ATRA resolves the differentiation block in t(15;17) acute myeloid leukemia by restoring PU.1 expression
Open accessAbstract
Tightly regulated expression of the transcription factor PU.1 is crucial for normal hematopoiesis. PU.1 knockdown mice develop acute myeloid leukemia (AML), and PU.1 mutations have been observed in some populations of patients with AML. Here we found that conditional expression of promyelocytic leukemia-retinoic acid receptor alpha (PML-RARA), the protein encoded by the t(15;17) translocation found in acute promyelocytic leukemia (APL), suppressed PU.1 expression, while treatment of APL cell lines and primary cells with all-trans retinoic acid (ATRA) restored PU.1 expression and induced neutrophil differentiation. ATRA-induced activation was mediated by a region in the PU.1 promoter to which CEBPB and OCT-1 binding were induced. Finally, conditional expression of PU.1 in human APL cells was sufficient to trigger neutrophil differentiation, whereas reduction of PU.1 by small interfering RNA (siRNA) blocked ATRA-induced neutrophil differentiation. This is the first report to show that PU.1 is suppressed in acute promyelocytic leukemia, and that ATRA restores PU.1 expression in cells harboring t(15;17).
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
ATRA restores myeloid differentiation by resolving PU.1 expression in AML.
“all-trans retinoic acid (ATRA) restores myeloid differentiation by resolving PU.1 expression in AML (31)”
From FBW7 Inhibits Myeloid Differentiation in Acute Myeloid Leukemia via GSK3-Dependent Ubiquitination of PU.1 (2021) · cites this paper as [31]
The Introduction and Discussion report that ATRA restores PU.1 expression and induces myeloid differentiation in PML-RARA-positive, t(15;17) acute promyelocytic leukemia cells. The claim extends that finding to AML generally, which the paper does not establish. (LLM, conf=0.88)
Experimental — accuracy not yet measuredModerate PU.1 inhibition is common in AML patients.
“yet moderate PU.1 inhibition is common in AML patients”
From Minimal PU.1 reduction induces a preleukemic state and promotes development of acute myeloid leukemia (2015) · cites this paper as [18]
The Results (page not available) report that the t(15;17) APL subgroup had approximately half the PU.1 RNA of AML-M2 and AML-M4 patients, although the difference was not statistically significant. The Discussion describes PU.1 suppression in APL, but the paper does not establish that moderate inhibition is common across AML patients. (LLM, conf=0.87)
Experimental — accuracy not yet measuredSeveral AML-typic mutations, such as NPM1c, FLT3-ITD/TDK, or AML1-ETO, moderately compromise the regulation or function of PU.1.
“Several AML-typic mutations, such as NPM1c, FLT3-ITD/TDK, or AML1-ETO, moderately compromise the regulation or function of PU.1 (19–22)”
From PU.1-Dependent Enhancer Inhibition Separates <i>Tet2</i> -Deficient Hematopoiesis from Malignant Transformation (2022) · cites this paper as [22]
The Discussion (page unavailable) reports that the AML-associated PML-RARA fusion suppresses PU.1, supporting the general point that an AML-associated genetic alteration can affect PU.1. The paper does not address NPM1c, FLT3-ITD/TDK, or AML1-ETO, or establish that those mutations moderately compromise PU.1 regulation or function. (LLM, conf=0.82)
Experimental — accuracy not yet measuredDespite moderately reduced PU.1 mRNA levels, its broader transcriptional network appears intact.
“Despite moderately reduced PU.1 mRNA levels, its broader transcriptional network appears intact, in line with the essentiality of the transcription factor in maintaining normal and malignant hematopoiesis (20, 22, 23, 46, 48).”
From PU.1-Dependent Enhancer Inhibition Separates <i>Tet2</i> -Deficient Hematopoiesis from Malignant Transformation (2022) · cites this paper as [22]
The Results report approximately half as much PU.1 RNA in t(15;17) AML samples as in AML-M2 and AML-M4 samples, although the difference was not statistically significant. The Discussion describes PU.1 as crucial to normal myeloid development and implicated in leukemia. The paper does not show that the broader PU.1 transcriptional network remains intact; its Results instead report loss of binding activity at a PU.1 target site in one APL cell line. Page numbers were not available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredPU.1 is inhibited in most patients with AML through various molecular pathways.
“PU.1 is also inhibited in most patients with AML through various molecular pathways (19, 20, 22, 46, 47).”
From PU.1-Dependent Enhancer Inhibition Separates <i>Tet2</i> -Deficient Hematopoiesis from Malignant Transformation (2022) · cites this paper as [22]
The Discussion reports PU.1 suppression in acute promyelocytic leukemia (APL) and mentions PU.1 mutations in patients with other AML subtypes. It does not establish that PU.1 is inhibited in most patients with AML; the Results found a nonsignificant difference in PU.1 RNA between the t(15;17) group and two other AML groups. (LLM, conf=0.87)
Experimental — accuracy not yet measured
ATRA restores PU.1 expression in AMLs bearing t(15;17).
“Moreover, because ATRA also restores PU.1 expression in AMLs bearing t(15;17) (31), we hypothesized that GSK3b negatively regulated PU.1 levels leading to AML”
From FBW7 Inhibits Myeloid Differentiation in Acute Myeloid Leukemia via GSK3-Dependent Ubiquitination of PU.1 (2021) · cites this paper as [31]
A wide array of myeloid leukemia-associated oncogenic lesions can interfere with PU.1 expression or function, including PML/RARA, AML1-ETO, NPM1c, CEBPA, and mitogenic kinase mutations in BCR/ABL and Flt3ITD.
“a wide array of myeloid leukemia–associated oncogenic lesions can interfere with PU.1 expression or function, including PML/RARA, AML1-ETO, NPM1c, CEBPA, and mitogenic kinase mutations in BCR/ABL and Flt3ITD (Gerloff et al., 2015; McKenzie et al., 2019; Mueller et al., 2006; Noguera et al., 2016; Vangala et al., 2003; Yang et al., 2012).”
From PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress (2021) · cites this paper as Mueller et al., 2006
In acute promyelocytic leukaemia, the PML-RAR-α fusion protein lowers PU.1 expression.
“Likewise, the expression of the PML-RAR-α fusion protein in acute promyelocytic leukaemia (APL) reduces PU.1 expression [122].”
From PU.1 and partners: regulation of haematopoietic stem cell fate in normal and malignant haematopoiesis (2009) · cites this paper as [122]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Cites
Requirement of transcription factor PU.1 in the development of multiple hematopoietic lineages
Scott, E. W., Simon, M. C., Anastasi, J., & Singh, H. (1994) · Science · doi:10.1126/science.8079170 · Cited by 1,532 · see citing works
Targeted disruption of the PU.1 gene results in multiple hematopoietic abnormalities
McKercher, S. R., Torbett, B. E., Anderson, K. L., Henkel, G. W., Vestal, D. J., Baribault, H., Klemsz, M., Feeney, A. J., Wu, G. E., Paige, C. J., et al. (1996) · The EMBO Journal · doi:10.1002/j.1460-2075.1996.tb00949.x · Cited by 1,130 · see citing works
Role of the histone deacetylase complex in acute promyelocytic leukaemia
Lin, R. J., Nagy, L., Inoue, S., Shao, W., Miller, W. H., & Evans, R. M. (1998) · Nature · doi:10.1038/35895 · Cited by 1,060 · see citing works
Melnick, A. M., & Licht, J. D. (1999) · Blood · doi:10.1182/blood.v93.10.3167.410k44_3167_3215 · Cited by 1,024 · see citing works
Grignani, F., Matteis, S. D., Nervi, C., Tomassoni, L., Gelmetti, V., Cioce, M., Fanelli, M., Ruthardt, M., Ferrara, F. F., Zamir, I., et al. (1998) · Nature · doi:10.1038/35901 · Cited by 1,004 · see citing works
The macrophage and B cell-specific transcription factor PU.1 is related to the ets oncogene
Klemsz, M. J., McKercher, S. R., Celada, A., Van Beveren, C., & Maki, R. A. (1990) · Cell · doi:10.1016/0092-8674(90)90219-5 · Cited by 954 · see citing works
Lanotte, M., Martin-Thouvenin, V., Najman, S. J., Balerini, P., Valensi, F., & Berger, R. (1991) · Blood · doi:10.1182/blood.v77.5.1080.1080 · Cited by 881 · see citing works
Transcription Factors, Normal Myeloid Development, and Leukemia
Tenen, D. G., Hromas, R., Licht, J. D., & Zhang, D.-E. (1997) · Blood · doi:10.1182/blood.v90.2.489 · Cited by 735 · see citing works
Self-citationGrignani, F., Ferrucci, P. F., Testa, U., Talamo, G., Fagioli, M., Alcalay, M., Mencarelli, A., Grignani, F., Peschle, C., Nicoletti, I., et al. (1993) · Cell · doi:10.1016/0092-8674(93)80044-f · Cited by 579 · see citing works
Acute myeloid leukemia induced by graded reduction of a lineage-specific transcription factor, PU.1.
Rosenbauer, F., Wagner, K., Kutok, J. L., Iwasaki, H., Le Beau, M. M., Okuno, Y., Akashi, K., Fiering, S., & Tenen, D. G. (2004) · Nature Genetics · doi:10.1038/ng1361 · Cited by 506 · see citing works
Self-citationPU.1 induces myeloid lineage commitment in multipotent hematopoietic progenitors
Nerlov, C., & Graf, T. (1998) · Genes & Development · doi:10.1101/gad.12.15.2403 · Cited by 449 · see citing works
Zhang, D. E., Hetherington, C. J., Chen, H. M., & Tenen, D. G. (1994) · Molecular and Cellular Biology · doi:10.1128/mcb.14.1.373 · Cited by 411 · see citing works
Self-citationZhang, D.-E., Hetherington, C. J., Chen, H.-M., & Tenen, D. G. (1994) · Molecular and Cellular Biology · doi:10.1128/mcb.14.1.373-381.1994 · Cited by 411 · see citing works
Self-citationSmith, L., Hohaus, S., Gonzalez, D., Dziennis, S., & Tenen, D. (1996) · Blood · doi:10.1182/blood.v88.4.1234.bloodjournal8841234 · Cited by 332 · see citing works
Self-citationDynamic regulation of PU.1 expression in multipotent hematopoietic progenitors
Nutt, S. L., Metcalf, D., D'Amico, A., Polli, M., & Wu, L. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20041535 · Cited by 325 · see citing works
Heterozygous PU.1 mutations are associated with acute myeloid leukemia
Mueller, B. U., Pabst, T., Osato, M., Asou, N., Johansen, L. M., Minden, M. D., Behre, G., Hiddemann, W., Ito, Y., & Tenen, D. G. (2002) · Blood · doi:10.1182/blood.v100.3.998 · Cited by 243 · see citing works
Self-citationNeutrophils and monocytes express high levels of PU.1 (Spi-1) but not Spi-B
