ArticleCancer research2021
Targeting an Inducible SALL4-Mediated Cancer Vulnerability with Sequential Therapy.
Article in Cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Inhibition of TRPC6 channel suppresses bladder cancer proliferation by disrupting store-operated calcium entry.Scientific reports · 2026Article
- E2F8-induced GRPEL2 promoted colorectal cancer progression via targeting TIGAR.Journal of translational medicine · 2025Article
- Magnetic drug-loaded microbubbles for treating lower limb venous thrombosis under controllable rotating magnetic field.Frontiers in bioengineering and biotechnology · 2025Article
- Cryptotanshinone targets tumor-immune-microbiome axis to suppress colorectal cancer.Frontiers in pharmacology · 2025Article
- Editorial: New insights into cancer immunology of refractory GU and liver tumors: therapy and mechanism.Frontiers in immunology · 2024Article
- SALL4 upregulates brain-derived neurotrophic factor to mediate Hedgehog signaling to inhibit carboplatin sensitivity in colon adenocarcinoma.Pharmacogenomics · 2024Article
- The new advance of SALL4 in cancer: Function, regulation, and implication.Journal of clinical laboratory analysis · 2023Review
- PROTACs in Epigenetic Cancer Therapy: Current Status and Future Opportunities.Molecules (Basel, Switzerland) · 2023Review
- Stapled peptide PROTAC induced significantly greater anti-PD-L1 effects than inhibitor in human cervical cancer cells.Frontiers in immunology · 2023Article
- Cervical cancer immune infiltration microenvironment identification, construction of immune scores, assisting patient prognosis and immunotherapy.Frontiers in immunology · 2023Article
- A novel necroptosis-related long noncoding RNA model for predicting clinical features, immune characteristics, and therapeutic response in clear cell renal cell carcinoma.Frontiers in immunology · 2023Article
- Restoration of WT1/miR-769-5p axis by HDAC1 inhibition promotes MMT reversal in mesenchymal-like mesothelial cells.Cell death & disease · 2022Article
- Review
- Study on the mechanism of SALL4 down-regulation in promoting the invasion and migration of oral squamous cell carcinoma and influencing the survival and prognosis of patients.Annals of translational medicine · 2022Article
- Demethylation and Up-Regulation of an Oncogene after Hypomethylating Therapy.The New England journal of medicine · 2022Article
- A review of recent advances on single use of antibody-drug conjugates or combination with tumor immunology therapy for gynecologic cancer.Frontiers in pharmacology · 2022Review
- The copper-associated protein STEAP2 correlated with glioma prognosis and immune infiltration.Frontiers in cellular neuroscience · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 6 institutions in 4 countries.
Funding
Abstract
Oncofetal protein SALL4 is critical for cancer cell survival. Targeting SALL4, however, is only applicable in a fraction of cancer patients who are positive for this gene. To overcome this limitation, we propose to induce a cancer vulnerability by engineering a partial dependency upon SALL4. Following exogenous expression of SALL4, SALL4-negative cancer cells became partially dependent on SALL4. Treatment of SALL4-negative cells with the FDA-approved hypomethylating agent 5-aza-2'-deoxycytidine (DAC) resulted in transient upregulation of SALL4. DAC pretreatment sensitized SALL4-negative cancer cells to entinostat, which negatively affected SALL4 expression through a microRNA, miRNA-205, both in culture and
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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.