Kipps TJ, Stevenson FK, Wu CJ, Croce CM, Packham G, Wierda WG, et al. Power lymphocytic leukaemia. Nat Rev Dis Prim. 2017;3:16096.
Vosoughi T, Bagheri M, Hosseinzadeh M, Ehsanpour A, Davari N, Saki N. CD markers variations in continual lymphocytic leukemia: New insights into prognosis. J Cell Physiol. 2019;234:19420–39.
Hallek M. Power lymphocytic leukemia: 2020 replace on prognosis, danger stratification and therapy. Am J Hematol. 2019;94:1266–87.
Eichhorst B, Robak T, Montserrat E, Ghia P, Niemann CU, Kater AP, et al. Power lymphocytic leukaemia: ESMO Scientific Follow Tips for prognosis, therapy and follow-up. Ann Oncol. 2021;32:23–33.
Nabhan C, Chaffee KG, Slager SL, Galanina N, Achenbach SJ, Schwager SM, et al. Evaluation of racial variations in illness traits, therapy patterns, and outcomes of sufferers with continual lymphocytic leukemia. Am J Hematol. 2016;91:677–80.
Wang Y, Tschautscher MA, Rabe KG, Name TG, Leis JF, Kenderian SS, et al. Scientific traits and outcomes of Richter transformation: expertise of 204 sufferers from a single middle. Haematologica. 2020;105:765–73.
Siegel RL, Miller KD, Fuchs HE, Jemal A. Most cancers statistics, 2021. CA Most cancers J Clin. 2021;71:7–33.
Yao Y, Lin X, Li F, Jin J, Wang H. The worldwide burden and attributable danger components of continual lymphocytic leukemia in 204 nations and territories from 1990 to 2019: evaluation based mostly on the worldwide burden of illness examine 2019. Biomed Eng On-line. 2022;21:4.
Shanafelt TD, Rabe KG, Kay NE, Zent CS, Jelinek DF, Reinalda MS, et al. Age at prognosis and the utility of prognostic testing in sufferers with continual lymphocytic leukemia. Most cancers. 2010;116:4777–87.
Delgado J, Villamor N. Power lymphocytic leukemia in younger people revisited. Haematologica. 2014;99:4–5.
Goldin LR, Slager SL. Familial CLL: genes and atmosphere. Hematology. 2007;2007:339–45.
Karakosta M, Delicha E-M, Kouraklis G, Manola KN. Affiliation of varied danger components with continual lymphocytic leukemia and its cytogenetic traits. Arch Environ Occup Well being. 2016;71:317–29.
Moore NS, Aldubayan SH, Taylor-Weiner A, Stilgenbauer S, Getz G, Wu CJ, et al. Inherited DNA restore and cell cycle gene defects in continual lymphocytic leukemia. J Clin Oncol. 2019;37:1508–1508.
Brown JR. Inherited susceptibility to continual lymphocytic leukemia: proof and prospects for the longer term. Ther Adv Hematol. 2013;4:298–308.
Ring A, Zenz T. Genetics of “high-risk” continual lymphocytic leukemia within the occasions of chemoimmunotherapy. Haematologica. 2020;105:1180–2.
Riches JC, O’Donovan CJ, Kingdon SJ, McClanahan F, Clear AJ, Neuberg DS, et al. Trisomy 12 continual lymphocytic leukemia cells exhibit upregulation of integrin signaling that’s modulated by NOTCH1 mutations. Blood. 2014;123:4101–10.
Rossi D, Gaidano G. The scientific implications of gene mutations in continual lymphocytic leukaemia. Br J Most cancers. 2016;114:849–54.
Xanthopoulos C, Kostareli E. Advances in epigenetics and epigenomics in continual lymphocytic leukemia. Curr Genet Med Rep. 2019;7:214–26.
Mallm J, Iskar M, Ishaque N, Klett LC, Kugler SJ, Muino JM, et al. Linking aberrant chromatin options in continual lymphocytic leukemia to transcription issue networks. Mol Syst Biol. 2019;15. https://doi.org/10.15252/msb.20188339.
Griffen TL, Hoff FW, Qiu Y, Lillard JW, Ferrajoli A, Thompson P, et al. Proteomic profiling based mostly classification of CLL gives prognostication for contemporary remedy and identifies novel therapeutic targets. Blood Most cancers J. 2022;12:43.
Alsagaby SA. Transcriptomics-based validation of the relatedness of heterogeneous nuclear ribonucleoproteins to continual lymphocytic leukemia as potential biomarkers of the illness aggressiveness. Saudi Med J. 2019;40:328–38.
Mayer RL, Schwarzmeier JD, Gerner MC, Bileck A, Mader JC, Meier-Menches SM, et al. Proteomics and metabolomics establish molecular mechanisms of ageing doubtlessly predisposing for continual lymphocytic leukemia. Mol Cell Proteom. 2018;17:290–303.
