^
    1d
    Results of the prospective EORTC Children Leukemia Group study 58081 in precursor B- and T-cell acute lymphoblastic leukemia. (PubMed, Hemasphere)
    Dexamethasone (DXM) was used in average-risk 2 (AR2) T-ALL and B-ALL during induction, 10 and 6 mg/m2/day, respectively. Leucovorin rescue was delayed to 42 h instead of 36 h after initiation of high-dose methotrexate, and a postconsolidation MRD time point was added to stratify patients...The HR was 2.15 (99% CI: 0.67-6.85) for very low-risk but 0.34 (99% CI: 0.13-0.89) for AR2. The particularly favorable results observed in the T-ALLs and AR2 subgroups suggest the benefit of using DXM in specific patient groups and highlight the importance of risk stratification.
    Journal
    |
    ABL1 (ABL proto-oncogene 1)
    |
    methotrexate • leucovorin calcium • methotrexate IV
    2d
    PU.1 eviction at lymphocyte-specific chromatin domains mediates glucocorticoid response in acute lymphoblastic leukemia. (PubMed, Nat Commun)
    Treatment with a PU.1 inhibitor enhances glucocorticoid sensitivity, demonstrating the clinical potential of targeting this pathway. This study uncovers a mechanism involving PU.1 and the glucocorticoid receptor, linking transcription factor activity with drug response, and suggesting potential therapeutic strategies for overcoming resistance.
    Journal
    |
    SPI1 (Spi-1 Proto-Oncogene)
    3d
    Mutations at BCL11B Exon 4 Associated with T Cell Acute Lymphoblastic Leukemia Are Facilitated by AID and Formation of Non-B DNA Conformations. (PubMed, Mol Cell Biol)
    Importantly, various lines of experimentation reveal that BCL11B FR could fold into parallel G-quadruplex, triplex, and hairpin structures, which could act as a replication/transcription block, causing mutagenesis. Thus, our results suggest that AID binds to BCL11B exon 4 due to non-B DNA formation, causing U:G mismatches or replication blocks, which, when repaired erroneously, generates deleterious mutations, resulting in loss of functionality of BCL11B, and thus becomes the cause of T-ALL.
    Journal
    |
    BCL11B (BAF Chromatin Remodeling Complex Subunit BCL11B)
    |
    BCL11B mutation
    3d
    A Novel NRAS Variant Near the Splice Junction in Moroccan Childhood Acute Lymphoblastic Leukemia: A Molecular Dynamics Study. (PubMed, Biochem Genet)
    Our findings suggest that the NRAS p.Arg97Thr variant may disrupt the splicing machinery and functions of the protein, thus playing a vital role in leukemogenesis. In addition, the highly druggable pocket may possibly be studied for its therapeutic implications.
    Journal
    |
    KRAS (KRAS proto-oncogene GTPase) • NRAS (Neuroblastoma RAS viral oncogene homolog) • RAS (Rat Sarcoma Virus)
    |
    KRAS mutation • NRAS mutation
    4d
    Delineating Notch1 and Notch2: Receptor-Specific Significance and Therapeutic Importance of Pinpoint Targeting Strategies for Hematological Malignancies. (PubMed, Eur J Haematol)
    In this review, we emphasize the importance of distinct tissue-specific expression patterns, functional divergence, disease-specific considerations, and the necessity to minimize off-target effects that collectively underscore the significance of "individualized" targeting for Notch1 and Notch2. This comprehensive review sheds light on the receptor-specific characteristics of Notch1 and Notch2, providing insights into their roles in cellular processes and offering opportunities for developing tailored therapeutic interventions in the fields of biomedical research and clinical practice.