Chen, H., Zhang, P., Voso, M., Hohaus, S., Gonzalez, D., Glass, C., Zhang, D., & Tenen, D. (1995) · Blood · doi:10.1182/blood.v85.10.2918.bloodjournal85102918 · Cited by 216 · see citing works
Self-citationHematopoietic lineage- and stage-restricted expression of the ETS oncogene family member PU.1
Hromas, R., Orazi, A., Neiman, R., Maki, R., Van Beveran, C., Moore, J., & Klemsz, M. (1993) · Blood · doi:10.1182/blood.v82.10.2998.2998 · Cited by 216 · see citing works
(1995) · PubMed · Cited by 206 · see citing works
Self-citationSpi-1/PU.1 Transgenic Mice Develop Multistep Erythroleukemias
Moreau-Gachelin, F., Wendling, F., Molina, T., Denis, N., Titeux, M., Grimber, G., Briand, P., Vainchenker, W., & Tavitian, A. (1996) · Molecular and Cellular Biology · doi:10.1128/mcb.16.5.2453 · Cited by 189 · see citing works
Park, D. J., Chumakov, A. M., Vuong, P. T., Chih, D. Y., Gombart, A. F., Miller, W. H., & Koeffler, H. P. (1999) · Journal of Clinical Investigation · doi:10.1172/jci2887 · Cited by 187 · see citing works
Devroe, E., & Silver, P. A. (2002) · BMC Biotechnology · doi:10.1186/1472-6750-2-15 · Cited by 185 · see citing works
Nervi, C., Ferrara, F. F., Fanelli, M., Rippo, M. R., Tomassini, B., Ferrucci, P. F., Ruthardt, M., Gelmetti, V., Gambacorti-Passerini, C. B., Diverio, D., et al. (1998) · PubMed · doi:10.1182/blood.v92.7.2244 · Cited by 171 · see citing works
C/EBPβ: a major PML–RARA‐responsive gene in retinoic acid‐induced differentiation of APL cells
Duprez, E., Wagner, K., Koch, H., & Tenen, D. G. (2003) · The EMBO Journal · doi:10.1093/emboj/cdg556 · Cited by 164 · see citing works
Self-citationNeutrophils Deficient in PU.1 Do Not Terminally Differentiate or Become Functionally Competent
Anderson, K. L., Smith, K. A., Pio, F., Torbett, B. E., & Maki, R. A. (1998) · Blood · doi:10.1182/blood.v92.5.1576 · Cited by 142 · see citing works
Inhibition of hematopoiesis by competitive binding of transcription factor PU.1
Voso, M. T., Burn, T. C., Wulf, G., Lim, B., Leone, G., & Tenen, D. G. (1994) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.91.17.7932 · Cited by 141 · see citing works
Self-citationCook, W. D., McCaw, B. J., Herring, C., John, D. L., Foote, S. J., Nutt, S. L., & Adams, J. M. (2004) · Blood · doi:10.1182/blood-2004-06-2234 · Cited by 140 · see citing works
CCAAT/Enhancer binding proteins repress the leukemic phenotype of acute myeloid leukemia
Truong, B.-T. H. (2002) · Blood · doi:10.1182/blood-2002-05-1374 · Cited by 103 · see citing works
Visualizing PU.1 activity during hematopoiesis
Back, J., Allman, D., Chan, S., & Kastner, P. (2005) · Experimental Hematology · doi:10.1016/j.exphem.2004.12.010 · Cited by 97 · see citing works
Suraweera, N., Meijne, E., Moody, J., Carvajal-Carmona, L. G., Yoshida, K., Pollard, P., Fitzgibbon, J., Riches, A., van Laar, T., Huiskamp, R., et al. (2005) · Oncogene · doi:10.1038/sj.onc.1208422 · Cited by 60 · see citing works
Octamer Binding Factors and Their Coactivator Can Activate the Murine PU.1 (spi-1) Promoter
Chen, H.-M., Zhang, P., Radomska, H. S., Hetherington, C. J., Zhang, D.-E., & Tenen, D. G. (1996) · Journal of Biological Chemistry · doi:10.1074/jbc.271.26.15743 · Cited by 59 · see citing works
Self-citationKishi, K., Toba, K., Azegami, T., Tsukada, N., Uesugi, Y., Masuko, M., Niwano, H., Hashimoto, S., Sakaue, M., Furukawa, T., et al. (1998) · PubMed · Cited by 48 · see citing works
Kistler, B., Pfisterer, P. H., & Wirth, T. C. (1995) · PubMed · Cited by 44 · see citing works
Are PU.1 mutations frequent genetic events in acute myeloid leukemia (AML)?
Lamandin, C., Sagot, C., Roumier, C., Lepelley, P., De Botton, S., Cosson, A., Fenaux, P., & Preudhomme, C. (2002) · Blood · doi:10.1182/blood-2002-08-2563 · Cited by 38 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Transcription factors in myeloid development: balancing differentiation with transformation
Rosenbauer, F., & Tenen, D. G. (2007) · Nature Reviews Immunology · doi:10.1038/nri2024 · Cited by 606 · see citing works
Self-citationDifferentiation therapy of leukemia: 3 decades of development.
