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TP53 in AML and MDS: The new (old) kid on the block
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“However, any clinical applications of these findings are, so far, restricted to just a few cancer types, such as chronic lymphocytic leukemia (CLL) or acute myeloid leukemia (AML) [83, 84].”
From The TP53 tumor suppressor gene: From molecular biology to clinical investigations (2025) · cites this paper as [83]
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Arber, D. A., Orazi, A., Hasserjian, R. P., Borowitz, M. J., Calvo, K. R., Kvasnicka, H.-M., Wang, S. A., Bagg, A., Barbui, T., Branford, S., et al. (2022) · Blood · doi:10.1182/blood.2022015850 · Cited by 2,945
Self-citationFenaux, P., Mufti, G. J., Hellstrom-Lindberg, E., Santini, V., Finelli, C., Giagounidis, A., Schoch, R., Gattermann, N., Sanz, G., List, A., et al. (2009) · The Lancet Oncology · doi:10.1016/s1470-2045(09)70003-8 · Cited by 2,663
Midostaurin plus Chemotherapy for Acute Myeloid Leukemia with a FLT3 Mutation
Stone, R. M., Mandrekar, S. J., Sanford, B. L., Laumann, K., Geyer, S., Bloomfield, C. D., Thiede, C., Prior, T. W., Döhner, K., Marcucci, G., et al. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1614359 · Cited by 2,250
TP53 mutations in human cancers: origins, consequences, and clinical use.
Olivier, M., Hollstein, M., & Hainaut, P. (2010) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a001008 · Cited by 2,199
Mutant p53 in Cancer: New Functions and Therapeutic Opportunities
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Bode, A. M., & Dong, Z. (2004) · Nature Reviews Cancer · doi:10.1038/nrc1455 · Cited by 1,270
Regulation of p53 in response to DNA damage
Lakin, N. D., & Jackson, S. P. (1999) · Oncogene · doi:10.1038/sj.onc.1203015 · Cited by 987
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Wolf, Y., Anderson, A. C., & Kuchroo, V. K. (2020) · Nature Reviews Immunology · doi:10.1038/s41577-019-0224-6 · Cited by 959
Role of TP53 mutations in the origin and evolution of therapy-related acute myeloid leukaemia
Wong, T. N., Ramsingh, G., Young, A. L., Miller, C. A., Touma, W., Welch, J. S., Lamprecht, T. L., Shen, D., Hundal, J., Fulton, R. S., et al. (2015) · Nature · doi:10.1038/nature13968 · Cited by 892
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Petitjean, A., Achatz, M. I. W., Borresen-Dale, A. L., Hainaut, P., & Olivier, M. (2007) · Oncogene · doi:10.1038/sj.onc.1210302 · Cited by 884
Research works printed but not linked: 149
- Papaemmanuil, 2016, Genomic classification and prognosis in acute myeloid leukemia, N Engl J Med, 374, 2209, 10.1056/NEJMoa1516192 · DOI · Paper page
- Sperling, 2017, The genetics of myelodysplastic syndrome: from clonal haematopoiesis to secondary leukaemia, Nat Rev Cancer, 17, 5, 10.1038/nrc.2016.112 · DOI · Paper page
- Sebaa, 2012, Incidence of 17p deletions and TP53 mutation in myelodysplastic syndrome and acute myeloid leukemia with 5q deletion, Genes Chromosomes Cancer, 51, 1086, 10.1002/gcc.21993 · DOI
- Ogawa, 2019, Genetics of MDS, Blood, 133, 1049, 10.1182/blood-2018-10-844621 · DOI · Paper page
- DiNardo, 2016, Mutations in AML: prognostic and therapeutic implications, Hematology Am Soc Hematol Educ Program, 2016, 348, 10.1182/asheducation-2016.1.348 · DOI · Paper page
- Bejar, 2014, Clinical and genetic predictors of prognosis in myelodysplastic syndromes, Haematologica, 99, 956, 10.3324/haematol.2013.085217 · DOI
- Daver, 2022, TP53-mutated myelodysplastic syndrome and acute myeloid leukemia: biology, current therapy, and future directions, Cancer Discov, OF1
- Vogelstein, 2000, Surfing the p53 network, Nature, 408, 307, 10.1038/35042675 · DOI · Paper page
- Zhang, 2017, The role of p53 in myelodysplastic syndromes and acute myeloid leukemia: molecular aspects and clinical implications, Leuk Lymphoma, 58, 1777, 10.1080/10428194.2016.1266625 · DOI
