Evidence map›Paper›PMID 15077155›Full record

ReviewOncogene2004

Apoptosis defects and chemotherapy resistance: molecular interaction maps and networks.

Yves Pommier, Olivier Sordet, Smitha Antony, Richard L Hayward, Kurt W Kohn

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed
34.2field-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

180 citing papers in PubMed, 558 citations in OpenAlex.

  1. Article
  2. Article
  3. Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Frontiers in systems biology · 2023
    Article
  10. Article
  11. Article
  12. Ferroptosis in tumor immunity and therapy.Journal of cellular and molecular medicine · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Functionalization of Nanomaterials for Skin Cancer Theranostics.Frontiers in bioengineering and biotechnology · 2022
    Review

120 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

5 authors at 3 institutions in 2 countries.

Yves PommierLaboratory of Molecular Pharmacology, Center for Cancer Research, NCI, NIH, DHHS, Bethesda, MD 20892, USA. pommiery@pasteur.fr
Olivier Sordet
Smitha Antony
Richard L Hayward
Kurt W Kohn
Center for Cancer Research · USUnited States Department of Health and Human Services · USWestern General Hospital · GB

Funding

DNA Repair, Cell Cycle Checkpoints and Apoptosis as Targets for Anticancer DrugsZIABC006150 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 2009 to 2025
$23.0M
Investigating Regulatory Networks that Control Cell Proliferation and ApoptosisZIABC006192 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KOHN, KURT · 2009 to 2014
$3.8M
PROTEIN-ASSOCIATED DNA BREAKS AS INDICATOR OF TOPOISOMERASE INHIBITIONZ01BC006150 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 1996 to 2008
$1.5M
Molecular regulatory network controling cell proliferatiZ01BC006192 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KOHN, KURT · 1996 to 2008
$969k
6 · The paper itself

Abstract

Intrinsic (innate) and acquired (adaptive) resistance to chemotherapy critically limits the outcome of cancer treatments. For many years, it was assumed that the interaction of a drug with its molecular target would yield a lethal lesion, and that determinants of intrinsic drug resistance should therefore be sought either at the target level (quantitative changes or/and mutations) or upstream of this interaction, in drug metabolism or drug transport mechanisms. It is now apparent that independent of the factors above, cellular responses to a molecular lesion can determine the outcome of therapy. This review will focus on programmed cell death (apoptosis) and on survival pathways (Bcl-2, Apaf-1, AKT, NF-kappaB) involved in multidrug resistance. We will present our molecular interaction mapping conventions to summarize the AKT and IkappaB/NF-kappaB networks. They complement the p53, Chk2 and c-Abl maps published recently. We will also introduce the 'permissive apoptosis-resistance' model for the selection of multidrug-resistant cells.

Indexed as

ApoptosisDrug Resistance, NeoplasmProtein Serine-Threonine KinasesAnimalsApoptotic Protease-Activating Factor 1HumansNeoplasmsNF-kappa BProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2AKT1 protein, humanAPAF1 protein, humanApoptotic Protease-Activating Factor 1NF-kappa BProteinsProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2

Identifiers

PMID15077155
OpenAlexW1984789674

What OpenQuestion holds

Textmetadata
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.