Nowak, D., Stewart, D., & Koeffler, H. P. (2009) · Blood · doi:10.1182/blood-2009-01-198911 · Cited by 348 · see citing works
Fukao, T., Fukuda, Y., Kiga, K., Sharif, J., Hino, K., Enomoto, Y., Kawamura, A., Nakamura, K., Takeuchi, T., & Tanabe, M. (2007) · Cell · doi:10.1016/j.cell.2007.02.048 · Cited by 292 · see citing works
Leukaemogenesis: more than mutant genes
Chen, J., Odenike, O. M., & Rowley, J. D. (2009) · Nature reviews. Cancer · doi:10.1038/nrc2765 · Cited by 314 · see citing works
Caiado, F., Pietras, E. M., & Manz, M. G. (2021) · Journal of Experimental Medicine · doi:10.1084/jem.20201541 · Cited by 289 · see citing works
Pulikkan, J. A., Dengler, V., Peramangalam, P. S., Zada, A. A. P., Müller‐Tidow, C., Bohlander, S. K., Tenen, D. G., & Behre, G. (2009) · Blood · doi:10.1182/blood-2009-08-240101 · Cited by 284 · see citing works
Self-citationNagy, L., Szántó, A., Szatmári, I., & Széles, L. (2012) · Physiological Reviews · doi:10.1152/physrev.00004.2011 · Cited by 215 · see citing works
The role of PU.1 and GATA-1 transcription factors during normal and leukemogenic hematopoiesis
Burda, P., Laslo, P., & Stopka, T. (2010) · Leukemia · doi:10.1038/leu.2010.104 · Cited by 184 · see citing works
Ebralidze, A. K., Guibal, F. C., Steidl, U. G., Zhang, P., Lee, S., Bartholdy, B., Alberich-Jordà, M., Petkova, V., Rosenbauer, F., Huang, G., et al. (2008) · Genes & Development · doi:10.1101/gad.1654808 · Cited by 176 · see citing works
Self-citationWang, K., Wang, P., Shi, J., Zhu, X., He, M., Jia, X., Yang, X., Qiu, F., Jin, W. Y., Qian, M., et al. (2010) · Cancer Cell · doi:10.1016/j.ccr.2009.12.045 · Cited by 162 · see citing works
Viny, A. D., Bowman, R. L., Liu, Y., Lavallée, V., Eisman, S. E., Xiao, W., Durham, B. H., Navitski, A., Park, J., Braunstein, S., et al. (2019) · Cell stem cell · doi:10.1016/j.stem.2019.08.003 · Cited by 163 · see citing works
Heuser, M., Argiropoulos, B., Kuchenbauer, F. C., Yung, E., Piper, J., Fung, S., Schlenk, R. F., Döhner, K., Hinrichsen, T., Rudolph, C., et al. (2007) · Blood · doi:10.1182/blood-2007-03-080523 · Cited by 148 · see citing works
Will, B., Vogler, T. O., Narayanagari, S., Bartholdy, B., Todorova, T. I., da Silva Ferreira, M., Chen, J., Yu, Y., Mayer, J., Barreyro, L., et al. (2015) · Nature Medicine · doi:10.1038/nm.3936 · Cited by 127 · see citing works
Guibal, F. C., Alberich-Jorda, M., Hirai, H., Ebralidze, A., Levantini, E., Di Ruscio, A., Zhang, P., Santana-Lemos, B. A., Neuberg, D., Wagers, A. J., et al. (2009) · Blood · doi:10.1182/blood-2008-10-182071 · Cited by 126 · see citing works
Self-citationPharmacological inhibition of the transcription factor PU.1 in leukemia
Antony-Debré, I., Paul, A., Leite, J., Mitchell, K., Kim, H. M., Carvajal, L. A., Todorova, T. I., Huang, K., Kumar, A., Farahat, A. A., et al. (2017) · Journal of Clinical Investigation · doi:10.1172/jci92504 · Cited by 120 · see citing works
C/EBPα binds and activates the PU.1 distal enhancer to induce monocyte lineage commitment
Yeamans, C., Wang, D., Paz-Priel, I., Torbett, B. E., Tenen, D. G., & Friedman, A. D. (2007) · Blood · doi:10.1182/blood-2007-03-080291 · Cited by 118 · see citing works
Self-citationSteidl, U., Steidl, C., Ebralidze, A., Chapuy, B., Han, H.-J., Will, B., Rosenbauer, F., Becker, A., Wagner, K., Koschmieder, S., et al. (2007) · Journal of Clinical Investigation · doi:10.1172/jci30525 · Cited by 114 · see citing works
Self-citationComplexity of CEBPA Dysregulation in Human Acute Myeloid Leukemia
Pabst, T., & Mueller, B. U. (2009) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-08-2941 · Cited by 115 · see citing works
Self-citationZeng, C., Yu, X., Lai, J., Yang, L., Chen, S., & Li, Y. (2015) · Journal of Hematology & Oncology · doi:10.1186/s13045-015-0223-4 · Cited by 105 · see citing works
Transcriptional dysregulation during myeloid transformation in AML
Pabst, T., & Mueller, B. U. (2007) · Oncogene · doi:10.1038/sj.onc.1210765 · Cited by 104 · see citing works
Self-citationPU.1: A crucial and versatile player in hematopoiesis and leukemia
Kastner, P., & Chan, S. (2008) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2007.01.026 · Cited by 101 · see citing works
The Transcription Factor PU.1 is a Critical Regulator of Cellular Communication in the Immune System
Turkistany, S. A., & DeKoter, R. P. (2011) · Archivum Immunologiae et Therapiae Experimentalis · doi:10.1007/s00005-011-0147-9 · Cited by 96 · see citing works
Koya, J., Kataoka, K., Sato, T., Bando, M., Kato, Y., Tsuruta-Kishino, T., Kobayashi, H., Narukawa, K., Miyoshi, H., Shirahige, K., et al. (2016) · Nature Communications · doi:10.1038/ncomms10924 · Cited by 95 · see citing works
Interconversion between Tumorigenic and Differentiated States in Acute Myeloid Leukemia
McKenzie, M. D., Ghisi, M., Oxley, E. P., Ngo, S., Cimmino, L., Esnault, C., Liu, R., Salmon, J. M., Bell, C. C., Ahmed, N., et al. (2019) · Cell Stem Cell · doi:10.1016/j.stem.2019.07.001 · Cited by 91 · see citing works
PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress
Chavez, J. S., Rabe, J. L., Loeffler, D., Higa, K. C., Hernandez, G., Mills, T. S., Ahmed, N., Gessner, R. L., Ke, Z., Idler, B. M., et al. (2021) · Journal of Experimental Medicine · doi:10.1084/jem.20201169 · Cited by 91 · see citing works
“On the other hand, loss-of function mutations in PU.1 itself are rarely observed in hematological malignancy, though a wide array of myeloid leukemia-associated oncogenic lesions can interfere with PU.1 expression or function, including PML/RARA, AML1-ETO, NPM1c, and mitogenic kinase mutations in BCR/ABL and Flt3ITD (…”
BackgroundTranscriptional Control of Natural Killer Cell Development and Function
Hesslein, D. G. T., & Lanier, L. L. (2011) · Advances in immunology · doi:10.1016/b978-0-12-387664-5.00002-9 · Cited by 86 · see citing works
Marchis, M. D. D., Ballarino, M., Salvatori, B., Puzzolo, M., Bozzoni, I., & Fatica, A. (2009) · Leukemia · doi:10.1038/leu.2008.372 · Cited by 89 · see citing works
Epigenetic gene regulation in stem cells and correlation to cancer
Mathews, L., Crea, F., & Farrar, W. L. (2009) · Differentiation · doi:10.1016/j.diff.2009.04.002 · Cited by 76 · see citing works
Gupta, P., Gurudutta, G. U., Saluja, D., & Tripathi, R. P. (2009) · Journal of Cellular and Molecular Medicine · doi:10.1111/j.1582-4934.2009.00757.x · Cited by 74 · see citing works
Is PU.1 a dosage-sensitive regulator of haemopoietic lineage commitment and leukaemogenesis?
