Farydak (panobinostat) / Secura Bio - LARVOL DELTA

An evolving landscape – how changing conditioning regimes can improve myelofibrosis transplant outcomes. (ASH 2025) - "Of the 16 cases, seven received Fludarabine/Busulphan/Antithymocyte globulin (Flu/Bu/ATG) conditioning (Fludarabine 30mg/m 2 day -9 to day -5, Busulphan 3.2mg/kg on day -4 and day -3 and rabbit ATG 2.5mg/kg on day -2 and day -1), seven underwent Fludarabine/Cyclophosphamide (Flu/Cy) conditioning (Fludarabine 25mg/m 2 day -6 to day -2 and Cyclophosphamide 1g/m 2 on day -3 and day -2), and two received Fludarabine/Melphalan (Flu/Mel) (Fludarabine 25mg/m 2 day -6 to day -2 and Melphalan 100mg/m 2 on day -2)...Therapies included Ruxolitnib, Momelotinib, splenic irradiation, Hydroxycarbamide, Danazol, Interferon, Cyclophosphamide, Anagrelide, Thalidomide, Panobinostat and Navitoclax...Although limited by a small sample size, these findings indicate that the Flu/Bu/ATG conditioning regimen may be associated with improved outcomes, thereby supporting its adoption as the preferred approach for patients undergoing allogeneic stem cell transplantation for myelofibrosis as per BSH..."

Acute Graft versus Host Disease • Chronic Graft versus Host Disease • Graft versus Host Disease • Immunology • Infectious Disease • Myelofibrosis • Pneumonia • Respiratory Diseases • Transplantation • ASXL1 • CALR • JAK2 • SF3B1 • U2AF1

Real-world treatment landscape after anti-BCMA CAR T-cell therapy in relapsed/refractory multiple myeloma: An international Study (ASH 2025) - "Novel BCMA-targeted therapies, such as CAR T-cells (cilta-cel from 2nd line, ide-cel from 3rd line) and bispecific T-cell engagers (e.g., teclistamab, elranatamab from 4th line), have become new standards of care...Abbreviations: K=carfilzomib; E=elotuzumab; Pom=pomalidomide; d=dexamethasone; Isa=isatuximab; F=panobinostat; R=lenalidomide; Tec=teclistamab; X=selinexor; Elra=elranatamab; Belamaf=belantamab mafodotin; Ixa=ixazomib... This real-world study of 100 MM patients relapsing after anti-BCMA CAR T-cell treatment shows that 91% were in their 4th or 5th line of therapy. A large majority were triple-class exposed, and 52% were lenalidomide-refractory. In the absence of a clear standard of care, common treatments were identified: elotuzumab- and isatuximab-based regimens in the 3rd line; teclistamab and elotuzumab-based options in the 4th line; and teclistamab, elranatamab, and belantamab mafodotin in the 5th line."

CAR T-Cell Therapy • Clinical • HEOR • Real-world • Real-world evidence • Cardiovascular • Diabetes • Dyslipidemia • Hematological Malignancies • Hypertension • Metabolic Disorders • Multiple Myeloma • Renal Disease

A functional precision medicine clinical trial in Relapsed/Refractory multiple myeloma: Prospective study of a high throughput drug sensitivity assay on correlation of drug sensitivity scores with treatment response (ASH 2025) - P=N/A | "All patients (100%) had prior exposure to lenalidomide, 97.5% to bortezomib, 85% to carfilzomib, 82% to daratumumab, 77.5% to pomalidomide, and 12.5% BCMA CAR-T therapy...From Oncopanel2 v1, the top drugs by DSS included bortezomib (median DSS 47.7), carfilzomib (median DSS 47.3), panobinostat (median DSS 47), and romidepsin (median DSS 45.4). From Oncopanel2 v2, the top drugs by DSS were marizomib (an investigational PI, with median DSS 46.1), carfilzomib (median DSS 40.2), ixazomib (median DSS 37.2), and oprozomib (an investigational PI, with median DSS 31.6)... The use of a high throughput drug sensitivity assay was feasible among patients with relapsed/refractory MM. In our analysis of drug-specific DSS thresholds for bortezomib and Selinexor, DSS performance varied by agent, highlighting the need for drug-specific threshold optimization. In the patients who received Selinexor, there was a non-significant tendency toward higher DSS scores in responders,..."