    Review • Journal
    |
    NOTCH1 (Notch 1) • NOTCH2 (Notch 2)
    4d
    Donor-Derived CD5 CAR T Cells in Subjects with Relapsed or Refractory T-Cell Acute Lymphoblastic Leukemia (clinicaltrials.gov)
    P1, N=19, Terminated, Beijing Boren Hospital | Recruiting --> Terminated; ethic commitee decision
    Trial termination
    |
    CD5 (CD5 Molecule)
    |
    CD5 positive
    |
    cyclophosphamide
    4d
    Donor-Derived CD5 CAR T (CT125B) Cells for Relapsed or Refractory T- Cell Acute Lymphoblastic Leukemia/Lymphoma (clinicaltrials.gov)
    P1, N=0, Withdrawn, Beijing Boren Hospital | N=18 --> 0 | Trial completion date: Jul 2024 --> Dec 2023 | Recruiting --> Withdrawn | Trial primary completion date: Jul 2024 --> Dec 2023
    Enrollment change • Trial completion date • Trial withdrawal • Trial primary completion date
    |
    CD5 (CD5 Molecule)
    |
    CD5 positive
    |
    cyclophosphamide • CD5 CAR T (CT125B)
    4d
    Phase I Clinical Trial of Autologous CD7-CAR T Cell Therapy for High-risk Acute T-cell Leukemia/lymphoma (clinicaltrials.gov)
    P1, N=16, Completed, Beijing Boren Hospital | Recruiting --> Completed
    Trial completion
    |
    CD7 (CD7 Molecule)
    |
    cyclophosphamide • autologous CD7-CAR T cells
    5d
    AALL1231: Combination Chemotherapy With or Without Bortezomib in Treating Younger Patients With Newly Diagnosed T-Cell Acute Lymphoblastic Leukemia or Stage II-IV T-Cell Lymphoblastic Lymphoma (clinicaltrials.gov)
    P3, N=847, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Sep 2024 --> Sep 2025
    Trial completion date
    |
    CD20 (Membrane Spanning 4-Domains A1) • CD8 (cluster of differentiation 8) • CD22 (CD22 Molecule) • CD34 (CD34 molecule) • CD5 (CD5 Molecule) • CD7 (CD7 Molecule) • CD2 (CD2 Molecule) • MPO (Myeloperoxidase)
    |
    CD22 expression
    |
    cytarabine • bortezomib • doxorubicin hydrochloride • cyclophosphamide • ifosfamide • etoposide IV • methotrexate • vincristine • daunorubicin • leucovorin calcium • Oncaspar liquid (pegaspargase) • mercaptopurine • thioguanine • Hemady (dexamethasone tablets) • Starasid (cytarabine ocfosfate)
    5d
    Demethylating Agents Combined with Venetoclax for High-risk T-Cell Lymphoma/leukemia Post-Transplant Relapse Prevention (clinicaltrials.gov)
    P2, N=59, Recruiting, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine
    New P2 trial • Post-transplantation
    |
    Venclexta (venetoclax) • azacitidine • decitabine
    6d
    CAR-20/19-T Cells in Patients With Relapsed/Refractory B Cell ALL (clinicaltrials.gov)
    P1, N=24, Suspended, Medical College of Wisconsin | Recruiting --> Suspended
    Trial suspension
    |
    CD20 positive
    |
    CAR-20/19-T Cells
    11d
    S1905: Study to Test AKR1C3-Activated Prodrug OBI-3424 (OBI-3424) in Patients With Relapsed/Refractory T-Cell Acute Lymphoblastic Leukemia (T-ALL) (clinicaltrials.gov)
    P2, N=39, Recruiting, SWOG Cancer Research Network | Trial completion date: Aug 2027 --> Aug 2032 | Trial primary completion date: Aug 2026 --> Aug 2028
    Trial completion date • Trial primary completion date
    |
    AKR1C3 (Aldo-Keto Reductase Family 1 Member C3)
    |
    AKR1C3 expression
    |
    OBI-3424
    11d
    The third generation AKR1C3-activated prodrug, ACHM-025, eradicates disease in preclinical models of aggressive T-cell acute lymphoblastic leukemia. (PubMed, Blood Cancer J)
    To exploit this finding, we developed a novel prodrug, ACHM-025, which is selectively activated by AKR1C3 to a nitrogen mustard DNA alkylating agent...ACHM-025 was significantly more effective than cyclophosphamide both as a single agent and when used in combination with cytarabine/6-mercaptopurine. Notably, ACHM-025 in combination with nelarabine was curative when used to treat a chemoresistant T-ALL PDX in vivo. The in vivo efficacy of ACHM-025 directly correlated with AKR1C3 expression levels, providing a predictive biomarker for response. Together, our work provides strong preclinical evidence highlighting the potential of ACHM-025 as a targeted and effective therapy for aggressive forms of T-ALL.