Dakic, A., Wu, L., & Nutt, S. L. (2007) · Trends in Immunology · doi:10.1016/j.it.2007.01.006 · Cited by 72 · see citing works
Retinoic acid receptors, hematopoiesis and leukemogenesis
Collins, S. J. (2008) · Current Opinion in Hematology · doi:10.1097/moh.0b013e3283007edf · Cited by 71 · see citing works
Genome-wide functions of PML–RARα in acute promyelocytic leukaemia
Saeed, S., Logie, C., Stunnenberg, H. G., & Martens, J. H. A. (2011) · British Journal of Cancer · doi:10.1038/sj.bjc.6606095 · Cited by 63 · see citing works
JMJD3 facilitates C/EBPβ-centered transcriptional program to exert oncorepressor activity in AML
Yu, S., Zhu, K.-Y., Chen, J., Liu, X.-Z., Xu, P., Zhang, W., Li, Y., Guo, H., & Zhu, J. (2018) · Nature Communications · doi:10.1038/s41467-018-05548-z · Cited by 63 · see citing works
Hamid, R., & Brandt, S. J. (2009) · Molecular Oncology · doi:10.1016/j.molonc.2009.07.004 · Cited by 57 · see citing works
PU.1 controls the expression of long noncoding RNA HOTAIRM1 during granulocytic differentiation
Wei, S., Zhao, M., Wang, X., Li, Y., & Wang, K. (2016) · Journal of Hematology & Oncology · doi:10.1186/s13045-016-0274-1 · Cited by 56 · see citing works
PU.1 is linking the glycolytic enzyme HK3 in neutrophil differentiation and survival of APL cells
Federzoni, E. A., Valk, P. J. M., Torbett, B. E., Haferlach, T., Löwenberg, B., Fey, M. F., & Tschan, M. P. (2012) · Blood · doi:10.1182/blood-2011-09-378117 · Cited by 55 · see citing works
Self-citationAn Effective Model of the Retinoic Acid Induced HL-60 Differentiation Program
Tasseff, R. A., Jensen, H. A., Congleton, J., Dai, D. L., Rogers, K. V., Sagar, A., Bunaciu, R. P., Yen, A., & Varner, J. D. (2017) · Scientific Reports · doi:10.1038/s41598-017-14523-5 · Cited by 54 · see citing works
PU.1 is essential for MLL leukemia partially via crosstalk with the MEIS/HOX pathway
Zhou, J., Wu, J., Li, B., Liu, D., Yu, J., Yan, X., Zheng, S., Wang, J., Zhang, L., Zhang, L., et al. (2014) · Leukemia · doi:10.1038/leu.2013.384 · Cited by 53 · see citing works
Self-citationPendino, F., Nguyen, É., Jonassen, I., Dysvik, B., Azouz, A., Lanotte, M., Ségal-Bendirdjian, E., & Lillehaug, J. R. (2009) · Blood · doi:10.1182/blood-2008-07-170035 · Cited by 51 · see citing works
All-transretinoic acid in the treatment of pediatric acute promyelocytic leukemia
Masetti, R., Vendemini, F., Zama, D., Biagi, C., Gasperini, P., & Pession, A. (2012) · Expert Review of Anticancer Therapy · doi:10.1586/era.12.101 · Cited by 51 · see citing works
Review: genetic models of acute myeloid leukaemia
McCormack, E., Bruserud, Ø., & Gjertsen, B. T. (2008) · Oncogene · doi:10.1038/onc.2008.16 · Cited by 48 · see citing works
Verbiest, T., Bouffler, S. D., Nutt, S. L., & Badie, C. (2015) · Carcinogenesis · doi:10.1093/carcin/bgv016 · Cited by 48 · see citing works
Epigenetic control of hematopoiesis: the PU.1 chromatin connection
van Riel, B., & Rosenbauer, F. (2014) · Biological Chemistry · doi:10.1515/hsz-2014-0195 · Cited by 47 · see citing works
Retinoid receptor signaling and autophagy in acute promyelocytic leukemia
Orfali, N., McKenna, S. L., Cahill, M. R., Gudas, L. J., & Mongan, N. P. (2014) · Experimental Cell Research · doi:10.1016/j.yexcr.2014.03.018 · Cited by 47 · see citing works
Curik, N., Burda, P., Vargová, K., Pospíšil, V., Beličková, M., Vlckova, P., Savvulidi, F. G., Nečas, E., Hajkova, H., Haškovec, C., et al. (2012) · Leukemia · doi:10.1038/leu.2012.47 · Cited by 45 · see citing works
CLEC5A (MDL-1) is a novel PU.1 transcriptional target during myeloid differentiation
Batliner, J., Mancarelli, M. M., Jenal, M., Reddy, V. A., Fey, M. F., Torbett, B. E., & Tschan, M. P. (2010) · Molecular Immunology · doi:10.1016/j.molimm.2010.10.016 · Cited by 44 · see citing works
Self-citationHuynh, T. T., Sultan, M., Vidovic, D., Dean, C. A., Cruickshank, B. M., Lee, K., Loung, C.-Y., Holloway, R. W., Hoskin, D. W., Waisman, D. M., et al. (2019) · Scientific Reports · doi:10.1038/s41598-019-45982-7 · Cited by 41 · see citing works
The anti-apoptotic gene BCL2A1 is a novel transcriptional target of PU.1
Jenal, M., Batliner, J., Reddy, V. A., Haferlach, T., Tobler, A., Fey, M. F., Torbett, B. E., & Tschan, M. P. (2010) · Leukemia · doi:10.1038/leu.2010.26 · Cited by 40 · see citing works
