Signaling lymphocytic activation molecules Slam and cancers: friends or foes?
Metrics: PDF 1240 views | HTML 2516 views | ?
Gregory Fouquet1,*, Ingrid Marcq1,*, Véronique Debuysscher1, Jagadeesh Bayry2, Amrathlal Rabbind Singh3, Abderrahmane Bengrine4, Eric Nguyen-Khac1,5, Mickael Naassila1 and Hicham Bouhlal1
1INSERM 1247-GRAP, Centre Universitaire de Recherche en Santé CURS, Université de Picardie Jules Verne, CHU Sud, Amiens, France
2INSERM UMRS 1138, Centre de Recherche des Cordeliers–Paris, Paris, France
3Department of Microbiology, Aravind Medical Research Foundation, Anna Nagar, Madurai-India
4Biobanque de Picardie, Centre Hospitalier Universitaire Sud, Amiens, France
5Service Hepato-Gastroenterologie, Centre Hospitalier Universitaire Sud, Amiens, France
*These authors contributed equally to this work
Hicham Bouhlal, email: email@example.com
Ingrid Marcq, email: Ingrid.firstname.lastname@example.org
Keywords: SLAMF molecules; cancer; pathophysiology; therapy
Received: October 19, 2016 Accepted: December 03, 2017 Epub: February 26, 2018 Published: March 23, 2018
Signaling Lymphocytic Activation Molecules (SLAM) family receptors are initially described in immune cells. These receptors recruit both activating and inhibitory SH2 domain containing proteins through their Immunoreceptor Tyrosine based Switch Motifs (ITSMs). Accumulating evidence suggest that the members of this family are intimately involved in different physiological and pathophysiological events such as regulation of immune responses and entry pathways of certain viruses. Recently, other functions of SLAM, principally in the pathophysiology of neoplastic transformations have also been deciphered. These new findings may prompt SLAM to be considered as new tumor markers, diagnostic tools or potential therapeutic targets for controlling the tumor progression. In this review, we summarize the major observations describing the implications and features of SLAM in oncology and discuss the therapeutic potential attributed to these molecules.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.