Delgado J, Nadeu F, Colomer D, Campo E. Power lymphocytic leukemia: from molecular pathogenesis to novel therapeutic methods. Haematologica. 2020;105:2205–17.
Molica S. Power lymphocytic leukemia prognostic fashions in actual life: nonetheless a good distance off. Knowledgeable Rev Hematol. 2021;14:137–41.
Crombie J, Davids MS. IGHV mutational standing testing in continual lymphocytic leukemia. Am J Hematol. 2017;92:1393–7.
Rozovski U, Keating MJ, Estrov Z. Why is the immunoglobulin heavy chain gene mutation standing a prognostic indicator in continual lymphocytic leukemia? Acta Haematol. 2018;140:51–54.
Burns A, Alsolami R, Becq J, Stamatopoulos B, Timbs A, Bruce D, et al. Entire-genome sequencing of continual lymphocytic leukaemia reveals distinct variations within the mutational panorama between IgHVmut and IgHVunmut subgroups. Leukemia. 2018;32:332–42.
Awwad MHS, Kriegsmann Okay, Plaumann J, Benn M, Hillengass J, Raab MS, et al. The prognostic and predictive worth of IKZF1 and IKZF3 expression in T-cells in sufferers with a number of myeloma. OncoImmunology. 2018;7:e1486356.
Ljungström V, Cortese D, Younger E, Pandzic T, Mansouri L, Plevova Okay, et al. Entire-exome sequencing in relapsing continual lymphocytic leukemia: scientific impression of recurrent RPS15 mutations. Blood. 2016;127:1007–16.
Messina M, Del Giudice I, Khiabanian H, Rossi D, Chiaretti S, Rasi S, et al. Genetic lesions related to continual lymphocytic leukemia chemo-refractoriness. Blood. 2014;123:2378–88.
Rossi D, Bruscaggin A, Spina V, Rasi S, Khiabanian H, Messina M, et al. Mutations of the SF3B1 splicing consider continual lymphocytic leukemia: affiliation with development and fludarabine-refractoriness. Blood. 2011;118:6904–8.
Zenz T, Häbe S, Denzel T, Mohr J, Winkler D, Bühler A, et al. Detailed evaluation of p53 pathway defects in fludarabine-refractory continual lymphocytic leukemia (CLL): dissecting the contribution of 17p deletion, TP53 mutation, p53-p21 dysfunction, and miR34a in a potential scientific trial. Blood. 2009;114:2589–97.
Tausch E, Shut W, Dolnik A, Bloehdorn J, Chyla B, Bullinger L, et al. Venetoclax resistance and purchased BCL2 mutations in continual lymphocytic leukemia. Haematologica. 2019;104:e434–e437.
Regulation PJ, Berndt SI, Speedy HE, Camp NJ, Sava GP, Skibola CF, et al. Genome-wide affiliation evaluation implicates dysregulation of immunity genes in continual lymphocytic leukaemia. Nat Commun. 2017;8:14175.
Speedy HE, Di Bernardo MC, Sava GP, Dyer MJS, Holroyd A, Wang Y, et al. A genome-wide affiliation examine identifies a number of susceptibility loci for continual lymphocytic leukemia. Nat Genet. 2014;46:56–60.
Berndt SI, Skibola CF, Joseph V, Camp NJ, Nieters A, Wang Z, et al. Genome-wide affiliation examine identifies a number of danger loci for continual lymphocytic leukemia. Nat Genet. 2013;45:868–76.
Berndt SI, Camp NJ, Skibola CF, Vijai J, Wang Z, Gu J, et al. Meta-analysis of genome-wide affiliation research discovers a number of loci for continual lymphocytic leukemia. Nat Commun. 2016;7:10933.
Crowther-Swanepoel D, Houlston RS. The molecular foundation of familial continual lymphocytic leukemia. Haematologica. 2009;94:606–9.
Lin W-Y, Fordham SE, Sunter N, Elstob C, Rahman T, Willmore E, et al. Genome-wide affiliation examine identifies danger loci for progressive continual lymphocytic leukemia. Nat Commun. 2021;12:665.
Yan H, Tian S, Kleinstern G, Wang Z, Lee J-H, Boddicker NJ, et al. Power lymphocytic leukemia (CLL) danger is mediated by a number of enhancer variants inside CLL danger loci. Hum Mol Genet. 2020;29:2761–74.
Alkan C, Coe BP, Eichler EE. Genome structural variation discovery and genotyping. Nat Rev Genet. 2011;12:363–76.