- Christiansen, 2001, Mutations with loss of heterozygosity of p53 are common in therapy-related myelodysplasia and acute myeloid leukemia after exposure to alkylating agents and significantly associated with deletion or loss of 5q, a complex karyotype, and a poor prognosis, J Clin Oncol, 19, 1405, 10.1200/JCO.2001.19.5.1405 · DOI · Paper page
- Ben-Yehuda, 1996, Microsatellite instability and p53 mutations in therapy-related leukemia suggest mutator phenotype, Blood, 88, 4296, 10.1182/blood.V88.11.4296.bloodjournal88114296 · doi:10.1182/blood.v88.11.4296.bloodjournal88114296 · Paper page
- Lee, 2019, Molecular pathogenesis of myelodysplastic syndromes with deletion 5q, Eur J Haematol, 102, 203, 10.1111/ejh.13207 · DOI
- Cumbo, 2020, TP53 in myelodysplastic syndromes: recent biological and clinical findings, Int J Mol Sci, 21, 10.3390/ijms21103432 · DOI
- Joerger, 2010, The tumor suppressor p53: from structures to drug discovery, Cold Spring Harb Perspect Biol, 2, 10.1101/cshperspect.a000919 · DOI · Paper page
- Stengel, 2017, The impact of TP53 mutations and TP53 deletions on survival varies between AML, ALL, MDS and CLL: an analysis of 3307 cases, Leukemia, 31, 705, 10.1038/leu.2016.263 · DOI · Paper page
- Assi, 2018, P53 protein overexpression in de novo acute myeloid leukemia patients with normal diploid karyotype correlates with FLT3 internal tandem duplication and worse relapse-free survival, Am J Hematol, 93, 1376, 10.1002/ajh.25255 · DOI
- Grob, 2022, Molecular characterization of mutant TP53 acute myeloid leukemia and high-risk myelodysplastic syndrome, Blood, 139, 2347, 10.1182/blood.2021014472 · DOI · Paper page
- Sallman, 2016, Impact of TP53 mutation variant allele frequency on phenotype and outcomes in myelodysplastic syndromes, Leukemia, 30, 666, 10.1038/leu.2015.304 · DOI · Paper page
- Jiang, 2021, TP53 in myelodysplastic syndromes, Cancers (Basel), 13, 10.3390/cancers13215392 · DOI
- Kadia, 2016, TP53 mutations in newly diagnosed acute myeloid leukemia: clinicomolecular characteristics, response to therapy, and outcomes, Cancer, 122, 3484, 10.1002/cncr.30203 · DOI · Paper page
- Khoury, 2022, The 5th edition of the World Health Organization classification of haematolymphoid tumours: myeloid and histiocytic/dendritic neoplasms, Leukemia, 36, 1703, 10.1038/s41375-022-01613-1 · DOI · Paper page
- Levine, 2020, p53: 800 million years of evolution and 40 years of discovery, Nat Rev Cancer, 20, 471, 10.1038/s41568-020-0262-1 · DOI · Paper page
- Klimovich, 2022, p53 partial loss-of-function mutations sensitize to chemotherapy, Oncogene, 41, 1011, 10.1038/s41388-021-02141-5 · DOI · Paper page
- Donehower, 2019, Integrated analysis of TP53 gene and pathway alterations in the cancer genome atlas, Cell Rep, 28, 3010, 10.1016/j.celrep.2019.08.061 · DOI · Paper page
- Prochazka, 2019, Clinical implications of subclonal TP53 mutations in acute myeloid leukemia, Haematologica, 104, 516, 10.3324/haematol.2018.205013 · DOI
- Surget, 2014, Uncovering the role of p53 splice variants in human malignancy: a clinical perspective, Onco Targets Ther, 7, 57
- El Marabti, 2018, The cancer spliceome: reprograming of alternative splicing in cancer, Front Mol Biosci, 5, 80, 10.3389/fmolb.2018.00080 · DOI · Paper page
- Rivlin, 2011, Mutations in the p53 tumor suppressor gene: important milestones at the various steps of tumorigenesis, Genes Cancer, 2, 466, 10.1177/1947601911408889 · DOI · Paper page
- Molica, 2020, TP53 mutations in acute myeloid leukemia: still a daunting challenge?, Front Oncol, 10
- Dohner, 2022, Diagnosis and management of AML in adults: 2022 ELN recommendations from an international expert panel, Blood, 140, 1345, 10.1182/blood.2022016867 · DOI · Paper page
- Arber, 2016, The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia, Blood, 127, 2391, 10.1182/blood-2016-03-643544 · DOI · Paper page
