ReviewTrends in pharmacological sciences2018
Combination Therapies Targeting HDAC and IKK in Solid Tumors.
Review in Trends in pharmacological sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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
34 citing papers in PubMed, 58 citations in OpenAlex.
- Dual Epigenetic and Chaperone Inhibition Disrupts Hypoxia Signaling and Tumor Progression in 3-D Models of Triple-Negative Breast Cancer.Research square · 2026Article
- Epigenetic modifications in cancer drug resistance: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Inflammatory milieu and role of epigenetic modifications in high-grade serous ovarian cancer.Clinical epigenetics · 2026Review
- HDAC3 inhibitors induce drug resistance by promoting IL-17 A production by T cells.Scientific reports · 2024Article
- Co-delivery Nano System of MS-275 and V-9302 Induces Pyroptosis and Enhances Anti-Tumor Immunity Against Uveal Melanoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Discovery of a novel hybrid coumarin-hydroxamate conjugate targeting the HDAC1-Sp1-FOSL2 signaling axis for breast cancer therapy.Cell communication and signaling : CCS · 2024Article
- Advances in targeting histone deacetylase for treatment of solid tumors.Journal of hematology & oncology · 2024Review
- New clinical trial design in precision medicine: discovery, development and direction.Signal transduction and targeted therapy · 2024Review
- Platinum(IV) Prodrugs Incorporating an Indole-Based Derivative, 5-Benzyloxyindole-3-Acetic Acid in the Axial Position Exhibit Prominent Anticancer Activity.International journal of molecular sciences · 2024Article
- CYLD induces high oxidative stress and DNA damage through class I HDACs to promote radiosensitivity in nasopharyngeal carcinoma.Cell death & disease · 2024Article
- Targeting Wnt signaling for improved glioma immunotherapy.Frontiers in immunology · 2024Article
- The Development of HDAC and Tubulin Dual-Targeting Inhibitors for Cancer Therapy.Mini reviews in medicinal chemistry · 2024Review
- Article
- Histone deacetylase 6's function in viral infection, innate immunity, and disease: latest advances.Frontiers in immunology · 2023Review
- Current Molecular Combination Therapies Used for the Treatment of Breast Cancer.International journal of molecular sciences · 2022Review
- Changes in the BTK/NF-κB signaling pathway and related cytokines in different stages of neuromyelitis optica spectrum disorders.European journal of medical research · 2022Article
- Harnessing anti-tumor and tumor-tropism functions of macrophages via nanotechnology for tumor immunotherapy.Exploration (Beijing, China) · 2022Review
- Targeting epigenetic modifiers to reprogramme macrophages in non-resolving inflammation-driven atherosclerosis.European heart journal open · 2021Article
- A Pan-Histone Deacetylase Inhibitor Enhances the Antitumor Activity of B7-H3-Specific CAR T Cells in Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Dual Kinase Targeting in Leukemia.Cancers · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The rationale for developing histone deacetylase (HDAC) inhibitors (HDACi) as anticancer agents was based on their ability to induce apoptosis and cell cycle arrest in cancer cells. However, while HDACi have been remarkably effective in the treatment of hematological malignancies, clinical studies with HDACi as single agents in solid cancers have been disappointing. Recent studies have shown that, in addition to inducing apoptosis in cancer cells, class I HDACi induce IκB kinase (IKK)-dependent expression of proinflammatory chemokines, such as interleukin-8 (IL8; CXCL8), resulting in the increased proliferation of tumor cells, and limiting the effectiveness of HDACi in solid tumors. Here, we discuss the mechanisms responsible for HDACi-induced CXCL8 expression, and opportunities for combination therapies targeting HDACs and IKK in solid tumors.
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.