Fillerova R, Petrackova A, Papajik T, Turcsanyi P, Behalek M, Gajdos P, et al. Subsequent-generation optical mapping reveals quite a few beforehand unrecognizable structural variants in continual lymphocytic leukemia. Blood. 2019;134:5450–5450.
Durak Aras B, Isik S, Uskudar Teke H, Aslan A, Yavasoglu F, Gulbas Z, et al. Which prognostic marker is chargeable for the scientific heterogeneity in CLL with 13q deletion? Mol Cytogenetics. 2021;14:2.
Calin GA, Dumitru CD, Shimizu M, Bichi R, Zupo S, Noch E, et al. Frequent deletions and down-regulation of micro- RNA genes miR15 and miR16 at 13q14 in continual lymphocytic leukemia. Proc Natl Acad Sci USA. 2002;99:15524–9.
Roberts AW, Davids MS, Pagel JM, Kahl BS, Puvvada SD, Gerecitano JF, et al. Concentrating on BCL2 with venetoclax in relapsed continual lymphocytic leukemia. N Engl J Med. 2016;374:311–22.
Abruzzo LV, Herling CD, Calin GA, Oakes C, Barron LL, Banks HE, et al. Trisomy 12 continual lymphocytic leukemia expresses a novel set of activated and targetable pathways. Haematologica. 2018;103:2069–78.
Athanasiadou A, Stamatopoulos Okay, Tsompanakou A, Gaitatzi M, Kalogiannidis P, Anagnostopoulos A, et al. Scientific, immunophenotypic, and molecular profiling of trisomy 12 in continual lymphocytic leukemia and comparability with different karyotypic subgroups outlined by cytogenetic evaluation. Most cancers Genet Cytogenetics. 2006;168:109–19.
Pepe F, Rassenti LZ, Pekarsky Y, Labanowska J, Nakamura T, Nigita G, et al. A big fraction of trisomy 12, 17p −, and 11q − CLL circumstances carry unidentified microdeletions of miR-15a/16-1. Proc Natl Acad Sci USA. 2022;119. https://doi.org/10.1073/pnas.2118752119.
Villamor N, Conde L, Martínez-Trillos A, Cazorla M, Navarro A, Beà S, et al. NOTCH1 mutations establish a genetic subgroup of continual lymphocytic leukemia sufferers with excessive danger of transformation and poor end result. Leukemia. 2013;27:1100–6.
Queirós AC, Villamor N, Clot G, Martinez-Trillos A, Kulis M, Navarro A, et al. A B-cell epigenetic signature defines three biologic subgroups of continual lymphocytic leukemia with scientific impression. Leukemia. 2015;29:598–605.
Kulis M, Heath S, Bibikova M, Queirós AC, Navarro A, Clot G, et al. Epigenomic evaluation detects widespread gene-body DNA hypomethylation in continual lymphocytic leukemia. Nat Genet. 2012;44:1236–42.
Wojdacz TK, Amarasinghe HE, Kadalayil L, Beattie A, Forster J, Blakemore SJ, et al. Scientific significance of DNA methylation in continual lymphocytic leukemia sufferers: outcomes from 3 UK scientific trials. Blood Adv. 2019;3:2474–81.
Kretzmer H, Biran A, Purroy N, Lemvigh CK, Clement Okay, Gruber M, et al. Preneoplastic alterations outline CLL DNA methylome and persist by illness development and remedy. Blood Most cancers Discov. 2021;2:54–69.
Tsagiopoulou M, Papakonstantinou N, Moysiadis T, Mansouri L, Ljungström V, Duran-Ferrer M, et al. DNA methylation profiles in continual lymphocytic leukemia sufferers handled with chemoimmunotherapy. Clin Epigenetics. 2019;11:177.
Bannister AJ, Kouzarides T. Regulation of chromatin by histone modifications. Cell Res. 2011;21:381–95.
Pastore A, Gaiti F, Lu SX, Model RM, Kulm S, Chaligne R, et al. Corrupted coordination of epigenetic modifications results in diverging chromatin states and transcriptional heterogeneity in CLL. Nat Commun. 2019;10:1874.
Kosmaczewska A, Ciszak L, Suwalska Okay, Wolowiec D, Frydecka I. CTLA-4 overexpression in CD19+/CD5+ cells correlates with the extent of cell cycle regulators and illness development in B-CLL sufferers. Leukemia. 2005;19:301–4.
Wang L, Shalek AK, Lawrence M, Ding R, Gaublomme JT, Pochet N, et al. Somatic mutation as a mechanism of Wnt/β-catenin pathway activation in CLL. Blood. 2014;124:1089–98.
Robertson LE, Plunkett W, McConnell Okay, Keating MJ, McDonnell TJ. Bcl-2 expression in continual lymphocytic leukemia and its correlation with the induction of apoptosis and scientific end result. Leukemia. 1996;10:456–9.