- Nguyen-Khac, 2022, The complex karyotype in hematological malignancies: a comprehensive overview by the Francophone Group of Hematological Cytogenetics (GFCH), Leukemia, 36, 1451, 10.1038/s41375-022-01561-w · DOI
- Schoch, 2004, Karyotype is an independent prognostic parameter in therapy-related acute myeloid leukemia (t-AML): an analysis of 93 patients with t-AML in comparison to 1091 patients with de novo AML, Leukemia, 18, 120, 10.1038/sj.leu.2403187 · DOI · Paper page
- Kuendgen, 2021, Therapy-related myelodysplastic syndromes deserve specific diagnostic sub-classification and risk-stratification-an approach to classification of patients with t-MDS, Leukemia, 35, 835, 10.1038/s41375-020-0917-7 · DOI
- Greenberg, 2012, Revised international prognostic scoring system for myelodysplastic syndromes, Blood J Am Soc Hematol., 120, 2454
- Weinberg, 2022, TP53 mutation defines a unique subgroup within complex karyotype de novo and therapy-related MDS/AML, Blood Adv, 6, 2847, 10.1182/bloodadvances.2021006239 · DOI · Paper page
- Rucker, 2012, TP53 alterations in acute myeloid leukemia with complex karyotype correlate with specific copy number alterations, monosomal karyotype, and dismal outcome, Blood, 119, 2114, 10.1182/blood-2011-08-375758 · DOI · Paper page
- Ebert, 2011, Molecular dissection of the 5q deletion in myelodysplastic syndrome, Semin Oncol, 38, 621, 10.1053/j.seminoncol.2011.04.010 · DOI
- Bersanelli, 2021, Classification and personalized prognostic assessment on the basis of clinical and genomic features in myelodysplastic syndromes, J Clin Oncol, 39, 1223, 10.1200/JCO.20.01659 · DOI · Paper page
- Zemanova, 2018, Chromothripsis in high-risk myelodysplastic syndromes: incidence, genetic features, clinical implications, and impact on survival of patients treated with azacytidine (data from Czech MDS Group), Blood, 132, 1815, 10.1182/blood-2018-99-114151 · doi:10.1182/blood-2018-99-114151
- Cluzeau, 2021, Personalized medicine for TP53 mutated myelodysplastic syndromes and acute myeloid leukemia, Int J Mol Sci, 22, 10.3390/ijms221810105 · DOI
- Quesada, 2019, DDX41 mutations in myeloid neoplasms are associated with male gender, TP53 mutations and high-risk disease, Am J Hematol, 94, 757, 10.1002/ajh.25486 · DOI
- Garber, 1991, Follow-up study of twenty-four families with Li-Fraumeni syndrome, Cancer Res, 51, 6094
- Kuendgen, 2006, Myelodysplastic syndromes in patients younger than age 50, J Clin Oncol, 24, 5358, 10.1200/JCO.2006.07.5598 · DOI
- Jaiswal, 2014, Age-related clonal hematopoiesis associated with adverse outcomes, N Engl J Med, 371, 2488, 10.1056/NEJMoa1408617 · DOI · Paper page
- Babushok, 2016, Genetic predisposition to myelodysplastic syndrome and acute myeloid leukemia in children and young adults, Leuk Lymphoma, 57, 520, 10.3109/10428194.2015.1115041 · DOI
- Klco, 2021, Advances in germline predisposition to acute leukaemias and myeloid neoplasms, Nat Rev Cancer, 21, 122, 10.1038/s41568-020-00315-z · DOI
- Singhal, 2017, Presence of rare germline variants in Fanconi anaemia pathway genes confers a poor prognosis comparable to TP53 mutations in therapy-related myeloid neoplasms, Blood, 130, 4231
- Swaminathan, 2019, Hematologic malignancies and Li-Fraumeni syndrome, Cold Spring Harb Mol Case Stud, 5, 10.1101/mcs.a003210 · DOI
- Leone, 2003, Inhibitors of DNA methylation in the treatment of hematological malignancies and MDS, Clin Immunol, 109, 89, 10.1016/S1521-6616(03)00207-9 · DOI
- Deng, 2020, The prognostic impact of variant allele frequency (VAF) in TP53 mutant patients with MDS: a systematic review and meta-analysis, Eur J Haematol, 105, 524, 10.1111/ejh.13483 · DOI
- Goel, 2016, High prevalence and allele burden-independent prognostic importance of p53 mutations in an inner-city MDS/AML cohort, Leukemia, 30, 1793, 10.1038/leu.2016.74 · DOI
