cytarabine / Generic mfg. - LARVOL DELTA

Safety and Efficacy of Condensed High-Dose Cytarabine Consolidation (HiDAC-123) Versus Standard HiDAC-135 in Adults with AML in First Remission (HOPA 2026) - "In this single-center cohort, HiDAC-123 demonstrated comparable OS and RFS to HiDAC-135 while providing improvements in ANC recovery, bacterial infection rates, and hospital utilization. Survival outcomes may reflect limited event counts and heterogeneity in post-consolidation therapies. These findings support HiDAC-123 as a safety-optimized, resource-efficient consolidation strategy."

Clinical • Acute Myelogenous Leukemia • Febrile Neutropenia • Hematological Disorders • Infectious Disease • Neutropenia

Impact of granulocyte-colony stimulating factor use on the incidence of febrile neutropenia in acute myeloid leukemia patients undergoing high dose cytarabine consolidation therapy (HOPA 2026) - "These risks may be even higher when patients receive certain concomitant tyrosine kinase inhibitors (TKI) and gemtuzumab ozogamicin (GO). A total of 41 patients were included in the initial analysis, however; only 33 patients met inclusion criteria for data analysis. The duration of neutropenia appeared to persist longer across all cycles in patients who did not receive G-CSF vs. those who received G-CSF."

Acute Myelogenous Leukemia • Febrile Neutropenia • Hematological Malignancies • Infectious Disease • Leukemia • Neutropenia

Evaluation of Outcomes for HiDAC-135 Versus HiDAC-123 (HOPA 2026) - "Pending Conclusions/ Pending"

Acute Myelogenous Leukemia • Febrile Neutropenia • Hematological Disorders • Hematological Malignancies • Leukemia • Neutropenia

Comparing Incidence of Febrile Neutropenia Following HyperCVAD Cycle 4 Part B vs. Previous Cycles: Evaluating Risk vs. Benefit of Final Cycle Omissions or Dose Reductions (HOPA 2026) - "Background/Rationale The HyperCVAD regimen, which alternates between two cytotoxic components—Part A (cyclophosphamide, vincristine, doxorubicin, and dexamethasone) and Part B (high-dose methotrexate and cytarabine)—is a cornerstone of therapy for adult patients with acute lymphoblastic leukemia (ALL) and Burkitt's lymphoma, producing high complete remission rates...Results Results are pending at the time of abstract submission. ConclusionsConclusions are pending completion of data analysis."

Acute Lymphocytic Leukemia • Burkitt Lymphoma • Febrile Neutropenia • Hematological Disorders • Hematological Malignancies • Human Immunodeficiency Virus • Infectious Disease • Leukemia • Lymphoma • Neutropenia

Assessing the Safety and Efficacy of Cladribine, Low-Dose Cytarabine Plus Venetoclax in Patients with Newly Diagnosed, and Relapsed/Refractory Acute Myeloid Leukemia (HOPA 2026) - "Despite this, complete remission rates with azacitidine and venetoclax remain modest at approximately 36.7%2, underscoring the ongoing need for additional effective and tolerable treatment options. Conclusion to be presented upon completion of final data analysis."

Clinical • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia

Impact of Granulocyte Colony Stimulating Factor on High Dose Cytarabine Consolidation in Acute Myeloid Leukemia (HOPA 2026) - "In progress."

Acute Myelogenous Leukemia • Chemotherapy-Induced Neutropenia • Febrile Neutropenia • Hematological Malignancies • Infectious Disease • Leukemia • Neutropenia

Incidence of Cytarabine Syndrome in High-Dose Cytarabine with and without Steroid Premedication (HOPA 2026) - "In February of 2018, Yale New Haven Health System (YNHHS) removed steroids as a premedication to HDAC consolidation regimen and switched to a neurokinin 1 receptor antagonist and ondansetron. Research in Progress"

Acute Myelogenous Leukemia • Hematological Malignancies • Infectious Disease • Leukemia • Musculoskeletal Pain

Real-World Effectiveness of Intensive Venetoclax plus Purine Analog-Based Induction (FLAG-IDA-Ven or CLIA-Ven) for Newly Diagnosed Acute Myeloid Leukemia (HOPA 2026) - "Background/rationale: Cytarabine plus daunorubicin (7+3) remains a standard induction regimen for adults with newly diagnosed acute myeloid leukemia (AML). research in progress"

Clinical • Real-world • Real-world effectiveness • Real-world evidence • Acute Myelogenous Leukemia • Bone Marrow Transplantation • Hematological Malignancies • Leukemia

