Evidence map›Paper›PMID 24295132›Full record

ReviewLeukemia & lymphoma2014

Targeting the apoptosis pathway in hematologic malignancies.

Shadia Zaman, Rui Wang, Varsha Gandhi

Open access · greenAbstract readReview
In one paragraph

Review in Leukemia & lymphoma, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

90 citing papers in PubMed, 1 synthesis or guideline pooled it, 216 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Targeting protein-protein interactions in the BCL-2 family: opportunities for precision oncology.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  4. Article
  5. Epigenetic Reactivation of <italic>SOCS-3</italic> and Inhibition of ERK1/2 Underlie Thymoquinone-Induced Apoptosis in a Chronic Myeloid Leukemia Xenograft Model.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2026
    Article
  6. Chemoresistance: The hidden barrier in cancer treatment.Cancer pathogenesis and therapy · 2026
    Review
  7. Review
  8. Food science & nutrition · 2025
    Article
  9. Design, synthesis, andRSC advances · 2025
    Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Globospiramine fromCells · 2024
    Article
  15. Heat-KilledJournal of microbiology and biotechnology · 2024
    Article
  16. Food science & nutrition · 2024
    Article
  17. Review
  18. Characterization, modes of interactions with DNA/BSA biomolecules and anti-tumor activity of newly synthesized dinuclear platinum(II) complexes with pyridazine bridging ligand.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2024
    Article
  19. Short Fragmented Peptides fromCurrent drug discovery technologies · 2024
    Article
  20. Journal of medicinal chemistry · 2023
    Article

30 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

3 authors at 2 institutions in 1 country.

Shadia ZamanDepartment of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center , Houston, TX , USA.
Rui Wang
Varsha Gandhi
The University of Texas MD Anderson Cancer Center · USSociety of Surgical Oncology · US

Funding

Tissue CoreP01CA081534 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KIPPS, THOMAS J · 2000 to 2016
$59.5M
NCI NIH HHS P01 CA081534NCI NIH HHS P01 CA81534
6 · The paper itself

Abstract

Apoptosis is a cell death program that is well-orchestrated for normal tissue homeostasis and for removal of damaged, old or infected cells. It is regulated by intrinsic and extrinsic pathways. The intrinsic pathway responds to signals such as ultraviolet radiation or DNA damage and activates "executioner" caspases through a mitochondria-dependent pathway. The extrinsic pathway is activated by death signals induced, for example, by an infection that activates the immune system or receptor-mediated pathways. The extrinsic pathway signals also cascade down to executioner caspases that cleave target proteins and lead to cell death. Strict control of cellular apoptosis is important for the hematopoietic system as it has a high turnover rate. However, the apoptosis program is often deregulated in hematologic malignancies leading to the accumulation of malignant cells. Therefore, apoptosis pathways have been identified for the development of anticancer therapeutics. We review here the proteins that have been targeted for anticancer drug development in hematologic malignancies. These include BCL-2 family proteins, death ligands and receptors, inhibitor of apoptosis family proteins and caspases. Except for caspase activators, drugs that target each of these classes of proteins have advanced into clinical trials.

Indexed as

AnimalsAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsHematologic NeoplasmsHumansMolecular Targeted TherapySignal TransductionAntineoplastic AgentsApoptosis Regulatory ProteinsApoptosiscancer therapeuticshematologic malignancies

Identifiers

PMID24295132
PMCPMC4152229
OpenAlexW1974543775

What OpenQuestion holds

Textmetadata
LicenceTDM
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.