ReviewOncotarget2012
Solid tumor differentiation therapy - is it possible?
Review in Oncotarget, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 118 citations in OpenAlex.
- Inhibition of WNT signaling sensitizes CRC cells to anti-tumor effects of retinoids: basis for new drug combinations in oncology.Cancer biology & therapy · 2026Article
- The Influences of RARγ on the Behavior of Normal and Cancer Stem Cells.International journal of molecular sciences · 2026Review
- Ephrin-A5 or EphA7 stimulation is anti-proliferative for human rhabdomyosarcoma in vitro.Skeletal muscle · 2025Article
- Inhibition of DKK-1 by WAY262611 Inhibits Osteosarcoma Metastasis.Molecular cancer therapeutics · 2025Article
- A novel clinically relevant antagonistic interplay between prolactin and oncogenic YAP-CCN2 pathways as a differentiation therapeutic target in breast cancer.Cell death & disease · 2025Article
- Targeting Androgen, Thyroid Hormone, and Vitamin A and D Receptors to Treat Prostate Cancer.International journal of molecular sciences · 2024Review
- Molecular Interactions of Selective Agonists and Antagonists with the Retinoic Acid Receptor γ.International journal of molecular sciences · 2024Review
- Antileukemia Activity of Human Natural Killer Cell-Derived Nanomagic Bullets against Acute Myeloid Leukemia (AML).International journal of hematology-oncology and stem cell research · 2024Article
- AI identifies potent inducers of breast cancer stem cell differentiation based on adversarial learning from gene expression data.Briefings in bioinformatics · 2024Article
- Prostate cancer research: tools, cell types, and molecular targets.Frontiers in oncology · 2024Review
- Deregulation of All-International journal of molecular sciences · 2023Review
- Single-cell profiling of alveolar rhabdomyosarcoma reveals RAS pathway inhibitors as cell-fate hijackers with therapeutic relevance.Science advances · 2023Article
- Epigenetic Priming and Development of New Combination Therapy Approaches.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Small Molecule-Induced Differentiation As a Potential Therapy for Liver Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Notch-Sox9 Axis Mediates Hepatocyte Dedifferentiation inInternational journal of molecular sciences · 2022Article
- ZNF117 regulates glioblastoma stem cell differentiation towards oligodendroglial lineage.Nature communications · 2022Article
- Mutation or not, what directly establishes a neoplastic state, namely cellular immortality and autonomy, still remains unknown and should be prioritized in our research.Journal of Cancer · 2022Review
- Engaging plasticity: Differentiation therapy in solid tumors.Frontiers in pharmacology · 2022Review
- Terminal differentiation and anti-tumorigenic effects of prolactin in breast cancer.Frontiers in endocrinology · 2022Review
- Alterations of Chromatin Regulators in the Pathogenesis of Urinary Bladder Urothelial Carcinoma.Cancers · 2021Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic and epigenetic events within a cell which promote a block in normal development or differentiation coupled with unregulated proliferation are hallmarks of neoplastic transformation. Differentiation therapy involves the use of agents with the ability to induce differentiation in cells that have lost this ability, i.e. cancer cells. The promise of differentiation-based therapy as a viable treatment modality is perhaps best characterized by the addition of retinoids in the treatment of acute promyelocytic leukemia (APML) revolutionizing the management of APML and dramatically improving survival. However, interest and application of differentiationbased therapy for the treatment of solid malignancies have lagged due to deficiencies in our understanding of differentiation pathways in solid malignancies. Over the past decade, a differentiation-based developmental model for solid tumors has emerged providing insights into the biology of various solid tumors as well as identification of targetable pathways capable of re-activating blocked terminal differentiation programs. Furthermore, a variety of agents including retinoids, histone deacetylase inhibitors (HDACI), PPARγ agonists, and others, currently in use for a variety of malignancies, have been shown to induce differentiation in solid tumors. Herein we discuss the relevancy of differentiation-based therapies in solid tumors, using soft tissue sarcomas (STS) as a biologic and clinical model, and review the preclinical data to support its role as a promising modality of therapy for the treatment of solid tumors.
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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.