Evidence map›Paper›PMID 26956768›Full record

ArticleJournal of proteome research2016

Distinct Metabolic Signature of Human Bladder Cancer Cells Carrying an Impaired Fanconi Anemia Tumor-Suppressor Signaling Pathway.

Jayabal Panneerselvam, Guoxiang Xie, Raymond Che, Mingming Su, Jun Zhang, Wei Jia, Peiwen Fei

Open access · greenAbstract read
In one paragraph

Article in Journal of proteome research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Focal Point of Fanconi Anemia Signaling.International journal of molecular sciences · 2021
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Multifaceted Fanconi Anemia Signaling.Trends in genetics : TIG · 2018
    Review
  13. Fanconi Anemia Signaling and Cancer.Trends in cancer · 2017
    Review
  14. Article
  15. FANCD2 and DNA Damage.International journal of molecular sciences · 2017
    Review
  16. Article
  17. Article
  18. Article
  19. 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

7 authors at 4 institutions in 1 country.

Jayabal PanneerselvamUniversity of Hawaii Cancer Center, University of Hawaii , Honolulu, Hawaii, 96813 United States.
Guoxiang XieUniversity of Hawaii Cancer Center, University of Hawaii , Honolulu, Hawaii, 96813 United States.
Raymond CheUniversity of Hawaii Cancer Center, University of Hawaii , Honolulu, Hawaii, 96813 United States.
Mingming SuUniversity of Hawaii Cancer Center, University of Hawaii , Honolulu, Hawaii, 96813 United States.
Jun ZhangDepartment of Laboratory Medicine and Pathology, Mayo Clinic Foundation , Rochester, Minnesota, 55905 United States.
Wei JiaUniversity of Hawaii Cancer Center, University of Hawaii , Honolulu, Hawaii, 96813 United States.
Peiwen FeiUniversity of Hawaii Cancer Center, University of Hawaii , Honolulu, Hawaii, 96813 United States.
University of Hawaiʻi at Mānoa · USUniversity of Hawaii Cancer CenterUniversity of Hawaii System · USMayo Clinic · US

Funding

University of Hawaii Cancer Center CCSGP30CA071789 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI Xin Chen · 1996 to 2026
$56.2M
Molecular Insights into the Fanconi Anemia Tumor Suppressor Signaling PathwayR01CA188251 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI FEI, PEIWEN · 2014 to 2018
$1.6M
Roles of the Fanconi Anemia Pathway in Bladder TumorigenesisR01CA136532 · NCI · UNIVERSITY OF MINNESOTA · PI FEI, PEIWEN · 2009 to 2013
$1.5M
NCI NIH HHS P30 CA071789NCI NIH HHS R01 CA136532NCI NIH HHS R01CA136532NCI NIH HHS R01 CA188251NCI NIH HHS R01CA188251
6 · The paper itself

Abstract

Metabolic profiling has great potential to help the diagnosis and prognosis of cancer patients. Fanconi Anemia (FA) tumor-suppressor signaling has been instrumental in understanding human tumorigenesis. However, this instrumental understanding has never been demonstrated at the metabolic level. Here, we show that impaired FA signaling can lead cells to exhibit metabolic signatures of tumorigenesis. This is consistent with our original studies of the roles of FA signaling in suppressing non-FA tumorigenesis at functional and genetic levels. Using ultraperformance liquid chromatography-mass spectroscopy and gas chromatography-mass spectrometry, we characterized metabolic alterations in bladder cancer cells carrying an intact or impaired FA pathway. The latter was obtained by ectopically expressing FAVL (FAVL-high), which we previously found to be capable of inactivating FA signaling. A total of 18 metabolites, end products of cell proliferation or apoptosis, were significantly different between FAVL-high and -low cells. Methionine, phenylalanine, and threonine, resulting from a tumorigenic process, were substantially increased in FAVL-high cells. With this study, we achieved genomic, functional, and metabolomic characterization of the roles of FA signaling in the development of human cancer. Furthermore, this study provides novel insights into how to translate FA basic research into strategies for producing effective biomarkers in human cancer diagnosis and prognosis.

Indexed as

MetabolomeSignal TransductionAlternative SplicingApoptosisCell Line, TumorCell ProliferationCell Transformation, NeoplasticChromatography, LiquidEpithelial CellsFanconi Anemia Complementation Group L ProteinGene ExpressionHumansMass SpectrometryMethioninePhenylalanineProtein IsoformsFANCL protein, humanFanconi Anemia Complementation Group L ProteinMethioninePhenylalanineProtein IsoformsThreoninebladder cancercell proliferationFA pathwayFAVLmetabolomics

Identifiers

PMID26956768
PMCPMC4874490
OpenAlexW2295182169

What OpenQuestion holds

Textmetadata
LicenceTDM
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.