Evidence map›Paper›PMID 19462467›Full record

ArticleHuman mutation2009

Molecular profiling of the "plexinome" in melanoma and pancreatic cancer.

Asha Balakrishnan, Junia Y Penachioni, Simona Lamba, Fonnet E Bleeker, Carlo Zanon, Monica Rodolfo, Viviana Vallacchi, Aldo Scarpa, Lara Felicioni, Matthias Buck and 4 more

Open access · greenAbstract read
In one paragraph

Article in Human mutation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. SEMAPHORINS and their receptors: focus on the crosstalk between melanoma and hypoxia.Journal of experimental & clinical cancer research : CR · 2021
    Review
  7. Article
  8. Article
  9. Frontiers in cell and developmental biology · 2021
    Article
  10. Article
  11. Review
  12. Novel somatic alterations underlie Chinese papillary thyroid carcinoma.Cancer biomarkers : section A of Disease markers · 2020
    Article
  13. Article
  14. Review
  15. Genes & development · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Loss of plexin-B3 in hepatocellular carcinoma.Experimental and therapeutic medicine · 2015
    Article
  20. 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

14 authors at 8 institutions in 3 countries.

Asha BalakrishnanLaboratory of Molecular Genetics, Institute for Cancer Research and Treatment, University of Torino Medical School, Candiolo, Italy.
Junia Y Penachioni
Simona Lamba
Fonnet E Bleeker
Carlo Zanon
Monica Rodolfo
Viviana Vallacchi
Aldo Scarpa
Lara Felicioni
Matthias Buck
Antonio Marchetti
Paolo M Comoglio
Alberto Bardelli
Luca Tamagnone
Candiolo Cancer Institute · ITFIRC Institute of Molecular Oncology · ITFondazione IRCCS Istituto Nazionale dei Tumori · ITUniversity of Chieti-Pescara · ITAcademic Medical Center · NLCase Western Reserve University · USMolecular Oncology (United States) · USUniversity of Verona · IT

Funding

Signaling Biophysics of Protein-GTPase InteractionsR01GM073071 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI BUCK, MATTHIAS · 2005 to 2009
$1.4M
NIGMS NIH HHS GM73071NIGMS NIH HHS R01 GM073071
6 · The paper itself

Abstract

Plexins are transmembrane high-affinity receptors for semaphorins, regulating cell guidance, motility, and invasion. Functional evidences implicate semaphorin signals in cancer progression and metastasis. Yet, it is largely unknown whether plexin genes are genetically altered in human tumors. We performed a comprehensive gene copy analysis and mutational profiling of all nine members of the plexin gene family (plexinome), in melanomas and pancreatic ductal adenocarcinomas (PDACs), which are characterized by high metastatic potential and poor prognosis. Gene copy analysis detected amplification of PLXNA4 in melanomas, whereas copy number losses of multiple plexin genes were seen in PDACs. Somatic mutations were detected in PLXNA4, PLXNB3, and PLXNC1; providing the first evidence that these plexins are mutated in human cancer. Functional assays in cellular models revealed that some of these missense mutations result in loss of plexin function. For instance, c.1613G>A, p.R538H mutation in the extracellular domain of PLXNB3 prevented binding of the ligand Sema5A. Moreover, although PLXNA4 signaling can inhibit tumor cell migration, the mutated c.5206C>T, p.H1736Y allele had lost this activity. Our study is the first systematic analysis of the "plexinome" in human tumors, and indicates that multiple mutated plexins may be involved in cancer progression.

Indexed as

Gene Expression ProfilingAdenocarcinomaHumansMelanomaMutationPancreatic NeoplasmsPhylogenyPolymerase Chain ReactionReceptors, Cell SurfaceReceptors, Cell Surface

Identifiers

PMID19462467
PMCPMC2989154
OpenAlexW2104393011

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.