Safety and Effectiveness of Micafungin Prophylaxis in Patients Receiving 7+3 Chemotherapy with FLT3 Inhibitor for Acute Myeloid Leukemia (HOPA 2026) - "Background/Rationale: FMS-like tyrosine kinase (FLT3) gene mutations occur in approximately 30% of patients with newly diagnosed acute myeloid leukemia (AML).1 Two FLT3 inhibitors (FLT3i), midostaurin and quizartinib, are approved for frontline treatment of FLT3-positive AML in combination with 7+3 (cytarabine plus daunorubicin/idarubicin).2 Grade 3 neutropenia is common with 7+3+FLTi therapy, necessitating invasive fungal infection (IFI) prophylaxis. These results demonstrate the safe and efficacious use of micafungin for IFI prophylaxis in patients with AML treated with 7+3+FLT3i therapy. Rates of IFIs in this cohort were similar to historical comparators utilizing mold-active azoles for antifungal prophylaxis. 5,6 Notably, most IFIs in this study were classified as possible, with rates of proven IFIs comparable to those previously reported with mold-active azoles.5,6 Additionally, rates of FLT3i dose change, induction response outcomes, and hematologic recovery were..."

Clinical • Acute Myelogenous Leukemia • Hematological Disorders • Hematological Malignancies • Infectious Disease • Leukemia • Neutropenia • FLT3

Efficacy of blinatumomab use in B-cell acute lymphoblastic leukemia (ALL) patients with discordant minimal residual disease (MRD) monitoring assays (HOPA 2026) - "Eligible patients received HyperCVAD as induction therapy, consisting of alternating A cycles (cyclophosphamide, mesna, doxorubicin, vincristine, and dexamethasone) and B cycles (high-dose methotrexate and cytarabine). The primary outcome was complete MRD response by NGS following one to two cycles of blinatumomab, assessed through manual chart review. Results/Discussion/Conclusion (State if not available): This study is ongoing therefore results, discussion, and conclusions are not yet available."

Clinical • Discordant • Minimal residual disease • Residual disease • Acute Lymphocytic Leukemia • B Acute Lymphoblastic Leukemia • Hematological Malignancies • Leukemia

A Study to Find the Highest Dose of SNDX-5613 (Revumenib) as a Treatment Option After Hematopoietic Stem Cell Transplant in Children With Acute Lymphoblastic Leukemia, Acute Myeloid Leukemia, and Mixed Phenotype Acute Leukemia (clinicaltrials.gov) - P1 | N=29 | Not yet recruiting | Sponsor: Children's Oncology Group

New P1 trial • Acute Lymphocytic Leukemia • Acute Myelogenous Leukemia • Bone Marrow Transplantation • Hematological Malignancies • Leukemia • Oncology • Pediatrics • Transplantation • CD4 • KMT2A • NUP98

Insights into chemotherapy-related cognitive impairment in childhood acute myeloid leukemia survivors (AACR 2026) - "Standard induction therapy for pediatric AML involves the use of high dose Ara-C intrathecal chemotherapy for CNS prophylaxis, sometimes combined with Methotrexate, both well-documented causal agents regarding neurotoxicity and their link to CRCI. A significant fraction of pediatric AML survivors experience CRCI may be suffering from unrecognized health conditions, and as such may largely benefit from increased neurocognitive monitoring and resources. As for future pediatric AML patients, careful consideration of these neurocognitive consequences could inform risk-stratified intensity adjustments and introduce targeted neuroprotective strategies during therapy, minimizing cognitive morbidity and allowing patients to not only live longer, but live better."

Clinical • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology

Multiomic state-transition framework reveals chemotherapy-induced metabolic reprogramming in acute myeloid leukemia (AACR 2026) - "Using a CBFB::MYH11 knock-in murine model of AML, we collected weekly peripheral blood samples before and after a "5+3" chemotherapy regimen consisting of cytarabine and daunorubicin, modeling the standard-of-care "7+3" regimen. Importantly, model simulations capture response followed by relapse similar to the mRNA and miRNA time-series data trajectories. Together, our findings demonstrate that a mathematically grounded, multiomic state-transition framework captures chemotherapy-induced transcriptomic and metabolic dynamics, offering a systematic approach to predict response and identify metabolic vulnerabilities in AML."

Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology

Cuproptosis induction in TP53-mutated acute myeloid leukemia (AACR 2026) - "In contrast, cytarabine, idarubicin, and venetoclax activity was substantially diminished in TP53-deficient cells, consistent with the known resistance of TP53-mutated AML to these standard therapies. Notably, combining low-dose elesclomol with the hypomethylating agent decitabine, which has established clinical efficacy in TP53-mutated AML, produced a synergistic increase in apoptosis in TP53-deficient AML cells.Together, these findings demonstrate that copper ionophores can bypass TP53-associated resistance to AML cell death by activating cuproptosis rather than relying on p53-dependent apoptotic pathways. The robust activity of copper ionophores across diverse TP53-deficient AML models, coupled with the enhanced efficacy observed in combination with decitabine, underscores cuproptosis induction as a promising therapeutic approach for TP53-deficient AML."

Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • TP53

A novel thioxanthenone activates p47phox to exploit redox vulnerabilities in acute myeloid leukemia (AACR 2026) - "06-30 induces robust and selective cytotoxicity across genetically diverse AML cell lines including models resistant to standard of care agents (cytarabine, azacitidine), and demonstrates strong activity in primary AML blasts with adverse molecular profiles. Thus, thioxanthenone 06-30 represents both a first-in-class mechanistic probe and a promising therapeutic lead for redox-based targeting in AML. Together, these findings provide strong rationale for the further preclinical development and eventually clinical investigation of 06-30 as a strategy to exploit redox vulnerabilities in leukemia and improve outcomes for patients with limited therapeutic options."

Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • CD34 • FLT3 • TP53

Synergistic antileukemic activity of JAK inhibition combined with cytarabine in acute megakaryoblastic leukemia (AACR 2026) - "Our results provide robust preclinical evidence that combining JAK inhibition with cytarabine yields synergistic antileukemic effects in AMKL, including in a niche-protected context, and significantly improves in vivo outcomes. This data strongly supports the rationale for clinical evaluation of this combination in AMKL patients, especially those with JAK-STAT pathway activation."

Hematological Malignancies • Leukemia • Oncology • ANXA5 • STAT3 • STAT5

LEDGF/p75 drives chemoresistance in CML via JAK/STAT pathway modulation (AACR 2026) - "In KMT2A-wild-type (WT) AML cell lines U-937 and Kasumi-1, LEDGF/p75 depletion did not alter cytarabine sensitivity and the same trend was observed in WT T-ALL cell lines Jurkat and SupT-1...Interestingly, LEDGF/p75 KD in two WT KMT2A CML cell lines, K-562 and JUR-MK1, led to a significant reduction in proliferation upon vincristine treatment (IC50 K-562 Mock/KD: 2.61 ± 0.10 nM / 0.81 ± 0.09 nM and IC50 JUR-MK1 Mock/KD: 3.93 ± 0.35 nM / 2.37 ± 0.30 nM) and increased apoptosis with elevated caspase3. Treatment of K-562 cells with BCR-ABL inhibitors Imatinib and Ponatinib also showed decreased proliferation upon LEDGF/p75 depletion...Taken together, our result indicates that the role of LEDGF/p75 in therapy resistance is context dependent and varies across leukemic subtypes. We identify a previously unknown function of LEDGF/p75 in mediating drug resistance in CML cells acting through the JAK/STAT Pathway."

Breast Cancer • Chronic Myeloid Leukemia • Hematological Malignancies • Leukemia • Oncology • Prostate Cancer • Solid Tumor • T Acute Lymphoblastic Leukemia • ABL1 • BCL2A1 • BCL2L1 • BCR • CASP3 • KMT2A • STAT2 • STAT5

Tenofovir Alafenamide Promotes Differentiation and Induces Apoptosis of AML Cells by Inhibiting Telomerase Reverse Transcriptase. (PubMed, Anticancer Res) - "TAF may serve as a promising novel therapeutic agent for the treatment of AML."

Journal • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • ITGAM • TERT

MSTN and TCF12 as Candidate Immunometabolic Signatures in Glioma-Associated Foam Cells: Insights from Integrated Multi-Omics Analysis. (PubMed, Curr Issues Mol Biol) - "Additionally, drug sensitivity prediction analysis demonstrated that MSTN expression was significantly associated with sensitivity to paclitaxel and VE-822, while TCF12 expression showed potential associations with sensitivity to cytarabine, olaparib, Wee1 inhibitor, paclitaxel, and VE-822. Immunofluorescence confirmed upregulated expression of MSTN and TCF12 in glioma tissues and their co-localization with macrophages. In conclusion, this study identified TAFCs as the central cells in the glioma microenvironment, with their signature genes MSTN and TCF12 representing candidate immunometabolic signatures associated with macrophage-mediated immunosuppression and metabolic reprogramming in glioma, suggesting their potential as biomarkers for patient stratification and as targets for immunometabolic therapies."

Journal • Brain Cancer • Glioma • Oncology • Solid Tumor • TCF12

Epigenetic Activity of Cancer Therapy Drugs Revealed by HeLa TI Cell-Based Assay. (PubMed, Epigenomes) - "Our findings show that many anticancer therapy agents modulate the epigenetic landscape of cancer cells, providing a rationale for expanding their therapeutic applications and enhancing the efficacy of combination strategies by overcoming epigenetically driven chemoresistance."

