<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE root>
<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="other" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Oncohematology</journal-id><journal-title-group><journal-title xml:lang="en">Oncohematology</journal-title><trans-title-group xml:lang="ru"><trans-title>Онкогематология</trans-title></trans-title-group></journal-title-group><issn publication-format="print">1818-8346</issn><issn publication-format="electronic">2413-4023</issn><publisher><publisher-name xml:lang="en">Publishing House ABV Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">1033</article-id><article-id pub-id-type="doi">10.17650/1818-8346-2025-20-2-87-103</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>BASIC RESEARCH</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>ФУНДАМЕНТАЛЬНЫЕ ИССЛЕДОВАНИЯ В ПРАКТИЧЕСКОЙ МЕДИЦИНЕ НА СОВРЕМЕННОМ ЭТАПЕ</subject></subj-group><subj-group subj-group-type="article-type"><subject></subject></subj-group></article-categories><title-group><article-title xml:lang="en">The significance of miR-142 in tumor progression of diffuse large B-cell lymphoma</article-title><trans-title-group xml:lang="ru"><trans-title>Значение miR-142 в опухолевой прогрессии диффузной В-клеточной крупноклеточной лимфомы</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-7542-7285</contrib-id><name-alternatives><name xml:lang="en"><surname>Voropaeva</surname><given-names>E. N.</given-names></name><name xml:lang="ru"><surname>Воропаева</surname><given-names>Е. Н.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>52 Krasny Prospekt, Novosibirsk 630091 </p><p>175/1 B. Bogatkova St., Novosibirsk 630089 </p></bio><bio xml:lang="ru"><p>Елена Николаевна Воропаева</p><p>630091 Новосибирск, Красный пр-кт, 52</p><p>630089 Новосибирск, ул. Б. Богаткова, 175/1 </p></bio><email>vena.81@mail.ru</email><xref ref-type="aff" rid="aff1"/><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-6110-4351</contrib-id><name-alternatives><name xml:lang="en"><surname>Seregina</surname><given-names>O. B.</given-names></name><name xml:lang="ru"><surname>Серегина</surname><given-names>О. Б.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>2 Krasny Prospekt, Novosibirsk 630091</p></bio><bio xml:lang="ru"><p>630091 Новосибирск, Красный пр-кт, 52</p></bio><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-5429-4011</contrib-id><name-alternatives><name xml:lang="en"><surname>Voytko</surname><given-names>M. S.</given-names></name><name xml:lang="ru"><surname>Войтко</surname><given-names>М. С.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>2 Krasny Prospekt, Novosibirsk 630091</p></bio><bio xml:lang="ru"><p>630091 Новосибирск, Красный пр-кт, 52</p></bio><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-2708-1133</contrib-id><name-alternatives><name xml:lang="en"><surname>Babaeva</surname><given-names>T. N.</given-names></name><name xml:lang="ru"><surname>Бабаева</surname><given-names>Т. Н.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>2 Krasny Prospekt, Novosibirsk 630091</p></bio><bio xml:lang="ru"><p>630091 Новосибирск, Красный пр-кт, 52</p></bio><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-6938-3802</contrib-id><name-alternatives><name xml:lang="en"><surname>Skvortsova</surname><given-names>N. V.</given-names></name><name xml:lang="ru"><surname>Скворцова</surname><given-names>Н. В.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>2 Krasny Prospekt, Novosibirsk 630091</p></bio><bio xml:lang="ru"><p>630091 Новосибирск, Красный пр-кт, 52</p></bio><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-7165-4496</contrib-id><name-alternatives><name xml:lang="en"><surname>Maksimov</surname><given-names>V. N.</given-names></name><name xml:lang="ru"><surname>Максимов</surname><given-names>В. Н.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>2 Krasny Prospekt, Novosibirsk 630091</p><p>175/1 B. Bogatkova St., Novosibirsk 630089 </p></bio><bio xml:lang="ru"><p>630091 Новосибирск, Красный пр-кт, 52</p><p>630089 Новосибирск, ул. Б. Богаткова, 175/1 </p></bio><xref ref-type="aff" rid="aff1"/><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-1261-5470</contrib-id><name-alternatives><name xml:lang="en"><surname>Pospelova</surname><given-names>T. I.</given-names></name><name xml:lang="ru"><surname>Поспелова</surname><given-names>Т. И.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>52 Krasny Prospekt, Novosibirsk 630091</p></bio><bio xml:lang="ru"><p>630091 Новосибирск, Красный пр-кт, 52</p></bio><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Novosibirsk State Medical University</institution></aff><aff><institution xml:lang="ru">ФГБОУ ВО «Новосибирский государственный медицинский университет» Минздрава России</institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en">The Institute of Internal and Preventive Medicine – branch of the Federal Research Center, Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences</institution></aff><aff><institution xml:lang="ru">НИИ терапии и профилактической медицины – филиал ФГБНУ «Федеральный исследовательский центр Институт цитологии и генетики СО РАН»</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2025-05-22" publication-format="electronic"><day>22</day><month>05</month><year>2025</year></pub-date><volume>20</volume><issue>2</issue><issue-title