PMID- 19519462
OWN - NLM
STAT- MEDLINE
DCOM- 20090715
LR  - 20210102
IS  - 1871-5303 (Print)
IS  - 1871-5303 (Linking)
VI  - 9
IP  - 2
DP  - 2009 Jun
TI  - Retinoids as critical modulators of immune functions: new therapeutic 
      perspectives for old compounds.
PG  - 113-31
AB  - Retinoids are vitamin A derivatives that critically regulate several 
      physiological and pathological processes, including immune functions and cancer 
      development. These biological response modifiers exert their pleiotropic effects 
      through the interaction with nuclear receptors, defined as retinoic acid 
      receptors (RARs) and retinoid X receptors (RXRs). These ligand-activated nuclear 
      receptors induce the transcription of target genes by binding to responsive 
      elements in the promoter regions. RARs and RXRs are also capable to interact with 
      other nuclear receptors, thus expanding their spectrum of action on gene 
      expression. Evidence has been accumulated indicating that retinoids may exert 
      beneficial effects in both immune-mediated disorders and tumors. With regard to 
      cancer, retinoids directly target neoplastic cells by inducing differentiation, 
      inhibiting cell growth or promoting survival. However, the efficacy of these 
      compounds in cancer treatment probably resides in their ability to modulate also 
      the function of immune effectors. Vitamin A derivatives are currently used in the 
      therapy of acute promyelocytic leukemia and of cutaneous T cell lymphomas, but 
      they could be effective also on B-cell malignancies. Clinical trials are ongoing 
      to test their efficacy in solid tumors. In this review, we give a broad depiction 
      of how retinoids influence the function of immune effectors and affect growth and 
      survival of hematological malignancies. This with the aim to better understand 
      the clinical effects of retinoid-based therapies and provide the rationale to 
      combine retinoids with other active compounds in new synergistic treatment 
      strategies.
FAU - Montrone, Michele
AU  - Montrone M
AD  - Cancer Bioimmunotherapy Unit, Department of Medical Oncology, Centro di 
      Riferimento Oncologico - IRCCS, National Cancer Institute, 33081, Aviano (PN), 
      Italy.
FAU - Martorelli, Debora
AU  - Martorelli D
FAU - Rosato, Antonio
AU  - Rosato A
FAU - Dolcetti, Riccardo
AU  - Dolcetti R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United Arab Emirates
TA  - Endocr Metab Immune Disord Drug Targets
JT  - Endocrine, metabolic & immune disorders drug targets
JID - 101269157
RN  - 0 (Retinoids)
SB  - IM
MH  - Animals
MH  - B-Lymphocytes/drug effects/physiology
MH  - Hematologic Neoplasms/drug therapy/immunology
MH  - Humans
MH  - Immune System/*drug effects/physiology
MH  - Multiple Myeloma/drug therapy/immunology
MH  - Neoplasms/drug therapy/immunology
MH  - Retinoids/*pharmacology
MH  - T-Lymphocytes/drug effects/physiology
RF  - 195
EDAT- 2009/06/13 09:00
MHDA- 2009/07/16 09:00
CRDT- 2009/06/13 09:00
PHST- 2009/06/13 09:00 [entrez]
PHST- 2009/06/13 09:00 [pubmed]
PHST- 2009/07/16 09:00 [medline]
AID - 10.2174/187153009788452435 [doi]
PST - ppublish
SO  - Endocr Metab Immune Disord Drug Targets. 2009 Jun;9(2):113-31. doi: 
      10.2174/187153009788452435.