Clinical • IO biomarker • Hematological Malignancies • Leukemia • Multiple Myeloma • Plasma Cell Leukemia • Plasmacytoma • SDC1

Profiling drug sensitivity in CLL B cells after BTK inhibitor progression using a novel drug panel (ASH 2025) - " Using the Mayo Clinic CLL Database and the Mayo Clinic CLL Tissue Bank, we identified 47 patients with RR CLL, all of whom experienced disease progressionon a BTKi (35 ibrutinib +/- CD20 antibody, 10 acalabrutinib +/- CD20 antibody, 2 other)...We also observed that RR CLL cohort exhibited significantly increased drug resistance to most of the tested drugs in the presence of BMSCs with corresponding increases in IC50s (with vs. without BMSCs, fold-change respectively): LP-118 3.92-fold, venetoclax 1.98-fold, carfilzomib 2.58-fold, TP-0903 1.65-fold, panobinostat 204.23-fold, TCIP1 1.91-fold, crenolanib 1.31-fold, idasanutlin 1.69-fold, belinostat 6.14-fold, LP-168 1.29-fold, eprenetapopt 3.44-fold and GTE 1.08-fold (11 out of 12 with p -values <0.05 except for GTE which was not significant, Mann-Whitney U test)... Our results highlight the spectrum of currently available drugs that show promise for therapeutic use in patients with RR CLL who experience disease..."

IO biomarker • Chronic Lymphocytic Leukemia • Hematological Malignancies • Leukemia • AXL • BCL2 • STAT6 • TP53

Efficacy of novel agents in the treatment of acute myeloid leukemia and myelodysplastic syndrome: A systematic review and meta-analysis (ASH 2025) - "Newer agents included for AML were Guadectiabine, Magrolimab, Alvocidib, Enasidenib, Flotetuzumab, Vadastuximab, Mitoxantrone, Pevonedistat, Entospletinib, Eprenetapopt, Belinostat, Onvansertib, Panobinostat, Cediranib Maleate, Nilotinib, Emavusertib, and anti-CD45 antibody (DOTA-BC8). The newer agents investigated for MDS included Rigosertib, Imetelstat, Pembrolizumab, Enasidenib, Sabatolimab, Ivosidenib, Elitercept, Pevonedistat, Emavusertib, Atezolizumab, and Olutasidenib...All patients were treated concomitantly with either azacitidine (77%) or decitabine (23%)... This meta-analysis and systematic review demonstrate promising efficacy for novel agents in AML and MDS patients. There is a need for prospective trials with larger patient populations to investigate these agents further."

Retrospective data • Review • Acute Myelogenous Leukemia • Hematological Disorders • Hematological Malignancies • Leukemia • Myelodysplastic Syndrome • Neutropenia • TP53

Developing epigenetic synergistic drug combinations with albendazole in paediatric acute myeloid leukaemia (ASH 2025) - "Similar anthelmintic agents, mebendazole (MBZ) and parbendazole (PBZ), have been reported to have effects on epigenetic regulators that alter C-MYB degradation (Walf-Vorderwülbecke et al...These epigenetic hits represent various target families such as HDAC inhibitors (vorinostat, panobinostat, and CUDC-101), BET inhibitors (OTX-015, PFI-1, and (-)-JQ), aurora kinase inhibitors (MK-8745 and JNJ-7706621), and DNA synthesis inhibitors (cytarabine)...HDAC inhibitors (vorinostat), BET inhibitors (OTX-015) and histone methyltransferase (MS023) were among the most represented epigenetic target families, indicating potential mechanism of action of the novel ABZ+epigenetic combination. The novel drug candidate ABZ was found to have remarkable anti-leukaemia efficacy in murine and human models of childhood AML in vitro and in vivo while having negligible effects in normal cells. Current work is focused on evaluating ABZ+epigenetic synergistic combinations that will be taken..."

Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Pediatrics • HOXA9 • IL1B • MEIS1

Multi‑omics analysis of Del20q reveals PHF20 haploinsufficiency and an HDAC2-centered epigenetic circuit in myeloid neoplasms (ASH 2025) - "Consistent with these roles,preliminary results in a PHF20 knockdown model in TF-1 cells showed accelerated proliferation andrendered the line cytokine-independent, functionally validating its leukemogenic potential.Transcriptome-wide analysis of del20q patient samples revealed an inverse correlation between PHF20and HDAC2 expression (r²=0.40, p=0.047); HDAC2 is the chief de-acetylase that removes H4K16ac, andloss of PHF20 appears to shift chromatin toward a heterochromatic, differentiation-blocked state.We screened six primary del20q AML samples and found marked BCL-2 dependence: venetoclax IC₅₀ 0.12µM versus 0.48 µM in diploid controls (ΔAUC –0.23, p=0.009) and a similar differential for ABT-737 (ΔAUC–0.21, p=0.012). In two tested samples, panobinostat showed promising activity (ΔAUC +0.17, p=0.17),suggesting that the PHF20–HDAC2 axis is therapeutically exploitable...These insights identify venetoclax-based regimens, potentiallypotentiated by HDAC..."

IO biomarker • Brain Cancer • Glioblastoma • Hematological Malignancies • Leukemia • Melanoma • Solid Tumor • BCL2 • CD34 • HDAC2 • TP53

Multiomics-guided ex vivo drug sensitivity testing in Relapsed/Refractory Acute Myeloid Leukemia (ASH 2025) - "DNMT3A mutation suggested response tonavitoclax and KPT-330 (OR 8.4, p=0.18; OR 4.2, p=0.5, respectively). Associations were also foundbetween FLT3 mutation or short relapse latency among navitoclax responders (OR 4.2, p=0.5; eachrespectively).FLT3 mutants were associated with ponatinib sensitivity which was linked to FGFR3/FGFR4 upregulationin responders (OR 4.2, p=0.5). Furthermore, samples of patients who relapsed quickly were sensitive toeprenetapopt, wherein responders had upregulation of target gene MDM2 (OR 2.7, p=0.6). All patientsamples were highly sensitive to Panobinostat...Crucially, this proof-of-concept results supports a precision-medicine framework combininggenomic insights with functional drug screening, might offer actionable options for a patient group that isotherwise limited to supportive care alone. Further validation in larger cohorts of specific targets andtranslating and repurposing drugs post exvivo DS through potential clinical trials are ongoing."

Preclinical • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • BCL2L1 • DNMT3A • FGFR3 • FGFR4 • FLT3 • IDH2 • MDM2 • MIR15A • MIR182

Phase I study of the histone deacetylase inhibitor panobinostat in sickle cell disease (ASH 2025) - P1 | "Introduction: Reactivation of HbF in adult life is a proven effective therapy for β-hemoglobinopathies.Hydroxyurea (HU) is the only FDA approved drug for sickle cell disease (SCD) that ameliorates diseaseseverity by inducing fetal hemoglobin (HbF). A third subject will be enrolled to complete Cohort 2, and if no DLTs areobserved, dose escalation to Cohort 3 (20 mg MWF continuous x 12 weeks) will be initiated, for a total of12 additional subjects to be enrolled. Our findings in both Cohorts support the ability of PAN to increaseHbF in vivo. The observation of an increase in HbF by HPLC in Cohort 2 is encouraging."

Epigenetic controller • P1 data • Beta-Thalassemia • Cardiovascular • Genetic Disorders • Hematological Disorders • Sickle Cell Disease • STAT5 • STAT5AWqe • TFRC

Azacitidine-panobinostat activates NF-kb signaling in the bone marrow microenvironment to chemosensitize KMT2A rearranged pediatric AML (ASH 2025) - "While IFN-a sensitizedNTPL-146 and DF-5 to cytarabine (cyt) and daunorubicin (dauno), exogenous IFN-a failed to mimic aza-pano mediated sensitivity in NTPL-377, indicating aza-pano mediated sensitivity is dependent on IFN-asignaling in NTPL-146 and DF-5 but not NTPL-377. If cell death induced by aza-pano is regulated by IFNsignaling, then inhibiting a downstream regulator of IFN receptor signaling with ruxolitinib (rux) shouldreverse chemosensitivity...These data confirm that thepresence of functional immune system promotes survival by aza-pano.Thus, transcriptional activation of inflammatory signaling and an immune response is responsible fortherapeutic efficacy of aza-pano. Mechanistically, we have shown that aza-pano primes KMT2Ar AML byhyperactivation of NFkB signaling."

