Evidence map›Paper›PMID 25013758›Full record

ReviewBioMed research international2014

Apoptosis and molecular targeting therapy in cancer.

Mohamed Hassan, Hidemichi Watari, Ali AbuAlmaaty, Yusuke Ohba, Noriaki Sakuragi

RetractedOpen access · hybridAbstract readReviewRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 492 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
492citing papers in PubMed, 1 pooled it
28.2field-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

492 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,106 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Pharmacological and Phytochemical Insights IntoFood science & nutrition · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Mohamed HassanBiotechnology Program, Department of Zoology, Port Said University, Faculty of Science, Port Said 42521, Egypt ; Department of Obstetrics and Gynecology, Graduate School of Medicine, Hokkaido University, Sapporo 060-8638, Japan.
Hidemichi WatariDepartment of Obstetrics and Gynecology, Graduate School of Medicine, Hokkaido University, Sapporo 060-8638, Japan.
Ali AbuAlmaatyBiotechnology Program, Department of Zoology, Port Said University, Faculty of Science, Port Said 42521, Egypt.
Yusuke OhbaDepartment of Cell Physiology, Graduate School of Medicine, Hokkaido University, Sapporo 060-8638, Japan.
Noriaki SakuragiDepartment of Obstetrics and Gynecology, Graduate School of Medicine, Hokkaido University, Sapporo 060-8638, Japan.
Hokkaido University · JPPort Said University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis is the programmed cell death which maintains the healthy survival/death balance in metazoan cells. Defect in apoptosis can cause cancer or autoimmunity, while enhanced apoptosis may cause degenerative diseases. The apoptotic signals contribute into safeguarding the genomic integrity while defective apoptosis may promote carcinogenesis. The apoptotic signals are complicated and they are regulated at several levels. The signals of carcinogenesis modulate the central control points of the apoptotic pathways, including inhibitor of apoptosis (IAP) proteins and FLICE-inhibitory protein (c-FLIP). The tumor cells may use some of several molecular mechanisms to suppress apoptosis and acquire resistance to apoptotic agents, for example, by the expression of antiapoptotic proteins such as Bcl-2 or by the downregulation or mutation of proapoptotic proteins such as BAX. In this review, we provide the main regulatory molecules that govern the main basic mechanisms, extrinsic and intrinsic, of apoptosis in normal cells. We discuss how carcinogenesis could be developed via defective apoptotic pathways or their convergence. We listed some molecules which could be targeted to stimulate apoptosis in different cancers. Together, we briefly discuss the development of some promising cancer treatment strategies which target apoptotic inhibitors including Bcl-2 family proteins, IAPs, and c-FLIP for apoptosis induction.

Indexed as

Molecular Targeted TherapyApoptosisCarcinogenesisCASP8 and FADD-Like Apoptosis Regulating ProteinGenes, bcl-2HumansInhibitor of Apoptosis ProteinsNeoplasmsSignal TransductionCASP8 and FADD-Like Apoptosis Regulating ProteinCFLAR protein, humanInhibitor of Apoptosis Proteins

Identifiers

PMID25013758
PMCPMC4075070
OpenAlexW2096306846

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.