Self-citationMarchwicka, A., Cebrat, M., Sampath, P., ewski, Å. Å. ⁄., & Marcinkowska, E. (2014) · Frontiers in Oncology · doi:10.3389/fonc.2014.00125 · Cited by 41 · see citing works
Wang, Y., Jin, W., Jia, X., Luo, R., Tan, Y., Zhu, X., Yang, X., Wang, X., & Wang, K. (2014) · Cell Death and Disease · doi:10.1038/cddis.2014.388 · Cited by 40 · see citing works
Commonly dysregulated genes in murine APL cells
Yuan, W., Payton, J. E., Holt, M. S., Link, D. C., Watson, M. A., DiPersio, J. F., & Ley, T. J. (2006) · Blood · doi:10.1182/blood-2006-07-036640 · Cited by 40 · see citing works
PU.1 is regulated by NF-κB through a novel binding site in a 17 kb upstream enhancer element
Bonadies, N., Neururer, C., Steege, A., Vallabhapurapu, S., Pabst, T., & Mueller, B. (2010) · Oncogene · doi:10.1038/onc.2009.371 · Cited by 41 · see citing works
Self-citationYan, Y., Hanse, E. A., Stedman, K., Benson, J. M., Lowman, X. H., Subramanian, S., & Kelekar, A. (2016) · Cell Death and Differentiation · doi:10.1038/cdd.2016.1 · Cited by 39 · see citing works
Oncolytic Virotherapy for Hematological Malignancies
Bais, S., Bartee, E., Rahman, M. M., McFadden, G., & Cogle, C. R. (2011) · Advances in Virology · doi:10.1155/2012/186512 · Cited by 37 · see citing works
Gibson, S. E., Dong, H. Y., Advani, A. S., & Hsi, E. D. (2006) · American Journal of Clinical Pathology · doi:10.1309/ujul60upup3yje93 · Cited by 37 · see citing works
The Runx-PU.1 pathway preserves normal and AML/ETO9a leukemic stem cells
Staber, P. B., Zhang, P., Ye, M., Welner, R. S., Levantini, E., Di Ruscio, A., Ebralidze, A. K., Bach, C., Zhang, H., Zhang, J., et al. (2014) · Blood · doi:10.1182/blood-2014-01-550855 · Cited by 36 · see citing works
Self-citationSignificance of oncogenes and tumor suppressor genes in AML prognosis
Kavianpour, M., Ahmadzadeh, A., Shahrabi, S., & Saki, N. (2016) · Tumor Biology · doi:10.1007/s13277-016-5067-1 · Cited by 36 · see citing works
Sanchez, P. V., Glantz, S. T., Scotland, S., Kasner, M. T., & Carroll, M. P. (2013) · Leukemia · doi:10.1038/leu.2013.202 · Cited by 36 · see citing works
Mankaï, A., Bordron, A., Renaudineau, Y., Martins-Carvalho, C., Takahashi, S., Ghédira, I., Berthou, C., & Youinou, P. (2008) · Cancer Research · doi:10.1158/0008-5472.can-07-6446 · Cited by 36 · see citing works
Wang, X., Jin, P., Zhang, Y., & Wang, K. (2021) · Cell Death and Disease · doi:10.1038/s41419-021-03566-2 · Cited by 33 · see citing works
Brugnoli, F., Lambertini, E., Varin‐Blank, N., Piva, R., Marchisio, M., Grassilli, S., Miscia, S., Capitani, S., & Bertagnolo, V. (2009) · Experimental Cell Research · doi:10.1016/j.yexcr.2009.09.004 · Cited by 35 · see citing works
Heterozygous deletion of the PU.1 locus in human AML
Bonadies, N., Pabst, T., & Mueller, B. U. (2010) · Blood · doi:10.1182/blood-2009-03-212225 · Cited by 33 · see citing works
Self-citationSenescence is a Spi1-induced anti-proliferative mechanism in primary hematopoietic cells
Delestré, L., Cui, H., Esposito, M., Quiveron, C., Mylonas, E., Penard-Lacronique, V., Bischof, O., & Guillouf, C. (2017) · Haematologica · doi:10.3324/haematol.2016.157636 · Cited by 32 · see citing works
Hu, L., Liu, J., Ye, M., Zheng, H., Ding, C., Wang, H., Charwudzi, A., Li, M., Li, J., Zhai, Z., et al. (2020) · RNA Biology · doi:10.1080/15476286.2020.1854520 · Cited by 33 · see citing works
Mishra, M., Thacker, G., Sharma, A., Singh, A. K., Upadhyay, V., Sanyal, S., Verma, S. P., Tripathi, A. K., Bhatt, M. L. B., & Trivedi, A. K. (2021) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-20-0268 · Cited by 30 · see citing works
Lentiviral PU.1 overexpression restores differentiation in myeloid leukemic blasts
Durual, S., Rideau, A., Ruault-Jungblut, S., Cossali, D., Beris, P., Piguet, V, & Matthes, T. (2007) · Leukemia · doi:10.1038/sj.leu.2404645 · Cited by 30 · see citing works
Zhang, J., Song, L., Huang, Y., Zhao, Q. L., Zhao, K.-W., & Chen, G. (2008) · Haematologica · doi:10.3324/haematol.13096 · Cited by 30 · see citing works
Miranda, M. B., Redner, R. L., & Johnson, D. E. (2007) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-07-0514 · Cited by 30 · see citing works
NDRG1 contributes to retinoic acid-induced differentiation of leukemic cells.