xml:lang="en"/><issue-title xml:lang="ru"/><fpage>87</fpage><lpage>103</lpage><history><date date-type="received" iso-8601-date="2025-05-20"><day>20</day><month>05</month><year>2025</year></date><date date-type="accepted" iso-8601-date="2025-05-20"><day>20</day><month>05</month><year>2025</year></date></history><permissions><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/></permissions><self-uri xlink:href="https://oncohematology.abvpress.ru/ongm/article/view/1033">https://oncohematology.abvpress.ru/ongm/article/view/1033</self-uri><abstract xml:lang="en"><p>In recent years, microRNAs have attracted the attention of researchers as potential markers for diagnosis, classification, prognosis of tumor progression and sensitivity to treatment, as well as their use as targets for therapy. The purpose of the review is to summarize data on the miR-142 role in the tumor progression of one of the most common lymphoproliferative diseases – diffuse large B-cell lymphoma.MicroRNA miR-142 has a broad spectrum of tumor-suppressor functions by targeting a number of important protooncogenes, the loss of control over which contributes to enhanced proliferation, blocking apoptosis, activating B-lymphocyte survival signaling pathways, metabolic reprogramming, creating an immunosuppressive microenvironment and tumor evasion of immune surveillance, as well as dissemination of malignant cells.Information on the nomenclature and mechanisms of miR-142 formation, the participation of miR-142 in hematopoiesis are provided, the pathogenetic role and relationship between the miR-142 expression profile and diffuse large B-cell lymphoma are analyzed, and miR-142 molecular genetic abnormalities in this disease are discussed.</p></abstract><trans-abstract xml:lang="ru"><p>В последние годы микроРНК привлекли внимание исследователей в области онкогематологии как потенциальные маркеры для диагностики, классификации, прогнозирования особенностей течения и чувствительности к лечению опухолей, а также их использования в качестве мишеней для таргетной терапии.Цель обзора – обобщение данных о роли miR-142 в опухолевой прогрессии одного из самых частых лимфопролиферативных заболеваний – диффузной В-клеточной крупноклеточной лимфомы.МикроРНК miR-142 обладает широким спектром опухоль-супрессорных функций за счет нацеливания на ряд важнейших протоонкогенов, утрата контроля над которыми способствует усилению пролиферации, блоку апоптоза, активации сигнальных путей выживания В-лимфоцитов, метаболическому перепрограммированию, созданию иммуносупрессивной микросреды и избеганию опухолью иммунного надзора, а также диссеминации злокачественных клеток.Приведена информация о номенклатуре и механизмах образования miR-142, участии miR-142 в гемопоэзе, проанализированы патогенетическая роль miR-142 и взаимосвязь между профилем экспрессии miR-142 и диффузной В-клеточной крупноклеточной лимфомой, а также обсуждаются молекулярно-генетические нарушения miR-142 при данном заболевании.</p></trans-abstract><kwd-group xml:lang="en"><kwd>diffuse large B-cell lymphoma</kwd><kwd>microRNA regulation</kwd><kwd>gene expression</kwd><kwd>microRNA-based cancer therapy</kwd><kwd>miR-142</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>диффузная В-клеточная крупноклеточная лимфома</kwd><kwd>регуляция микроРНК</kwd><kwd>экспрессия генов</kwd><kwd>терапия рака на основе микроРНК</kwd><kwd>miR-142</kwd></kwd-group><funding-group><funding-statement xml:lang="en">The work was performed at the expense of the Russian Science Foundation grant No. 25-25-00068.</funding-statement><funding-statement xml:lang="ru">Работа выполнена за счет средств гранта Российского научного фонда № 25-25-00068.</funding-statement></funding-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Cheng M., Zhu Y., Yu H. et al. Non-coding RNA notations, regulations and interactive resources. Funct Integr Genomics 2024;24(6):217. DOI: 10.1007/s10142-024-01494-w</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Di Bella S., La Ferlita A., Carapezza G. et al. A benchmarking of pipelines for detecting ncRNAs from RNA-Seq data. Brief Bioinform 2020;21(6):1987–98. DOI: 10.1093/bib/bbz110</mixed-citation></ref><ref id="B3"><label>3.</label><mixed-citation>Marguerat S., Bähler J. RNA-seq: from technology to biology. Cell Mol Life Sci 2010;67(4):569–79. DOI: 10.1007/s00018-009-0180-6</mixed-citation></ref><ref id="B4"><label>4.</label><mixed-citation>Saliminejad K., Khorram Khorshid H.R., Soleymani Fard S., Ghaffari S.H. An overview of microRNAs: biology, functions, therapeutics, and analysis methods. J Cell Physiol 2019;234(5):5451–65. DOI: 10.1002/jcp.27486</mixed-citation></ref><ref id="B5"><label>5.</label><mixed-citation>Acunzo M., Romano G., Wernicke D., Croce C.M. MicroRNA and cancer – a brief overview [published correction appears in Adv Biol Regul 2015;58:53]. Adv Biol Regul 2015;57:1–9. DOI: 10.1016/j.jbior.2014.09.013</mixed-citation></ref><ref id="B6"><label>6.</label><mixed-citation>Menegatti J., Nakel J., Stepanov Y.K. et al. Changes of protein expression after CRISPR/Cas9 knockout of miRNA-142 in cell lines derived from diffuse large B-cell lymphoma. Cancers (Basel) 2022;14(20):5031. DOI: 10.3390/cancers14205031</mixed-citation></ref><ref id="B7"><label>7.