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©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Clin Oncol. Oct 10, 2014; 5(4): 621-632
Published online Oct 10, 2014. doi: 10.5306/wjco.v5.i4.621
Published online Oct 10, 2014. doi: 10.5306/wjco.v5.i4.621
C4.4A as a biomarker in pulmonary adenocarcinoma and squamous cell carcinoma
Benedikte Jacobsen, Mette Camilla Kriegbaum, Michael Ploug, The Finsen Laboratory, Rigshospitalet, Copenhagen Biocenter, 2200 Copenhagen, Denmark
Benedikte Jacobsen, Mette Camilla Kriegbaum, Michael Ploug, Biotech Research and Innovation Centre, University of Copenhagen, 2200 Copenhagen, Denmark
Eric Santoni-Rugiu, Department of Pathology, Diagnostic Center, Rigshospitalet, Copenhagen University Hospital, 2100 Copenhagen, Denmark
Michael Ploug, 2nd Danish-Chinese Centre for Proteases and Cancer (This is a virtual centre without a defined address)
Author contributions: All authors contributed equally to manuscript preparation.
Supported by Copenhagen University Hospital (Rigshospitalets Forskningspuljer), The Danish National Research Foundation (Danish-Chinese Centre for Proteases and Cancer), Harboefonden, Torben og Alice Frimodts Fond, Fabrikant Einar Willumsens Mindelegat, Holger Rabitz and hustrus Legat, The Lundbeck Foundation
Correspondence to: Michael Ploug, PhD, DSc, The Finsen Laboratory, Rigshospitalet, Copenhagen Biocenter, Ole Maaløes Vej 5, Room 3.3.31, 2200 Copenhagen, Denmark. m-ploug@finsenlab.dk
Telephone: +45-35456037 Fax: +45-35453797
Received: January 4, 2014
Revised: June 4, 2014
Accepted: June 14, 2014
Published online: October 10, 2014
Processing time: 209 Days and 15.1 Hours
Revised: June 4, 2014
Accepted: June 14, 2014
Published online: October 10, 2014
Processing time: 209 Days and 15.1 Hours
Core Tip
Core tip: C4.4A is a new biomarker with potential prognostic value in pulmonary adenocarcinoma. High levels of protein expression correlate with poor patient survival and a histological growth pattern of the solid type. Recent data suggest that C4.4A is negatively regulated by the tumor suppressor liver kinase B1 (LKB1), which is inactivated in a fraction of adenocarcinomas of the lung. Such an inverse association between C4.4A and LKB1 could possibly render C4.4A a candidate predictive biomarker for therapeutic intervention targeting components of the LKB1 pathway, such as mammalian target of rapamycin.