Cells from patients with T-cell PLL often contain large electron-dense granules. T-cell PLL cells are generally CD4+ and CD8-; however, other patterns may exist in about one-third of patients.204 Inversion in the long arm of chromosome 14 and trisomy of the long arm of chromosome 8 have been reported in at least one-half of the cases of T-cell PLL.205 Whether a human lymphotrophic retrovirus is involved in the pathogen-esis of T-PLL is controversial.206

The higher density of surface immunoglobulins and pattern of heavy chain overexpression suggests that the prolymphocyte is immunologically more mature than the B lymphocyte of CLL. Therefore, the word "prolymphocyte" is misleading. About one-third of patients with PLL display circulating monoclonal immunoglobulin compared to about 5 percent in those with CLL.201 Despite the apparent derivation from a more mature B cell, the clinical course in patients with B-cell PLL is much more aggressive than observed in patients with typical CLL.199 Some cases of apparent B-cell PLL exhibit the t(11;14)(q13;q32) cytogenetic abnormality typical of mantle cell lymphoma.207

Prolymphocytic transformation may rarely occur in patients with CLL. Careful observation of blood smears from patients with CLL suggest that many do contain at least some prolym-phocytes.201 Prolymphocytic transformation is arbitrarily defined as the presence of more than 55 percent prolymphocytes in the blood. Spleens from patients with PLL are infiltrated with neoplastic lymphoid cells that replace both the red and white pulp (both diffuse and nodular areas).208 The bone marrow usually shows a diffuse and nodular pattern of involvement with almost total replacement of normal marrow elements. A pseudonodular pattern may be noted in lymph nodes and is associated with almost complete obliteration of architecture. The liver and almost every other organ, including the heart,209 may also be diffusely infiltrated with neoplastic prolymphocytes in advanced cases.208

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