Evidence map›Paper›PMID 38424164›Full record

ReviewBritish journal of cancer2024

Ranolazine: a potential anti-metastatic drug targeting voltage-gated sodium channels.

Mustafa B A Djamgoz

Open access · hybridAbstract readReview
In one paragraph

Review in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.4field-weighted citation impact, top 3% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 23 citations in OpenAlex.

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  12. Metal Ion Signaling in Biomedicine.Chemical reviews · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 2 countries.

Mustafa B A DjamgozDepartment of Life Sciences, Imperial College London, South Kensington Campus, London, SW7 2AZ, UK. m.djamgoz@imperial.ac.uk.ORCID 0000-0003-1435-8540
Cyprus International University · CY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMulti-faceted evidence from a range of cancers suggests strongly that de novo expression of voltage-gated sodium channels (VGSCs) plays a significant role in driving cancer cell invasiveness. Under hypoxic conditions, common to growing tumours, VGSCs develop a persistent current (I

methodsSeveral different carcinomas were examined. We used data from a range of experimental approaches relating to cellular invasiveness and metastasis. These were supplemented by survival data mined from cancer patients.

resultsIn vitro, ranolazine inhibited invasiveness of cancer cells especially under hypoxia. In vivo, ranolazine suppressed the metastatic abilities of breast and prostate cancers and melanoma. These data were supported by a major retrospective epidemiological study on breast, colon and prostate cancer patients. This showed that risk of dying from cancer was reduced by ca.60% among those taking ranolazine, even if this started 4 years after the diagnosis. Ranolazine was also shown to reduce the adverse effects of chemotherapy on heart and brain. Furthermore, its anti-cancer effectiveness could be boosted by co-administration with other drugs.

conclusionsRanolazine, alone or in combination with appropriate therapies, could be reformulated as a safe anti-metastatic drug offering many potential advantages over current systemic treatment modalities.

Indexed as

RanolazineAnimalsAntineoplastic AgentsFemaleHumansMaleNeoplasm InvasivenessNeoplasm MetastasisNeoplasmsVoltage-Gated Sodium Channel BlockersVoltage-Gated Sodium ChannelsAntineoplastic AgentsRanolazineVoltage-Gated Sodium Channel BlockersVoltage-Gated Sodium Channels

Identifiers

PMID38424164
PMCPMC11058819
OpenAlexW4392298197

What OpenQuestion holds

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Registered trials

None linked

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.