</label><mixed-citation>Anastasiadou E., Jacob L.S., Slack F.J. Non-coding RNA networks in cancer. Nat Rev Cancer 2018;18(1):5–18. DOI: 10.1038/nrc.2017.99</mixed-citation></ref><ref id="B8"><label>8.</label><mixed-citation>Tan Y.F., Chen Z.Y., Wang L. et al. MiR-142-3p functions as an oncogene in prostate cancer by targeting FOXO1. J Cancer 2020;11(6):1614–24. DOI: 10.7150/jca.41888</mixed-citation></ref><ref id="B9"><label>9.</label><mixed-citation>Yang L., Wang Z.F., Wu H., Wang W. miR-142-5p improves neural differentiation and proliferation of adipose-derived stem cells. Cell Physiol Biochem 2018;50(6):2097–107. DOI: 10.1159/000495054</mixed-citation></ref><ref id="B10"><label>10.</label><mixed-citation>Bandrés E., Cubedo E., Agirre X. et al. Identification by real-time PCR of 13 mature microRNAs differentially expressed in colorectal cancer and non-tumoral tissues. Mol Cancer 2006;5:29. DOI: 10.1186/1476-4598-5-29</mixed-citation></ref><ref id="B11"><label>11.</label><mixed-citation>Fu Y., Sun L.Q., Huang Y. et al. miR-142-3p inhibits the metastasis of hepatocellular carcinoma cells by regulating HMGB1 gene expression. Curr Mol Med 2018;18(3):135–41. DOI: 10.2174/1566524018666180907161124</mixed-citation></ref><ref id="B12"><label>12.</label><mixed-citation>Mansoori B., Mohammadi A., Ghasabi M. et al. miR-142-3p as tumor suppressor miRNA in the regulation of tumorigenicity, invasion and migration of human breast cancer by targeting Bach-1 expression. J Cell Physiol 2019;234(6):9816–25. DOI: 10.1002/jcp.27670</mixed-citation></ref><ref id="B13"><label>13.</label><mixed-citation>Wang Z., Liu Z., Fang X., Yang H. MiR-142-5p suppresses tumorigenesis by targeting PIK3CA in non-small cell lung cancer. Cell Physiol Biochem 2017;43(6):2505–15. DOI: 10.1159/000484459</mixed-citation></ref><ref id="B14"><label>14.</label><mixed-citation>Zhang X., Yan Z., Zhang J. et al. Combination of hsa-miR-375 and hsa-miR-142-5p as a predictor for recurrence risk in gastric cancer patients following surgical resection. Ann Oncol 2011;22(10):2257–66. DOI: 10.1093/annonc/mdq758</mixed-citation></ref><ref id="B15"><label>15.</label><mixed-citation>Kawano S., Araki K., Bai J. et al. A gain-of-function mutation in microRNA 142 is sufficient to cause the development of T-cell leukemia in mice. Cancer Sci 2023;114(7):2821–34. DOI: 10.1111/cas.15794</mixed-citation></ref><ref id="B16"><label>16.</label><mixed-citation>Mildner A., Chapnik E., Varol D. et al. MicroRNA-142 controls thymocyte proliferation. Eur J Immunol 2017;47(7):1142–52. DOI: 10.1002/eji.201746987</mixed-citation></ref><ref id="B17"><label>17.</label><mixed-citation>Hezaveh K., Kloetgen A., Bernhart S.H. et al. Alterations of microRNA and microRNA-regulated messenger RNA expression in germinal center B-cell lymphomas determined by integrative sequencing analysis. Haematologica 2016;101(11):1380–9. DOI: 10.3324/haematol.2016.143891</mixed-citation></ref><ref id="B18"><label>18.</label><mixed-citation>Morin R.D., Assouline S., Alcaide M. et al. Genetic landscapes of relapsed and refractory diffuse large B-cell lymphomas. Clin Cancer Res 2016;22(9):2290–300. DOI: 10.1158/1078-0432.CCR-15-2123</mixed-citation></ref><ref id="B19"><label>19.</label><mixed-citation>Soltani S., Zakeri A., Tabibzadeh A. et al. A review on EBV encoded and EBV-induced host microRNAs expression profile in different lymphoma types. Mol Biol Rep 2021;48(2):1801–17. DOI: 10.1007/s11033-021-06152-z</mixed-citation></ref><ref id="B20"><label>20.</label><mixed-citation>PLOS ONE editors. Expression of concern: overexpression of miR-142-5p and miR-155 in gastric mucosa-associated lymphoid tissue (MALT) lymphoma resistant to Helicobacter pylori eradication. PLoS One 2023;18(1):e0278797. DOI: 10.1371/journal.pone.0278797</mixed-citation></ref><ref id="B21"><label>21.</label><mixed-citation>Dahlhaus M., Roolf C., Ruck S. et al. Expression and prognostic significance of hsa-miR-142-3p in acute leukemias. Neoplasma 2013;60(4):432–8. DOI: 10.4149/neo_2013_056</mixed-citation></ref><ref id="B22"><label>22.</label><mixed-citation>Bellon M., Lepelletier Y., Hermine O., Nicot C. Deregulation of microRNA involved in hematopoiesis and the immune response in HTLV-I adult T-cell leukemia. Blood 2009;113(20):4914–7. DOI: 10.1182/blood-2008-11-189845</mixed-citation></ref><ref id="B23"><label>23.</label><mixed-citation>Lv M., Zhang X., Jia H. et al. An oncogenic role of miR-142-3p in human T-cell acute lymphoblastic leukemia (T-ALL) by targeting glucocorticoid receptor-α and cAMP/PKA pathways. Leukemia 2012;26(4):769–77. DOI: 10.1038/leu.2011.273</mixed-citation></ref><ref id="B24"><label>24.</label><mixed-citation>Huang W., Paul D., Calin G.A., Bayraktar R. miR-142: a master regulator in hematological malignancies and therapeutic opportunities. Cells 2023;13(1):84. DOI: 10.3390/cells13010084</mixed-citation></ref><ref id="B25"><label>25.</label><mixed-citation>Pahlavan Y., Mohammadi Nasr M., Dalir Abdolahinia E. et al. Prominent roles of microRNA-142 in cancer. Pathol Res Pract 2020;216(11):153220. DOI: 10.1016/j.prp.2020.153220</mixed-citation></ref><ref id="B26"><label>26.</label><mixed-citation>Schwarzenbach H., Nishida N., Calin G.A., Pantel K. Clinical relevance of circulating cell-free microRNAs in cancer. Nat Rev Clin Oncol 2014;11(3):145–56. DOI: 10.1038/nrclinonc.2014.5</mixed-citation></ref><ref id="B27"><label>27.