- Döhner, 2017, Diagnosis and management of AML in adults: 2017 ELN recommendations from an international expert panel, Blood, 129, 424, 10.1182/blood-2016-08-733196 · DOI · Paper page
- Zeidan, 2023, Prognostic implications of mono-hit and multi-hit TP53 alterations in patients with acute myeloid leukemia and higher risk myelodysplastic syndromes treated with azacitidine-based therapy, Leukemia, 37, 240, 10.1038/s41375-022-01766-z · DOI
- Ebert, 2008, Identification of RPS14 as a 5q- syndrome gene by RNA interference screen, Nature, 451, 335, 10.1038/nature06494 · DOI · Paper page
- Shahjahani, 2019, Complex karyotype in myelodysplastic syndromes: diagnostic procedure and prognostic susceptibility, Oncol Rev, 13, 389, 10.4081/oncol.2019.389 · DOI
- Akkari, 2022, Guiding the global evolution of cytogenetic testing for hematologic malignancies, Blood, 139, 2273, 10.1182/blood.2021014309 · DOI
- Duncavage, 2022, Genomic profiling for clinical decision making in myeloid neoplasms and acute leukemia, Blood, 140, 2228, 10.1182/blood.2022015853 · DOI · Paper page
- Peterson, 2018, The utilization of chromosomal microarray technologies for hematologic neoplasms: an ACLPS critical review, Am J Clin Pathol, 150, 375, 10.1093/ajcp/aqy076 · DOI
- Chauffaille, 2020, Detection of somatic TP53 mutations and 17p deletions in patients with chronic lymphocytic leukemia: a review of the current methods, Hematol Transfus Cell Ther, 42, 261, 10.1016/j.htct.2020.05.005 · DOI
- Greenberg, 2022, NCCN guidelines(R) insights: myelodysplastic syndromes, version 3.2022, J Natl Compr Canc Netw, 20, 106, 10.6004/jnccn.2022.0009 · DOI
- Heuser, 2021, 2021 update on MRD in acute myeloid leukemia: a consensus document from the European LeukemiaNet MRD Working Party, Blood, 138, 2753, 10.1182/blood.2021013626 · DOI · Paper page
- Bacher, 2018, Challenges in the introduction of next-generation sequencing (NGS) for diagnostics of myeloid malignancies into clinical routine use, Blood Cancer J, 8, 113, 10.1038/s41408-018-0148-6 · DOI
- Soussi, 2022, Benign SNPs in the coding region of TP53: finding the needles in a haystack of pathogenic variants, Cancer Res, 82, 3420, 10.1158/0008-5472.CAN-22-0172 · DOI
- Malcikova, 2018, ERIC recommendations for TP53 mutation analysis in chronic lymphocytic leukemia-update on methodological approaches and results interpretation, Leukemia, 32, 1070, 10.1038/s41375-017-0007-7 · DOI · Paper page
- Miura, 2021, A simple method to estimate the in-house limit of detection for genetic mutations with low allele frequencies in whole-exome sequencing analysis by next-generation sequencing, BMC Genom Data, 22, 8, 10.1186/s12863-020-00956-x · DOI
- Bally, 2014, Detection of TP53 mutations in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). A comparison between a functional method (FASAY) and next generation sequencing (NGS), Blood, 124, 3266, 10.1182/blood.V124.21.3266.3266 · doi:10.1182/blood.v124.21.3266.3266
- Tonisson, 2002, Evaluating the arrayed primer extension resequencing assay of TP53 tumor suppressor gene, Proc Natl Acad Sci U S A, 99, 5503, 10.1073/pnas.082100599 · DOI
- Kantorova, 2015, TP53 mutation analysis in chronic lymphocytic leukemia: comparison of different detection methods, Tumour Biol, 36, 3371, 10.1007/s13277-014-2971-0 · DOI
- Malcikova, 2015, Detailed analysis of therapy-driven clonal evolution of TP53 mutations in chronic lymphocytic leukemia, Leukemia, 29, 877, 10.1038/leu.2014.297 · DOI
- Kringen, 2005, Evaluation of arrayed primer extension for TP53 mutation detection in breast and ovarian carcinomas, Biotechniques, 39, 755, 10.2144/000112000 · DOI
- Seifert, 2009, The prognostic impact of 17p (p53) deletion in 2272 adults with acute myeloid leukemia, Leukemia, 23, 656, 10.1038/leu.2008.375 · DOI · Paper page
- Merlat, 1999, Therapy-related myelodysplastic syndrome and acute myeloid leukemia with 17p deletion. A report on 25 cases, Leukemia, 13, 250, 10.1038/sj.leu.2401298 · DOI
