PMID- 17725806
OWN - NLM
STAT- MEDLINE
DCOM- 20071214
LR  - 20070926
IS  - 1349-7006 (Electronic)
IS  - 1347-9032 (Linking)
VI  - 98
IP  - 11
DP  - 2007 Nov
TI  - Lack and restoration of sensitivity of lung cancer cells to cellular attack with 
      special reference to expression of human leukocyte antigen class I and/or major 
      histocompatibility complex class I chain related molecules A/B.
PG  - 1795-802
AB  - Both cytotoxic T lymphocytes (CTL) and natural killer (NK) cells may play major 
      roles in the host defense against cancer. However, their relationship against the 
      same tumor remains to be elucidated. Among 26 human lung cancer cell lines 
      established in our laboratory, 10 (38%) exhibited human leukocyte antigen 
      (HLA)-class I haplotype loss and three (12%) lost HLA-class I expression totally 
      by flow cytometry analysis. The two cell lines (E522L and C831L) that lost their 
      expression of HLA-class I in vitro and in vivo were applied for further 
      evaluations. Genetic abnormalities of beta2-microglobulin gene were observed in 
      both E522L (loss of mRNA) and C831L (point mutation). Transduction of the 
      wild-type beta2-microglobulin gene rendered them positive for HLA-class I 
      expression. The CTL were induced from autologous peripheral blood mononuclear 
      cells or regional lymph node lymphocytes by stimulation with wild-type 
      beta2-microglobulin transduced-E522L or -C831L, and they showed tumor-specific 
      cytotoxicity against wild-type beta2-microglobulin-transductant, but not parental 
      cells. In NK cell cytotoxicity, E522L showed high sensitivity to NK cells; 
      however, C831L showed resistance despite loss of HLA-class I expression. E522L 
      expressed MHC class I chain related molecules A/B, but C831L did not. The 
      transduction of the MHC class I chain related molecule A gene from E522L rendered 
      C831L positive for expression and sensitive to NK cell cytotoxicity. 
      Reconstruction of HLA-class I and MHC class I chain related molecules A 
      expression could abrogate evasion from cellular attack by CTL and NK cells, and 
      it may lead to a breakthrough in the development of cancer immunotherapy.
FAU - Baba, Tetsuro
AU  - Baba T
AD  - Department of Surgery II, School of Medicine, University of Occupational and 
      Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan.
FAU - Hanagiri, Takeshi
AU  - Hanagiri T
FAU - Ichiki, Yoshinobu
AU  - Ichiki Y
FAU - Kuroda, Koji
AU  - Kuroda K
FAU - Shigematsu, Yoshiki
AU  - Shigematsu Y
FAU - Mizukami, Makiko
AU  - Mizukami M
FAU - Sugaya, Masakazu
AU  - Sugaya M
FAU - Takenoyama, Mitsuhiro
AU  - Takenoyama M
FAU - Sugio, Kenji
AU  - Sugio K
FAU - Yasumoto, Kosei
AU  - Yasumoto K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070828
PL  - England
TA  - Cancer Sci
JT  - Cancer science
JID - 101168776
RN  - 0 (HLA-A Antigens)
RN  - 0 (HLA-B Antigens)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (beta 2-Microglobulin)
SB  - IM
MH  - Carcinoma, Large Cell/genetics/immunology/pathology
MH  - Cell Line, Tumor
MH  - Genotype
MH  - HLA-A Antigens/genetics/*immunology
MH  - HLA-B Antigens/genetics/*immunology
MH  - Histocompatibility Antigens Class I/genetics/*immunology
MH  - Humans
MH  - Killer Cells, Natural/immunology
MH  - Lung Neoplasms/genetics/*immunology/pathology
MH  - Male
MH  - Middle Aged
MH  - T-Lymphocytes, Cytotoxic/immunology
MH  - beta 2-Microglobulin/genetics/immunology
EDAT- 2007/08/30 09:00
MHDA- 2007/12/15 09:00
CRDT- 2007/08/30 09:00
PHST- 2007/08/30 09:00 [pubmed]
PHST- 2007/12/15 09:00 [medline]
PHST- 2007/08/30 09:00 [entrez]
AID - CAS586 [pii]
AID - 10.1111/j.1349-7006.2007.00586.x [doi]
PST - ppublish
SO  - Cancer Sci. 2007 Nov;98(11):1795-802. doi: 10.1111/j.1349-7006.2007.00586.x. Epub 
      2007 Aug 28.