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Growth vs. DNA strand breaks in Hodgkin's disease: Impaired proliferative ability of Hodgkin and Reed‐Sternberg cells
Author(s) -
Spina Donatella,
Leoncini Lorenzo,
Close Pauline,
Megha Tiziana,
Pacenti Lorenzo,
Tosi Piero,
Pileri Stefano,
Sabattini Elena,
Kraft Rainer,
Laissue Jean A.,
Cottier Hans
Publication year - 1996
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19960410)66:2<179::aid-ijc7>3.0.co;2-#
Subject(s) - reed–sternberg cell , dna , cancer research , medicine , biology , pathology , hodgkin lymphoma , genetics , lymphoma
We re‐appraised the cell renewal pattern in Hodgkin's disease (HD), considering that most, though not all, Hodgkin/Reed‐Sternberg (H‐RS) cells exhibit abortive mitoses and that a substantial fraction of these exhibits DNA damage suggestive of imminent or actual cell death. Using combined immunohistochemistry and in situ end‐labeling to detect strand breaks, the percentage per case of CD30 + (mainly H‐RS) cells with DNA fragmentation (DNA fragmentation index [DFI]) was estimated. For each case, we registered the mitotic index (MI) of CD30 + cells and the percentage of Ki‐67 + atypical large cells. To quantify the sum of our parameters for mitosis, whether successful or not, and DNA damage, we introduced the kinetic event index (KEI = MI + DFI). Only DFI and KEI distinguished significantly between mixed cellularity and nodular sclerosis HD. The values for MI and DFI, and therefore for KEI, of CD30 + and CD30 − small lymphoid cells were proportional. The percentages of Ki‐67 + large atypical cells (median 50%) did not correlate significantly with either MIs or DFIs of CD30 + cells. Cluster analysis revealed the existence, independent of histological subtype, of 2 large groups of HD with different KEIs. Our findings suggest that cell deletion plays an important role in HD. Further, it appears that proliferation‐associated antigens in H‐RS cells do not reflect successful cell production in this disorder. © 1996 Wiley‐Liss, Inc.