Yoo KH, Hennighausen L. EZH2 methyltransferase and H3K27 methylation in breast most cancers. Int J Biol Sci. 2012;8:59–65.
Papakonstantinou N, Ntoufa S, Chartomatsidou E, Kotta Okay, Agathangelidis A, Giassafaki L, et al. The histone methyltransferase EZH2 as a novel prosurvival consider clinically aggressive continual lymphocytic leukemia. Oncotarget. 2016;7:35946–59.
Puente XS, Beà S, Valdés-Mas R, Villamor N, Gutiérrez-Abril J, Martín-Subero JI, et al. Non-coding recurrent mutations in continual lymphocytic leukaemia. Nature. 2015;526:519–24.
Rodríguez D, Bretones G, Quesada V, Villamor N, Arango JR, López-Guillermo A, et al. Mutations in CHD2 trigger faulty affiliation with lively chromatin in continual lymphocytic leukemia. Blood. 2015;126:195–202.
Parker H, Rose-Zerilli MJJ, Larrayoz M, Clifford R, Edelmann J, Blakemore S, et al. Genomic disruption of the histone methyltransferase SETD2 in continual lymphocytic leukaemia. Leukemia. 2016;30:2179–86.
Zhang P, Wu W, Chen Q, Chen M. Non-Coding RNAs and their Built-in Networks. J Integr Bioinform. 2019;16. https://doi.org/10.1515/jib-2019-0027.
Vigorito E, Perks KL, Abreu-Goodger C, Bunting S, Xiang Z, Kohlhaas S, et al. microRNA-155 regulates the era of immunoglobulin class-switched plasma cells. Immunity. 2007;27:847–59.
Elton TS, Selemon H, Elton SM, Parinandi NL. Regulation of the MIR155 host gene in physiological and pathological processes. Gene. 2013;532:1–12.
Pekarsky Y, Balatti V, Croce CM. BCL2 and miR-15/16: from gene discovery to therapy. Cell Demise Differ. 2018;25:21–26.
Lin X, Guan H, Huang Z, Liu J, Li H, Wei G, et al. Downregulation of Bcl-2 expression by miR-34a mediates palmitate-induced min6 cells apoptosis. J Diab Res. 2014;2014:1–7.
Shanesazzade Z, Peymani M, Ghaedi Okay, Nasr Esfahani MH. miR-34a/BCL-2 signaling axis contributes to apoptosis in MPP + -induced SH-SY5Y cells. Mol Genet Genom Med. 2018;6:975–81.
Ferracin M, Zagatti B, Rizzotto L, Cavazzini F, Veronese A, Ciccone M, et al. MicroRNAs involvement in fludarabine refractory continual lymphocytic leukemia. Mol Most cancers. 2010;9:123.
Qian Y, Shi L, Luo Z. Lengthy non-coding RNAs in most cancers: implications for prognosis, prognosis, and remedy. Entrance Med. 2020;7. https://doi.org/10.3389/fmed.2020.612393.
Marín-Béjar O, Mas AM, González J, Martinez D, Athie A, Morales X, et al. The human lncRNA LINC-PINT inhibits tumor cell invasion by a extremely conserved sequence component. Genome Biol. 2017;18:202.
Blume CJ, Hotz-Wagenblatt A, Hüllein J, Sellner L, Jethwa A, Stolz T, et al. p53-dependent non-coding RNA networks in continual lymphocytic leukemia. Leukemia. 2015;29:2015–23.
Dal Bo M, Rossi FM, Rossi D, Deambrogi C, Bertoni F, Del Giudice I, et al. 13q14 Deletion dimension and variety of deleted cells each affect prognosis in continual lymphocytic leukemia. Genes Chromosomes Most cancers. 2011;50:633–43.
Garding A, Bhattacharya N, Claus R, Ruppel M, Tschuch C, Filarsky Okay, et al. Epigenetic upregulation of lncRNAs at 13q14.3 in leukemia is linked to the in cis downregulation of a gene cluster that targets NF-kB. PLoS Genet. 2013;9:e1003373.
Martin FJ, Amode MR, Aneja A, Austine-Orimoloye O, Azov AG, Barnes I, et al. Ensembl 2023. Nucleic Acids Res. 2023;51:D933–D941.
Bradner JE, Hnisz D, Younger RA. Transcriptional habit in most cancers. Cell. 2017;168:629–43.
Burger JA, Chiorazzi N. B cell receptor signaling in continual lymphocytic leukemia. Tendencies Immunol. 2013;34:592–601.
Pede V, Rombout A, Vermeire J, Naessens E, Mestdagh P, Robberecht N, et al. CLL cells reply to B-cell receptor stimulation with a microRNA/mRNA signature related to MYC activation and cell cycle development. PLoS ONE. 2013;8:e60275.
