Advances in the Understanding of EBV Associated Lymphoproliferative Disorders

Abstract

Neoplasia may be defined as the uncontrolled growth of a specific population of cells which, in the absence of therapeutic intervention, will eventuate in the death of the patient. Progressive accumulation of neoplastic cells at primary and secondary sites, is dependent upon both a pathological intrinsic drive to proliferation and the failure of extracellular mechanisms which normally suppress proliferation or destroy proliferating cells. Thus, a pathological proliferative drive alone (of the kind, for example, that may be induced by certain viral infections) is not sufficient to give rise to neoplasia. For uncontrolled proliferation to occur, there must be accompanying intracellular changes which permit the cell to escape host regulatory mechanisms, or failure of the external regulatory mechanisms themselves. Thus, neoplasia is generally - perhaps always - the result of genetic changes which, result in both abnormal proliferation and escape from those mechanisms that normally regulate proliferation. When a partially transformed cell, i.e one which is not able to proliferate indefinitely in the presence of normal host regulatory factors, encounters a host with impaired ability to regulate cellular proliferation, the net result is likely to be the development of a cellular process that is indistinguishable from a genetically induced neoplasm at histological and clinical levels.