Clinical • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Pediatrics • IL1B • IL2 • KMT2A • MEF2C • MLLT1 • MLLT10 • MLLT3 • NFKBIA • STAT5 • TNFAIP3

Identifying common transcriptional mechanisms in treatment-resistant glioma. (SNO 2025) - "Background: Glioma, the most common primary brain tumor, shows poor prognosis and resistance to first-line therapies, like temozolomide (TMZ), lomustine (LOM) and panobinostat-marizomib (PM), complicating treatment and diminishing disease-free survival. RNA-sequencing identified common genes linked to TMZ, LOM, and PM chemoresistance, revealing key genetic networks involved in acquiring and maintaining drug resistance. Targeting these pathways, along with epigenetic silencing and/or combinatorial therapies, may resensitize chemoresistant cells and allow for effective treatment of glioma."

Brain Cancer • Glioma • High Grade Glioma • Solid Tumor • ERBB4 • FOXA1 • PDGFRA • SOX2

Medical Writing Bias in Myeloma Clinical Research: A Comprehensive Analysis (ASH 2023) - "Methods Clinical study papers from PubMed between January 2000 and March 2023 were analyzed if at least 1 of the 10 following drugs were evaluated: bortezomib (BORT), carfilzomib (CARF), daratumumab (DARA, elotuzumab (ELO), isatuximab (ISA), ixazomib (IXA), lenalidomide (LEN), panobinostat (PAN), pomalidomide (POM), and selinexor (SELI), and the manufacturer of the drug(s) sponsored the study (N=1466). Specific journals including Blood and British Journal of Haematology both show high numbers of papers with potential writing bias; and, furthermore, a high percentage of papers published in high impact journals such as the New England Journal of Medicine and Lancet show this type of potential bias. This practice of allowing medical writing to be carried out by those with direct ties to the pharmaceutical company is likely to result in the publication of papers with results and conclusions regarding the efficacy and safety of drugs that are biased which compromises their..."

Clinical • Hematological Disorders • Hematological Malignancies • Multiple Myeloma • Oncology

Belantamab Mafodotin + Bortezomib + Dexamethasone Versus 2L+ Relapsed/Refractory Multiple Myeloma Regimens: Lenalidomide-Exposed, Lenalidomide-Refractory, High-Risk Cytogenic, and 2L-Only Subpopulations: A Network Meta-Analysis (ASH 2024) - P3 | "The phase III DREAMM-7 study (NCT04246047) evaluated belantamab mafodotin (B), an antibody-drug conjugate targeting B-cell maturation antigen, with bortezomib (V)+dexamethasone (d; BVd) vs daratumumab (D)+Vd (DVd) in patients with RRMM who had ≥1 prior line of therapy (2L+) and included patients who were len-exposed/refractory (Hungria et al...NMAs were constructed based on the availability of regimen data within the networks for each subpopulation of interest (2L+ len-exposed, len-refractory, 2L-only and high-risk cytogenetic).Results : All regimens compared with BVd were PI-based regimens.The len-exposed subpopulation network comprised 8 RCTs and included the following regimens : BVd, DVd, carfilzomib (K)+ d (Kd; plus an alternative dosage), DKd, isatuximab (Isa)+ Kd (IsaKd), pomalidomide (P)+ Vd (PVd), selinexor (S)+Vd (SVd), and Vd...HRs (95% credible interval [CrI]) for BVd compared with anti-CD38 regimens included 0.34 (0.17-0.71) vs DKd, 0.29 (0.13-0.64) vs..."

IO biomarker • Retrospective data • Hematological Malignancies • Multiple Myeloma • Oncology

Establishment of a stable replicon cell line of Tembusu virus (TMUV) for high-throughput antiviral screening. (PubMed, Poult Sci) - "Using the Vero-TMUV replicon system, three compounds, Panobinostat, Floxuridine, and 5-Fluorouracil were screened out as promising antiviral candidates, along with the known flavivirus inhibitor, Lycorine. The development of this stable replicon cell line for TMUV cluster 3 may provide a versatile platform for screening antiviral drugs and also for understanding the host-virus interaction."