- Sanchez-Castro, 2013, Characterization and prognostic implication of 17 chromosome abnormalities in myelodysplastic syndrome, Leuk Res, 37, 769, 10.1016/j.leukres.2013.04.010 · doi:10.1016/j.leukres.2013.04.010
- Sanchez-Castro, 2015, Fluorescence in situ hybridization of TP53 for the detection of chromosome 17 abnormalities in myelodysplastic syndromes, Leuk Lymphoma, 56, 3183, 10.3109/10428194.2015.1028053 · DOI
- Malcovati, 2013, Diagnosis and treatment of primary myelodysplastic syndromes in adults: recommendations from the European LeukemiaNet, Blood, 122, 2943, 10.1182/blood-2013-03-492884 · DOI · Paper page
- Ribeiro, 2021, Genomic variations in patients with myelodysplastic syndrome and karyotypes without numerical or structural changes, Sci Rep, 11, 2783, 10.1038/s41598-021-81467-2 · DOI
- Berry, 2019, Clinical use of SNP-microarrays for the detection of genome-wide changes in haematological malignancies, Crit Rev Oncol Hematol, 142, 58, 10.1016/j.critrevonc.2019.07.016 · DOI
- Arenillas, 2013, Single nucleotide polymorphism array karyotyping: a diagnostic and prognostic tool in myelodysplastic syndromes with unsuccessful conventional cytogenetic testing, Genes Chromosomes Cancer, 52, 1167, 10.1002/gcc.22112 · DOI
- Yang, 2022, High-resolution structural variant profiling of myelodysplastic syndromes by optical genome mapping uncovers cryptic aberrations of prognostic and therapeutic significance, Leukemia, 36, 2306, 10.1038/s41375-022-01652-8 · DOI
- Raffone, 2020, Diagnostic accuracy of p53 immunohistochemistry as surrogate of TP53 sequencing in endometrial cancer, Pathol Res Pract, 216, 10.1016/j.prp.2020.153025 · DOI
- Kortekaas, 2020, Performance of the pattern-based interpretation of p53 immunohistochemistry as a surrogate for TP53 mutations in vulvar squamous cell carcinoma, Histopathology, 77, 92, 10.1111/his.14109 · DOI
- Yu, 2021, TP53 co-mutational features and NGS-calibrated immunohistochemistry threshold in gastric cancer, Onco Targets Ther, 14, 4967, 10.2147/OTT.S321949 · DOI
- McGraw, 2016, Immunohistochemical pattern of p53 is a measure of TP53 mutation burden and adverse clinical outcome in myelodysplastic syndromes and secondary acute myeloid leukemia, Haematologica, 101, e320, 10.3324/haematol.2016.143214 · DOI
- Ruzinova, 2019, TP53 immunohistochemistry correlates with TP53 mutation status and clearance in decitabine-treated patients with myeloid malignancies, Haematologica, 104, e345, 10.3324/haematol.2018.205302 · DOI
- Fitzpatrick, 2022, Correlation of p53 immunohistochemistry with TP53 mutational status and overall survival in newly diagnosed acute myeloid leukaemia, Histopathology, 81, 496, 10.1111/his.14726 · DOI
- Fernandez-Pol, 2017, Immunohistochemistry for p53 is a useful tool to identify cases of acute myeloid leukemia with myelodysplasia-related changes that are TP53 mutated, have complex karyotype, and have poor prognosis, Mod Pathol, 30, 382, 10.1038/modpathol.2016.206 · DOI
- Chui, 2022, Somatic intronic TP53 c.375+5G mutations are a recurrent but under-recognized mode of TP53 inactivation, J Pathol Clin Res, 8, 14, 10.1002/cjp2.242 · doi:10.1002/cjp2.242
- Fang, 2022, Pure erythroid leukemia is characterized by biallelic TP53 inactivation and abnormal p53 expression patterns in de novo and secondary cases, Haematologica, 107, 2232, 10.3324/haematol.2021.280487 · DOI
- Sangoi, 2022, p53 null phenotype is a "positive result" in urothelial carcinoma in situ, Mod Pathol, 35, 1287, 10.1038/s41379-022-01062-2 · doi:10.1038/s41379-022-01062-2
- Orachum, 2022, Clinical outcomes of immunohistochemistry of the p53 staining pattern in high-grade serous ovarian carcinoma, Obstet Gynecol Sci, 65, 459, 10.5468/ogs.22102 · DOI
- Salomao, 2022, Reduced murine double minute 2 and 4 protein, but not messenger RNA, expression is associated with more severe disease in myelodysplastic syndromes and acute myeloblastic leukaemia, Br. J. Haematol.