</label><mixed-citation>Anandagoda N., Willis J.C., Hertweck A. et al. microRNA-142- mediated repression of phosphodiesterase 3B critically regulates peripheral immune tolerance. J Clin Invest 2019;129(3):1257–71. DOI: 10.1172/JCI124725</mixed-citation></ref><ref id="B28"><label>28.</label><mixed-citation>Shrestha A., Mukhametshina R.T., Taghizadeh S. et al. MicroRNA-142 is a multifaceted regulator in organogenesis, homeostasis, and disease. Dev Dyn 2017;246(4):285–90. DOI: 10.1002/dvdy.24477</mixed-citation></ref><ref id="B29"><label>29.</label><mixed-citation>Nimmo R., Ciau-Uitz A., Ruiz-Herguido C. et al. MiR-142-3p controls the specification of definitive hemangioblasts during ontogeny. Dev Cell 2013;26(3):237–49. DOI: 10.1016/j.devcel.2013.06.023</mixed-citation></ref><ref id="B30"><label>30.</label><mixed-citation>GeneCaRNA. The human ncRNA GENE DATABASE. Available at: https://www.genecards.org/cgi-bin/carddisp.pl?gene=MIR142&amp;keywords=mir-142</mixed-citation></ref><ref id="B31"><label>31.</label><mixed-citation>Landgraf P., Rusu M., Sheridan R. et al. A mammalian microRNA expression atlas based on small RNA library sequencing. Cell 2007;129(7):1401–14. DOI: 10.1016/j.cell.2007.04.040</mixed-citation></ref><ref id="B32"><label>32.</label><mixed-citation>Liu R., Zheng S., Yu K. et al. Prognostic value of miR-142 in solid tumors: a meta-analysis. Biosci Rep 2021;41(2):BSR20204043. DOI: 10.1042/BSR20204043</mixed-citation></ref><ref id="B33"><label>33.</label><mixed-citation>Rivkin N., Chapnik E., Mildner A. et al. Erythrocyte survival is controlled by microRNA-142. Haematologica 2017;102(4):676–85. DOI: 10.3324/haematol.2016.156109</mixed-citation></ref><ref id="B34"><label>34.</label><mixed-citation>Ding S., Liang Y., Zhao M. et al. Decreased microRNA-142-3p/5p expression causes CD4+ T cell activation and B cell hyperstimulation in systemic lupus erythematosus. Arthritis Rheum 2012;64(9):2953–63. DOI: 10.1002/art.34505</mixed-citation></ref><ref id="B35"><label>35.</label><mixed-citation>Talebi F., Ghorbani S., Chan W.F. et al. MicroRNA-142 regulates inflammation and T cell differentiation in an animal model of multiple sclerosis. J Neuroinflammation 2017;14(1):55. DOI: 10.1186/s12974-017-0832-7</mixed-citation></ref><ref id="B36"><label>36.</label><mixed-citation>Kramer N.J., Wang W.L., Reyes E.Y. et al. Altered lymphopoiesis and immunodeficiency in miR-142 null mice. Blood 2015;125(24):3720–30. DOI: 10.1182/blood-2014-10-603951</mixed-citation></ref><ref id="B37"><label>37.</label><mixed-citation>Xu S., Guo K., Zeng Q. et al. The RNase III enzyme dicer is essential for germinal center B-cell formation. Blood 2012;119(3):767–76. DOI: 10.1182/blood-2011-05-355412</mixed-citation></ref><ref id="B38"><label>38.</label><mixed-citation>Skoufos G., Kakoulidis P., Tastsoglou S. et al. TarBase-v9.0 extends experimentally supported miRNA-gene interactions to cell-types and virally encoded miRNAs. Nucleic Acids Res 2024;52(D1):D304–10. DOI: 10.1093/nar/gkad1071</mixed-citation></ref><ref id="B39"><label>39.</label><mixed-citation>Klümper T., Bruckmueller H., Diewock T. et al. Expression differences of miR-142-5p between treatment-naïve chronic myeloid leukemia patients responding and non-responding to imatinib therapy suggest a link to oncogenic ABL2, SRI, cKIT and MCL1 signaling pathways critical for development of therapy resistance. Exp Hematol Oncol 2020;9:26. DOI: 10.1186/s40164-020-00183-1</mixed-citation></ref><ref id="B40"><label>40.</label><mixed-citation>Zareifar P., Ahmed H.M., Ghaderi P. et al. miR-142-3p/5p role in cancer: from epigenetic regulation to immunomodulation. Cell Biochem Funct 2024;42(2):e3931. DOI: 10.1002/cbf.3931</mixed-citation></ref><ref id="B41"><label>41.</label><mixed-citation>Hashmi A.A., Iftikhar S.N., Nargus G. et al. Double-expressor phenotype (BCL-2/c-MYC co-expression) of diffuse large B-cell lymphoma and its clinicopathological correlation. Cureus 2021;13(2):e13155. DOI: 10.7759/cureus.13155</mixed-citation></ref><ref id="B42"><label>42.</label><citation-alternatives><mixed-citation xml:lang="en">Babicheva L.G., Poddubnaya I.V. Heterogeneous diffuse large B-cell lymphoma: accurate diagnosis as a key to successful therapy. A review. Sovremennaya onkologiya = Journal of Modern Oncology 2023;25(2):168–77. (In Russ.). DOI: 10.26442/18151434.2023.2.202237</mixed-citation><mixed-citation xml:lang="ru">Бабичева Л.Г., Поддубная И.В. Гетерогенная диффузная В-клеточная крупноклеточная лимфома: правильный диагноз как залог успешной терапии. Современная онкология 2023;25(2):168–77. DOI: 10.26442/18151434.2023.2.202237</mixed-citation></citation-alternatives></ref><ref id="B43"><label>43.</label><mixed-citation>Bisso A., Sabò A., Amati B. MYC in germinal center-derived lymphomas: mechanisms and therapeutic opportunities. Immunol Rev 2019;288(1):178–97. DOI: 10.1111/imr.12734</mixed-citation></ref><ref id="B44"><label>44.</label><mixed-citation>Shen R., Fu D., Dong L. et al. Simplified algorithm for genetic subtyping in diffuse large B-cell lymphoma. Signal Transduct Target Ther 2023;8(1):145. DOI: 10.1038/s41392-023-01358-y</mixed-citation></ref><ref id="B45"><label>45.</label><mixed-citation>Wenzel S.S., Grau M., Mavis C. et al. MCL1 is deregulated in subgroups of diffuse large B-cell lymphoma. Leukemia 2013;27(6):1381–90. DOI: 10.1038/leu.2012.367</mixed-citation></ref><ref id="B46"><label>46.