Journal • Preclinical • CNS Disorders • Infectious Disease

Machine learning-driven glycolytic subtyping and exosome-based PKM splicing modulation overcome drug resistance in hyper-glycolytic myeloid leukemia. (PubMed, NPJ Digit Med) - "These subtypes exhibited distinct drug sensitivities (C1 sensitive to panobinostat, MK-2206, 17-AAG; C2 sensitive to venetoclax) and predicted immunotherapy responses (C1 potentially benefiting more from anti-PD-1)...Crucially, aberrant PKM2 overexpression was linked to imatinib (IM) resistance...To mitigate vMO toxicity, IL3-Lamp2b-engineered exosomes were developed, demonstrating efficient vMO loading, targeted delivery to leukemia cells, potent PKM splicing correction, significant IM resistance reversal, and minimal stromal cell toxicity. This work defines glycolysis-based AML subtypes with therapeutic implications and establishes engineered exosome-delivered vMO as a promising strategy to overcome drug resistance in hyper-glycolytic myeloid leukemia."

IO biomarker • Journal • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • HIF1A • PKM

Pharmacological inhibition of or reduced EZH2 levels sensitized diffuse intrinsic pontine gliomas (DIPG) to ONC201, leading to synthetic lethality (SNO 2025) - "RNA-seq showed that ONC201 and EHZ2 inhibitor tazemetostat-treated cells exhibited similar transcriptional profiles, sharing top-regulated genes...In contrast, there was no overlap in the transcription or cytokine profiles obtained after ONC201 and Panobinostat (an HDAC inhibitor) treatment... ONC201 and EHZ2 inhibition converge on nodes within the same linear pathway and exhibit synthetic lethal interactions. These findings bear therapeutic implications and provide the foundation for drug combinations with ONC201."

Synthetic lethality • Brain Cancer • Diffuse Intrinsic Pontine Glioma • Glioma • Solid Tumor • EZH2

Targeting H3K27M protein with inhibitors of histone deacetylases in H3K27-altered diffuse midline gliomas (SNO 2025) - "Importantly, we have recently shown that some HDACi (including panobinostat, pracinostat/SB939, vorinostat and entinostat) lead to the reduction in the H3K27M protein levels. We are hoping that our studies may pave the way for new therapeutic strategies for patients with DMGs, aiming at eradication of detrimental H3K27M oncohistone protein. The study is supported by the Sonata Bis-14 grant (2024/54/E/NZ3/00480) awarded by the National Science Centre, Poland."

Epigenetic controller • Brain Cancer • Diffuse Midline Glioma • Glioma • High Grade Glioma • Solid Tumor

Comparative Study of Histone Deacetylase Inhibitors for Radiation Protection Using Survival Outcomes in a Mouse Model. (PubMed, Biol Pharm Bull) - "Male ICR mice received 7.5 Gy TBI followed by a single administration of valproic acid (VPA; 300 or 600 mg/kg), sodium butyrate (NaB; 500 or 1000 mg/kg), trichostatin A (TSA; 0.5 or 1.0 mg/kg), vorinostat (10 or 50 mg/kg), panobinostat (25 or 50 mg/kg), givinostat (5 or 10 mg/kg), or entinostat (25 or 50 mg/kg). VPA's efficacy may reflect a combination of effects on DNA repair, inflammation, and redox regulation rather than HDAC inhibition alone. These findings suggest VPA to be a promising candidate for radioprotection and emphasize the need for further studies to optimize dosing and explore underlying mechanisms."

Clinical • Journal • Preclinical • Inflammation

The histone modifier KANSL2 is an actionable biomarker in multiple myeloma. (PubMed, Mol Cancer Ther) - "High KANSL2 levels increased sensitivity to the histone deacetylase (HDAC) inhibitor panobinostat and bromodomain and extra-terminal motif (BET) inhibitor OTX-015 and their combination. Ex vivo drug response profiling in relapsed/refractory MM patient samples confirmed that high KANSL2 expression is associated with selective MM cell killing by HDAC and BET inhibitors. Collectively, these findings position KANSL2 as a mediator of chemotherapy resistance and actionable biomarker for response to drugs targeting its epigenetic program."

Biomarker • Journal • Hematological Malignancies • Multiple Myeloma • Oncology • KAT8

Trends in Medicare Spending on Multiple Myeloma Drugs, 2013 to 2021 (ASH 2023) - "Lenalidomide (68%) and pomalidomide (52%) had the largest price increases...Spending on the three myeloma drugs approved via accelerated approval but subsequently withdrawn from the market following confirmatory trials was $85,328,842 (melflufen: $859,764, belantamab: $31,749,711, panobinostat: $52,719,367). Spending data demonstrate prescriber sensitivity to route-of-administration-specific toxicities: almost no intravenous bortezomib was prescribed, and in 2021, >60% of patients on daratumumab received subcutaneous Darzalex Faspro. Second-in-class anti-CD38 antibody isatuximab offered daratumumab little competition (623 beneficiaries received isatuximab vs 20,573 receiving daratumumab)...Our analysis underscores why the Inflation Reduction Act—and its key provisions of inflationary rebates and Medicare price negotiation—are vital to rein in Medicare spending. Generic competition, particularly for lenalidomide and bortezomib, whose patents expired recently, may also..."