    Preclinical • Journal
    |
    AKR1C3 (Aldo-Keto Reductase Family 1 Member C3)
    |
    AKR1C3 expression
    |
    cytarabine • cyclophosphamide • nelarabine • mercaptopurine • ACHM-025 • Mustargen (mechlorethamine)
    12d
    Comprehensive Genomic Profiling (CGP) of Acute Lymphoblastic Leukemias with Foundation One Heme Identifies Actionable Genomic Alterations and Biomarkers (ASH 2024)
    This analysis of 2,637 samples comprising a variety of molecular subtypes of ALL demonstrated that the F1H assay detects pathogenic genomic alterations with diagnostic, prognostic, and therapeutic significance. As both the treatment landscape and disease classification system in ALL have continued to evolve over time, CGP assays such as F1H can play a critical role in clinical decision making by simultaneously assessing the presence and absence of numerous actionable genomic alterations and biomarkers with a single assay.
    KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • ABL1 (ABL proto-oncogene 1) • NRAS (Neuroblastoma RAS viral oncogene homolog) • PTEN (Phosphatase and tensin homolog) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • NOTCH1 (Notch 1) • JAK2 (Janus kinase 2) • RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • ETV6 (ETS Variant Transcription Factor 6) • CRLF2 (Cytokine Receptor Like Factor 2) • IKZF1 (IKAROS Family Zinc Finger 1) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • FBXW7 (F-Box And WD Repeat Domain Containing 7) • PAX5 (Paired Box 5) • TCF3 (Transcription Factor 3) • P2RY8 (P2Y Receptor Family Member 8) • PBX1 (PBX Homeobox 1) • ABL2 (ABL Proto-Oncogene 2, Non-Receptor Tyrosine Kinase)
    |
    TP53 mutation • KRAS mutation • NRAS mutation • PTEN mutation • CDKN2A deletion
    |
    FoundationOne® Heme CDx
    12d
    ECOG-ACRIN EA9152: Venetoclax and Vincristine in Treating Patients With Relapsed or Refractory T-cell or B-cell Acute Lymphoblastic Leukemia (clinicaltrials.gov)
    P1/2, N=74, Active, not recruiting, ECOG-ACRIN Cancer Research Group | Recruiting --> Active, not recruiting
    Enrollment closed • Combination therapy • IO biomarker
    |
    BCL2 (B-cell CLL/lymphoma 2)
    |
    BCL2 expression
    |
    Venclexta (venetoclax) • vincristine • Marqibo (vincristine liposomal)
    13d
    BuCy Vs. TBICy for Allo-HSCT in T-ALL Patients (clinicaltrials.gov)
    P3, N=430, Not yet recruiting, The First Affiliated Hospital of Soochow University
    New P3 trial
    |
    cytarabine • cyclophosphamide • busulfan
    15d
    Transcriptional regulatory program controlled by MYB in T-cell acute lymphoblastic leukemia. (PubMed, Leukemia)
    Their expression can be recovered at later time-points, suggesting the presence of a negative feedback loop mechanism. In contrast, late response genes, which are continuously downregulated after MYB depletion, includes many genes involved in cell proliferation as well as TAL1 targets, thereby affecting the cellular phenotype.
