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International Journal of Surgical Oncology
Volume 2012, Article ID 834852, 4 pages
Clinical Study

Clinical Behavior in Metastatic Brain Disease Is Not Influenced by the Immunological Defense Mediated by CD57+ NK-Cells

1Laboratory of Experimental Neuro-Oncology, Neuroscience Research Unit, Puerta de Hierro Hospital, Autonomous University, 28222 Madrid, Spain
2Neurosurgical Service, Puerta de Hierro Hospital, Autonomous University, 28222 Madrid, Spain
3Department of Pathology, Central Defense Hospital, 28047 Madrid, Spain

Received 21 April 2011; Revised 22 May 2011; Accepted 24 May 2011

Academic Editor: Russell Lonser

Copyright © 2012 J. Vaquero et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Objectives. The purpose of the present study is to verify if the degree of immunological response against metastatic tumors, measured by the number of CD57+ NK-cells in the tissue of a brain metastasis, influences the later development of new brain metastases or tumor recurrence. Patients and Methods. CD57+ NK-cells were immunohistochemically identified in the resected tumor, in a series of twenty patients operated on by a single brain metastasis secondary to lung adenocarcinoma. In each case, the degree of CD57+ NK-cells infiltration within the tumor tissue and the period free of new intracranial disease after brain surgery were recorded. Results. All the studied tumors showed variable number of CD57+ NK-cells (mean ± standard deviation: per microscopical field, at 200x). The period free of intracranial disease ranged between 10 and 52 weeks (mean ± standard deviation: ). Statistical analysis showed that there was no correlation between the degree of NK-cells infiltration within the resected tumor and the period free of intracranial disease after surgery ( ). Conclusion. This finding supports that clinical behavior in metastatic brain disease is not influenced by the immunological response mediated by CD57+ NK-cells.