Ferreira PG, Jares P, Rico D, Gómez-López G, Martínez-Trillos A, Villamor N, et al. Transcriptome characterization by RNA sequencing identifies a serious molecular and scientific subdivision in continual lymphocytic leukemia. Genome Res. 2014;24:212–26.
Griffen TL, Dammer EB, Dill CD, Carey KM, Younger CD, Nunez SK, et al. Multivariate transcriptome evaluation identifies networks and key drivers of continual lymphocytic leukemia relapse danger and affected person survival. BMC Med Genomics. 2021;14:171.
Sbarrato T, Horvilleur E, Pöyry T, Hill Okay, Chaplin LC, Spriggs RV, et al. A ribosome-related signature in peripheral blood CLL B cells is linked to decreased survival following therapy. Cell Demise Dis. 2016;7:e2249–e2249.
Anastasiadou E, Jacob LS, Slack FJ. Non-coding RNA networks in most cancers. Nat Rev Most cancers. 2018;18:5–18.
Krek A, Grün D, Poy MN, Wolf R, Rosenberg L, Epstein EJ, et al. Combinatorial microRNA goal predictions. Nat Genet. 2005;37:495–500.
Balatti V, Acunzo M, Pekarky Y, Croce CM. Novel mechanisms of regulation of miRNAs in CLL. Tendencies Most cancers. 2016;2:134–43.
Rossi S, Shimizu M, Barbarotto E, Nicoloso MS, Dimitri F, Sampath D, et al. microRNA fingerprinting of CLL sufferers with chromosome 17p deletion establish a miR-21 rating that stratifies early survival. Blood. 2010;116:945–52.
Cui B, Chen L, Zhang S, Mraz M, Fecteau J-F, Yu J, et al. MicroRNA-155 influences B-cell receptor signaling and associates with aggressive illness in continual lymphocytic leukemia. Blood. 2014;124:546–54.
Carrà G, Panuzzo C, Torti D, Parvis G, Crivellaro S, Familiari U, et al. Therapeutic inhibition of USP7-PTEN community in continual lymphocytic leukemia: a method to beat TP53 mutated/deleted clones. Oncotarget. 2017;8:35508–22.
Fathullahzadeh S, Mirzaei H, Honardoost MA, Sahebkar A, Salehi M. Circulating microRNA-192 as a diagnostic biomarker in human continual lymphocytic leukemia. Most cancers Gene Ther. 2016;23:327–32.
Li S, Moffett HF, Lu J, Werner L, Zhang H, Ritz J, et al. MicroRNA expression profiling identifies activated B cell standing in continual lymphocytic leukemia cells. PLoS ONE. 2011;6:e16956.
Deneberg S, Kanduri M, Ali D, Bengtzen S, Karimi M, Qu Y, et al. microRNA-34b/c on chromosome 11q23 is aberrantly methylated in continual lymphocytic leukemia. Epigenetics. 2014;9:910–7.
Cimmino A, Calin GA, Fabbri M, Iorio MV, Ferracin M, Shimizu M, et al. miR-15 and miR-16 induce apoptosis by concentrating on BCL2. Proc Natl Acad Sci USA. 2005;102:13944–9.
Calin GA, Cimmino A, Fabbri M, Ferracin M, Wojcik SE, Shimizu M, et al. MiR-15a and miR-16-1 cluster features in human leukemia. Proc Natl Acad Sci. 2008;105:5166–71.
Wang H, Guo M, Wei H, Chen Y. Concentrating on MCL-1 in most cancers: present standing and views. J Hematol Oncol. 2021;14:67.
O’Leary NA, Wright MW, Brister JR, Ciufo S, Haddad D, McVeigh R, et al. Reference sequence (RefSeq) database at NCBI: present standing, taxonomic enlargement, and practical annotation. Nucleic Acids Res. 2016;44:D733–D745.
Hanlon Okay, Rudin CE, Harries LW. Investigating the targets of MIR-15a and MIR-16-1 in sufferers with continual lymphocytic leukemia (CLL). PLoS ONE. 2009;4:e7169.
Linsley PS, Schelter J, Burchard J, Kibukawa M, Martin MM, Bartz SR, et al. Transcripts focused by the MicroRNA-16 household cooperatively regulate cell cycle development. Mol Cell Biol. 2007;27:2240–52.
Turk A, Calin GA, Kunej T. MicroRNAs in leukemias: a clinically annotated compendium. IJMS. 2022;23:3469.
Visone R, Veronese A, Rassenti LZ, Balatti V, Pearl DK, Acunzo M, et al. miR-181b is a biomarker of illness development in continual lymphocytic leukemia. Blood. 2011;118:3072–9.