    Journal
    |
    RUNX1 (RUNX Family Transcription Factor 1) • CXCR4 (Chemokine (C-X-C motif) receptor 4) • IKZF2 (IKAROS family zinc finger 2) • GATA3 (GATA binding protein 3)
    |
    CXCR4 expression
    17d
    A dual role for PSIP1/LEDGF in T cell acute lymphoblastic leukemia. (PubMed, Sci Adv)
    In cell lines, PSIP1 down-regulation leads to a reduction of COX20, an assembly factor of the cytochrome c oxidase in the mitochondria, and to a reduction in mitochondrial respiration. This indicates that PSIP1 can exert a dual role in the context of T-ALL, either as a tumor suppressor gene during tumor initiation or as a dependency factor in tumor maintenance.
    Journal
    |
    KMT2A (Lysine Methyltransferase 2A)
    |
    MLL rearrangement
    24d
    Super-Enhancer-Driven IRF2BP2 is Activated by Master Transcription Factors and Sustains T-ALL Cell Growth and Survival. (PubMed, Adv Sci (Weinh))
    Cleavage under targets and tagmentation (CUT&Tag) assays and immunoprecipitation revealed that IRF2BP2 cooperates with the master TFs of T-ALL cells, targeting the enhancer of the T-ALL susceptibility gene recombination activating 1 (RAG1) and modulating its expression. These findings provide new insights into the regulatory network within T-ALL cells, identifying potential new targets for therapeutic intervention.
    Journal
    |
    ERG (ETS Transcription Factor ERG) • ETS1 (ETS Proto-Oncogene 1) • IRF2 (Interferon Regulatory Factor 2) • ELF1 (E74 Like ETS Transcription Factor 1) • RAG1 (Recombination Activating 1)
    25d
    Branching NOTCH1 to DNA damage in T-cell acute lymphoblastic leukemia. (PubMed, Haematologica)
    Not available.
    Journal
    |
    NOTCH1 (Notch 1)
    26d
    A comprehensive consolidation of data on the connection between CDKN2A polymorphisms and the susceptibility to childhood acute lymphoblastic leukemia. (PubMed, Hematol Transfus Cell Ther)
    The aggregated data revealed that the rs3731217 variation offers protection against the development of pediatric acute lymphoblastic leukemia and the rs3731249 polymorphism is significantly correlated with susceptibility.
    Review • Journal
    |
    CDKN2A (Cyclin Dependent Kinase Inhibitor 2A)
    26d
    ALKBH5 promotes T-cell acute lymphoblastic leukemia growth via m6A-guided epigenetic inhibition of miR-20a-5p. (PubMed, Exp Cell Res)
    miR-20a-5p suppressed DDX5 transcription. In conclusion, ALKBH5-mediated m6A demethylation decreases DGCR8 binding to pri-miR-20a, thereby repressing miR-20a-5p expression and enhancing DDX5 expression, ultimately inhibiting T-ALL cell apoptosis and promoting proliferation.
    Journal
    |
    DDX5 (DEAD-Box Helicase 5) • ALKBH5 (AlkB Homolog 5, RNA Demethylase) • MIR20A (MicroRNA 20a)
    |
    DDX5 overexpression
    26d
    DARATALL-VHR: Daratumumab in VHR T-ALL Treated According to the ALL National Treatment Program (clinicaltrials.gov)
    P2, N=31, Recruiting, Gruppo Italiano Malattie EMatologiche dell'Adulto | Not yet recruiting --> Recruiting | Trial completion date: Jan 2029 --> Oct 2029 | Initiation date: May 2024 --> Oct 2024 | Trial primary completion date: Jan 2029 --> Oct 2029
    Enrollment open • Trial completion date • Trial initiation date • Trial primary completion date
    |
    cyclophosphamide • Darzalex Faspro (daratumumab and hyaluronidase-fihj)
    1m
    Single-cell sequencing technology to characterize stem T-cell subpopulations in acute T-lymphoblastic leukemia and the role of stem T-cells in the disease process. (PubMed, Aging (Albany NY))
    Stem T cells were involved in the development of Pre-T-ALL through the regulatory effects of transcription factors (TFs) KLF2 and FOS and multiple ligand-receptor pairs.
