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Evidence and Clinical Implications

Arch Dermatol. 2004;140:1156-1160.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

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 . . . [Full Text of this Article]

WHAT ARE STEM CELLS, LYMPHOID PRECURSOR CELLS, AND NEOPLASTIC STEM CELLS?


WHAT IS THE ORIGIN OF NEOPLASTIC STEM CELLS?

WHAT IS THE EVIDENCE FOR PRECURSOR CELL TRANSFORMATION IN CUTANEOUS LYMPHOMA?

DOES THE CONCEPT OF LSC ACCOUNT FOR THE CLINICAL FEATURES OF CUTANEOUS LYMPHOMA?

IS THERE EVIDENCE AGAINST THE EXISTENCE OF LSC?

CONCLUSIONS
Robert Gniadecki, MD

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Arch Dermatol. 2004;140(9):1057-1061.
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