Zenz T, Mohr J, Eldering E, Kater AP, Bühler A, Kienle D, et al. miR-34a as a part of the resistance community in continual lymphocytic leukemia. Blood. 2009;113:3801–8.
Pekarsky Y, Santanam U, Cimmino A, Palamarchuk A, Efanov A, Maximov V, et al. Tcl1 expression in continual lymphocytic leukemia is regulated by miR-29 and miR-181. Most cancers Res. 2006;66:11590–3.
Ferrajoli A, Shanafelt TD, Ivan C, Shimizu M, Rabe KG, Nouraee N, et al. Prognostic worth of miR-155 in people with monoclonal B-cell lymphocytosis and sufferers with B continual lymphocytic leukemia. Blood. 2013;122:1891–9.
Wiestner A. BCR pathway inhibition as remedy for continual lymphocytic leukemia and lymphoplasmacytic lymphoma. Hematology. 2014;2014:125–34.
Sandhu SK, Fassan M, Volinia S, Lovat F, Balatti V, Pekarsky Y, et al. B-cell malignancies in microRNA Eμ-miR-17∼92 transgenic mice. Proc Natl Acad Sci USA. 2013;110:18208–13.
Bagnara D, Kaufman MS, Calissano C, Marsilio S, Patten PEM, Simone R, et al. A novel adoptive switch mannequin of continual lymphocytic leukemia suggests a key function for T lymphocytes within the illness. Blood. 2011;117:5463–72.
Ahmadi A, Kaviani S, Yaghmaie M, Pashaiefar H, Ahmadvand M, Jalili M, et al. Altered expression of MALAT1 lncRNA in continual lymphocytic leukemia sufferers, correlation with cytogenetic findings. Blood Res. 2018;53:320.
Gutschner T, Hämmerle M, Eißmann M, Hsu J, Kim Y, Hung G, et al. The noncoding RNA MALAT1 is a essential regulator of the metastasis phenotype of lung most cancers cells. Most cancers Res. 2013;73:1180–9.
Wang LQ, Wong KY, Li ZH, Chim CS. Epigenetic silencing of tumor suppressor lengthy non-coding RNA BM742401 in continual lymphocytic leukemia. Oncotarget. 2016;7:82400–10.
Fabris L, Juracek J, Calin G. Non-coding RNAs as most cancers hallmarks in continual lymphocytic leukemia. IJMS. 2020;21:6720.
Tschumper RC, Shanafelt TD, Kay NE, Jelinek DF. Function of lengthy non-coding RNAs in illness development of early stage unmutated continual lymphocytic leukemia. Oncotarget. 2019;10:60–75.
Zhang Y, Hu X, Xu H, Li Y, Zhang L, Feng L, et al. Complete profiling of the epitranscriptomic N6-methyladenosine RNA methylation in continual lymphocytic leukemia. Blood. 2020;136:17–18.
Gassner FJ, Zaborsky N, Buchumenski I, Levanon EY, Gatterbauer M, Schubert M, et al. RNA modifying contributes to epitranscriptome range in continual lymphocytic leukemia. Leukemia. 2021;35:1053–63.
Johnston HE, Carter MJ, Larrayoz M, Clarke J, Garbis SD, Oscier D, et al. Proteomics profiling of CLL versus wholesome B-cells identifies putative therapeutic targets and a subtype-independent signature of spliceosome dysregulation. Mol Cell Proteom. 2018;17:776–91.
Meier-Abt F, Lu J, Cannizzaro E, Pohly MF, Kummer S, Pfammatter S, et al. The protein panorama of continual lymphocytic leukemia. Blood. 2021;138:2514–25.
Woyach JA, Johnson AJ, Byrd JC. The B-cell receptor signaling pathway as a therapeutic goal in CLL. Blood. 2012;120:1175–84.
Fallah-Arani F, Schweighoffer E, Vanes L, Tybulewicz VLJ. Redundant function for Zap70 in B cell improvement and activation. Eur J Immunol. 2008;38:1721–33.
Chen L, Widhopf G, Huynh L, Rassenti L, Rai KR, Weiss A, et al. Expression of ZAP-70 is related to elevated B-cell receptor signaling in continual lymphocytic leukemia. Blood. 2002;100:4609–14.
Buchner M, Fuchs S, Prinz G, Pfeifer D, Bartholomé Okay, Burger M, et al. Spleen tyrosine kinase is overexpressed and represents a possible therapeutic goal in continual lymphocytic leukemia. Most cancers Res. 2009;69:5424–32.
Contri A, Brunati AM, Trentin L, Cabrelle A, Miorin M, Cesaro L, et al. Power lymphocytic leukemia B cells comprise anomalous Lyn tyrosine kinase, a putative contribution to faulty apoptosis. J Clin Investig. 2005;115:369–78.
