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The relationship between membrane characteristics, functional reactivity of T‐lymphocytes, and the progression rate of B‐cell chronic lymphocytic leukemia
Author(s) -
Vitale Branko,
Antica Mariastefania,
Benković Borka,
Burek Blanka,
Jakšić Branimir
Publication year - 1985
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19850901)56:5<1075::aid-cncr2820560519>3.0.co;2-r
Subject(s) - chronic lymphocytic leukemia , medicine , leukemia , immunology , complete remission , complete response , oncology , chemotherapy
Study performed on 192 patients has demonstrated that the progression rate of chronic lymphocytic leukemia (CLL) is associated with the existence of T‐cell defect(s). A dynamic classification system based on evaluation of tumor mass growth rate, response to therapy, and myelopoietic failure (MF) has been devised for evaluation of progression rate of CLL. Besides four basic groups (Group 1: CLL without therapẏ; Group 2: CLL on therapy, without remission; Group 3: CLL on therapy, partial remission; Group 4: CLL on therapy, complete remission) patients were further classified into phase (type) A (stable, indolent CLL) or phase (type) B (active, progressive CLL). The major criteria for phase A were: total tumor mass (TTM) doubling time (DT) longer than 12 months, no MF, and/or good response to therapy. The major criteria for phase B were: TTM DT less than 12 months and/or accompanying MF and/or no response to therapy. The following major findings have been demonstrated: (1) altered quantitative relationship between active and nonactive parts of T‐cell compartment (E/A ratio) in the progressive phase of CLL; (2) altered B/Tγ ratio in the progressive phase of CLL; (3) more than 50% increased percentage of Tγ cells in the stable phase of CLL; (4) very low stable and absent seeding efficiency of T‐cells in the progressive phase of CLL; (5) altered (delayed) DNA synthesis pattern in the progressive phase of CLL; and (6) negative local xenogeneic graft versus host reaction in the progressive phase of CLL. Based on reported results, a hypothesis regarding the possible role of T‐cells in the pathogenesis of CLL was suggested.