- Loschi, 2022, How I treat TP53-mutated acute myeloid leukemia and myelodysplastic syndromes, Cancers, 14, 4519, 10.3390/cancers14184519 · DOI
- Granowicz, 2022, Targeting TP53-mutated acute myeloid leukemia: research and clinical developments, Onco Targets Ther, 15, 423, 10.2147/OTT.S265637 · DOI
- Kuykendall, 2018, Acute myeloid leukemia: the good, the bad, and the ugly, Am Soc Clin Oncol Educ Book, 38, 555, 10.1200/EDBK_199519 · DOI
- Bowen, 2009, TP53 gene mutation is frequent in patients with acute myeloid leukemia and complex karyotype, and is associated with very poor prognosis, Leukemia, 23, 203, 10.1038/leu.2008.173 · DOI · Paper page
- Goldberg, 2018, TP53 mutations predict poorer responses to CPX-351 in acute myeloid leukemia, Blood, 132, 1433, 10.1182/blood-2018-99-117772 · DOI
- Hills, 2014, Addition of gemtuzumab ozogamicin to induction chemotherapy in adult patients with acute myeloid leukaemia: a meta-analysis of individual patient data from randomised controlled trials, Lancet Oncol, 15, 986, 10.1016/S1470-2045(14)70281-5 · DOI · Paper page
- Muller-Thomas, 2014, Response to azacitidine is independent of p53 expression in higher-risk myelodysplastic syndromes and secondary acute myeloid leukemia, Haematologica, 99, e179, 10.3324/haematol.2014.104760 · DOI
- Dohner, 2018, Cytogenetics and gene mutations influence survival in older patients with acute myeloid leukemia treated with azacitidine or conventional care, Leukemia, 32, 2546, 10.1038/s41375-018-0257-z · DOI
- Middeke, 2021, Decitabine treatment in 311 patients with acute myeloid leukemia: outcome and impact of TP53 mutations - a registry based analysis, Leuk Lymphoma, 62, 1432, 10.1080/10428194.2020.1864354 · DOI
- Boddu, 2018, Outcomes with lower intensity therapy in TP53-mutated acute myeloid leukemia, Leuk Lymphoma, 59, 2238, 10.1080/10428194.2017.1422864 · DOI
- DiNardo, 2020, Azacitidine and venetoclax in previously untreated acute myeloid leukemia, N Engl J Med, 383, 617, 10.1056/NEJMoa2012971 · DOI · Paper page
- DiNardo, 2019, Venetoclax combined with decitabine or azacitidine in treatment-naive, elderly patients with acute myeloid leukemia, Blood, 133, 7, 10.1182/blood-2018-08-868752 · DOI · Paper page
- Aldoss, 2019, Venetoclax and hypomethylating agents in TP53-mutated acute myeloid leukaemia, Br J Haematol, 187, e45, 10.1111/bjh.16166 · DOI
- DiNardo, 2020, 10-day decitabine with venetoclax for newly diagnosed intensive chemotherapy ineligible, and relapsed or refractory acute myeloid leukaemia: a single-Centre, phase 2 trial, Lancet Haematol, 7, e724, 10.1016/S2352-3026(20)30210-6 · DOI · Paper page
- Cluzeau, 2021, Eprenetapopt plus azacitidine in TP53-mutated myelodysplastic syndromes and acute myeloid leukemia: a phase II study by the Groupe Francophone des Myelodysplasies (GFM), J Clin Oncol, 39, 1575, 10.1200/JCO.20.02342 · DOI · Paper page
- Daver, 2022, Tolerability and efficacy of the first-in-class anti-CD47 antibody magrolimab combined with azacitidine in frontline TP53m AML patients: phase 1b results, J Clin Oncol, 40, 7020, 10.1200/JCO.2022.40.16_suppl.7020 · DOI
- Daver, 2021, Phase I/II study of azacitidine (AZA) with venetoclax (VEN) and magrolimab (Magro) in patients (pts) with newly diagnosed older/unfit or high-risk acute myeloid leukemia (AML) and relapsed/refractory (R/R) AML, Blood, 138, 371, 10.1182/blood-2021-153638 · DOI
- Brunner, 2021, Efficacy and safety of sabatolimab (MBG453) in combination with hypomethylating agents (HMAs) in patients (Pts) with very high/high-risk myelodysplastic syndrome (vHR/HR-MDS) and acute myeloid leukemia (AML): final analysis from a phase Ib study, Blood, 138, 244, 10.1182/blood-2021-146039 · DOI
- Vadakekolathu, 2020, TP53 abnormalities correlate with immune infiltration and associate with response to flotetuzumab immunotherapy in AML, Blood Adv, 4, 5011, 10.1182/bloodadvances.2020002512 · DOI
- Uy, 2021, Flotetuzumab as salvage immunotherapy for refractory acute myeloid leukemia, Blood, 137, 751, 10.1182/blood.2020007732 · DOI · Paper page