IO biomarker • Journal • Oncology

Small-molecule inhibitors as salvage therapy for CBFB::MYH11-associated acute myeloid leukemia (AACR 2026) - "Although chemotherapy with cytarabine and an anthracycline induces high remission rates, it often causes severe side effects, and relapse is common...Ongoing studies will assess SM1's impact on animal survival and aim to extend both in vitro and in vivo analyses to additional lead compounds identified in our in-silico screening. The success of this study could enable the development of a small-molecule therapeutic toolkit for chemoresistant AML harboring CBFB::MYH11 and support future applications in other AML subtypes with oncogenic fusions."

Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • RUNX1

G3BP1 knockdown sensitizes the acute myeloid leukemia cell line HL60 to venetoclax by inducing apoptosis (AACR 2026) - "HL60/shG3BP1 cells exhibited reduced sensitivity to Ara-C compared to control cells (IC50 value: 7 µM, 0.5 µM, respectively), while conversely demonstrating increased sensitivity to venetoclax (IC50 value: 4nM, 900nM, respectively). Sensitivity to other tested agents, including daunorubicin, etoposide, and Decitabine, remained unchanged. Knockdown of G3BP1 in HL60 cells resulted in enhanced sensitivity to venetoclax. This enhanced sensitivity might be explained by the impairment of G3BP1-mediated SG formation."

IO biomarker • Preclinical • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • BCL2 • CASP3 • G3BP1 • WT1

Regulation of ribosomal RNA synthesis in acute myeloid leukemia (AACR 2026) - "This synergy did not extend to other AML chemotherapy agents, such as daunorubicin or cytarabine, indicating a unique, synthetically lethal interaction between the rRNA synthesis and Bcl-2 signaling pathways in AML cells.In summary, we demonstrate that rRNA synthesis and Pol1 expression are amplified in AML cells to sustain an oncogenic, stem-like state that renders them more resistant to apoptotic stimuli. Notably, our findings identify rRNA synthesis as a therapeutic vulnerability in AML cells and uncover a novel synthetic lethality with Bcl-2 inhibition."

IO biomarker • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • HOXA9

Leukemia Cutis: Clinicopathologic and Genomic Correlation in Skin–Marrow Pairs (USCAP 2026) - "Most c-AML cases (80%) received 7+3 chemotherapy while CMN treatments varied, including inqovi, tyrosine kinase inhibitors, hypomethylating agents alone or with venetoclax...Results Table: Table 1: Clinicopathologic and Genomic Correlation among myeloid neoplasms (acute and chronic) involving skin and bone marrow BM- bone marrow, CML- chronic myeloid leukemia, MPN- myeloproliferative neoplasm, CMML- chronic myelomonocytic leukemia, a CML- atypical chronic myeloid leukemia, BCR::ABL1 negative, MDS/MPN- myelodysplastic/myeloproliferative neoplasm, MDS- myelodysplastic syndrome, WBC- white blood cell count, Hb- hemoglobin, PLT- platelet count, MR-myelodysplasia related, NOS- not otherwise specified, 7 + 3 therapy- cytarabine + anthracycline, HMA- hypomethlating agents, Ven-venetoclax, FLAG-Ida-Ven- fludarabine + cytarabine+ granulocyte colony-stimulating factor (G-CSF)+ idarubicin+ venetoclax, TKI-tyrosine kinase inhibitor, BMT-bone marrow transplant, CR- clinical..."

Clinical • Acute Myelogenous Leukemia • Atypical Chronic Myeloid Leukemia • Bone Marrow Transplantation • Chronic Myeloid Leukemia • Chronic Myelomonocytic Leukemia • Hematological Disorders • Hematological Malignancies • Leukemia • Myelodysplastic Syndrome • Myeloproliferative Neoplasm • ABL1 • ASXL1 • DNMT3A • ETV6 • FLT3 • JAK2 • KMT2A • KRAS • NPM1 • NRAS • PTPN11 • RUNX1 • TET2 • TP53 • WT1

Beyond Blast Clearance: Pilot Study of Morphologic Trajectories after Venetoclax-based Therapy in Acute Myeloid Leukemia (AML) (USCAP 2026) - "Background: Venetoclax (VEN) with a hypomethylating agent or low-dose cytarabine is widely used as initial therapy for adults with newly diagnosed AML who are ineligible/not candidates for intensive induction chemotherapy. At the first post-VEN assessment most patients entered morphologic remission, yet a meaningful minority had persistent AML with erythroid or monocytic shifts. EH was common in remission and with persistence, underscoring the need to distinguish reactive EH from blast-equivalent ES during response evaluation. While underpowered for definitive genomic associations, this study highlights pitfalls in post-VEN interpretation and supports prospective studies with standardized timepoints, genomics, MRD, and focus on erythroid events."

Clinical • Acute Myelogenous Leukemia • Hematological Disorders • Hematological Malignancies • Leukemia • DNMT3A • NPM1 • RUNX1 • TP53