Chen, S., Han, Y.-H., Zheng, Y., Zhao, M., Yan, H., Zhao, Q., Chen, G.-Q., & Li, D. (2009) · Leukemia research : a Forum for Studies on Leukemia and Normal Hemopoiesis · doi:10.1016/j.leukres.2008.10.016 · Cited by 25 · see citing works
Intrinsic disorder controls two functionally distinct dimers of the master transcription factor PU.1
Xhani, S., Lee, S., Kim, H. M., Wang, S., Esaki, S., Ha, V. L., Khanezarrin, M., Fernandez, G. L., Albrecht, A. V., Aramini, J. M., et al. (2020) · Science Advances · doi:10.1126/sciadv.aay3178 · Cited by 29 · see citing works
Burda, P., Čuřík, N., Kokavec, J., Bašová, P., Mikulenková, D., Skoultchi, A. I., Zavadil, J., & Stopka, T. (2009) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-09-0031 · Cited by 28 · see citing works
Vezzali, F., Grassilli, S., Lambertini, E., Brugnoli, F., Patergnani, S., Nika, E., Piva, R., Pinton, P., Capitani, S., & Bertagnolo, V. (2018) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.13594 · Cited by 26 · see citing works
Matsushita, H., Nakajima, H., Nakamura, Y., Tsukamoto, H., Tanaka, Y., Gui-lan, J., Yabe, M., Asai, S., Ono, R., Nosaka, T., et al. (2008) · Oncogene · doi:10.1038/onc.2008.285 · Cited by 25 · see citing works
Orfali, N. M., O’Donovan, T. R., Cahill, M. R., Benjamin, D., Nanus, D. M., McKenna, S. L., Gudas, L. J., & Mongan, N. P. (2019) · European Journal Of Haematology · doi:10.1111/ejh.13367 · Cited by 25 · see citing works
Humbert, M., Federzoni, E. A., Britschgi, A., Schläfli, A. M., Valk, P. J. M., Kaufmann, T., Haferlach, T., Behre, G., Simon, H., Torbett, B. E., et al. (2013) · Journal of Leukocyte Biology · doi:10.1189/jlb.1112608 · Cited by 25 · see citing works
Self-citationNoguera, N. I., Piredda, M. L., Taulli, R., Catalano, G., Angelini, G., Gaur, G., Nervi, C., Voso, M. T., Lunardi, A., Pandolfi, P. P., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.11964 · Cited by 25 · see citing works
PU.1 and Junb: suppressing the formation of acute myeloid leukemia stem cells.
Somervaille, T. C. P., & Cleary, M. L. (2006) · Cancer Cell · doi:10.1016/j.ccr.2006.11.009 · Cited by 25 · see citing works
Nakazaki, E., Tsolmon, S., Han, J., & Isoda, H. (2011) · European Journal of Nutrition · doi:10.1007/s00394-011-0282-4 · Cited by 24 · see citing works
Yuan, R., Zhu, X., Radich, J. P., & Ao, P. (2016) · Scientific Reports · doi:10.1038/srep24307 · Cited by 23 · see citing works
Haimovici, A., Humbert, M., Federzoni, E. A., Shan, D., Brunner, T., Frese, S., Kaufmann, T., Torbett, B. E., & Tschan, M. P. (2017) · Cell Death and Differentiation · doi:10.1038/cdd.2017.40 · Cited by 23 · see citing works
Aivalioti, M. M., Bartholdy, B. A., Pradhan, K., Bhagat, T. D., Zintiridou, A., Jeong, J. J., Thiruthuvanathan, V. J., Pujato, M., Paranjpe, A., Zhang, C., et al. (2022) · Blood Cancer Discovery · doi:10.1158/2643-3230.bcd-21-0226 · Cited by 22 · see citing works
“1 mRNA levels, its broader transcriptional network appears intact, in line with the essentiality of the transcription factor in maintaining normal and malignant hematopoiesis (20, 22, 23, 46, 48).”
BackgroundMai, S., Hodges, A., Chen, H.-M., Zhang, J., Wang, Y.-L., Liu, Y., Nakatsu, F., Wang, X., Fang, J., Xu, Y., et al. (2023) · Cancer Research · doi:10.1158/0008-5472.can-22-2483 · Cited by 22 · see citing works
Jensen, H. A., Yourish, H. B., Bunaciu, R. P., Varner, J. D., & Yen, A. (2015) · FEBS Open Bio · doi:10.1016/j.fob.2015.09.008 · Cited by 23 · see citing works
Retinoic acid signaling in myelopoiesis
Drumea, K. C., Yang, Z., & Rosmarin, A. G. (2008) · Current Opinion in Hematology · doi:10.1097/moh.0b013e3282f20a9c · Cited by 22 · see citing works
Targeting of leukemia-initiating cells in acute promyelocytic leukemia.