</label><mixed-citation>Uddin S., Hussain A.R., Siraj A.K. et al. Role of phosphatidylinositol 3’-kinase/AKT pathway in diffuse large B-cell lymphoma survival. Blood 2006;108(13):4178–86. DOI: 10.1182/blood-2006-04-016907</mixed-citation></ref><ref id="B47"><label>47.</label><mixed-citation>Wang L., Qin W., Huo Y.J. et al. Advances in targeted therapy for malignant lymphoma. Sig Transduct Target Ther 2020;5(1):15. DOI: 10.1038/s41392-020-0113-2</mixed-citation></ref><ref id="B48"><label>48.</label><mixed-citation>Batlevi C.L., Morschhauser F. Novel targeted agents for follicular lymphoma. Ann Lymphoma 2021;5:3. DOI: 10.21037/aol-20-45</mixed-citation></ref><ref id="B49"><label>49.</label><mixed-citation>Zhou N., Choi J., Grothusen G. et al. DLBCL-associated NOTCH2 mutations escape ubiquitin-dependent degradation and promote chemoresistance. Blood 2023;142(11):973–88. DOI: 10.1182/blood.2022018752</mixed-citation></ref><ref id="B50"><label>50.</label><mixed-citation>Ren J., Li W., Pan G. et al. miR-142-3p modulates cell invasion and migration via PKM2-mediated aerobic glycolysis in colorectal cancer. Anal Cell Pathol (Amst) 2021;2021:9927720. DOI: 10.1155/2021/9927720</mixed-citation></ref><ref id="B51"><label>51.</label><mixed-citation>Zhang Y., Zhai Z., Duan J. et al. Lactate: the mediator of metabolism and immunosuppression. Front Endocrinol (Lausanne) 2022;13:901495. DOI: 10.3389/fendo.2022.901495</mixed-citation></ref><ref id="B52"><label>52.</label><citation-alternatives><mixed-citation xml:lang="en">Jabara H.H., Ohsumi T., Chou J. et al. A homozygous mucosa- associated lymphoid tissue 1 (MALT1) mutation in a family with combined immunodeficiency. J Allergy Clin Immunol 2013;132(1):151–8. DOI: 10.1016/j.jaci.2013.04.047</mixed-citation><mixed-citation xml:lang="ru">Jabara H.H., Ohsumi T., Chou J. et al. A homozygous mucosa-associated lymphoid tissue 1 (MALT1) mutation in a family with combined immunodeficiency. J Allergy Clin Immunol 2013;132(1):151–8. DOI: 10.1016/j.jaci.2013.04.047</mixed-citation></citation-alternatives></ref><ref id="B53"><label>53.</label><mixed-citation>Guldenpfennig C., Teixeiro E., Daniels M. NF-κB’s contribution to B cell fate decisions. Front Immunol 2023;14:1214095. DOI: 10.3389/fimmu.2023.1214095</mixed-citation></ref><ref id="B54"><label>54.</label><mixed-citation>Gehring T., Seeholzer T., Krappmann D. BCL10 – bridging CARDs to immune activation. Front Immunol 2018;9:1539. DOI: 10.3389/fimmu.2018.01539</mixed-citation></ref><ref id="B55"><label>55.</label><mixed-citation>Li T., Li X., Zamani A. et al. c-Rel is a myeloid checkpoint for cancer immunotherapy. Nat Cancer 2020;1(5):507–17. DOI: 10.1038/s43018-020-0061-3</mixed-citation></ref><ref id="B56"><label>56.</label><mixed-citation>Fruman D.A., Chiu H., Hopkins B.D. et al. The PI3K pathway in human disease. Cell 2017;170(4):605–35. DOI: 10.1016/j.cell.2017.07.029</mixed-citation></ref><ref id="B57"><label>57.</label><mixed-citation>De la Cruz López K.G., Toledo Guzmán M.E., Sánchez E.O., García Carrancá A. mTORC1 as a regulator of mitochondrial functions and a therapeutic target in cancer. Front Oncol 2019;9:1373. DOI: 10.3389/fonc.2019.01373</mixed-citation></ref><ref id="B58"><label>58.</label><citation-alternatives><mixed-citation xml:lang="en">Shurygina I.A., Shurygin M.G. Mitogen-activated protein kinases as a target for regulating of the connective tissue growth. Patologicheskaya fiziologiya i eksperimental’naya terapiya = Pathological Physiology and Experimental Therapy 2018;63(4):151–7. (In Russ.). DOI: 10.25557/0031-2991.2019.04.151-157</mixed-citation><mixed-citation xml:lang="ru">Шурыгина И.А., Шурыгин М.Г. Митогенактивируемые протеинкиназы как мишень для регуляции роста соединительной ткани. Патологическая физиология и экспериментальная терапия 2018;63(4):151–7. DOI: 10.25557/0031-2991.2019.04.151-157</mixed-citation></citation-alternatives></ref><ref id="B59"><label>59.</label><mixed-citation>Kiu H., Nicholson S.E. Biology and significance of the JAK/STAT signalling pathways. Growth Factors 2012;30(2):88–106. DOI: 10.3109/08977194.2012.660936</mixed-citation></ref><ref id="B60"><label>60.</label><mixed-citation>Lewis K.L., Trotman J. Integration of PET in DLBCL. Semin Hematol 2023;60(5):291–304. DOI: 10.1053/j.seminhematol.2023.12.003</mixed-citation></ref><ref id="B61"><label>61.</label><mixed-citation>Halford S.E.R., Walter H., McKay P. et al. Phase I expansion study of the first-in-class monocarboxylate transporter 1 (MCT1) inhibitor AZD3965 in patients with diffuse large B-cell lymphoma (DLBCL) and Burkitt lymphoma (BL). J Clin Oncol 2021;39(15 suppl). DOI: 10.1200/JCO.2021.39.15_suppl.3115</mixed-citation></ref><ref id="B62"><label>62.</label><mixed-citation>Bhalla K., Jaber S., Nahid M.N. et al. Role of hypoxia in diffuse large B-cell lymphoma: metabolic repression and selective translation of HK2 facilitates development of DLBCL. Sci Rep 2018;8(1):744. DOI: 10.1038/s41598-018-19182-8</mixed-citation></ref><ref id="B63"><label>63.</label><mixed-citation>Shi X., Wu C., Deng W., Wu J. Prognostic value of lactate dehydrogenase to absolute lymphocyte count ratio and albumin to fibrinogen ratio in diffuse large B-cell lymphoma. Medicine (Baltimore) 2024;103(30):e39097. DOI: 10.1097/MD.0000000000039097</mixed-citation></ref><ref id="B64"><label>64.