    Journal
    |
    CD74 (CD74 Molecule) • HAVCR2 (Hepatitis A Virus Cellular Receptor 2) • CCR7 (Chemokine (C-C motif) receptor 7) • TGFB1 (Transforming Growth Factor Beta 1) • LGALS9 (Galectin 9) • KLRD1 (Killer Cell Lectin Like Receptor D1)
    1m
    Isatuximab in Adult Patients With Cytologic or Molecular Relapsed/Refractory CD38 Positive T-cell Acute Lymphoblastic Leukemia (clinicaltrials.gov)
    P2, N=40, Not yet recruiting, Goethe University
    New P2 trial
    |
    bortezomib • Sarclisa (isatuximab-irfc)
    1m
    TARDBP drives T-cell acute lymphoblastic leukemia progression by binding MDM2 mRNA, involving β-catenin pathway. (PubMed, FASEB J)
    Moreover, XAV-939, a β-catenin inhibitor, was capable of suppressing the malignant phenotypes in TARDBP-overexpressed T-ALL cells...In aggregate, we explored a promising biomarker, TARDBP, for T-ALL treatment. The underlying mechanisms might involve the interaction with MDM2 mRNA and the regulation of the β-catenin pathway.
    Journal
    |
    TARDBP (TAR DNA Binding Protein)
    |
    XAV-939
    1m
    Ruxolitinib combined with venetoclax and azacitidine in the treatment of refractory T-ALL patients with JAK1, JAK3, and STAT5B gene mutations: a case report and literature review (PubMed, Zhonghua Xue Ye Xue Za Zhi)
    Notably, pleural effusion and mediastinal mass significantly improved the post-chest cavity infusion of dexamethasone combined with etoposide at the same stage. The patient also underwent allogeneic hematopoietic stem cell transplantation upon achieving bone marrow remission and was followed up until January 2024. Ruxolitinib combined with venetoclax and azacytidine has shown promising efficacy and safety in treating refractory T-ALL harboring the JAK1, JAK3, and STAT5B mutations, providing a novel therapeutic approach for such patients.
    Review • Journal
    |
    JAK1 (Janus Kinase 1) • JAK3 (Janus Kinase 3) • STAT5B (Signal Transducer And Activator Of Transcription 5B)
    |
    JAK3 mutation
    |
    Venclexta (venetoclax) • azacitidine • Jakafi (ruxolitinib) • etoposide IV • dexamethasone
    1m
    Biallelic Loss of 7q34 (TRB) and 9p21.3 (CDKN2A/2B) in Adult Ph-Negative Acute T-Lymphoblastic Leukemia. (PubMed, Int J Mol Sci)
    A clonal rearrangement of the TRB gene was revealed in 6 out of 7 cases with 7q34 biallelic loss. Both biallelic deletions can be considered favorable prognostic factors, with an association with 9p21 being statistically significant (p = 0.01) and a trend for 7q34 (p = 0.12) being observed.
    Journal
    |
    CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • PRSS1 (Serine Protease 1)
    |
    CDKN2A negative
    1m
    Enhancer looping protein LDB1 modulates MYB expression in T-ALL cell lines in vitro by cooperating with master transcription factors. (PubMed, J Exp Clin Cancer Res)
    To sum up, our research establishes the pivotal fuction of LDB1 in the tumorigenesis and progression of T-ALL cell lines. Mechanistic insights reveal that LDB1 cooperates with ERG, ETV6, and IRF1 to modulate the expression of downstream effector genes. Furthermore, LDB1 controls MYB through remote enhancer modulation, providing valuable mechanistic insights into its involvement in the progression of T-ALL.
