PMID- 28864616
OWN - NLM
STAT- MEDLINE
DCOM- 20170925
LR  - 20181219
IS  - 1535-5667 (Electronic)
IS  - 0161-5505 (Linking)
VI  - 58
IP  - Suppl 2
DP  - 2017 Sep
TI  - CXCR4 Ligands: The Next Big Hit?
PG  - 77S-82S
LID - 10.2967/jnumed.116.186874 [doi]
AB  - The G protein-coupled protein receptor C-X-C chemokine receptor 4 (CXCR4) is an 
      attractive target for cancer diagnosis and treatment, as it is overexpressed in 
      many solid and hematologic cancers. Binding of its ligand, C-X-C chemokine ligand 
      12 (CXCL12), results in receptor internalization and activation of several signal 
      transduction pathways, such as phosphoinositide 3-kinase/protein kinase B, which 
      are critical in cell proliferation, angiogenesis, development of metastasis, and 
      survival. Also, the CXCR4-CXCL12 axis is involved in the interaction between 
      hematopoietic stem cells (as well as hematologic and solid tumor cells) and their 
      protective microenvironment. This interaction can be disrupted by CXCR4 
      antagonists. This concept is being used clinically to harvest hematopoietic stem 
      or progenitor cells from bone marrow and to sensitize cancer cells to 
      conventional chemotherapy and radiotherapy, and the potential to overcome tumor 
      microenvironment-driven immunosuppression is being explored. This review focuses 
      on new strategies for improvement of cancer treatment by targeting of the 
      CXCR4-CXCL12 interaction. Because of its critical role in cancer, many peptidic 
      and nonpeptidic ligands with different modes of antagonistic activity against the 
      CXCR4-CXCL12 axis have been developed, with some of them reaching clinical 
      trials. Molecular imaging with recently developed radiolabeled CXCR4 ligands 
      could facilitate the selection of patients who might benefit from directed 
      targeted therapy, including CXCR4-directed endoradiotherapy.
CI  - (c) 2017 by the Society of Nuclear Medicine and Molecular Imaging.
FAU - Walenkamp, Annemiek M E
AU  - Walenkamp AME
AD  - Department of Medical Oncology, University Medical Center Groningen, University 
      of Groningen, Groningen, The Netherlands a.walenkamp@umcg.nl.
FAU - Lapa, Constantin
AU  - Lapa C
AD  - Department of Nuclear Medicine, University Hospital Wurzburg, Wurzburg, Germany.
FAU - Herrmann, Ken
AU  - Herrmann K
AD  - Department of Nuclear Medicine, University Hospital Essen, Essen, Germany.
AD  - Department of Molecular and Medical Pharmacology, David Geffen School of 
      Medicine, UCLA, Los Angeles, California.
FAU - Wester, Hans-Jurgen
AU  - Wester HJ
AD  - Pharmaceutical Radiochemistry, Technische Universitat Munchen, Munich, Germany; 
      and.
AD  - Scintomics GmbH, Fuerstenfeldbruck, Germany.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - J Nucl Med
JT  - Journal of nuclear medicine : official publication, Society of Nuclear Medicine
JID - 0217410
RN  - 0 (Chemokine CXCL12)
RN  - 0 (Ligands)
RN  - 0 (Receptors, CXCR4)
SB  - IM
MH  - Animals
MH  - Chemokine CXCL12/metabolism
MH  - Humans
MH  - Ligands
MH  - Molecular Targeted Therapy/*methods
MH  - Neoplasms/drug therapy/immunology/pathology/radiotherapy
MH  - Receptors, CXCR4/*metabolism
MH  - Tumor Microenvironment/drug effects/radiation effects
OTO - NOTNLM
OT  - CXCR4
OT  - endoradiotherapy
OT  - immunotherapy
OT  - tumor microenvironment
EDAT- 2017/09/03 06:00
MHDA- 2017/09/26 06:00
CRDT- 2017/09/03 06:00
PHST- 2017/03/24 00:00 [received]
PHST- 2017/06/02 00:00 [accepted]
PHST- 2017/09/03 06:00 [entrez]
PHST- 2017/09/03 06:00 [pubmed]
PHST- 2017/09/26 06:00 [medline]
AID - jnumed.116.186874 [pii]
AID - 10.2967/jnumed.116.186874 [doi]
PST - ppublish
SO  - J Nucl Med. 2017 Sep;58(Suppl 2):77S-82S. doi: 10.2967/jnumed.116.186874.