</label><mixed-citation>Garcia-Lacarte M., Grijalba S.C., Melchor J. et al. The PD-1/PD-L1 checkpoint in normal germinal centers and diffuse large B-cell lymphomas. Cancers (Basel) 2021;13(18):4683. DOI: 10.3390/cancers13184683</mixed-citation></ref><ref id="B65"><label>65.</label><mixed-citation>Wang L., Cao C., Qiu J. et al. Correlation between PD-1 and sPD-L1 expression levels in peripheral blood of DLBCL patients and their clinicopathological characteristics. Cell Mol Biol (Noisy-le-grand) 2024;70(2):44–50. DOI: 10.14715/cmb/2024.70.2.7</mixed-citation></ref><ref id="B66"><label>66.</label><mixed-citation>Zhang T., Liu H., Jiao L. et al. Genetic characteristics involving the PD-1/PD-L1/L2 and CD73/A2aR axes and the immunosuppressive microenvironment in DLBCL. J Immunother Cancer 2022;10(4):e004114. DOI: 10.1136/jitc-2021-004114</mixed-citation></ref><ref id="B67"><label>67.</label><mixed-citation>Wei Y., Zhou K., Wang C. et al. Exosomal miR-142-3p from M1-polarized macrophages suppresses cell growth and immune escape in glioblastoma through regulating HMGB1-mediated PD-1/PD-L1 checkpoint. J Neurochem 2025;169(1):e16224. DOI: 10.1111/jnc.16224</mixed-citation></ref><ref id="B68"><label>68.</label><mixed-citation>Amornsupak K., Thongchot S., Thinyakul C. et al. HMGB1 mediates invasion and PD-L1 expression through RAGE-PI3K/ AKT signaling pathway in MDA-MB-231 breast cancer cells. BMC Cancer 2022;22(1):578. DOI: 10.1186/s12885-022-09675-1</mixed-citation></ref><ref id="B69"><label>69.</label><mixed-citation>Chen F., Zhao D., Xu Y. et al. miR-142 deficit in T cells during blast crisis promotes chronic myeloid leukemia immune escape. Nat Commun 2025;16(1):1253. DOI: 10.1038/s41467-025-56383-y</mixed-citation></ref><ref id="B70"><label>70.</label><mixed-citation>Ling J., Sun Q., Tian Q. et al. Human papillomavirus 16 E6/E7 contributes to immune escape and progression of cervical cancer by regulating miR-142-5p/PD-L1 axis. Arch Biochem Biophys 2022;731:109449. DOI: 10.1016/j.abb.2022.109449</mixed-citation></ref><ref id="B71"><label>71.</label><mixed-citation>Zhou C., Zhang Y., Yan R. et al. Exosome-derived miR-142-5p remodels lymphatic vessels and induces IDO to promote immune privilege in the tumour microenvironment. Cell Death Differ 2021;28(2):715–29. DOI: 10.1038/s41418-020-00618-6</mixed-citation></ref><ref id="B72"><label>72.</label><mixed-citation>Motsch N., Alles J., Imig J. et al. MicroRNA profiling of Epstein– Barr virus-associated NK/T-cell lymphomas by deep sequencing. PLoS One 2012;7(8):e42193. DOI: 10.1371/journal.pone.0042193</mixed-citation></ref><ref id="B73"><label>73.</label><mixed-citation>Berrien-Elliott M.M., Sun Y., Neal C. et al. MicroRNA-142 is critical for the homeostasis and function of type 1 innate lymphoid cells. Immunity 2019;51(3):479–90.e6. DOI: 10.1016/j.immuni.2019.06.016</mixed-citation></ref><ref id="B74"><label>74.</label><mixed-citation>Wu X., Li T., Jiang R. et al. Targeting MHC-I molecules for cancer: function, mechanism, and therapeutic prospects. Mol Cancer 2023;22(1):194. DOI: 10.1186/s12943-023-01899-4</mixed-citation></ref><ref id="B75"><label>75.</label><mixed-citation>Damania B., Kenney S.C., Raab-Traub N. Epstein–Barr virus: biology and clinical disease. Cell 2022;185(20):3652–70. DOI: 10.1016/j.cell.2022.08.026</mixed-citation></ref><ref id="B76"><label>76.</label><mixed-citation>Bednarska K., Chowdhury R., Tobin J.W.D. et al. Epstein–Barr virus-associated lymphomas decoded. Br J Haematol 2024;204(2):415–33. DOI: 10.1111/bjh.19255</mixed-citation></ref><ref id="B77"><label>77.</label><mixed-citation>Fitzsimmons L., Cartlidge R., Chang C. et al. BCL-2 homologue BHRF1 drives chemoresistance and lymphomagenesis by inhibiting multiple cellular pro-apoptotic proteins. Cell Death Differ 2020;27(5):1554–68. DOI: 10.1038/s41418-019-0435-1</mixed-citation></ref><ref id="B78"><label>78.</label><mixed-citation>Okuno Y., Murata T., Sato Y. et al. Defective Epstein–Barr virus in chronic active infection and haematological malignancy. Nat Microbiol 2019;4(3):404–13. DOI: 10.1038/s41564-019-0387-8</mixed-citation></ref><ref id="B79"><label>79.</label><mixed-citation>Chen Y., Kincaid R.P., Bastin K. et al. MicroRNA-focused CRISPR/Cas9 screen identifies miR-142 as a key regulator of Epstein–Barr virus reactivation. PLoS Pathog 2024;20(6):e1011970. DOI: 10.1371/journal.ppat.1011970</mixed-citation></ref><ref id="B80"><label>80.</label><citation-alternatives><mixed-citation xml:lang="en">Ambrosio M.R., Navari M., Di Lisio L. et al. The Epstein Barr- encoded BART-6-3p microRNA affects regulation of cell growth and immuno response in Burkitt lymphoma. Infect Agent Cancer 2014;9:12. DOI: 10.1186/1750-9378-9-12</mixed-citation><mixed-citation xml:lang="ru">Ambrosio M.R., Navari M., Di Lisio L. et al. The Epstein Barr-encoded BART-6-3p microRNA affects regulation of cell growth and immuno response in Burkitt lymphoma. Infect Agent Cancer 2014;9:12. DOI: 10.1186/1750-9378-9-12</mixed-citation></citation-alternatives></ref><ref id="B81"><label>81.</label><mixed-citation>Urbanek-Trzeciak M.O., Galka-Marciniak P., Nawrocka P.M. et al. Pan-cancer analysis of somatic mutations in miRNA genes. EBioMedicine 2020;61:103051. DOI: 10.1016/j.ebiom.2020.103051</mixed-citation></ref><ref id="B82"><label>82.