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Relevant bibliographies by topics / Myeloid Cell Leukemia 1 (MCL1)

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Dissertations / Theses
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Academic literature on the topic 'Myeloid Cell Leukemia 1 (MCL1)'

Author: Grafiati

Published: 7 September 2021

Last updated: 29 July 2025

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Journal articles on the topic "Myeloid Cell Leukemia 1 (MCL1)"

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Luo, Hui, Jennifer A. Cain, AnnaLynn Molitoris, Joseph Opferman, and Michael H. Tomasson. "Myc Induces Acute Myeloid Leukemia by Conferring Self-Renewal Activity to Committed Myeloid Progenitor Cells That Resist Apoptosis Via Endogenous Mcl-1." Blood 110, no. 11 (2007): 2634. http://dx.doi.org/10.1182/blood.v110.11.2634.2634.

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Abstract Ectopic expression of Myc in most primary cell types induces apoptosis, and cancer development typically requires additional, anti-apoptotic mutations. We reported previously that ectopic expression of Myc in unfractionated murine bone marrow cells induced rapid onset acute myeloid leukemia (AML) without detectable anti-apoptotic mutations. We hypothesized that AML developed in our model because a subset of normal primary bone marrow cells were inherently resistant to Myc-induced apoptosis. Consistent with this model, seven days of Myc activation in the bone marrow of mice caused the

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Sevin, Margaux, Franck Debeurme, Lucie Laplane, et al. "Cytokine-like protein 1–induced survival of monocytes suggests a combined strategy targeting MCL1 and MAPK in CMML." Blood 137, no. 24 (2021): 3390–402. http://dx.doi.org/10.1182/blood.2020008729.

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Abstract Mouse models of chronic myeloid malignancies suggest that targeting mature cells of the malignant clone disrupts feedback loops that promote disease expansion. Here, we show that in chronic myelomonocytic leukemia (CMML), monocytes that accumulate in the peripheral blood show a decreased propensity to die by apoptosis. BH3 profiling demonstrates their addiction to myeloid cell leukemia-1 (MCL1), which can be targeted with the small molecule inhibitor S63845. RNA sequencing and DNA methylation pattern analysis both point to the implication of the mitogen-activated protein kinase (MAPK)

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Acton, Alexus, and William J. Placzek. "Myeloid Cell Leukemia 1 Small Molecule Inhibitor S63845 Synergizes with Cisplatin in Triple-Negative Breast Cancer." Cancers 15, no. 18 (2023): 4481. http://dx.doi.org/10.3390/cancers15184481.

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Triple-negative breast cancer (TNBC) is an aggressive cancer that lacks specific molecular targets that are often used for therapy. The refractory rate of TNBC to broad-spectrum chemotherapy remains high; however, the combination of newly developed treatments with the current standard of care has delivered promising anti-tumor effects. One mechanism employed by TNBC to avoid cell death is the increased expression of the anti-apoptotic protein, myeloid cell leukemia 1 (MCL1). Multiple studies have demonstrated that increased MCL1 expression enables resistance to platinum-based chemotherapy. In

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Mukai, Risa, and Takayuki Ohshima. "Enhanced Stabilization of MCL1 by the Human T-Cell Leukemia Virus Type 1 bZIP Factor Is Modulated by Blocking the Recruitment of Cullin 1 to the SCF Complex." Molecular and Cellular Biology 36, no. 24 (2016): 3075–85. http://dx.doi.org/10.1128/mcb.00450-16.

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Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus that is the etiological agent of adult T-cell leukemia (ATL). The HTLV-1 basic leucine zipper factor (HBZ), which is encoded by the minus strand of the provirus, is constitutively expressed in all ATL patient cells and likely contributes to the development and maintenance of ATL. Furthermore, the overexpression of the myeloid cell leukemia 1 (MCL1) protein is frequently observed in hematological cancers as well as several other types of cancers. Here, we found that the expression of HBZ in cells stabilized MCL1 protein expr

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Moujalled, Donia M., Giovanna Pomilio, Thomas Morley, et al. "CD74 Antibody Conjugated to an MCL1 Inhibitor (S227928) Combines Synergistically with Venetoclax to Enhance Killing of Acute Myeloid Leukemia." Blood 144, Supplement 1 (2024): 4136. https://doi.org/10.1182/blood-2024-202691.

