Evidence map›Paper›PMID 38589288›Full record

ReviewBiomolecules & therapeutics2024

Unlocking the Therapeutic Potential of BCL-2 Associated Protein Family: Exploring BCL-2 Inhibitors in Cancer Therapy.

Bisan El Dakkak, Jalal Taneera, Waseem El-Huneidi, Eman Abu-Gharbieh, Rifat Hamoudi, Mohammad H Semreen, Nelson C Soares, Eman Y Abu-Rish, Mahmoud Y Alkawareek, Alaaldin M Alkilany and 1 more

Abstract readReview
In one paragraph

Review in Biomolecules & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. A new era in cancer therapy: targeting the Proteasome-Bcl-2 axis.Journal of experimental & clinical cancer research : CR · 2025
    Review
  7. Article
  8. Review
  9. Investigating Andrographis paniculata Compounds for Apoptosis Induction in Cancer.Asian Pacific journal of cancer prevention : APJCP · 2025
    Article
  10. Article
  11. Review
  12. Review
  13. ElevatedJournal of thoracic disease · 2024
    Article
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

11 authors.

Bisan El DakkakResearch Institute of Medical and Health Sciences, University of Sharjah, Sharjah 27272, United Arab Emirates.
Jalal TaneeraResearch Institute of Medical and Health Sciences, University of Sharjah, Sharjah 27272, United Arab Emirates.
Waseem El-HuneidiResearch Institute of Medical and Health Sciences, University of Sharjah, Sharjah 27272, United Arab Emirates.
Eman Abu-GharbiehResearch Institute of Medical and Health Sciences, University of Sharjah, Sharjah 27272, United Arab Emirates.
Rifat HamoudiResearch Institute of Medical and Health Sciences, University of Sharjah, Sharjah 27272, United Arab Emirates.
Mohammad H SemreenResearch Institute of Medical and Health Sciences, University of Sharjah, Sharjah 27272, United Arab Emirates.
Nelson C SoaresResearch Institute of Medical and Health Sciences, University of Sharjah, Sharjah 27272, United Arab Emirates.
Eman Y Abu-RishSchool of Pharmacy, The University of Jordan, Amman 11942, Jordan.
Mahmoud Y AlkawareekSchool of Pharmacy, The University of Jordan, Amman 11942, Jordan.
Alaaldin M AlkilanyCollege of Pharmacy, QU Health, Qatar University, Doha 2713, Qatar.
Yasser BustanjiResearch Institute of Medical and Health Sciences, University of Sharjah, Sharjah 27272, United Arab Emirates.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis, programmed cell death pathway, is a vital physiological mechanism that ensures cellular homeostasis and overall cellular well-being. In the context of cancer, where evasion of apoptosis is a hallmark, the overexpression of anti-apoptotic proteins like Bcl2, Bcl-xL and Mcl-1 has been documented. Consequently, these proteins have emerged as promising targets for therapeutic interventions. The BCL-2 protein family is central to apoptosis and plays a significant importance in determining cellular fate serving as a critical determinant in this biological process. This review offers a comprehensive exploration of the BCL-2 protein family, emphasizing its dual nature. Specifically, certain members of this family promote cell survival (known as anti-apoptotic proteins), while others are involved in facilitating cell death (referred to as pro-apoptotic and BH3-only proteins). The potential of directly targeting these proteins is examined, particularly due to their involvement in conferring resistance to traditional cancer therapies. The effectiveness of such targeting strategies is also discussed, considering the tumor's propensity for anti-apoptotic pathways. Furthermore, the review highlights emerging research on combination therapies, where BCL-2 inhibitors are used synergistically with other treatments to enhance therapeutic outcomes. By understanding and manipulating the BCL-2 family and its associated pathways, we open doors to innovative and more effective cancer treatments, offering hope for resistant and aggressive cases.

Indexed as

ApoptosisBCL-2 proteinBH3-mimetic drugsNanotechnologyNatural compoundsVenetoclax

Identifiers

PMID38589288
PMCPMC11063480

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.