Schiattone L, Ghia P, Scarfò L. The evolving therapy panorama of continual lymphocytic leukemia. Curr Opin Oncol. 2019;31:568–73.
Mavridou D, Psatha Okay, Aivaliotis M. Proteomics and drug repurposing in CLL in direction of precision medication. Cancers. 2021;13:3391.
Li Q, Verma IM. NF-κB regulation within the immune system. Nat Rev Immunol. 2002;2:725–34.
Loiarro M, Ruggiero V, Sette C. Concentrating on the Toll-like receptor/interleukin 1 receptor pathway in human ailments: rational design of MyD88 inhibitors. Clin Lymphoma Myeloma Leuk. 2013;13:222–6.
Ngo VN, Younger RM, Schmitz R, Jhavar S, Xiao W, Lim Okay-H, et al. Oncogenically lively MYD88 mutations in human lymphoma. Nature. 2011;470:115–9.
Westin JR. Standing of PI3K/Akt/mTOR pathway inhibitors in lymphoma. Clin Lymphoma Myeloma Leuk. 2014;14:335–42.
Hus I, Puła B, Robak T. PI3K inhibitors for the therapy of continual lymphocytic leukemia: present standing and future views. Cancers. 2022;14:1571.
Arruga F, Gizdic B, Serra S, Vaisitti T, Ciardullo C, Coscia M, et al. Purposeful impression of NOTCH1 mutations in continual lymphocytic leukemia. Leukemia. 2014;28:1060–70.
Music H, Liu D, Dong S, Zeng L, Wu Z, Zhao P, et al. Epitranscriptomics and epiproteomics in most cancers drug resistance: therapeutic implications. Sig Transduct Goal Ther. 2020;5:193.
Schmidt DR, Patel R, Kirsch DG, Lewis CA, Vander Heiden MG, Locasale JW. Metabolomics in most cancers analysis and rising purposes in scientific oncology. CA A Most cancers J Clin. 2021;71:333–58.
Piszcz J, Armitage EG, Ferrarini A, Rupérez FJ, Kulczynska A, Bolkun L, et al. To deal with or to not deal with: metabolomics reveals biomarkers for therapy indication in continual lymphocytic leukaemia sufferers. Oncotarget. 2016;7:22324–38.
Chen J-Y, Huang H-H, Yu S-Y, Wu S-J, Kannagi R, Khoo Okay-H. Concerted mass spectrometry-based glycomic method for precision mapping of sulfo sialylated N-glycans on human peripheral blood mononuclear cells and lymphocytes. Glycobiology. 2018;28:9–20.
Thurgood LA, Dwyer ES, Decrease KM, Chataway TK, Kuss BJ. Altered expression of metabolic pathways in CLL detected by unlabelled quantitative mass spectrometry evaluation. Br J Haematol. 2019;185:65–78.
Zalba S, ten Hagen TLM. Cell membrane modulation as adjuvant in most cancers remedy. Most cancers Deal with Rev. 2017;52:48–57.
Larson R, Yachnin S. Mevalonic acid induces DNA synthesis in continual lymphocytic leukemia cells. Blood. 1984;64:257–62.
Podhorecka M, Halicka D, Klimek P, Kowal M, Chocholska S, Dmoszynska A. Simvastatin and purine analogs have a synergic impact on apoptosis of continual lymphocytic leukemia cells. Ann Hematol. 2010;89:1115–24.
Bloehdorn J, Braun A, Taylor-Weiner A, Jebaraj BMC, Robrecht S, Krzykalla J, et al. Multi-platform profiling characterizes molecular subgroups and resistance networks in continual lymphocytic leukemia. Nat Commun. 2021;12:5395.
Thijssen R, Tian L, Anderson MA, Flensburg C, Jarratt A, Garnham AL, et al. Single-cell multiomics reveal the size of multilayered diversifications enabling CLL relapse throughout venetoclax remedy. Blood. 2022;140:2127–41.
Hirayama AV, Zheng Y, Dowling MR, Sheih A, Phi T-D, Kirchmeier DR, et al. Lengthy-term follow-up and single-cell multiomics traits of infusion merchandise in sufferers with continual lymphocytic leukemia handled with CD19 CAR-T cells. Blood. 2021;138:1749–1749.
Lu J, Cannizzaro E, Meier-Abt F, Scheinost S, Bruch P-M, Giles HAR, et al. Multi-omics reveals clinically related proliferative drive related to mTOR-MYC-OXPHOS exercise in continual lymphocytic leukemia. Nat Most cancers. 2021;2:853–64.
Largeot A, Klapp V, Viry E, Gonder S, Fernandez Botana I, Blomme A, et al. Inhibition of MYC translation by concentrating on of the newly recognized PHB-eIF4F complicated as therapeutic technique in CLL. Blood J. 2023;141:3166–83. blood.2022017839.
