Evidence map›Paper›PMID 15550937›Full record

ReviewCancer gene therapy2005

Mechanisms of resistance to TRAIL-induced apoptosis in cancer.

Lidong Zhang, Bingliang Fang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cancer gene therapy, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 282 papers.

0numbers the graph read from it
0cells of the map it votes in
282citing papers in PubMed
11.3field-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

282 citing papers in PubMed, 690 citations in OpenAlex.

  1. Review
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  9. Pharmaceutical biology · 2025
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  17. Endoplasmic reticulum stress regulates apoptosis and chemotherapeutic via enhancing TNFRSF10B recycling to the cell membrane in triple-negative breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
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  19. Review
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222 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

2 authors at 2 institutions in 1 country.

Lidong ZhangDepartment of Thoracic and Cardiovascular Surgery, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Bingliang Fang
The University of Texas MD Anderson Cancer Center · USThoracic Surgery Foundation · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is regarded as a potential anticancer agent. However, considerable numbers of cancer cells, especially some highly malignant tumors, are resistant to apoptosis induction by TRAIL, and some cancer cells that were originally sensitive to TRAIL-induced apoptosis can become resistant after repeated exposure (acquired resistance). Understanding the mechanisms underlying such resistance and developing strategies to overcome it are important for the successful use of TRAIL for cancer therapy. Resistance to TRAIL can occur at different points in the signaling pathways of TRAIL-induced apoptosis. Dysfunctions of the death receptors DR4 and DR5 due to mutations can lead to resistance. The adaptor protein Fas-associated death domain (FADD) and caspase-8 are essential for assembly of the death-inducing signaling complex, and defects in either of these molecules can lead to TRAIL resistance. Overexpression of cellular FADD-like interleukin-1beta-converting enzyme-inhibitory protein (cFLIP) correlates with TRAIL resistance in several types of cancer. Overexpression of Bcl-2 or Bcl-X(L), loss of Bax or Bak function, high expression of inhibitor of apoptosis proteins, and reduced release of second mitochondria-derived activator of caspases (Smac/Diablo) from the mitochondria to the cytosol have all been reported to result in TRAIL resistance in mitochondria-dependent type II cancer cells. Finally, activation of different subunits of mitogen-activated protein kinases or nuclear factor-kappa B can lead to development of either TRAIL resistance or apoptosis in certain types of cancer cells.

Indexed as

ApoptosisApoptosis Regulatory ProteinsArabidopsis Proteinsbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinCASP8 and FADD-Like Apoptosis Regulating ProteinDrug Resistance, NeoplasmFatty Acid DesaturasesGenetic TherapyHumansInhibitor of Apoptosis ProteinsIntracellular Signaling Peptides and ProteinsMembrane GlycoproteinsMembrane ProteinsMitogen-Activated Protein KinasesMutationApoptosis Regulatory ProteinsArabidopsis ProteinsBAK1 protein, humanBAX protein, humanbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinCASP8 and FADD-Like Apoptosis Regulating ProteinCFLAR protein, humanFad7 protein, ArabidopsisFatty Acid DesaturasesInhibitor of Apoptosis ProteinsIntracellular Signaling Peptides and ProteinsMembrane GlycoproteinsMembrane ProteinsMitogen-Activated Protein KinasesNF-kappa BProteinsProto-Oncogene Proteins c-bcl-2Receptors, TNF-Related Apoptosis-Inducing LigandReceptors, Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandTNFRSF10B protein, humanTNFSF10 protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID15550937
OpenAlexW2094570524

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.