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Background: BCL2 pro-survival proteins (BCL2, MCL1, BCL-XL) function as key regulators of oncogenic survival. BH3-mimetic drugs bind to pro-survival proteins (e.g. venetoclax to BCL2), enhancing BH3-only proteins to induce BAX/BAK dependent apoptosis. MCL1 is overexpressed in acute myeloid leukemia (AML) and increased expression has been observed in leukemias resistant to venetoclax-based therapy. Co-targeting BCL2 and MCL1 with selective BH3-mimetics has synergistic activity in diverse AML cases, including TP53-mutated disease (Thijssen, Blood, 2021). Clinical development of MCL1 inhibitors h

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Powell, Jason A., Alexander C. Lewis, Wenying Zhu, et al. "Targeting sphingosine kinase 1 induces MCL1-dependent cell death in acute myeloid leukemia." Blood 129, no. 6 (2017): 771–82. http://dx.doi.org/10.1182/blood-2016-06-720433.

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Key Points Inhibition of SPHK1 in human AML cells induces MCL1 degradation and caspase-dependent cell death. SPHK1 inhibitors reduce leukemic burden and prolong survival in orthotopic patient-derived xenografts of AML.

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Garzon, Ramiro, Flavia Pichiorri, Guido Marcucci, Steve Kornblau, Michael Andreeff, and Carlo Croce. "MiRNA-29b Targets MCL-1 and Is Down-Regulated in Chemotherapy-Resistant Acute Myeloid Leukemia (AML)." Blood 110, no. 11 (2007): 717. http://dx.doi.org/10.1182/blood.v110.11.717.717.

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Abstract AML is a heterogeneous disorder that includes several differently biologic entities. Patients with intermediate and poor-risk cytogenetics represent the majority of AML and chemotherapy-based regimens fail to cure most of these patients that are either resistant to or relapse shortly after treatment. Therefore, it is crucial to understand the biology of chemotherapy resistance in AML. Here, we proposed to investigate the relation between chemoresistance and miRNA expression in AML. First, using a miRNA microarray platform, we analyzed the miRNA profiles in pretreatment samples from a

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Golla, Upendarrao, Satyam Patel, Jeremy Hengst, et al. "Abstract 7227: Isatin analogs potentiate the cytotoxicity of venetoclax in acute myeloid leukemia cells." Cancer Research 84, no. 6_Supplement (2024): 7227. http://dx.doi.org/10.1158/1538-7445.am2024-7227.

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Abstract Acute Myeloid Leukemia (AML) is a rare but common hematological malignancy in children and adults. AML is a highly heterogeneous disease caused by the acquisition of several mutations affecting multiple cellular processes, thus requiring concomitant targeting of key survival nodes to treat effectively. As current first-line therapies for AML suffer with poor outcomes, drug resistance, and high relapse rates, there is an immediate need for new combinatorial therapies that are both safe and effective. Venetoclax (VEN), a selective inhibitor of antiapoptotic protein B-cell lymphoma-2 (BC

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Lazzari, Elisa, Leslie A. Crews, Christina Wu, et al. "Targeting Cancer Stem Cell Survival in Plasma Cell Leukemia with a Pan-BCL2 Inhibitor." Blood 126, no. 23 (2015): 5351. http://dx.doi.org/10.1182/blood.v126.23.5351.5351.

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Abstract INTRODUCTION Representing ten percent of all hematologic malignancies, multiple myeloma (MM) is typified by clonal plasma cell proliferation in the bone marrow (BM) and may progress to a therapy-resistant stage characterized by circulating malignant plasma cells, which is termed plasma cell leukemia, (PCL). Notably, copy number amplification involving the myeloid cell leukemia (MCL)-1 locus, and translocations at the BCL2 locus have been described in high-risk MM. Moreover, BCL2 family members, including both MCL1 and BCL2, are highly expressed in relapsed MM. Finally, downregulation

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Chakraborty, Samarpana, Claudia Morganti, Joyoti Dey, et al. "A STAT3 Degrader Demonstrates Pre-Clinical Efficacy in Venetoclax Resistant Acute Myeloid Leukemia." Blood 142, Supplement 1 (2023): 2787. http://dx.doi.org/10.1182/blood-2023-186947.

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Introduction: Acute Myeloid leukemia (AML) is an aggressive hematological malignancy resulting from the transformation of immature myeloid progenitor cells followed by an uncontrolled clonal proliferation and accumulation of the transformed cells. AML is the most common myeloid malignancy in the elderly [1]. Venetoclax (Ven) is a selective inhibitor of the anti-apoptotic BCL2 protein. Ven is FDA approved in combination with hypomethylating agents (HMA's) or low dose cytarabine for the treatment of de-novo AML in patients &gt; 75 years or those ineligible for standard induction therapies. D

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Dissertations / Theses on the topic "Myeloid Cell Leukemia 1 (MCL1)"

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Xiao, Kang. "Investigating the functional roles of Mcl-1 in apoptosis in mammalian cells /." View abstract or full-text, 2009. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202009%20XIAO.