Elnair R, Ellithi M, Kallam A, Shostrom V, Bociek RG. Outcomes of Richter’s transformation of continual lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL): an evaluation of the SEER database. Ann Hematol. 2021;100:2513–9.
Briski R, Taylor J. Remedy of richter transformation of continual lymphocytic leukemia within the trendy period. Cancers. 2023;15:1857.
Rossi D, Spina V, Gaidano G. Biology and therapy of Richter syndrome. Blood. 2018;131:2761–72.
Chigrinova E, Rinaldi A, Kwee I, Rossi D, Rancoita PMV, Strefford JC, et al. Two primary genetic pathways result in the transformation of continual lymphocytic leukemia to Richter syndrome. Blood. 2013;122:2673–82.
Fabbri G, Khiabanian H, Holmes AB, Wang J, Messina M, Mullighan CG, et al. Genetic lesions related to continual lymphocytic leukemia transformation to Richter syndrome. J Exp Med. 2013;210:2273–88.
De Paoli L, Cerri M, Monti S, Rasi S, Spina V, Bruscaggin A, et al. MGA, a suppressor of MYC, is recurrently inactivated in excessive danger continual lymphocytic leukemia. Leuk Lymphoma. 2013;54:1087–90.
Rossi D, Spina V, Deambrogi C, Rasi S, Laurenti L, Stamatopoulos Okay, et al. The genetics of Richter syndrome reveals illness heterogeneity and predicts survival after transformation. Blood. 2011;117:3391–401.
Rossi D, Cerri M, Capello D, Deambrogi C, Rossi FM, Zucchetto A, et al. Organic and scientific danger components of continual lymphocytic leukaemia transformation to Richter syndrome. Br J Haematol. 2008;142:202–15.
Timár B, Fülöp Z, Csernus B, Angster C, Bognár Á, Szepesi Á, et al. Relationship between the mutational standing of VH genes and pathogenesis of diffuse massive B-cell lymphoma in Richter’s syndrome. Leukemia. 2004;18:326–30.
Rasi S, Spina V, Bruscaggin A, Vaisitti T, Tripodo C, Forconi F, et al. A variant of the LRP4 gene impacts the chance of continual lymphocytic leukaemia transformation to Richter syndrome: Host Genetic Background and Danger of Richter Transformation. Br J Haematol. 2011;152:284–94.
Rinaldi A, Mensah AA, Kwee I, Forconi F, Orlandi EM, Lucioni M, et al. Promoter methylation patterns in Richter syndrome have an effect on stem-cell upkeep and cell cycle regulation and differ from de novo diffuse massive B-cell lymphoma. Br J Haematol. 2013;163:194–204.
Broséus J, Hergalant S, Vogt J, Tausch E, Kreuz M, Mottok A, et al. Molecular characterization of Richter syndrome identifies de novo diffuse massive B-cell lymphomas with poor prognosis. Nat Commun. 2023;14:309.
Van Roosbroeck Okay, Bayraktar R, Calin S, Bloehdorn J, Dragomir MP, Okubo Okay, et al. The involvement of microRNA within the pathogenesis of Richter syndrome. Haematologica. 2019;104:1004–15.
Klintman J, Appleby N, Stamatopoulos B, Ridout Okay, Eyre TA, Robbe P, et al. Genomic and transcriptomic correlates of Richter transformation in continual lymphocytic leukemia. Blood. 2021;137:2800–16.
Nadeu F, Royo R, Massoni-Badosa R, Playa-Albinyana H, Garcia-Torre B, Duran-Ferrer M, et al. Detection of early seeding of Richter transformation in continual lymphocytic leukemia. Nat Med. 2022;28:1662–71.
Kohlhaas V, Blakemore SJ, Al-Maarri M, Nickel N, Pal M, Roth A, et al. Lively Akt signaling triggers CLL towards Richter transformation by way of overactivation of Notch1. Blood. 2021;137:646–60.
Rozovski U, Hazan-Halevy I, Barzilai M, Keating MJ, Estrov Z. Metabolism pathways in continual lymphocytic leukemia. Leuk Lymphoma. 2016;57:758–65.
Falchi L, Keating MJ, Marom EM, Truong MT, Schlette EJ, Sargent RL, et al. Correlation between FDG/PET, histology, traits, and survival in 332 sufferers with continual lymphoid leukemia. Blood. 2014;123:2783–90.
Iyer P, Zhang B, Liu T, Jin M, Hart Okay, Music JY, et al. Disrupting MGA-MYC pushed metabolic reprogramming in Richter’s syndrome pre-clinical fashions by way of novel therapeutic approaches. Blood. 2022;140:9842–3.
