PMID- 23832118
OWN - NLM
STAT- MEDLINE
DCOM- 20140729
LR  - 20211021
IS  - 1476-5403 (Electronic)
IS  - 1350-9047 (Print)
IS  - 1350-9047 (Linking)
VI  - 21
IP  - 1
DP  - 2014 Jan
TI  - Multimodal immunogenic cancer cell death as a consequence of anticancer cytotoxic 
      treatments.
PG  - 39-49
LID - 10.1038/cdd.2013.84 [doi]
AB  - Apoptotic cell death generally characterized by a morphologically homogenous 
      entity has been considered to be essentially non-immunogenic. However, apoptotic 
      cancer cell death, also known as type 1 programmed cell death (PCD), was recently 
      found to be immunogenic after treatment with several chemotherapeutic agents and 
      oncolytic viruses through the emission of various danger-associated molecular 
      patterns (DAMPs). Extensive studies have revealed that two different types of 
      immunogenic cell death (ICD) inducers, recently classified by their distinct 
      actions in endoplasmic reticulum (ER) stress, can reinitiate immune responses 
      suppressed by the tumor microenvironment. Indeed, recent clinical studies have 
      shown that several immunotherapeutic modalities including therapeutic cancer 
      vaccines and oncolytic viruses, but not conventional chemotherapies, culminate in 
      beneficial outcomes, probably because of their different mechanisms of ICD 
      induction. Furthermore, interests in PCD of cancer cells have shifted from its 
      classical form to novel forms involving autophagic cell death (ACD), programmed 
      necrotic cell death (necroptosis), and pyroptosis, some of which entail 
      immunogenicity after anticancer treatments. In this review, we provide a brief 
      outline of the well-characterized DAMPs such as calreticulin (CRT) exposure, 
      high-mobility group protein B1 (HMGB1), and adenosine triphosphate (ATP) release, 
      which are induced by the morphologically distinct types of cell death. In the 
      latter part, our review focuses on how emerging oncolytic viruses induce 
      different forms of cell death and the combinations of oncolytic virotherapies 
      with further immunomodulation by cyclophosphamide and other immunotherapeutic 
      modalities foster dendritic cell (DC)-mediated induction of antitumor immunity. 
      Accordingly, it is increasingly important to fully understand how and which ICD 
      inducers cause multimodal ICD, which should aid the design of reasonably 
      multifaceted anticancer modalities to maximize ICD-triggered antitumor immunity 
      and eliminate residual or metastasized tumors while sparing autoimmune diseases.
FAU - Inoue, H
AU  - Inoue H
AD  - 1] Division of Molecular and Clinical Genetics, Medical Institute of 
      Bioregulation, Kyushu University, Fukuoka, Japan [2] Research Institute for 
      Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, 
      Fukuoka, Japan [3] Department of Advanced Molecular and Cell Therapy, Kyushu 
      University Hospital,Kyushu University, Fukuoka, Japan.
FAU - Tani, K
AU  - Tani K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20130705
PL  - England
TA  - Cell Death Differ
JT  - Cell death and differentiation
JID - 9437445
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Calreticulin)
RN  - 0 (HMGB1 Protein)
SB  - IM
MH  - Animals
MH  - Antineoplastic Agents/therapeutic use/*toxicity
MH  - Calreticulin/metabolism
MH  - Cell Death/*drug effects
MH  - Endoplasmic Reticulum Stress/drug effects
MH  - HMGB1 Protein/metabolism
MH  - Humans
MH  - Neoplasms/drug therapy/*immunology
MH  - Oncolytic Viruses/physiology
PMC - PMC3857623
EDAT- 2013/07/09 06:00
MHDA- 2014/07/30 06:00
PMCR- 2015/01/01
CRDT- 2013/07/09 06:00
PHST- 2013/03/11 00:00 [received]
PHST- 2013/05/06 00:00 [revised]
PHST- 2013/05/14 00:00 [accepted]
PHST- 2013/07/09 06:00 [entrez]
PHST- 2013/07/09 06:00 [pubmed]
PHST- 2014/07/30 06:00 [medline]
PHST- 2015/01/01 00:00 [pmc-release]
AID - cdd201384 [pii]
AID - 10.1038/cdd.2013.84 [doi]
PST - ppublish
SO  - Cell Death Differ. 2014 Jan;21(1):39-49. doi: 10.1038/cdd.2013.84. Epub 2013 Jul 
      5.