ReviewInternational journal of molecular sciences2017
Aberrant Signaling Pathways in T-Cell Acute Lymphoblastic Leukemia.
Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06855810 (Chinese Children's Cancer Group T-cell Acute Lymphoblastic Leukemia -2025 Project), which is not on this map. Cited by 41 papers.
What it found
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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.
Chinese Children's Cancer Group T-cell Acute Lymphoblastic Leukemia -2025 Project
Who cites it
41 citing papers in PubMed.
- CD40LG/CD28-Mediated Rho GTPase Signaling Drives Survival and Chemoresistance in Non-ETP T-ALL.International journal of molecular sciences · 2026Article
- Article
- Molecular screening of natural compounds targeting KRAS(G12C): a multi-parametric strategy against acute lymphoblastic leukemia.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- Novel Therapeutic Approaches in Pediatric Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2025Review
- Cytogenetic landscape aberrations in paediatric acute lymphoblastic leukaemia - a polish paediatric population treated according to ALL-IC BFM 2009 protocol.Scientific reports · 2025Article
- BCAT1 is a NOTCH1 target and sustains the oncogenic function of NOTCH1.Haematologica · 2025Article
- BCAT1 Associates with DNA Repair Proteins KU70 and KU80 and Contributes to Regulate DNA Repair in T-Cell Acute Lymphoblastic Leukemia (T-ALL).International journal of molecular sciences · 2024Article
- BIRC5 upregulation enhances DNMT3A-mutant T-ALL cell survival and pathogenesis.Blood neoplasia · 2024Article
- Review
- Leveraging altered lipid metabolism in treating B cell malignancies.Progress in lipid research · 2024Review
- Pathway of LCK Tyrosine Kinase and mTOR Signaling in Children with T-Cell Acute Lymphoblastic Leukemia.The application of clinical genetics · 2024Review
- PLK1 as a cooperating partner for BCL2-mediated antiapoptotic program in leukemia.Blood cancer journal · 2023Article
- Venetoclax-Resistant T-ALL Cells Display Distinct Cancer Stem Cell Signatures and Enrichment of Cytokine Signaling.International journal of molecular sciences · 2023Article
- Understanding the Roles of the Hedgehog Signaling Pathway during T-Cell Lymphopoiesis and in T-Cell Acute Lymphoblastic Leukemia (T-ALL).International journal of molecular sciences · 2023Review
- Targeted Treatment and Immunotherapy in High-risk and Relapsed/ Refractory Pediatric Acute Lymphoblastic Leukemia.Current pediatric reviews · 2023Review
- Article
- miRNAs in Lymphocytic Leukaemias-The miRror of Drug Resistance.International journal of molecular sciences · 2022Review
- Update from the 5th Edition of the World Health Organization Classification of Head and Neck Tumors: Hematolymphoid Proliferations and Neoplasia.Head and neck pathology · 2022Article
- Long noncoding RNA endogenous bornavirus-like nucleoprotein acts as an oncogene by regulating microRNA-655-3p expression in T-cell acute lymphoblastic leukemia.Bioengineered · 2022Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive disease caused by the malignant transformation of immature progenitors primed towards T-cell development. Clinically, T-ALL patients present with diffuse infiltration of the bone marrow by immature T-cell blasts high blood cell counts, mediastinal involvement, and diffusion to the central nervous system. In the past decade, the genomic landscape of T-ALL has been the target of intense research. The identification of specific genomic alterations has contributed to identify strong oncogenic drivers and signaling pathways regulating leukemia growth. Notwithstanding, T-ALL patients are still treated with high-dose multiagent chemotherapy, potentially exposing these patients to considerable acute and long-term side effects. This review summarizes recent advances in our understanding of the signaling pathways relevant for the pathogenesis of T-ALL and the opportunities offered for targeted therapy.
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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.