    Preclinical • Journal
    |
    ETV6 (ETS Variant Transcription Factor 6) • MYB (MYB Proto-Oncogene, Transcription Factor) • ERG (ETS Transcription Factor ERG) • IRF1 (Interferon Regulatory Factor 1)
    |
    IRF1 expression
    1m
    Targeting CD5 CAR-T Cells in the Treatment of r/r CD5+ T-ALL (clinicaltrials.gov)
    P1, N=30, Recruiting, Zhejiang University
    New P1 trial
    1m
    The DHODH inhibitor teriflunomide impedes cell proliferation and enhances chemosensitivity to daunorubicin (DNR) in T-cell acute lymphoblastic leukemia. (PubMed, Ann Hematol)
    Moreover, combined treatment with TRF and daunorubicin (DNR) significantly reduced cell viability and promoted apoptosis in DNR-resistant T-ALL cells. Our study provides valuable insights into the critical role of TRF in treating T-ALL while increasing the sensitivity of DNR-resistant T-ALL cells to DNR.
    Journal
    |
    TP53 (Tumor protein P53) • BTG2 (BTG Anti-Proliferation Factor 2)
    |
    TP53 expression
    |
    daunorubicin
    2ms
    Molecular profiling of myeloid/natural killer (NK) cell precursor acute leukemia (PubMed, Rinsho Ketsueki)
    Our retrospective case study uncovered that outcomes of MNKPL are unsatisfactory, even with hematopoietic cell transplantation. Multi-omics analysis and in vitro drug sensitivity assays revealed increased sensitivity to L-asparaginase and reduced levels of asparagine synthetase, supporting the clinically observed effectiveness of L-asparaginase.
    Journal
    |
    NOTCH1 (Notch 1) • RUNX3 (RUNX Family Transcription Factor 3) • BCL11B (BAF Chromatin Remodeling Complex Subunit BCL11B)
    2ms
    Allogeneic CD5-specific CAR-T therapy for relapsed/refractory T-ALL: a phase 1 trial. (PubMed, Nat Med)
    This study provides insights that could help to optimize this promising intervention. ClinicalTrials.gov registration: NCT05032599 .
    P1 data • Journal
    |
    CD5 (CD5 Molecule) • CD7 (CD7 Molecule)
    2ms
    The NF-κB1/p50 Subunit Influences the Notch/IL-6-Driven Expansion of Myeloid-Derived Suppressor Cells in Murine T-Cell Acute Lymphoblastic Leukemia. (PubMed, Int J Mol Sci)
    Mechanistically, IL-6 increase relies on loss of the negative control exerted by the p50 subunit on the IL-6 promoter. Our results reveal the Notch/NF-κB cross-talk in regulating myeloid-derived suppressor cell biology in T-cell leukemia, highlighting the need to consider carefully the pleiotropic effects of NF-κB-based therapy on the tumor microenvironment.
    Preclinical • Journal
    |
    IL6 (Interleukin 6) • NOTCH3 (Notch Receptor 3)
    |
    NOTCH mutation
    2ms
    A Study to Investigate LP-118, Ponatinib, Vincristine and Dexamethasone in Relapsed/Refractory Acute Lymphoblastic Leukemia (ALL) or Lymphoblastic Lymphoma (LBL) (clinicaltrials.gov)
    P1/2, N=15, Recruiting, University of Chicago | Active, not recruiting --> Recruiting
    Enrollment open
    |
    Iclusig (ponatinib) • vincristine • Xatmep (methotrexate oral solution)
    2ms
    Focal deletions of a promoter tether activate the IRX3 oncogene in T-cell acute lymphoblastic leukemia. (PubMed, Blood)
    Unexpectedly, the CRNDE super-enhancer interacts with the IRX3 promoter with no transcriptional output until it is untethered from the FTO intronic site. We propose that 'promoter tethering' of oncogenes to inert regions of the genome is a previously unappreciated biological mechanism preventing tumorigenesis.
