Evidence map›Paper›PMID 33270750›Full record

ArticlePloS one2020

Activated leukocyte cell adhesion molecule expression correlates with the WNT subgroup in medulloblastoma and is involved in regulating tumor cell proliferation and invasion.

Takamune Achiha, Noriyuki Kijima, Yoshinori Kodama, Naoki Kagawa, Manabu Kinoshita, Yasunori Fujimoto, Masahiro Nonaka, Junya Fukai, Akihiro Inoue, Namiko Nishida and 16 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Primary leptomeningeal medulloblastoma: a case-based review.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2022
    Review
  5. Review
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

26 authors at 15 institutions in 2 countries.

Takamune AchihaDepartment of Neurosurgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Noriyuki KijimaDepartment of Neurosurgery, Osaka University Graduate School of Medicine, Osaka, Japan.ORCID 0000-0003-2103-1909
Yoshinori KodamaKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Naoki KagawaDepartment of Neurosurgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Manabu KinoshitaDepartment of Neurosurgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Yasunori FujimotoDepartment of Neurosurgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Masahiro NonakaKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Junya FukaiKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.ORCID 0000-0001-7103-8493
Akihiro InoueKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Namiko NishidaKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Takumi YamanakaKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Atsuko HaradaKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Kanji MoriKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Naohiro TsuyuguchiKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Takehiro UdaKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Kenichi IshibashiKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Yusuke TomoganeKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Daisuke SakamotoKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Tomoko ShofudaKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Ema YoshiokaKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Daisuke KanematsuKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Masayuki ManoKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Betty LuuDevelopmental and Stem Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario, Canada.
Michael D TaylorDevelopmental and Stem Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario, Canada.
Yonehiro KanemuraKansai Molecular Diagnosis Network for Central Nervous System Tumors, Osaka, Japan.
Haruhiko KishimaDepartment of Neurosurgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Osaka National Hospital · JPThe University of Osaka · JPHyogo Medical University · JPKyoto Prefectural University of Medicine · JPEhime University · JPHospital for Sick Children · CAKansai Medical University · JPKansai Rosai Hospital · JPKindai University · JPKitano Hospital · JPOsaka City General Hospital · JPOsaka City University · JPTakatsuki General Hospital · JPUniversity of Toronto · CAWakayama Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cluster of differentiation (CD) 166 or activated leukocyte cell adhesion molecule (ALCAM) is a transmembrane molecule known to be an intercellular adhesion factor. The expression and function of ALCAM in medulloblastoma (MB), a pediatric brain tumor with highly advanced molecular genetics, remains unclear. Therefore, this study aimed to clarify the significance and functional role of ALCAM expression in MB. ALCAM expression in 45 patients with MB was evaluated by immunohistochemical analysis of formalin-fixed paraffin-embedded clinical specimens and the relationship between ALCAM expression and pathological type/molecular subgroup, such as WNT, SHH, Group 3, and Group 4, was examined. Eight ALCAM positive (18%), seven partially positive (16%), and 30 negative (67%) cases were detected. All seven cases of the WNT molecular subgroup were ALCAM positive and ALCAM expression strongly correlated with this subgroup (P < 0.0001). In addition, functional studies using MB cell lines revealed ALCAM expression affected proliferation and migration as a positive regulator in vitro. However, ALCAM silencing did not affect survival or the formation of leptomeningeal dissemination in an orthotopic mouse model, but did induce a malignant phenotype with increased tumor cell invasion at the dissemination sites (P = 0.0029). In conclusion, our results revealed that ALCAM exhibited highly specific expression in the WNT subgroup of MB. Furthermore, we demonstrated that the cell kinetics of MB cell lines can be altered by the expression of ALCAM.

Indexed as

Activated-Leukocyte Cell Adhesion MoleculeAdolescentAnimalsAntigens, CDBiomarkers, TumorBrain NeoplasmsCell AdhesionCell Adhesion Molecules, NeuronalCell MovementCell ProliferationCerebellar NeoplasmsChildChild, PreschoolFemaleFetal ProteinsGene ExpressionActivated-Leukocyte Cell Adhesion MoleculeALCAM protein, humanAntigens, CDBiomarkers, TumorCell Adhesion Molecules, NeuronalFetal ProteinsRNA, MessengerWnt Proteins

Identifiers

PMID33270750
PMCPMC7714159
OpenAlexW3109724579

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.