- Takahashi, 2016, Clinical implications of TP53 mutations in myelodysplastic syndromes treated with hypomethylating agents, Oncotarget, 7, 14172, 10.18632/oncotarget.7290 · DOI
- Chang, 2017, TP53 mutations predict decitabine-induced complete responses in patients with myelodysplastic syndromes, Br J Haematol, 176, 600, 10.1111/bjh.14455 · DOI
- Welch, 2016, TP53 and decitabine in acute myeloid leukemia and myelodysplastic syndromes, N Engl J Med, 375, 2023, 10.1056/NEJMoa1605949 · DOI · Paper page
- Bazinet, 2022, Azacitidine plus venetoclax in patients with high-risk myelodysplastic syndromes or chronic myelomonocytic leukaemia: phase 1 results of a single-centre, dose-escalation, dose-expansion, phase 1–2 study, Lancet Haematol, 9, e756, 10.1016/S2352-3026(22)00216-2 · DOI
- Zeidan, 2023, A phase 1b study of venetoclax and azacitidine combination in patients with relapsed or refractory myelodysplastic syndromes, Am J Hematol, 98, 272, 10.1002/ajh.26771 · DOI
- Sallman, 2022, Magrolimab in combination with azacitidine for untreated higher-risk myelodysplastic syndromes (HR-MDS): 5F9005 phase 1b study results, J Clin Oncol, 40, 7017, 10.1200/JCO.2022.40.16_suppl.7017 · DOI
- Mishra, 2021, Phase II trial of eprenetapopt (APR-246) in combination with azacitidine (AZA) as maintenance therapy for TP53 mutated AML or MDS following allogeneic stem cell transplantation (SCT), Blood, 138, 409, 10.1182/blood-2021-147962 · DOI
- Hou, 2015, TP53 mutations in de novo acute myeloid leukemia patients: longitudinal follow-ups show the mutation is stable during disease evolution, Blood Cancer J, 5, 10.1038/bcj.2015.59 · DOI · Paper page
- Lancet, 2018, CPX-351 (cytarabine and daunorubicin) liposome for injection versus conventional cytarabine plus daunorubicin in older patients with newly diagnosed secondary acute myeloid leukemia, J Clin Oncol, 36, 2684, 10.1200/JCO.2017.77.6112 · DOI · Paper page
- Wei, 2020, Oral azacitidine maintenance therapy for acute myeloid leukemia in first remission, N Engl J Med, 383, 2526, 10.1056/NEJMoa2004444 · DOI · Paper page
- Jin, 2020, 5-azacitidine induces NOXA to prime AML cells for venetoclax-mediated apoptosis, Clin Cancer Res, 26, 3371, 10.1158/1078-0432.CCR-19-1900 · DOI · Paper page
- Bogenberger, 2015, Ex vivo activity of BCL-2 family inhibitors ABT-199 and ABT-737 combined with 5-azacytidine in myeloid malignancies, Leuk Lymphoma, 56, 226, 10.3109/10428194.2014.910657 · DOI
- Garcia, 2020, Safety, efficacy, and patient-reported outcomes of venetoclax in combination with azacitidine for the treatment of patients with higher-risk myelodysplastic syndrome: a phase 1b study, Blood, 136, 55, 10.1182/blood-2020-139492 · DOI
- Poire, 2017, Allogeneic stem cell transplantation in adult patients with acute myeloid leukaemia and 17p abnormalities in first complete remission: a study from the Acute Leukemia Working Party (ALWP) of the European Society for Blood and Marrow Transplantation (EBMT), J Hematol Oncol, 10, 20, 10.1186/s13045-017-0393-3 · DOI
- Gilleece, 2018, Am J Hematol, 93, 1142, 10.1002/ajh.25211 · DOI
- Walter, 2013, Significance of minimal residual disease before myeloablative allogeneic hematopoietic cell transplantation for AML in first and second complete remission, Blood, 122, 1813, 10.1182/blood-2013-06-506725 · DOI · Paper page
- Gilleece, 2021, Measurable residual disease status and outcome of transplant in acute myeloid leukemia in second complete remission: a study by the acute leukemia working party of the EBMT, Blood Cancer J, 11, 88, 10.1038/s41408-021-00479-3 · DOI
- Chan, 2019, Impact of TP53 gene mutation clearance and conditioning intensity on outcome in MDS or AML patients prior to allogeneic stem cell transplantation, Blood, 134, 149, 10.1182/blood-2019-131530 · doi:10.1182/blood-2019-131530
- Scott, 2020, Allogeneic stem cell transplantation for high-risk acute leukemia and maintenance therapy: no time to waste, Blood Adv, 4, 3200, 10.1182/bloodadvances.2019000388 · doi:10.1182/bloodadvances.2019000388
- Burchert, 2020, Sorafenib maintenance after allogeneic hematopoietic stem cell transplantation for acute myeloid leukemia with FLT3-internal tandem duplication mutation (SORMAIN), J Clin Oncol, 38, 2993, 10.1200/JCO.19.03345 · DOI · Paper page