    Journal
    |
    FTO (Alpha-Ketoglutarate-Dependent Dioxygenase FTO) • CRNDE (Colorectal Neoplasia Differentially Expressed)
    2ms
    Targeting BTN2A1 enhances Vγ9Vδ2 T-cell effector functions and triggers tumor cell pyroptosis. (PubMed, Cancer Immunol Res)
    Together, these data demonstrate that targeting BTN2A1 with 107G3B5 enhances the Vγ9Vδ2 T-cell antitumor response by triggering the pyroptosis-induced immunogenic cell death. These new pyroptosis-based therapies have great potential to stimulate the immune system to fight cancer, especially "cold" tumors.
    Journal • Tumor cell
    |
    CASP3 (Caspase 3) • BTN2A1 (Butyrophilin Subfamily 2 Member A1) • CASP7 (Caspase 7)
    2ms
    Dual role of BCL11B in T-cell malignancies. (PubMed, Blood Sci)
    The antitumor effect of BCL11B suppression might be strengthened by generation of induced T to NK cells (ITNK). Therefore, there is an urgent need to develop a specific BCL11B inhibitor.
    Review • Journal
    |
    BCL11B (BAF Chromatin Remodeling Complex Subunit BCL11B)
    2ms
    CD123-Directed Autologous T-Cell Therapy for Acute Myelogenous Leukemia (CATCHAML) (clinicaltrials.gov)
    P1, N=32, Recruiting, St. Jude Children's Research Hospital | Active, not recruiting --> Recruiting
    Enrollment open
    |
    CD123 (Interleukin 3 Receptor Subunit Alpha) • IL3RA (Interleukin 3 Receptor Subunit Alpha)
    |
    Rituxan (rituximab) • cyclophosphamide • fludarabine IV • mesna • CD123-CAR T cell therapy
    2ms
    A Phase II Study of the Combination of Ponatinib with Mini-hyper CVD Chemotherapy and Venetoclax in Patients with Relapsed or Refractory T-cell Acute Lymphoblastic Leukemia (clinicaltrials.gov)
    P2, N=26, Active, not recruiting, M.D. Anderson Cancer Center | Recruiting --> Active, not recruiting
    Enrollment closed
    |
    BCL2 (B-cell CLL/lymphoma 2)
    |
    Venclexta (venetoclax) • Iclusig (ponatinib)
    2ms
    Total Marrow and Lymphoid Irradiation and Chemotherapy Before Donor Transplant in Treating Patients with Myelodysplastic Syndrome or Acute Leukemia (clinicaltrials.gov)
    P1, N=24, Active, not recruiting, City of Hope Medical Center | Trial completion date: Jun 2024 --> Dec 2024 | Trial primary completion date: Jun 2024 --> Dec 2024
    Trial completion date • Trial primary completion date • Post-transplantation
    |
    FLT3 (Fms-related tyrosine kinase 3) • HLA-DRB1 (Major Histocompatibility Complex, Class II, DR Beta 1)
    |
    MLL rearrangement • Chr t(9;11)
    |
    cyclophosphamide • fludarabine IV
    2ms
    A Study to Investigate LP-118, Ponatinib, Vincristine and Dexamethasone in Relapsed/Refractory Acute Lymphoblastic Leukemia (ALL) or Lymphoblastic Lymphoma (LBL) (clinicaltrials.gov)
    P1/2, N=15, Active, not recruiting, University of Chicago | Not yet recruiting --> Active, not recruiting | N=33 --> 15 | Initiation date: Apr 2025 --> Sep 2024
    Enrollment closed • Enrollment change • Trial initiation date
    |
    Iclusig (ponatinib) • vincristine • Xatmep (methotrexate oral solution)