PMID- 22671924
OWN - NLM
STAT- MEDLINE
DCOM- 20130308
LR  - 20191027
IS  - 1873-5576 (Electronic)
IS  - 1568-0096 (Linking)
VI  - 12
IP  - 7
DP  - 2012 Sep
TI  - Targeting of adhesion molecules as a therapeutic strategy in multiple myeloma.
PG  - 776-96
AB  - Multiple myeloma (MM) is a clonal disorder of plasma cells that remains, for the 
      most part, incurable despite the advent of several novel therapeutic agents. 
      Tumor cells in this disease are cradled within the bone marrow (BM) 
      microenvironment by an array of adhesive interactions between the BM cellular 
      residents, the surrounding extracellular matrix (ECM) components such as 
      fibronectin (FN), laminin, vascular cell adhesion molecule-1 (VCAM-1), 
      proteoglycans, collagens and hyaluronan, and a variety of adhesion molecules on 
      the surface of MM cells including integrins, hyaluronan receptors (CD44 and 
      RHAMM) and heparan sulfate proteoglycans. Several signaling responses are 
      activated by these interactions, affecting the survival, proliferation and 
      migration of MM cells. An important consequence of these direct adhesive 
      interactions between the BM/ECM and MM cells is the development of drug 
      resistance. This phenomenon is termed "cell adhesion-mediated drug resistance" 
      (CAM-DR) and it is thought to be one of the major mechanisms by which MM cells 
      escape the cytotoxic effects of therapeutic agents. This review will focus on the 
      adhesion molecules involved in the cross-talk between MM cells and components of 
      the BM microenvironment. The complex signaling networks downstream of these 
      adhesive molecules mediated by direct ligand binding or inside-out soluble 
      factors signaling will also be reviewed. Finally, novel therapeutic strategies 
      targeting these molecules will be discussed. Identification of the mediators of 
      MM-BM interaction is essential to understand MM biology and to elucidate novel 
      therapeutic targets for this disease.
FAU - Neri, Paola
AU  - Neri P
AD  - Division of Hematology, University of Calgary, AB, Canada.
FAU - Bahlis, Nizar J
AU  - Bahlis NJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Netherlands
TA  - Curr Cancer Drug Targets
JT  - Current cancer drug targets
JID - 101094211
RN  - 0 (Cell Adhesion Molecules)
SB  - IM
MH  - Animals
MH  - Bone Marrow/*drug effects/metabolism
MH  - Cell Adhesion/*drug effects
MH  - Cell Adhesion Molecules/*metabolism
MH  - Clinical Trials as Topic
MH  - Drug Evaluation, Preclinical
MH  - Humans
MH  - Molecular Targeted Therapy/*methods
MH  - Multiple Myeloma/*drug therapy/*metabolism/pathology
MH  - Signal Transduction/drug effects
EDAT- 2012/06/08 06:00
MHDA- 2013/03/09 06:00
CRDT- 2012/06/08 06:00
PHST- 2011/04/25 00:00 [received]
PHST- 2011/12/16 00:00 [revised]
PHST- 2011/12/30 00:00 [accepted]
PHST- 2012/06/08 06:00 [entrez]
PHST- 2012/06/08 06:00 [pubmed]
PHST- 2013/03/09 06:00 [medline]
AID - CCDT-EPUB-20120605-1 [pii]
AID - 10.2174/156800912802429337 [doi]
PST - ppublish
SO  - Curr Cancer Drug Targets. 2012 Sep;12(7):776-96. doi: 10.2174/156800912802429337.