of reactive oxygen species may be an important factor in <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> development. The transcription factor <jats:styled-content style=\"fixed-case\">NRF<\/jats:styled-content>2 can regulate the transcription of a battery of antioxidant and detoxificant genes after heterodimerizing with small\u2010<jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>af proteins. Although the participation of <jats:styled-content style=\"fixed-case\">NRF<\/jats:styled-content>2 in the development of chronic degenerative diseases has been thoroughly studied, the role of small\u2010<jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>af genes has not been documented. We have identified polymorphisms in the three <jats:italic><jats:styled-content style=\"fixed-case\">MAF<\/jats:styled-content><\/jats:italic> genes (<jats:italic><jats:styled-content style=\"fixed-case\">F<\/jats:styled-content><\/jats:italic>,<jats:italic> <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content><\/jats:italic> and <jats:italic><jats:styled-content style=\"fixed-case\">K<\/jats:styled-content><\/jats:italic>) and assessed their association with <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content>. Over 266 subjects with <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> and 399 unrelated healthy donors have been studied. After sequencing each <jats:italic><jats:styled-content style=\"fixed-case\">MAF<\/jats:styled-content><\/jats:italic> gene by Sanger technology, we found 17 variants in <jats:italic><jats:styled-content style=\"fixed-case\">MAFF<\/jats:styled-content><\/jats:italic> gene, eight in <jats:italic><jats:styled-content style=\"fixed-case\">MAFG<\/jats:styled-content><\/jats:italic> and seven in <jats:italic><jats:styled-content style=\"fixed-case\">MAFK<\/jats:styled-content><\/jats:italic>. In the case\u2010control study, the homozygote genotype <jats:styled-content style=\"fixed-case\">CC<\/jats:styled-content> for the rs9610915 <jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content> of <jats:italic><jats:styled-content style=\"fixed-case\">MAFF<\/jats:styled-content><\/jats:italic> was significantly associated with <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content>. The frequency of the <jats:styled-content style=\"fixed-case\">ACC<\/jats:styled-content> haplotype from <jats:italic><jats:styled-content style=\"fixed-case\">MAFK<\/jats:styled-content><\/jats:italic> was significantly lower than controls. After stratification by gender, the <jats:styled-content style=\"fixed-case\">ACC<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">GTG<\/jats:styled-content> haplotypes were associated only with males with <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content>. These novel data suggest an association between <jats:italic><jats:styled-content style=\"fixed-case\">MAFF<\/jats:styled-content><\/jats:italic> and <jats:italic><jats:styled-content style=\"fixed-case\">MAFG<\/jats:styled-content><\/jats:italic> and the development of <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/ejh.12211","type":"journal-article","created":{"date-parts":[[2013,10,14]],"date-time":"2013-10-14T05:06:40Z","timestamp":1381727200000},"page":"35-41","source":"Crossref","is-referenced-by-count":12,"title":["<i>Small <scp>MAF<\/scp><\/i> genes variants and chronic myeloid leukemia"],"prefix":"10.1111","volume":"92","author":[{"given":"Angelica","family":"Mart\u00ednez\u2010Hern\u00e1ndez","sequence":"first","affiliation":[{"name":"Immunogenomics and Metabolic Diseases Laboratory Instituto Nacional de Medicina Gen\u00f3mica, SS M\u00e9xico City M\u00e9xico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Humberto","family":"Gutierrez\u2010Malacatt","sequence":"additional","affiliation":[{"name":"Biological Science Program Universidad Nacional Aut\u00f3noma de M\u00e9xico M\u00e9xico City M\u00e9xico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karol","family":"Carrillo\u2010S\u00e1nchez","sequence":"additional","affiliation":[{"name":"Sequencing Unit Instituto Nacional de Medicina Gen\u00f3mica, SS M\u00e9xico City M\u00e9xico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yolanda","family":"Salda\u00f1a\u2010Alvarez","sequence":"additional","affiliation":[{"name":"Immunogenomics and Metabolic Diseases Laboratory Instituto Nacional de Medicina Gen\u00f3mica, SS M\u00e9xico City M\u00e9xico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alberto","family":"Rojas\u2010Ochoa","sequence":"additional","affiliation":[{"name":"Neurochemical Laboratory Instituto 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