The Oncogene AF1Q is Associated with WNT and STAT Signaling and Offers a Novel Independent Prognostic Marker in Patients with Resectable Esophageal Cancer.
Adult
Aged
Aged, 80 and over
Biomarkers, Tumor
/ metabolism
Esophageal Neoplasms
/ metabolism
Esophagectomy
/ mortality
Female
Follow-Up Studies
Gene Expression Regulation, Neoplastic
Humans
Hyaluronan Receptors
/ metabolism
Male
Middle Aged
Neoplasm Proteins
/ metabolism
Neoplasm Recurrence, Local
/ metabolism
Oncogenes
Prognosis
Proto-Oncogene Proteins
/ metabolism
Retrospective Studies
STAT1 Transcription Factor
/ metabolism
Survival Rate
Wnt1 Protein
/ metabolism
AF1Q
MLLT11
STAT
WNT
esophageal cancer
prognosis
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
30 10 2019
30 10 2019
Historique:
received:
04
10
2019
revised:
24
10
2019
accepted:
29
10
2019
entrez:
2
11
2019
pubmed:
2
11
2019
medline:
17
7
2020
Statut:
epublish
Résumé
AF1q impairs survival in hematologic and solid malignancies. AF1q expression is associated with tumor progression, migration, and chemoresistance, and acts as a transcriptional co-activator in WNT and STAT signaling. This study evaluates the role of AF1q in patients with resectable esophageal cancer (EC). A total of 278 patients operated on for esophageal cancer were retrospectively included, and the expression of AF1q, CD44, and pYSTAT3 was analyzed following immunostaining. Quantified data were processed to correlational and survival analysis. In EC patients, an elevated expression of AF1q was associated with CD44 (
Identifiants
pubmed: 31671695
pii: cells8111357
doi: 10.3390/cells8111357
pmc: PMC6912824
pii:
doi:
Substances chimiques
Biomarkers, Tumor
0
CD44 protein, human
0
Hyaluronan Receptors
0
MLLT11 protein, human
0
Neoplasm Proteins
0
Proto-Oncogene Proteins
0
STAT1 Transcription Factor
0
STAT1 protein, human
0
WNT1 protein, human
0
Wnt1 Protein
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Commentaires et corrections
Type : ErratumIn
Déclaration de conflit d'intérêts
M.G. has received institutional research support from AstraZeneca, Roche, Novartis, and Pfizer, and has received lecture fees, honoraria for participation on advisory boards, and travel support from Amgen, AstraZeneca, Celgene, EliLilly, Invectys, Pfizer, Nanostring, Novartis, Roche, and Medison. He has served as a consultant for AstraZeneca and EliLilly, and an immediate family member is employed by Sandoz. None of the other authors have financial and personal relationships with individuals or organizations that could inappropriately influence their work.
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