Evidence map›Paper›PMID 26775709›Full record

ReviewCell death & disease2016

Potential of apoptotic pathway-targeted cancer therapeutic research: Where do we stand?

S Baig, I Seevasant, J Mohamad, A Mukheem, H Z Huri, T Kamarul

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
19.1field-weighted citation impact, top 1% 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

125 citing papers in PubMed, 282 citations in OpenAlex.

  1. Trial
  2. Ubiquitin-Specific Protease 49 Interacts with Bax to Modulate Apoptosis.International journal of molecular sciences · 2026
    Article
  3. Drug design, development and therapy · 2026
    Review
  4. Review
  5. Article
  6. The cross-talk between NRF2 and apoptosis in cancer.Medical molecular morphology · 2025
    Review
  7. Article
  8. Article
  9. Anticancer Potential of Bioactive Compounds inCancer management and research · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Design of semisynthetic derivatives of the Amaryllidaceae alkaloid ambelline and exploration of theirSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
    Article
  20. Article

65 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

S BaigDepartment of Orthopaedic Surgery, Tissue Engineering Group, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia.
I SeevasantDepartment of Orthopaedic Surgery, Tissue Engineering Group, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia.
J MohamadInstitute of Biological Sciences, Faculty of Science, University of Malaysia, Kuala Lumpur 50603, Malaysia.
A MukheemDepartment of Orthopaedic Surgery, Tissue Engineering Group, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia.
H Z HuriClinical Investigation Centre, University of Malaya Medical Centre, Kuala Lumpur 50603, Malaysia.
T KamarulDepartment of Orthopaedic Surgery, Tissue Engineering Group, Faculty of Medicine, University of Malaya, Kuala Lumpur 50603, Malaysia.
University of Malaya · MYUniversity Malaya Medical Centre · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Underneath the intricacy of every cancer lies mysterious events that impel the tumour cell and its posterity into abnormal growth and tissue invasion. Oncogenic mutations disturb the regulatory circuits responsible for the governance of versatile cellular functions, permitting tumour cells to endure deregulated proliferation, resist to proapoptotic insults, invade and erode normal tissues and above all escape apoptosis. This disruption of apoptosis has been highly implicated in various malignancies and has been exploited as an anticancer strategy. Owing to the fact that apoptosis causes minimal inflammation and damage to the tissue, apoptotic cell death-based therapy has been the centre of attraction for the development of anticancer drugs. Increased understanding of the molecular pathways underlying apoptosis has enabled scientists to establish unique approaches targeting apoptosis pathways in cancer therapeutics. In this review, we reconnoitre the two major pathways (intrinsic and extrinsic) targeted cancer therapeutics, steering toward chief modulators of these pathways, such as B-cell lymphoma 2 protein family members (pro- and antiapoptotic), inhibitor of apoptosis proteins, and the foremost thespian of extrinsic pathway regulator, tumour necrosis factor-related apoptosis-inducing agent. Together, we also will have a look from clinical perspective to address the agents (drugs) and therapeutic strategies adopted to target these specific proteins/pathways that have entered clinical trials.

Indexed as

Therapeutic Human ExperimentationApoptosisHumansNeoplasms

Identifiers

PMID26775709
PMCPMC4816162
OpenAlexW2233407520

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.