Testa, U., & Lo‐Coco, F. (2015) · Europe PMC (PubMed Central) · doi:10.3978/j.issn.2306-9759.2015.04.03 · Cited by 22 · see citing works
Papetti, M., & Skoultchi, A. I. (2007) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-07-0145 · Cited by 22 · see citing works
Iriyama, N., Yuan, B., YOSHINO, Y., Hatta, Y., Horikoshi, A., Aizawa, S., Takei, M., Takeuchi, J., Takagi, N., & Toyoda, H. (2013) · International Journal of Oncology · doi:10.3892/ijo.2013.2236 · Cited by 21 · see citing works
Vav1 in differentiation of tumoral promyelocytes
Bertagnolo, V., Brugnoli, F., Grassilli, S., Nika, E., & Capitani, S. (2011) · Cellular Signalling · doi:10.1016/j.cellsig.2011.11.017 · Cited by 22 · see citing works
The significance of low PU.1 expression in patients with acute promyelocytic leukemia
Zhu, X., Zhang, H., Qian, M., Zhao, X., Yang, W., Wang, P., Zhang, J., & Wang, K. (2012) · Journal of Hematology & Oncology · doi:10.1186/1756-8722-5-22 · Cited by 21 · see citing works
Weng, X., Sheng, Y., Ge, D.-Z., Wu, J., Shi, L., & Cai, X. (2016) · Leukemia Research · doi:10.1016/j.leukres.2016.03.008 · Cited by 21 · see citing works
Induction of the autophagy-associated gene MAP1S via PU.1 supports APL differentiation
Haimovici, A., Brigger, D., Torbett, B. E., Fey, M. F., & Tschan, M. P. (2014) · Leukemia Research · doi:10.1016/j.leukres.2014.06.010 · Cited by 20 · see citing works
Self-citationWang, P., Tang, Z., Lee, B., Zhu, J. J., Cai, L., Szałaj, P., Tian, S. Z., Zheng, M., Plewczyński, D., Ruan, X., et al. (2020) · Genome biology · doi:10.1186/s13059-020-02030-2 · Cited by 20 · see citing works
Brown, N., Finnon, R., Manning, G., Bouffler, S. D., & Badie, C. (2015) · Mutation Research/Genetic Toxicology and Environmental Mutagenesis · doi:10.1016/j.mrgentox.2015.07.012 · Cited by 19 · see citing works
Watanabe‐Okochi, N., Yoshimi, A., Sato, T., Ikeda, T., Kumano, K., Taoka, K., Satoh, Y., Shinohara, A., Tsuruta-Kishino, T., Masuda, A., et al. (2013) · Blood · doi:10.1182/blood-2011-07-368654 · Cited by 19 · see citing works
Chronic inflammation can transform the fate of normal and mutant hematopoietic stem cells
Li, J., Malouf, C., Miles, L. A., Willis, M., Pietras, E. M., & King, K. Y. (2023) · Experimental Hematology · doi:10.1016/j.exphem.2023.08.008 · Cited by 18 · see citing works
Gaillard, C., Tokuyasu, T. A., Rosen, G. P., Sotzen, J. R., Vitaliano-Prunier, A., Roy, R., Passegue, E. A., de Thé, H., Figueroa, M. E., & Kogan, S. C. (2015) · Haematologica · doi:10.3324/haematol.2014.123018 · Cited by 18 · see citing works
Shao, X., Xiang, S., Fu, H., Chen, Y., Xu, A., Liu, Y., Qi, X., Cao, J., Zhu, H., Yang, B., et al. (2019) · Pharmacological Research · doi:10.1016/j.phrs.2019.104545 · Cited by 18 · see citing works
Effects of PPAR γ Ligands on Leukemia
Tabe, Y., Konopleva, M. Y., Andreeff, M., & Ohsaka, A. (2012) · PPAR Research · doi:10.1155/2012/483656 · Cited by 17 · see citing works
Sive, J. I., Basilico, S., Hannah, R., Kinston, S., Calero‐Nieto, F. J., & Göttgens, B. (2015) · Leukemia · doi:10.1038/leu.2015.172 · Cited by 17 · see citing works
Mikesch, J., Gronemeyer, H., & So, C. W. E. (2010) · Cancer Cell · doi:10.1016/j.ccr.2010.01.012 · Cited by 17 · see citing works
- Authors
- Mueller, B. U., Pabst, T., Fos, J., Petkovic, V., Fey, M. F., Asou, N., Buergi, U., & Tenen, D. G.
- Affiliations
- Harvard University (US)
- From the Department of Internal Medicine and the Department of Clinical Research, University Hospital, Bern, Switzerland; the Institute of Medical Oncology, University Hospital, Bern, Switzerland; Kumamoto University Hospital, Kumamoto, Japan; and Harvard Institutes of Medicine, Harvard Medical School, Boston, MA.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2006-04-15
- Volume
- 107
- Issue
- 8
- Pages
- 3330-3338
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC1895760
- OpenAlex
- W2135132221
- Cited by
- 207
- References
- 33
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 2 · 2023: 10 · 2022: 7 · 2021: 6 · 2020: 14 · 2019: 13 · 2018: 6 · 2017: 9 · 2016: 14 · 2015: 11 · 2014: 11 · 2013: 12 · 2012: 9
- FWCI
- 4.41
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Blood (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- BORIS (University Library Bern) (submittedVersion)
- Funders
- National Cancer Institute (CA 41456, #CA66996, R01CA041456, P01CA066996)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- PU.1, acute promyelocytic leukemia, PML-RARA fusion, all-trans retinoic acid, granulocytic differentiation, differentiation block, CEBPB, Oct-1, transcriptional regulation, hematopoiesis
- MeSH terms
- Proto-Oncogene Protein Spi-1, Animals, Antineoplastic Agents, Cell Differentiation, Chromosomes, Human, Pair 15, Chromosomes, Human, Pair 17, Humans, Neoplasm Proteins, Neutrophils, Proto-Oncogene Proteins, Translocation, Genetic, Tretinoin, Leukemia, Myeloid, Acute, Oncogene Proteins, Fusion, Trans-Activators, Gene Expression Regulation, Leukemic, Mice, Knockout, Cell Line, Tumor, Octamer Transcription Factor-1, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
