PMID- 14983503
OWN - NLM
STAT- MEDLINE
DCOM- 20040318
LR  - 20151119
IS  - 0008-543X (Print)
IS  - 0008-543X (Linking)
VI  - 100
IP  - 5
DP  - 2004 Mar 1
TI  - Major histocompatibility antigens and antigen-processing molecules in 
      retinoblastoma.
PG  - 1059-69
AB  - BACKGROUND: Malignant transformation of cells is frequently associated with 
      abnormalities in human leukocyte antigen (HLA) expression. These abnormalities 
      may play a role in the clinical course of the disease, because HLAs mediate 
      interactions of tumor cells with cytotoxic T lymphocytes (CTLs) and natural 
      killer (NK) cells. Retinoblastoma is the most common intraocular malignant tumor 
      in childhood and is characterized by direct spread to the optic nerve and orbit 
      as well as hematogeneous and lymphatic spread. Little is known about the role of 
      HLA expression in the progression of this malignant disease. METHODS: HLA Class I 
      antigen, beta2-microglobulin (beta2-m), HLA Class II antigens, and the 
      antigen-processing molecules (APMs) of the HLA Class I pathway, including 
      proteasomal subunits (low-molecular mass polypeptide 2 [LMP-2] and LMP-10), the 
      transporter-associated protein (TAP-1) subunit, the binding protein tapasin, and 
      the chaperone molecule calnexin, were studied in 30 archival retinoblastoma 
      specimens by immunohistochemistry. Immunoanalysis was performed based on the 
      International Histocompatibility Working Group Project Description. RESULTS: HLA 
      Class I antigen, beta2-m, HLA Class II antigen, and APMs were positive in 12 
      tumors with no invasion and were decreased in 13 tumors with choroidal and optic 
      nerve invasion. The difference in HLA and APM expression between the 2 groups was 
      statistically significant (P < 0.001). CONCLUSIONS: Decreased expression of HLA 
      was observed in aggressive tumors and in poorly differentiated tumors. The 
      current findings support a role for both CTLs and NK cell-mediated control of 
      tumor growth in the clinical course of retinoblastoma.
CI  - Copyright 2004 American Cancer Society.
FAU - Krishnakumar, Subramanian
AU  - Krishnakumar S
AD  - Department of Ocular Pathology, Medical and Vision Research Foundations, Chennai, 
      India. drkrishnakumar_2002@yahoo.com
FAU - Sundaram, Amirthalakshmi
AU  - Sundaram A
FAU - Abhyankar, Dhiraj
AU  - Abhyankar D
FAU - Krishnamurthy, Vanitha
AU  - Krishnamurthy V
FAU - Shanmugam, Mahesh Palanivelu
AU  - Shanmugam MP
FAU - Gopal, Lingam
AU  - Gopal L
FAU - Sharma, Tarun
AU  - Sharma T
FAU - Biswas, Jyotirmay
AU  - Biswas J
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer
JT  - Cancer
JID - 0374236
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Histocompatibility Antigens Class II)
SB  - IM
MH  - Biomarkers, Tumor/analysis
MH  - Cell Transformation, Neoplastic
MH  - Child
MH  - Child, Preschool
MH  - Culture Techniques
MH  - Female
MH  - Histocompatibility Antigens Class I/*analysis/immunology
MH  - Histocompatibility Antigens Class II/*analysis/immunology
MH  - Humans
MH  - Male
MH  - Neoplasm Invasiveness/*pathology
MH  - Probability
MH  - Prognosis
MH  - Retinal Neoplasms/*immunology/pathology
MH  - Retinoblastoma/*immunology/pathology
MH  - Sampling Studies
MH  - Sensitivity and Specificity
MH  - Statistics, Nonparametric
MH  - T-Lymphocytes, Cytotoxic/immunology
EDAT- 2004/02/26 05:00
MHDA- 2004/03/19 05:00
CRDT- 2004/02/26 05:00
PHST- 2004/02/26 05:00 [pubmed]
PHST- 2004/03/19 05:00 [medline]
PHST- 2004/02/26 05:00 [entrez]
AID - 10.1002/cncr.20062 [doi]
PST - ppublish
SO  - Cancer. 2004 Mar 1;100(5):1059-69. doi: 10.1002/cncr.20062.