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Choudhary, Gaurav Sudhakar. "Role of Myeloid Cell Leukemia 1 (MCL-1) in mediating chemoresistance towards BCL-2 homology 3 (BH3) mimetics in lymphoid malignancies." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1448024862.

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Benabderrahmane, Mohammed. "Etude de la structure et la dynamique de Mcl-1 : application en cancérologie Binding mode of Pyridoclax to myeloid cell leukemia-1 (Mcl-1) revealed by nuclear magnetic resonance spectroscopy, docking and molecular dynamics approaches Insights into Mcl-1 Conformational States and Allosteric Inhibition Mechanism from Molecular Dynamics Simulations, Enhanced Sampling, and Pocket Crosstalk Analysis." Thesis, Normandie, 2020. http://www.theses.fr/2020NORMC426.

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Ce travail ayant pour objet l’étude de la structure et la dynamique de Mcl-1, une protéine anti-apoptotique d’intérêt en cancérologie, est scindé en trois parties.Une première étude concerne une caractérisation du mode d’interaction du Pyridoclax (un inhibiteur BH3-mimétique) avec Mcl-1 par des approches expérimentales (RMN) et théoriques (simulations de dynamique moléculaire). Une deuxième partie est consacrée à l’étude et à la caractérisation des espaces conformationnels de Mcl-1 et son mode d’inhibition allostérique. Le troisième volet de ce travail, traite d’une approche d’analyse, basée s

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Perrod, Chiara. "Epigenetic PU.1 silencing in myeloid leukemia by mimicrying a T cell specific chromatin loop." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2013. http://dx.doi.org/10.18452/16863.

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Veränderungen in der lokalen Chromatinstruktur beeinflussen die dynamische Regulation von Genen, welche für die Differenzierung notwendig sind. PU.1 ist ein Master-Transkriptionsfaktor in der Hämatopoese und wird streng reguliert, um ein zelllinienspezifisches Expressionsmuster zu erzielen. Hohe Konzentrationen von PU.1 sind für myeloische Differenzierung erforderlich. In B-Zellen wird PU.1 mittelstark exprimiert und muss aktiv runterreguliert werden, um eine Ausdifferenzierung der multipotenten Vorläuferzellen zu T-Zellen zu ermöglichen. Derzeit ist wenig über die Regulierung von PU.1 in T-

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Dimberg, Anna. "The role of Stat 1 in retinoic acid-induced myelomonocytic differentiation of human leukemia cells /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2002. http://publications.uu.se/theses/91-554-5224-8/.

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Shaw, Jeremy Joseph Porter. "The Implications Of Gap Junction Inhibition In Jurkat Cell-CellCommunication And Proliferation." Kent State University Honors College / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ksuhonors1398988837.

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Perrod, Chiara [Verfasser], Achim [Akademischer Betreuer] Leutz, Harald [Akademischer Betreuer] Saumweber, and Matthias [Akademischer Betreuer] Selbach. "Epigenetic PU.1 silencing in myeloid leukemia by mimicrying a T cell specific chromatin loop / Chiara Perrod. Gutachter: Achim Leutz ; Harald Saumweber ; Matthias Selbach." Berlin : Humboldt Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2013. http://d-nb.info/1045951420/34.

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Herrmann, Monika [Verfasser], and Karl-Peter [Akademischer Betreuer] Hopfner. "Development of a novel T cell engaging antibody derivative for local PD-1/PD-L1 immune checkpoint blockade in acute myeloid leukemia / Monika Herrmann ; Betreuer: Karl-Peter Hopfner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1204827575/34.

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David, Laure. "Etude de nouvelles fonctions de la protéine checkpoint kinase 1 (Chk1) au cours de la différenciation myéloïde normale et leucémique." Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30179/document.

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Le cycle cellulaire est l'ensemble des étapes qui conduisent une cellule mère à se diviser en deux cellules filles. La protéine Checkpoint kinase 1 (Chk1) est importante pour sa progression. Nous avons d'une part cherché à savoir si Chk1 intervenait lors des mécanismes de production des plaquettes, car ces cellules permettant la coagulation du sang sont issues d'un cycle cellulaire particulier. Par ailleurs, nous avons étudié le rôle de Chk1 dans la Leucémie Aiguë Myéloïde (LAM), cancer des cellules sanguines. Les patients atteints de LAM sont traités par une chimiothérapie visant à endommager

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Kutsenko, Olena Oleksandrivna. "Regulation of MCL1 3' UTR-APA-derived mRNA isoforms." Master's thesis, 2018. http://hdl.handle.net/10773/24292.

