Evidence map›Paper›PMID 23334322›Full record

ReviewOncogene2013

Effects of vitamin B6 metabolism on oncogenesis, tumor progression and therapeutic responses.

L Galluzzi, E Vacchelli, J Michels, P Garcia, O Kepp, L Senovilla, I Vitale, G Kroemer

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

77 citing papers in PubMed, 158 citations in OpenAlex.

  1. Trial
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  6. From Fly to Human: Translational Relevance ofInternational journal of molecular sciences · 2026
    Review
  7. Article
  8. Review
  9. Review
  10. Inhibition of NAD-GPx4 axis and MEK triggers ferroptosis to suppress pancreatic ductal adenocarcinoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
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  14. Review
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  17. MR1 presents vitamin B6-related compounds for recognition by MR1-reactive T cells.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. Article
  19. Article
  20. Article

17 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

8 authors at 5 institutions in 1 country.

L Galluzzi1] Université Paris Descartes/Paris V, Sorbonne Paris Cité, Paris, France [2] Institut Gustave Roussy, Villejuif, France.
E Vacchelli
J Michels
P Garcia
O Kepp
L Senovilla
I Vitale
G Kroemer
Institut Gustave Roussy · FRUniversité Paris-Sud · FRHôpital Européen · FRInserm · FRUniversité Paris-Saclay · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pyridoxal-5'-phosphate (PLP), the bioactive form of vitamin B6, reportedly functions as a prosthetic group for >4% of classified enzymatic activities of the cell. It is therefore not surprising that alterations of vitamin B6 metabolism have been associated with multiple human diseases. As a striking example, mutations in the gene coding for antiquitin, an evolutionary old aldehyde dehydrogenase, result in pyridoxine-dependent seizures, owing to the accumulation of a metabolic intermediate that inactivates PLP. In addition, PLP is required for the catabolism of homocysteine by transsulfuration. Hence, reduced circulating levels of B6 vitamers (including PLP as well as its major precursor pyridoxine) are frequently paralleled by hyperhomocysteinemia, a condition that has been associated with an increased risk for multiple cardiovascular diseases. During the past 30 years, an intense wave of clinical investigation has attempted to dissect the putative links between vitamin B6 and cancer. Thus, high circulating levels of vitamin B6, as such or as they reflected reduced amounts of circulating homocysteine, have been associated with improved disease outcome in patients bearing a wide range of hematological and solid neoplasms. More recently, the proficiency of vitamin B6 metabolism has been shown to modulate the adaptive response of tumor cells to a plethora of physical and chemical stress conditions. Moreover, elevated levels of pyridoxal kinase (PDXK), the enzyme that converts pyridoxine and other vitamin B6 precursors into PLP, have been shown to constitute a good, therapy-independent prognostic marker in patients affected by non-small cell lung carcinoma (NSCLC). Here, we will discuss the clinical relevance of vitamin B6 metabolism as a prognostic factor in cancer patients.

Indexed as

AnimalsBiomarkers, TumorCarcinogenesisCarcinoma, Non-Small-Cell LungHumansLung NeoplasmsNeoplasmsPrognosisPyridoxal KinasePyridoxal PhosphateVitamin B 6Biomarkers, TumorPyridoxal KinasePyridoxal PhosphateVitamin B 6

Identifiers

PMID23334322
OpenAlexW2032094408

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.