</label><mixed-citation>Kansakar U., Gambardella J., Varzideh F. et al. miR-142 targets TIM-1 in human endothelial cells: potential implications for stroke, COVID-19, Zika, Ebola, dengue, and other viral infections. Int J Mol Sci 2022;23(18):10242. DOI: 10.3390/ijms231810242</mixed-citation></ref><ref id="B83"><label>83.</label><mixed-citation>Angiari S., Donnarumma T., Rossi B. et al. TIM-1 glycoprotein binds the adhesion receptor P-selectin and mediates T cell trafficking during inflammation and autoimmunity. Immunity 2014;40(4):542–53. DOI: 10.1016/j.immuni.2014.03.004</mixed-citation></ref><ref id="B84"><label>84.</label><mixed-citation>Yuan S., Liu K.J., Qi Z. Occludin regulation of blood-brain barrier and potential therapeutic target in ischemic stroke. Brain Circ 2020;6(3):152–62. DOI: 10.4103/bc.bc_29_20</mixed-citation></ref><ref id="B85"><label>85.</label><mixed-citation>Chen Z., Li G. Immune response and blood-brain barrier dysfunction during viral neuroinvasion. Innate Immun 2021;27(2):109–17. DOI: 10.1177/1753425920954281</mixed-citation></ref><ref id="B86"><label>86.</label><mixed-citation>Lenze D., Leoncini L., Hummel M. et al. The different epidemiologic subtypes of Burkitt lymphoma share a homogenous micro RNA profile distinct from diffuse large B-cell lymphoma. Leukemia 2011;25(12):1869–76. DOI: 10.1038/leu.2011.156</mixed-citation></ref><ref id="B87"><label>87.</label><mixed-citation>Ayoubian H., Ludwig N., Fehlmann T. et al. Epstein–Barr virus infection of cell lines derived from diffuse large B-cell lymphomas alters microRNA loading of the Ago2 complex. J Virol 2019;93(3):e01297–18. DOI: 10.1128/JVI.01297-18</mixed-citation></ref><ref id="B88"><label>88.</label><mixed-citation>Bahashwan S., Alsaadi M., Barefah A. et al. Profiling of microRNAs by next-generation sequencing: potential biomarkers for diffuse large B-cell lymphoma. J Taibah Univ Med Sci 2024;19(3):619–27. DOI: 10.1016/j.jtumed.2024.04.010</mixed-citation></ref><ref id="B89"><label>89.</label><mixed-citation>Lawrie C.H., Chi J., Taylor S. et al. Expression of microRNAs in diffuse large B cell lymphoma is associated with immunophenotype, survival and transformation from follicular lymphoma. J Cell Mol Med 2009;13(7):1248–60. DOI: 10.1111/j.1582-4934.2008.00628.x</mixed-citation></ref><ref id="B90"><label>90.</label><mixed-citation>Voropaeva E.N., Orlov Y.L., Loginova A.B. et al. Deregulation mechanisms and therapeutic opportunities of p53-responsive microRNAs in diffuse large B-cell lymphoma. PeerJ 2025;13:e18661. DOI: 10.7717/peerj.18661</mixed-citation></ref><ref id="B91"><label>91.</label><mixed-citation>Galka-Marciniak P., Urbanek-Trzeciak M.O., Nawrocka P.M., Kozlowski P. A pan-cancer atlas of somatic mutations in miRNA biogenesis genes. Nucleic Acids Res 2021;49(2):601–20. DOI: 10.1093/nar/gkaa1223</mixed-citation></ref><ref id="B92"><label>92.</label><mixed-citation>Machowska M., Galka-Marciniak P., Kozlowski P. Consequences of genetic variants in miRNA genes. Comput Struct Biotechnol J 2022;20:6443–57. DOI: 10.1016/j.csbj.2022.11.036</mixed-citation></ref><ref id="B93"><label>93.</label><mixed-citation>Kwanhian W., Lenze D., Alles J. et al. MicroRNA-142 is mutated in about 20 % of diffuse large B-cell lymphoma. Cancer Med 2012;1(2):141–55. DOI: 10.1002/cam4.29</mixed-citation></ref><ref id="B94"><label>94.</label><mixed-citation>Hornshøj H., Nielsen M.M., Sinnott-Armstrong N.A. et al. Pan-cancer screen for mutations in non-coding elements with conservation and cancer specificity reveals correlations with expression and survival. NPJ Genom Med 2018;3:1. DOI: 10.1038/s41525-017-0040-5</mixed-citation></ref><ref id="B95"><label>95.</label><mixed-citation>Bouska A., Zhang W., Gong Q. et al. Combined copy number and mutation analysis identifies oncogenic pathways associated with transformation of follicular lymphoma. Leukemia 2017;31(1):83–91. DOI: 10.1038/leu.2016.175</mixed-citation></ref><ref id="B96"><label>96.</label><citation-alternatives><mixed-citation xml:lang="en">Rheinbay E., Nielsen M.M., Abascal F. et al. Analyses of non- coding somatic drivers in 2,658 cancer whole genomes. Nature 2020;578(7793):102–11. DOI: 10.1038/s41586-020-1965-x</mixed-citation><mixed-citation xml:lang="ru">Rheinbay E., Nielsen M.M., Abascal F. et al. Analyses of non-coding somatic drivers in 2,658 cancer whole genomes. Nature 2020;578(7793):102–11. DOI: 10.1038/s41586-020-1965-x</mixed-citation></citation-alternatives></ref><ref id="B97"><label>97.</label><mixed-citation>Puente X.S., Beà S., Valdés-Mas R. et al. Non-coding recurrent mutations in chronic lymphocytic leukaemia. Nature 2015;526(7574):519–24. DOI: 10.1038/nature14666</mixed-citation></ref><ref id="B98"><label>98.</label><mixed-citation>Cancer Genome Atlas Research Network; Ley T.J., Miller C., Ding L. et al. Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia. N Engl J Med 2013;368(22):2059–74. DOI: 10.1056/NEJMoa1301689</mixed-citation></ref><ref id="B99"><label>99.</label><mixed-citation>Thol F., Scherr M., Kirchner A. et al. Clinical and functional implications of microRNA mutations in a cohort of 935 patients with myelodysplastic syndromes and acute myeloid leukemia. Haematologica 2015;100(4):e122–4. DOI: 10.3324/haematol.2014.120345</mixed-citation></ref><ref id="B100"><label>100.