Evidence map›Paper›PMID 39557802›Full record

ReviewMedical oncology (Northwood, London, England)2024

Thapsigargin and its prodrug derivatives: exploring novel approaches for targeted cancer therapy through calcium signaling disruption.

Iqra Khurram, Muhammad Umer Khan, Saooda Ibrahim, Muhammad Usman Ghani, Iram Amin, Luca Falzone, Jesús Herrera-Bravo, William N Setzer, Javad Sharifi-Rad, Daniela Calina

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Inter-Organellar CaCells · 2025
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
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

10 authors.

Iqra KhurramInstitute of Molecular Biology and Biotechnology, The University of Lahore, Lahore, Pakistan.
Muhammad Umer KhanInstitute of Molecular Biology and Biotechnology, The University of Lahore, Lahore, Pakistan. muhammad.umer4@mlt.uol.edu.pk.
Saooda IbrahimInstitute of Molecular Biology and Biotechnology, The University of Lahore, Lahore, Pakistan.
Muhammad Usman GhaniCentre for Applied Molecular Biology, University of the Punjab, Lahore, Pakistan.
Iram AminCentre of Excellence in Molecular Biology, University of the Punjab, Lahore, Pakistan.
Luca FalzoneDepartment of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Jesús Herrera-BravoDepartamento de Ciencias Básicas, Facultad de Ciencias, Universidad Santo Tomas, Santiago, Chile. jesusherrerabr@santotomas.cl.
William N SetzerAromatic Plant Research Center, 230 N 1200 E, Suite 102, Lehi, UT, 84043, USA.
Javad Sharifi-RadUniversidad Espíritu Santo, Samborondón, Ecuador. javad.sharifirad@gmail.com.
Daniela CalinaDepartment of Clinical Pharmacy, University of Medicine and Pharmacy of Craiova, 200349, Craiova, Romania. calinadaniela@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thapsigargin, a sesquiterpene lactone derived from Thapsia garganica L., has demonstrated mixed potential as an anticancer agent due to its potent ability to disrupt calcium signaling and induce apoptosis. This review evaluates the chemopreventive and chemotherapeutic potential of thapsigargin, focusing on its molecular mechanisms and toxicity. An extensive literature review of studies published since 2015 was conducted using databases such as PubMed/MedLine and Science Direct. Findings indicate that thapsigargin's primary mechanism is the inhibition of sarco/endoplasmic reticulum calcium ATPase, leading to endoplasmic reticulum stress and cell death in various cancer types. Despite these effects, thapsigargin's non-specific cytotoxicity results in significant side effects, including organ damage and histamine-related reactions. Recent advances in targeted delivery, especially with the prodrug mipsagargin, initially suggested promise in minimizing these toxicities by selectively activating in cancer cells expressing prostate-specific membrane antigen (PSMA). However, the completion of clinical trials with no ongoing studies suggests that the viability of mipsagargin and other prodrugs remains uncertain, especially in light of the toxicities observed. While thapsigargin and its derivatives present a potential pathway in cancer treatment, their future role in oncology requires careful re-evaluation.

Indexed as

Calcium SignalingNeoplasmsProdrugsThapsigarginAnimalsAntineoplastic AgentsHumansAntineoplastic AgentsProdrugsThapsigarginAnticancerApoptosisDrug toxicityEndoplasmic reticulum stressInhibitionMipsagargin (G-202)Sarco/endoplasmic reticulum calcium ATPase (SERCA)Thapsigargin

Identifiers

PMID39557802

What Socratic holds

Textmetadata
Read underepoch 390

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 Socratic graph.