Evidence map›Paper›PMID 33557398›Full record

ReviewCancers2021

Tumor Suppressor Protein p53 and Inhibitor of Apoptosis Proteins in Colorectal Cancer-A Promising Signaling Network for Therapeutic Interventions.

Ömer Güllülü, Stephanie Hehlgans, Claus Rödel, Emmanouil Fokas, Franz Rödel

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.9field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Molecules (Basel, Switzerland) · 2026
    Article
  4. Article
  5. Ambiguous Role of p53 in Transcription-Dependent Tumor Cell Death.International journal of molecular sciences · 2026
    Review
  6. Review
  7. Review
  8. Article
  9. Change of Expression of Ki 67, P53, and Cyclin D1 Immunoreactivity afterMiddle East journal of digestive diseases · 2025
    Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. NLRC4, inflammation and colorectal cancer (Review).International journal of oncology · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Ömer GüllülüDepartment of Radiotherapy and Oncology, University Hospital Frankfurt, Theodor-Stern-Kai 7, 60590 Frankfurt am Main, Germany.ORCID 0000-0003-0218-7721
Stephanie HehlgansDepartment of Radiotherapy and Oncology, University Hospital Frankfurt, Theodor-Stern-Kai 7, 60590 Frankfurt am Main, Germany.ORCID 0000-0002-6816-3450
Claus RödelDepartment of Radiotherapy and Oncology, University Hospital Frankfurt, Theodor-Stern-Kai 7, 60590 Frankfurt am Main, Germany.
Emmanouil FokasDepartment of Radiotherapy and Oncology, University Hospital Frankfurt, Theodor-Stern-Kai 7, 60590 Frankfurt am Main, Germany.
Franz RödelDepartment of Radiotherapy and Oncology, University Hospital Frankfurt, Theodor-Stern-Kai 7, 60590 Frankfurt am Main, Germany.ORCID 0000-0001-6057-1022
Goethe University Frankfurt · DE

Funding

Bundesministerium für Bildung und Forschung 02NUK050DDeutsche Forschungsgemeinschaft GRK1657
6 · The paper itself

Abstract

Despite recent advances in the treatment of colorectal cancer (CRC), patient's individual response and clinical follow-up vary considerably with tumor intrinsic factors to contribute to an enhanced malignancy and therapy resistance. Among these markers, upregulation of members of the inhibitor of apoptosis protein (IAP) family effects on tumorigenesis and radiation- and chemo-resistance by multiple pathways, covering a hampered induction of apoptosis/autophagy, regulation of cell cycle progression and DNA damage response. These mechanisms are tightly controlled by the tumor suppressor p53 and thus transcriptional and post-translational regulation of IAPs by p53 is expected to occur in malignant cells. By this, cellular IAP1/2, X-linked IAP, Survivin, BRUCE and LIVIN expression/activity, as well as their intracellular localization is controlled by p53 in a direct or indirect manner via modulating a multitude of mechanisms. These cover, among others, transcriptional repression and the signal transducer and activator of transcription (STAT)3 pathway. In addition, p53 mutations contribute to deregulated IAP expression and resistance to therapy. This review aims at highlighting the mechanistic and clinical importance of IAP regulation by p53 in CRC and describing potential therapeutic strategies based on this interrelationship.

Indexed as

BRUCEcIAP1/2colorectal carcinomainhibitor of apoptosis protein familyLIVINSurvivinTP53XIAP

Identifiers

PMID33557398
PMCPMC7916307
OpenAlexW3128227683

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.