- Sahasrabudhe, 2022, Novel investigational approaches for high-risk genetic subsets of AML: TP53, KMT2A, FLT3, Hematology Am Soc Hematol Educ Program, 2022, 15, 10.1182/hematology.2022000325 · DOI
- Bykov, 2016, Targeting of mutant p53 and the cellular redox balance by APR-246 as a strategy for efficient cancer therapy, Front Oncol, 6, 21, 10.3389/fonc.2016.00021 · DOI · Paper page
- Takimoto, 2019, The macrophage ‘Do not eat me’ signal, CD47, is a clinically validated cancer immunotherapy target, Ann Oncol, 30, 486, 10.1093/annonc/mdz006 · DOI
- Swoboda, 2020, The promise of macrophage directed checkpoint inhibitors in myeloid malignancies, Best Pract Res Clin Haematol, 33, 10.1016/j.beha.2020.101221 · DOI
- Daver, 2022, Phase I/II study of azacitidine (AZA) with venetoclax (VEN) and magrolimab (Magro) in patients (pts) with newly diagnosed (ND) older/unfit or high-risk acute myeloid leukemia (AML) and relapsed/refractory (R/R) AML, Blood, 140, 141, 10.1182/blood-2022-170188 · DOI
- Chao, 2019, Therapeutic targeting of the macrophage immune checkpoint CD47 in myeloid malignancies, Front Oncol, 9, 1380, 10.3389/fonc.2019.01380 · DOI · Paper page
- Brierley, 2019, The effects of monoclonal anti-CD47 on RBCs, compatibility testing, and transfusion requirements in refractory acute myeloid leukemia, Transfusion, 59, 2248, 10.1111/trf.15397 · DOI
- Sallman, 2019, The first-in-class anti-CD47 antibody magrolimab (5F9) in combination with azacitidine is effective in MDS and AML patients: ongoing phase 1b results, Blood, 134, 569, 10.1182/blood-2019-126271 · DOI · Paper page
- Zeidan, 2021, TIM-3 pathway dysregulation and targeting in cancer, Expert Rev Anticancer Ther, 21, 523, 10.1080/14737140.2021.1865814 · DOI
- Zeidan, 2021, Sabatolimab (MBG453) combination treatment regimens for patients (pts) with higher-risk myelodysplastic syndromes (HR-MDS): the MDS studies in the stimulus immuno-myeloid clinical trial program, Blood, 138, 4669, 10.1182/blood-2021-145626 · doi:10.1182/blood-2021-145626
- Al-Hussaini, 2016, Targeting CD123 in acute myeloid leukemia using a T-cell-directed dual-affinity retargeting platform, Blood, 127, 122, 10.1182/blood-2014-05-575704 · DOI · Paper page
- Chichili, 2015, A CD3xCD123 bispecific DART for redirecting host T cells to myelogenous leukemia: preclinical activity and safety in nonhuman primates, Sci Transl Med, 7, 289, 10.1126/scitranslmed.aaa5693 · DOI · Paper page
- Erba, 2019, Phase 1b study of the MDM2 inhibitor AMG 232 with or without trametinib in relapsed/refractory acute myeloid leukemia, Blood Adv, 3, 1939, 10.1182/bloodadvances.2019030916 · DOI · Paper page
- Mirgayazova, 2020, Therapeutic editing of the TP53 gene: is CRISPR/Cas9 an option?, Genes (Basel), 11, 10.3390/genes11060704 · DOI
- Maute, 2022, CD47-SIRPalpha-targeted therapeutics: status and prospects, Immunooncol Technol, 13
- Abaigar, 2016, Chromothripsis is a recurrent genomic abnormality in high-risk myelodysplastic syndromes, PLoS One, 11, 10.1371/journal.pone.0164370 · DOI
- Forment, 2012, Chromothripsis and cancer: causes and consequences of chromosome shattering, Nat Rev Cancer, 12, 663, 10.1038/nrc3352 · DOI · Paper page
Cited by
The TP53 tumor suppressor gene: From molecular biology to clinical investigations
Baliakas, P., & Soussi, T. (2025) · Journal of Internal Medicine · doi:10.1111/joim.20106 · Cited by 50
Metadata
- Authors
- Marks, J. A., Wang, X., Fenu, E. M., Bagg, A., & Lai, C.
- Venue
- Blood Reviews
- Publisher
- Elsevier BV
- Published
- 2023-07
- Volume
- 60
- Pages
- 101055
- ISSN
- 0268-960X
- Cited by
- 20
- References
- 31
- Language
- en
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
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- The paper
- Marks, J. A., Wang, X., Fenu, E. M., Bagg, A., & Lai, C. (2023). TP53 in AML and MDS: The new (old) kid on the block. Blood Reviews. https://doi.org/10.1016/j.blre.2023.101055
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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