ReviewSignal transduction and targeted therapy2020
Targeting multiple signaling pathways: the new approach to acute myeloid leukemia therapy.
Review in Signal transduction and targeted therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
130 citing papers in PubMed, 1 synthesis or guideline pooled it, 212 citations in OpenAlex.
- Targeting AraC-Resistant Acute Myeloid Leukemia by Dual Inhibition of CDK9 and Bcl-2: A Systematic Review and Meta-Analysis.Journal of healthcare engineering · 2022Pooled it
- RBM15 in leukemogenesis: an emerging regulator at the interface of RNA biology and hematopoiesis.Trends in cancer · 2026Review
- PI3Kδ inhibitor YY‑20394 is effective alone or in combination with Bcl‑2 inhibitor ABT199 in acute myeloid leukemia cells.Oncology reports · 2026Article
- Review
- Effects of BCL-2 and MCL-1 Inhibition on Apoptotic and Transcriptional Profiles in Acute Myeloid Leukemia.Medicina (Kaunas, Lithuania) · 2026Article
- Cardiotoxicity of Targeted Therapies in Hematologic Malignancies: From Molecular Mechanisms to Clinical Management.Current treatment options in oncology · 2026Review
- CPT1B promotes acute myeloid leukemia progression via fatty acid oxidation-dependent metabolic reprogramming.Translational oncology · 2026Article
- Predicting response to hypomethylating agents in myeloid neoplasms: a robust model.Annals of hematology · 2026Article
- Diagnosis-Driven Targeted Therapy in Acute Myeloid Leukemia: Clinical Integration of Tyrosine Kinase, BCL-2, and CD33-Directed Strategies with Midostaurin, Venetoclax, and Gemtuzumab Ozogamicin.Journal of clinical medicine · 2026Review
- Differential Expression and Target Gene Analysis of PBMC-Derived microRNAs as Prognostic Biomarkers in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2026Article
- Integrative transcriptomics defines CD36 as a key regulator of immunometabolic signaling in acute myeloid leukemia.Genes & genomics · 2026Article
- Solubility based mechanistic profiling of combinatorial drug therapy.Nature communications · 2026Article
- Biomarkers and advances in AML-MRC: from bench to bedside.Annals of hematology · 2026Review
- Review
- Dynamic heterogeneity towards drug resistance in AML cells is primarily driven by epigenomic mechanism unveiled by multi-omics analysis.Journal of advanced research · 2026Article
- Homoharringtonine and Gilteritinib Synergistically Induce Apoptosis and Suppress Viability in FLT3-ITD-Positive AML Cells.Biomedicines · 2026Article
- Enhancing the Nucleoside Analog Response with Translational Therapeutic Approaches to Overcome Resistance.Cells · 2026Review
- Dual relevance ofFrontiers in oncology · 2026Article
- UBC9 silencing-mediated PPARα deSUMOylation induces inhibition of cell proliferation by ferroptosis in acute myeloid leukemia.Archives of medical science : AMS · 2026Article
- Mutant NPM1 modulates PDCD4 ubiquitination degradation and facilitates leukemogenesis.iScience · 2025Article
70 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 2 countries.
Funding
Abstract
Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults and the second most common form of acute leukemia in children. Despite this, very little improvement in survival rates has been achieved over the past few decades. This is partially due to the heterogeneity of AML and the need for more targeted therapeutics than the traditional cytotoxic chemotherapies that have been a mainstay in therapy for the past 50 years. In the past 20 years, research has been diversifying the approach to treating AML by investigating molecular pathways uniquely relevant to AML cell proliferation and survival. Here we review the development of novel therapeutics in targeting apoptosis, receptor tyrosine kinase (RTK) signaling, hedgehog (HH) pathway, mitochondrial function, DNA repair, and c-Myc signaling. There has been an impressive effort into better understanding the diversity of AML cell characteristics and here we highlight important preclinical studies that have supported therapeutic development and continue to promote new ways to target AML cells. In addition, we describe clinical investigations that have led to FDA approval of new targeted AML therapies and ongoing clinical trials of novel therapies targeting AML survival pathways. We also describe the complexity of targeting leukemia stem cells (LSCs) as an approach to addressing relapse and remission in AML and targetable pathways that are unique to LSC survival. This comprehensive review details what we currently understand about the signaling pathways that support AML cell survival and the exceptional ways in which we disrupt them.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.