PMID- 20178101
OWN - NLM
STAT- MEDLINE
DCOM- 20100622
LR  - 20210103
IS  - 1097-0215 (Electronic)
IS  - 0020-7136 (Linking)
VI  - 127
IP  - 2
DP  - 2010 Jul 15
TI  - "Hard" and "soft" lesions underlying the HLA class I alterations in cancer cells: 
      implications for immunotherapy.
PG  - 249-56
LID - 10.1002/ijc.25270 [doi]
AB  - The ability of cancer cells to escape from the natural or immunotherapy-induced 
      antitumor immune response is often associated with alterations in the tumor cell 
      surface expression of Major Histocompatibility Complex (MHC) Class I antigens. 
      Considerable knowledge has been gained on the prevalence of various patterns of 
      MHC Class I defects and the underlying molecular mechanisms in different types of 
      cancer. In contrast, few data are available on the changes in MHC Class I 
      expression happening during the course of cancer immunotherapy. We have recently 
      proposed that the progression or regression of a tumor lesion in cancer patients 
      undergoing immunotherapy could be predetermined by the molecular mechanism 
      responsible for the MHC Class I alteration and not by the type of immunotherapy 
      used, i.e., interleukin-2 (IL-2), Bacillus Calmette-Guerin (BCG), 
      interferon-alpha (IFN-alpha), peptides alone, dendritic cells loaded with 
      peptides, protein-bound polysaccharide etc. If the molecular alteration 
      responsible for the changes in MHC Class I expression is reversible by cytokines 
      ("soft" lesion), the MHC Class I expression will be upregulated, the specific T 
      cell-mediated response will increase and the lesion will regress. However, if the 
      molecular defect is structural ("hard" lesion), the MHC Class I expression will 
      remain low, the escape mechanism will prevail and the primary tumor or the 
      metastatic lesion will progress. According to this idea, the nature of the 
      preexisting MHC Class I lesion in the cancer cell has a crucial impact 
      determining the final outcome of cancer immunotherapy. In this article, we 
      discuss the importance of these two types of molecular mechanisms of MHC Class 
      I-altered expression.
FAU - Garrido, Federico
AU  - Garrido F
AD  - Departamento de Bioquimica, Universidad de Granada, Granada, Spain. 
      federico.garrido.sspa@juntadeandalucia.es
FAU - Cabrera, Teresa
AU  - Cabrera T
FAU - Aptsiauri, Natalia
AU  - Aptsiauri N
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - 0 (Cancer Vaccines)
RN  - 0 (Histocompatibility Antigens Class I)
SB  - IM
MH  - Cancer Vaccines/therapeutic use
MH  - Histocompatibility Antigens Class I/*immunology
MH  - Humans
MH  - *Immunotherapy
MH  - Neoplasms/immunology/*therapy
MH  - Tumor Escape/*physiology
RF  - 72
EDAT- 2010/02/24 06:00
MHDA- 2010/06/23 06:00
CRDT- 2010/02/24 06:00
PHST- 2010/02/24 06:00 [entrez]
PHST- 2010/02/24 06:00 [pubmed]
PHST- 2010/06/23 06:00 [medline]
AID - 10.1002/ijc.25270 [doi]
PST - ppublish
SO  - Int J Cancer. 2010 Jul 15;127(2):249-56. doi: 10.1002/ijc.25270.