The development of many cancers and hematologic neoplasms is driven by neoplastic stem cells. These cells constitute a small proportion of the tumor mass and have low mitotic activity but demonstrate ability of efficient self-renewal.
It has long been recognized that many lymphomas and leukemias share phenotypic features with normal lymphocytes or their immature precursors. Realization of this fact provided a rationale for the classification of lymphomas and suggested their pathogenesis. Neoplastic transformation has been thought to occur at specific points during lymphoid development. The transformed cell becomes arrested at a certain stage of normal differentiation and this point corresponds to the event of malignant conversion.1 For example, lymphomas bearing the mature T-cell phenotype are supposed to result from the neoplastic transformation and clonal expansion of a single mature T cell. The same scheme has been applied for cutaneous lymphomas. It is widely accepted that the so-called primary cutaneous lymphomas originate directly from the lymphocytes recirculating through the skin, possibly from the lymphocytes belonging to the skin-associated lymphoid tissue.2,3 However, despite decades of research, this theory has not been experimentally confirmed and the nature of the initial steps of development of cutaneous lymphomas remains enigmatic.