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Favorable outcome in clinically stage II melanoma patients is associated with the presence of activated tumor infiltrating T‐lymphocytes and preserved MHC class I antigen expression
Author(s) -
van Houdt Inge S.,
Sluijter Berbel J.R.,
Moesbergen Laura M.,
Vos Wim M.,
de Gruijl Tanja D.,
Molenkamp Barbara G.,
van den Eertwegh Alfons J.M.,
Hooijberg Erik,
van Leeuwen Paul A.M.,
Meijer Chris J.L.M.,
Oudejans Joost J.
Publication year - 2008
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.23543
Subject(s) - antigen , melanoma , tumor infiltrating lymphocytes , cd8 , immunology , mhc class i , major histocompatibility complex , mhc class ii , medicine , tumor antigen , cancer research , immune system , biology , immunotherapy
In this study we investigated whether the presence of specific populations of tumor infiltrating lymphocytes (TILs) in diagnostic primary melanoma biopsies are related to outcome in clinically stage II melanoma patients. Moreover, we investigated whether the presence of TILs correlates with expression of MHC class I antigen and MHC class II antigen on tumor cells and/or tumor infiltrating antigen presenting cells. Diagnostic primary melanoma samples of 15 patients with an unfavorable outcome were compared with 20 patients with favorable outcome. Patients were matched for age, gender and Breslow thickness. Biopsies were examined for the presence of granzyme B + , CD8 + , CD4 + and CD56 + TILs and for expression of MHC class I antigen and MHC class II antigen on tumor and/or tumor infiltrating cells. A favorable clinical outcome was strongly associated with the presence of GrB + and CD4 + TILs, with expression of MHC class I antigen on tumor cells and with expression of MHC class II antigen on intratumoral antigen presenting cells. These data strongly support the notion that in melanoma patients the cellular immune response is a major factor in preventing melanoma cell dissemination. © 2008 Wiley‐Liss, Inc.