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Selective changes in expression of HLA class I polymorphic determinants in human solid tumors.

P G Natali1, M R Nicotra, A Bigotti

  • 1Department of Immunology, Regina Elena Cancer Institute, Rome, Italy.

Proceedings of the National Academy of Sciences of the United States of America
|September 1, 1989
PubMed
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Cancer cells often lose major histocompatibility complex class I (MHC I) molecules, crucial for immune recognition. This study reveals selective loss of specific MHC I (HLA-A2) epitopes in many tumors, potentially helping cancer evade immune surveillance.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Malignant transformation is often linked to reduced expression of major histocompatibility complex class I (MHC I) molecules.
  • The study investigates whether selective losses of MHC I expression occur, rather than a general decrease.

Purpose of the Study:

  • To determine if specific MHC I (HLA-A2) epitopes are selectively lost in various tumor types.
  • To understand the implications of selective MHC I loss for tumor immune evasion.

Main Methods:

  • Analysis of surgical biopsies from 13 tumor types using monoclonal antibodies (mAbs).
  • mAb BB7.2 was used to detect a polymorphic HLA-A2 epitope.
  • mAb W6/32 assessed overall HLA class I (HLA-A,B,C) expression.

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Main Results:

  • Selective loss or reduction of HLA-A2 expression was observed in 70-80% of endometrial, colorectal, mammary, and renal tumors.
  • Significant HLA-A2 loss also occurred in soft-tissue, skin, ovary, bladder, prostate, and stomach tumors (40-60%), and melanomas and lung carcinomas (25-30%).
  • All tested tumors retained expression of the framework HLA-A,B,C determinant.

Conclusions:

  • Selective loss of the HLA-A2 epitope, recognized by mAb BB7.2, is common in various cancers.
  • This selective loss may enable tumor cells to evade cytotoxic T cell recognition.
  • The findings suggest a mechanism for tumor cells to escape both T-cell and natural killer cell surveillance.