Medicare • Reimbursement • US reimbursement • Hematological Malignancies • Multiple Myeloma • Oncology

Targeting RNA polymerase I to boost natural killer cell anticancer activity in multiple myeloma. (PubMed, Cell Death Dis) - "Our study examined two "first-in-class" RNA Pol I inhibitors, CX-5461 and BMH-21, which differentially regulate NK cell-activating and inhibitory ligand expression in MM. This effect was modulated by Lenalidomide and Panobinostat. Moreover, RNA Pol I inhibition enhanced Daratumumab-mediated antibody-dependent cellular cytotoxicity (ADCC) of NK cells against MM, uncovering novel immuno-mediated antitumor mechanisms."

Journal • Hematological Malignancies • Multiple Myeloma • Oncology • HLA-E • IFNG • TNFA

Targeting H3K27M protein with inhibitors of histone deacetylases in H3K27-altered diffuse midline gliomas (WFNOS 2025) - "Importantly, we have recently shown that some HDACi (including panobinostat, pracinostat/SB939, vorinostat and entinostat) lead to the reduction in the H3K27M protein levels. We are hoping that our studies may pave the way for new therapeutic strategies for patients with DMGs, aiming at eradication of detrimental H3K27M oncohistone protein. The study is supported by the Sonata Bis-14 grant (2024/54/E/NZ3/00480) awarded by the National Science Centre, Poland."

Epigenetic controller • Brain Cancer • Diffuse Midline Glioma • Solid Tumor

Single-Cell Profiling of HDAC Inhibitor-Induced EBV Lytic Heterogeneity Defines Abortive and Refractory States in B Lymphoblasts. (PubMed, bioRxiv) - "We therefore characterized the impact of pan-HDAC inhibitor, panobinostat, and class I HDAC inhibitor, nanatinostat, on the growth, survival, and lytic reactivation of four EBV-positive cell lines: P3HR1-ZHT BL, Jijoye BL, IBL-1 immunoblastic lymphoma, and de novo infection derived lymphoblastoid cell lines (LCL). Single-cell RNA sequencing provided evidence of upregulated immune signaling pathways in this abortive lytic population. This study provides in depth characterization of lytic reactivation with a biologically relevant stimulus."

Heterogeneity • IO biomarker • Journal • Burkitt Lymphoma • Epstein-Barr Virus Infections • Gastric Cancer • Hematological Malignancies • Hodgkin Lymphoma • Immunology • Infectious Disease • Lymphoma • Nasopharyngeal Carcinoma • Oncology • Solid Tumor • TNFRSF9

Classifying the tumor immune microenvironment in cervical cancer based on nuclear cytoplasmic consistent genes. (PubMed, Sci Rep) - "LRG also showed greater sensitivity to PD-1/CTLA4 inhibitors and chemotherapeutic agents (e.g., Panobinostat and Doxorubicin). This study reveals the molecular mechanisms and clinical significance of NCCGs in CC and epithelial-origin cancers. NCCGs hold value in molecular classification, prognostic assessment, and predicting therapeutic responses, offering new markers and targets for precision medicine."

Biomarker • IO biomarker • Journal • Cervical Cancer • Oncology • Solid Tumor • BRCA • CD4 • CD8

The oncogenic role of BCL2L12 associated with immune status in the prognosis of human hepatocellular carcinoma. (PubMed, Naturwissenschaften) - "Panobinostat, Pirinixic acid, and Fluorouracil were predicted to be the potential BCL2L12-targeted drug for HCC. Our findings offer an understanding of the Oncogenic Role of BCL2L12 associated with immune status in the prognosis of HCC and provide potential strategies for currently limited treatment."

IO biomarker • Journal • Hepatocellular Cancer • Oncology • Solid Tumor • BCL2L12 • CYTOR • miR-125b • MIR4435-2HG • TNFRSF4