Evidence map›Paper›PMID 31118427›Full record

ArticleScientific reports2019

CD271 is a molecular switch with divergent roles in melanoma and melanocyte development.

Fabian V Filipp, Chen Li, Alexander D Boiko

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. A CD24BMC biology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. p53 Family in Resistance to Targeted Therapy of Melanoma.International journal of molecular sciences · 2022
    Review
  9. Tracking of Melanoma Cell Plasticity by Transcriptional Reporters.International journal of molecular sciences · 2022
    Article
  10. Article
  11. Article
  12. Review
  13. Targeting Genome Stability in Melanoma-A New Approach to an Old Field.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Review
  16. Review
  17. 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

3 authors at 2 institutions in 2 countries.

Fabian V FilippCancer Systems Biology, Institute of Computational Biology, Helmholtz Zentrum München, Ingolstädter Landstraße 1, D-85764, München, Germany. fabian.filipp@helmholtz-muenchen.de.ORCID http://orcid.org/0000-0001-9889-5727
Chen LiSue and Bill Gross Research Stem Cell Center, University of California Irvine, 845 Health Sciences Road, Irvine, CA, 92697, USA.
Alexander D BoikoSue and Bill Gross Research Stem Cell Center, University of California Irvine, 845 Health Sciences Road, Irvine, CA, 92697, USA. aboiko@uci.edu.
University of California, Irvine · USUniversity of California, Merced · US

Funding

Fresno State and UC Merced Bridges to the Doctorate Program in Biomedical and Behavioral SciencesR25GM115293 · NIGMS · CALIFORNIA STATE UNIVERSITY FRESNO · PI KRISHNAN, VISWANATHAN V, LIWANG, ANDY · 2015 to 2019
$1.2M
Tumor pyruvate kinase as key regulator of cancer metabolismR00CA154887 · NCI · UNIVERSITY OF CALIFORNIA, MERCED · PI FILIPP, FABIAN VOLKER · 2012 to 2014
$725k
Isolation and Characterization of Tumor Stem Cells from Melanoma PatientsR00CA154960 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI BOIKO, ALEXANDER D · 2013 to 2015
$716k
Tumor pyruvate kinase as key regulator of cancer metabolismK99CA154887 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI FILIPP, FABIAN VOLKER · 2011 to 2012
$177k
NCI NIH HHS K99 CA154887NCI NIH HHS R00 CA154887NCI NIH HHS R00 CA154960NIGMS NIH HHS R25 GM115293
6 · The paper itself

Abstract

Dysregulation of signaling networks controlling self-renewal and migration of developmental cell lineages is closely linked to the proliferative and invasive properties of tumors. Identification of such signaling pathways and their critical regulators is vital for successful design of effective targeted therapies against neoplastic tissue growth. The neurotrophin receptor (CD271/NGFR/p75NTR) is a key regulator of the melanocytic cell lineage through its ability to mediate cell growth, survival, and differentiation. Using clinical melanoma samples, normal melanocytes and global gene expression profiling we have investigated the role of CD271 in rewiring signal transduction networks of melanoma cells during neoplastic transformation. Our analysis demonstrates that depending on the cell fate of tumor initiation vs normal development, elevated levels of CD271 can serve as a switch between proliferation/survival and differentiation/cell death. Two divergent arms of neurotrophin signaling hold the balance between positive regulators of tumor growth controlled by E2F, MYC, SREBP1 and AKT3 pathways on the one hand, and differentiation, senescence, and apoptosis controlled by TRAF6/IRAK-dependent activation of AP1 and TP53 mediated processes on the other hand. A molecular network map revealed in this study uncovers CD271 as a context-specific molecular switch between normal development and malignant transformation.

Indexed as

Cell SurvivalCell Transformation, NeoplasticDisease ProgressionDNA RepairGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansMelanocytesMelanomaNeoplasm ProteinsNerve Tissue ProteinsReal-Time Polymerase Chain ReactionReceptors, Nerve Growth FactorSignal TransductionTranscriptomeNeoplasm ProteinsNerve Tissue ProteinsNGFR protein, humanReceptors, Nerve Growth Factor

Identifiers

PMID31118427
PMCPMC6531451
OpenAlexW2946724192

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.