PMID- 11883844
OWN - NLM
STAT- MEDLINE
DCOM- 20020329
LR  - 20201219
IS  - 0022-3085 (Print)
IS  - 0022-3085 (Linking)
VI  - 96
IP  - 3
DP  - 2002 Mar
TI  - Apoptosis of T lymphocytes invading glioblastomas multiforme: a possible tumor 
      defense mechanism.
PG  - 580-4
AB  - OBJECT: The goal of this study was to investigate whether apoptosis occurs in T 
      lymphocytes that invade Fas ligand (FasL)-expressing glioblastomas multiforme 
      (GBMs) and if its induction could be mediated by Fas. METHODS: Apoptotic T 
      lymphocytes were detected in GBMs by using detection of cell-type markers 
      combined with active caspase-3 immunohistochemical analysis, a recently 
      introduced apoptosis-specific in situ ligation assay, as well as by examining 
      morphological criteria. Apoptotic T cells expressed Fas and were localized in the 
      vicinity or in direct contact with FasL-expressing tumor cells. The T lymphocytes 
      were undergoing apoptosis in spite of Bcl-2 expression. Expression of Bax was 
      also detected in dying T cells, which can explain the absence of the protective 
      effect of Bcl-2. because Bax inhibits Bcl-2 death-repressor activity. 
      CONCLUSIONS: On the basis of the data presented in this paper, the authors 
      suggest that GBM cells that express FasL can induce apoptosis in invading immune 
      cells. This phenomenon may play an important role in these tumors' maintenance of 
      immune privilege and evasion of immune attacks. Awareness of this phenomenon 
      should be helpful for the development of novel strategies for treatment of 
      malignant gliomas.
FAU - Didenko, Vladimir V
AU  - Didenko VV
AD  - Department of Neurosurgery, Baylor College of Medicine, Houston, Texas, USA.
FAU - Ngo, Hop N
AU  - Ngo HN
FAU - Minchew, Candace
AU  - Minchew C
FAU - Baskin, David S
AU  - Baskin DS
LA  - eng
GR  - R03 AG022664/AG/NIA NIH HHS/United States
GR  - R01 CA78912-01/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosurg
JT  - Journal of neurosurgery
JID - 0253357
RN  - 0 (BAX protein, human)
RN  - 0 (FASLG protein, human)
RN  - 0 (Fas Ligand Protein)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (bcl-2-Associated X Protein)
SB  - IM
MH  - Apoptosis/genetics/*immunology
MH  - Brain Neoplasms/genetics/*immunology/pathology
MH  - Fas Ligand Protein
MH  - Glioblastoma/genetics/*immunology/pathology
MH  - Humans
MH  - Membrane Glycoproteins/genetics/physiology
MH  - Proto-Oncogene Proteins/genetics
MH  - Proto-Oncogene Proteins c-bcl-2/genetics
MH  - T-Lymphocytes/*immunology/pathology
MH  - Tumor Cells, Cultured/immunology/pathology
MH  - bcl-2-Associated X Protein
PMC - PMC1853267
MID - NIHMS20083
EDAT- 2002/03/09 10:00
MHDA- 2002/03/30 10:01
PMCR- 2008/02/02
CRDT- 2002/03/09 10:00
PHST- 2002/03/09 10:00 [pubmed]
PHST- 2002/03/30 10:01 [medline]
PHST- 2002/03/09 10:00 [entrez]
PHST- 2008/02/02 00:00 [pmc-release]
AID - 10.3171/jns.2002.96.3.0580 [doi]
PST - ppublish
SO  - J Neurosurg. 2002 Mar;96(3):580-4. doi: 10.3171/jns.2002.96.3.0580.