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A poliadenilação alternativa (APA) é uma etapa de processamento de pre-mRNA em que isoformas alternativas de mRNA são formadas com base na escolha de um sinal de poliadenilação (pA) sobre o outro. Quando confinada à Região 3’ não-Traduzida (3’ UTR), a APA gera mRNAs que variam somente no comprimento das suas 3’ UTRs (3’UTR-APA). Vários estudos têm demonstrado o papel da APA na regulação da expressão genética. Nos mamíferos, cerca de 70% de genes são sujeitos a APA, aumentando substancialmente a diversidade do transcriptoma. APA é relevante tanto em processos fisiológicos como patológicos, modu

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Book chapters on the topic "Myeloid Cell Leukemia 1 (MCL1)"

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, et al. "MCL-1 (Myeloid Cell Leukemia-1), BCL2L3 (BCL-2 like 3)." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100778.

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Popat, Uday, and Sergio Giralt. "Hematopoietic Cell Transplantation for Chronic Myeloid Leukemia." In Hematopoietic Stem Cell Transplantation. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-438-4_5.

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Lee, Dean Anthony, Laurence James Neil Cooper, and Elizabeth J. Shpall. "NK-Cell Immunotherapy for AML." In Targeted Therapy of Acute Myeloid Leukemia. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_40.

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Bishop, Michael R. "Stem Cell Transplantation for Chronic Myeloid Leukemia." In Current Controversies in Bone Marrow Transplantation. Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-657-7_6.

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Lee, Dean Anthony, Laurence James Neil Cooper, and Elizabeth J. Shpall. "Erratum to: NK-Cell Immunotherapy for AML." In Targeted Therapy of Acute Myeloid Leukemia. Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-1393-0_44.

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Booth, Christopher H., Lysette Mutkus, Karen Bussard, Erika Spaeth, Michael Andreeff, and Frank C. Marini. "Mesenchymal Stem/Stromal Cell-Targeted Therapies for Solid Tumors and Hematological Malignancies." In Targeted Therapy of Acute Myeloid Leukemia. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_43.

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Weber, Gerrit, Catherine M. Bollard, and Austin John Barrett. "Allogeneic and Autologous T cell Strategies to Enhance Targeting of Acute Myeloid Leukemias." In Targeted Therapy of Acute Myeloid Leukemia. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_41.

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Liao, Mickey, and Gary J. Schiller. "The Role of Transplantation in Favorable-Risk Acute Myeloid Leukemia." In Allogeneic Stem Cell Transplantation. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-478-0_12.

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Hoang, Van T., Isabel Hoffmann, Karina Borowski, et al. "Identification and Separation of Normal Hematopoietic Stem Cells and Leukemia Stem Cells from Patients with Acute Myeloid Leukemia." In Stem Cell Niche. Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-508-8_19.

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Vlachou, Thalia, Marco S. Nobile, Chiara Ronchini, Daniela Besozzi, and Pier Giuseppe Pelicci. "An Experimental and Computational Protocol to Study Cell Proliferation in Human Acute Myeloid Leukemia Xenografts." In Leukemia Stem Cells. Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0810-4_14.

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Conference papers on the topic "Myeloid Cell Leukemia 1 (MCL1)"

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Gagliardi, M., G. Chauhan, MK Pitner, et al. "Abstract P5-03-06: Overcoming MEK inhibitor resistance in triple-negative breast cancer by targeting myeloid cell leukemia-1 (MCL1), an anti-apoptotic protein." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p5-03-06.

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Bauer, M., M. Michalski, C. Kunst, M. Müller-Schilling, and K. Gülow. "Inhibition von Mcl-1 (Myeloid-Cell Leukemia 1) und Bcl-2 (B-Cell Lymphoma 2) - Ein neuer Therapieansatz bei Hepatozellulärem Karzinom (HCC)." In Viszeralmedizin 2021 Gemeinsame Jahrestagung Deutsche Gesellschaft für Gastroenterologie, Verdauungs- und Stoffwechselkrankheiten (DGVS), Sektion Endoskopie der DGVS, Deutsche Gesellschaft für Allgemein und Viszeralchirurgie (DGAV). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1733615.

