ReviewPflugers Archiv : European journal of physiology2014
T-type calcium channels blockers as new tools in cancer therapies.
Review in Pflugers Archiv : European journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.
- Meta-Analysis of Public Microarray Datasets Reveals Voltage-Gated Calcium Gene Signatures in Clinical Cancer Patients.PloS one · 2015Pooled it
- Hydrogel-Based Delivery of Ion Channel Modulators for Cancer Therapy: Current Advances and Future Perspectives.Gels (Basel, Switzerland) · 2026Review
- Pro-tumoral CaScientific reports · 2026Article
- Investigation of the antitumor activity of lapatinib and NNC 55-0396 dihydrochloride combination in gastric adenocarcinoma.Medical oncology (Northwood, London, England) · 2025Article
- OZ-001 Suppresses the Growth of Triple-Negative Breast Cancer and Pancreatic Cancer by Targeting STAT3 Phosphorylation and the Calcium Signaling Pathway.Biomolecules & therapeutics · 2025Article
- Repurposing of nervous system drugs for cancer treatment: recent advances, challenges, and future perspectives.Discover oncology · 2025Review
- Voltage-Gated Calcium Channels and the Parity-Dependent Differential Uterine Response to Oxytocin in Rats.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- CaThe Journal of biological chemistry · 2025Article
- Inhibition of the oncogenic channel Kv10.1 by the antipsychotic drug penfluridol.Frontiers in pharmacology · 2025Article
- Targeting the Renin-angiotensin-aldosterone System (RAAS) for Cardiovascular Protection and Enhanced Oncological Outcomes: Review.Current treatment options in oncology · 2024Review
- The L-type calcium channel CaV1.3: A potential target for cancer therapy.Journal of cellular and molecular medicine · 2024Review
- CACNA1H restrains chemotherapy resistance in ovarian clear cell carcinoma cells by repressing autophagy.Molecular genetics and genomics : MGG · 2024Article
- Nanotechnology and Cancer Bioelectricity: Bridging the Gap Between Biology and Translational Medicine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Exploring biological activities of novel Schiff bases derived from amlodipine andFuture medicinal chemistry · 2024Article
- Calcium channels as therapeutic targets in head and neck squamous cell carcinoma: current evidence and clinical trials.Frontiers in oncology · 2024Review
- Selective adhesion inhibition and hyaluronan envelope reduction of dermal tumor cells by cold plasma-activated medium.Cell adhesion & migration · 2023Article
- Modulation of FDG Uptake by Cell Cycle Synchronization Using a T-Type Calcium Channel Inhibitor.Cancers · 2023Article
- Evaluation of the Anticancer Activity of Calcium Ions Introduced into Human Breast Adenocarcinoma Cells MCF-7/WT and MCF-7/DOX by Electroporation.Pharmaceuticals (Basel, Switzerland) · 2023Article
- From HDAC to Voltage-Gated Ion Channels: What's Next? The Long Road of Antiepileptic Drugs Repositioning in Cancer.Cancers · 2022Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
T-type calcium channels are involved in a multitude of cellular processes, both physiological and pathological, including cancer. T-type channels are also often aberrantly expressed in different human cancers and participate in the regulation of cell cycle progression, proliferation, migration, and survival. Here, we review the recent literature and discuss the controversies, supporting the role of T-type Ca(2+) channels in cancer cells and the proposed use of channels blockers as anticancer agents. A growing number of reports show that pharmacological inhibition or RNAi-mediated downregulation of T-type channels leads to inhibition of cancer cell proliferation and increased cancer cell death. In addition to a single agent activity, experimental results demonstrate that T-type channel blockers enhance the anticancer effects of conventional radio- and chemotherapy. At present, the detailed biological mechanism(s) underlying the anticancer activity of these channel blockers is not fully understood. Recent findings and ideas summarized here identify T-type Ca(2+) channels as a molecular target for anticancer therapy and offer new directions for the design of novel therapeutic strategies employing channels blockers. Physiological relevance: T-type calcium channels are often aberrantly expressed or deregulated in cancer cells, supporting their proliferation, survival, and resistance to treatment; therefore, T-type Ca(2+) channels could be attractive molecular targets for anticancer therapy.
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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.