</label><mixed-citation>Marshall A., Kasturiarachchi J., Datta P. et al. Mir142 loss unlocks IDH2R140-dependent leukemogenesis through antagonistic regulation of HOX genes [published correction appears in Sci Rep 2021;11(1):6974]. Sci Rep 2020;10(1):19390. DOI: 10.1038/s41598-020-76218-8</mixed-citation></ref><ref id="B101"><label>101.</label><mixed-citation>Kozomara A., Birgaoanu M., Griffiths-Jones S. miRBase: from microRNA sequences to function. Nucleic Acids Res 2019;47(D1):D155–62. DOI: 10.1093/nar/gky1141</mixed-citation></ref><ref id="B102"><label>102.</label><mixed-citation>Chen Y., Wang X. miRDB: an online database for prediction of functional microRNA targets. Nucleic Acids Res 2020;48(D1):D127–31. DOI: 10.1093/nar/gkz757</mixed-citation></ref><ref id="B103"><label>103.</label><mixed-citation>Trissal M.C., Wong T.N., Yao J.C. et al. MIR142 loss-of-function mutations derepress ASH1L to increase HOXA gene expression and promote leukemogenesis. Cancer Res 2018;78(13):3510–21. DOI: 10.1158/0008-5472.CAN-17-3592</mixed-citation></ref><ref id="B104"><label>104.</label><mixed-citation>Khvorova A., Reynolds A., Jayasena S.D. Functional siRNAs and miRNAs exhibit strand bias [published correction appears in Cell 2003;115(4):505]. Cell 2003;115(2):209–16. DOI: 10.1016/s0092-8674(03)00801-8</mixed-citation></ref><ref id="B105"><label>105.</label><mixed-citation>Cheng Z., Liu G., Huang C., Zhao X. Upregulation of circRNA_100395 sponges miR-142-3p to inhibit gastric cancer progression by targeting the PI3K/AKT axis. Oncol Lett 2021;21(5):419. DOI: 10.3892/ol.2021.12680</mixed-citation></ref><ref id="B106"><label>106.</label><mixed-citation>Yin Z., Shen H., Gu C.M. et al. MiRNA-142-3P and FUS can be sponged by long noncoding RNA DUBR to promote cell proliferation in acute myeloid leukemia. Front Mol Biosci 2021;8:754936. DOI: 10.3389/fmolb.2021.754936</mixed-citation></ref><ref id="B107"><label>107.</label><mixed-citation>Gauwerky C.E., Huebner K., Isobe M. et al. Activation of MYC in a masked t(8;17) translocation results in an aggressive B-cell leukemia. Proc Natl Acad Sci USA 1989;86(22):8867–71. DOI: 10.1073/pnas.86.22.8867</mixed-citation></ref><ref id="B108"><label>108.</label><mixed-citation>Robbiani D.F., Bunting S., Feldhahn N. et al. AID produces DNA double-strand breaks in non-Ig genes and mature B cell lymphomas with reciprocal chromosome translocations. Mol Cell 2009;36(4):631–41. DOI: 10.1016/j.molcel.2009.11.007</mixed-citation></ref><ref id="B109"><label>109.</label><mixed-citation>Kuriyama K., Enomoto Y., Suzuki R. et al. Enforced expression of MIR142, a target of chromosome translocation in human B-cell tumors, results in B-cell depletion. Int J Hematol 2018;107(3):345–54. DOI: 10.1007/s12185-017-2360-8</mixed-citation></ref><ref id="B110"><label>110.</label><mixed-citation>Mitelman database of chromosome aberrations and gene fusions in cancer. Eds.: F. Mitelman, B. Johansson, F. Mertens. 2025. Available at: https://mitelmandatabase.isb-cgc.org</mixed-citation></ref><ref id="B111"><label>111.</label><mixed-citation>Andreopoulos B., Anastassiou D. Integrated analysis reveals hsa-miR-142 as a representative of a lymphocyte-specific gene expression and methylation signature. Cancer Inform 2012;11:61–75. DOI: 10.4137/CIN.S9037</mixed-citation></ref><ref id="B112"><label>112.</label><mixed-citation>Zhao H., Zhang L.E., Guo S. et al. Overexpression of DNA methyltransferase 1 as a negative independent prognostic factor in primary gastrointestinal diffuse large B-cell lymphoma treated with CHOP-like regimen and rituximab. Oncol Lett 2015;9(5):2307–12. DOI: 10.3892/ol.2015.3038</mixed-citation></ref><ref id="B113"><label>113.</label><mixed-citation>Amara K., Ziadi S., Hachana M. et al. DNA methyltransferase DNMT3b protein overexpression as a prognostic factor in patients with diffuse large B-cell lymphomas. Cancer Sci 2010;101(7):1722–30. DOI: 10.1111/j.1349-7006.2010.01569.x</mixed-citation></ref><ref id="B114"><label>114.</label><mixed-citation>Voropaeva E.N., Pospelova T.I., Orlov Y.L. et al. The methylation of the p53 targets the genes MIR-203, MIR-129-2, MIR-34A and MIR-34B/C in the tumor tissue of diffuse large B-cell lymphoma. Genes (Basel) 2022;13(8):1401. DOI: 10.3390/genes13081401</mixed-citation></ref><ref id="B115"><label>115.</label><citation-alternatives><mixed-citation xml:lang="en">Voropaeva E.N., Pospelova T.I., Berezina O.V. et al. Methylation of p53- responsive oncosuppressive microRNA genes in hemoblastosis. Sibirskiy onkologicheskiy zhurnal = Siberian Journal of Oncology 2022;21(2): 130–42. (In Russ.). DOI: 10.21294/1814-4861-2022-21-2-130-142</mixed-citation><mixed-citation xml:lang="ru">Воропаева Е.Н., Поспелова Т.И., Березина О.В. и др. Метилирование генов р53-респонзивных онкосупрессорных микроРНК при гемобластозах. Сибирский онкологический журнал 2022;21(2):130–42. DOI: 10.21294/1814-4861-2022-21-2-130-142</mixed-citation></citation-alternatives></ref><ref id="B116"><label>116.</label><mixed-citation>Bartel D.P. MicroRNAs: target recognition and regulatory functions. Cell 2009;136(2):215–33. DOI: 10.1016/j.cell.2009.01.002</mixed-citation></ref><ref id="B117"><label>117.</label><mixed-citation>Mazan-Mamczarz K., Gartenhaus R.B. Role of microRNA deregulation in the pathogenesis of diffuse large B-cell lymphoma (DLBCL). Leuk Res 2013;37(11):1420–8. DOI: 10.1016/j.leukres.2013.08.020</mixed-citation></ref></ref-list></back></article>