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Bauer, M., M. Michalski, C. Kunst, M. Müller-Schilling, and K. Gülow. "Inhibition von Mcl-1 (Myeloid-Cell Leukemia 1) und Bcl-2 (B-Cell Lymphoma 2) - Ein neuer Therapieansatz bei Hepatozellulärem Karzinom (HCC)." In Viszeralmedizin 2021 Gemeinsame Jahrestagung Deutsche Gesellschaft für Gastroenterologie, Verdauungs- und Stoffwechselkrankheiten (DGVS), Sektion Endoskopie der DGVS, Deutsche Gesellschaft für Allgemein und Viszeralchirurgie (DGAV). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1733615.

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Simijonović, Dušica, Marko Antonijević, Edina Avdović, Zorica Petrović, and Zoran Marković. "INHIBITORY EFFECT OF COUMARIN BENZOYLHYDRAZONES ON MCL-1 PROTEIN." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.442s.

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The protein that controls cell differentiation in acute myeloid leukemia is MCL-1. High-level of this protein causes the carcinogenesis. In this paper inhibitory effect of two coumarin benzoylhydrazones,(E)-2-hydroxy-N’-(1-(2-oxo-2H-chromen-3-yl)ethylidene)benzohydrazide (A) and (E)-4-hydroxy-N’-(1-(2-oxo-2H-chromen-3-yl)ethylidene)benzohydrazide (B) against MCL-1 protein was investigated. For this purpose, a molecular docking simulations were used. The obtained results showed that compound A showed better activity than compound B. Also, the docking simulations against MCL-1 protein were perfo

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Bauer, Magdalena, Marlen Michalski, Martina Müller-Schilling, and Karsten Gülow. "Combination of Mcl-1 (Myeloid-Cell Leukemia 1) and Bcl-2 (B-Cell Lymphoma 2) inhibition – A novel treatment approach for Hepatocellular Carcinoma (HCC)." In 38. Jahrestagung der Deutsche Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0041-1740759.

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Xia, Lijuan, Janice Gabrilove, and Yongkui Jing. "Abstract 3501: Flavopiridol decreases Mcl-1 and XIAP in acute myeloid leukemia cell resulting in augmentation of sorafenib-induced apoptosis." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3501.

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Tron, Adriana E., Matthew A. Belmonte, Steven Criscione, et al. "Abstract 302: Selective Mcl-1 inhibition by AZD5991 induces on-target cell death and achieves antitumor activity in multiple myeloma and acute myeloid leukemia." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-302.

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Guo, Jun, Lisa Roberts, Jeffrey B. Kraft, Philip J. Merta, Keith B. Glaser, and Omar J. Shah. "Abstract 12:JAK2V617Fdrives Mcl-1 expression and sensitizes acute myeloid leukemia cells to dual inhibition of JAK2 and Bcl-XL." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-12.

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Rosenbluth, Michael J., Wilbur A. Lam, and Daniel A. Fletcher. "Contribution of Cell Mechanics to Acute Leukemia." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-59881.

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Leukostasis is a life-threatening condition that occurs when leukemia cells accumulate in the vasculature of organs such as the brain and lungs. Recent evidence has shown that leukostasis is not simply due to the physical overcrowding of leukemia cells, as previously thought, but may result from specific mechanical properties of the cells and interactions between cells. Using atomic force microscopy (AFM), we obtained direct measurements of two mechanical properties that are likely involved in this condition: (1) stiffness of individual leukemia cells and (2) non-specific adhesion forces betwe

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Wang, Rui, Lijuan Xia, Janice Gabrilove, Samuel Waxman, and Yongkui Jing. "Abstract 799: Diminishing Mcl-1 protein leads to apoptosis of acute myeloid leukemia cells responding to all trans retinoic acid differentiation." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-799.

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Reports on the topic "Myeloid Cell Leukemia 1 (MCL1)"

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Kungwankiattichai, Smith, Ben Ponvilawa, Claudie Roy, Pattaraporn Tunsing, Florian Kuchenbauer, and Weerapat Owattanapanich. Maintenance with Hypomethylating Agents after Allogeneic Stem Cell Transplantation in Acute Myeloid Leukemia and Myelodysplastic Syndrome: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2021. http://dx.doi.org/10.37766/inplasy2021.11.0078.

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Review question / Objective: P: Patients with AML or MDS after allo-SCT; I: Hypomethylating agents after allo-SCT; C: Observation after allo-SCT; O: Overall survival rates. Condition being studied: Hypomethylating agents (HMAs) seem to have a range of properties favorable to post-allogeneic hematopoietic stem cell transplantation (allo-SCT) maintenance in acute myeloid leukemia (AML) patients. This meta-analysis was performed to review all relevant studies to compare the outcomes of patients undergoing allo-SCT for AML or MDS receiving HMA maintenance therapy with observation only. Information

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