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  , . 185: 116 (1998)
LETTER TO THE EDITOR
MUMMIFIED HODGKIN CELLS AND APOPTOSIS
The study by Lorenzen et al.1 is worthy of note, since
the mummified cells of Hodgkin’s disease (HD) have
long remained an enigma, being loosely considered as
degenerating Hodgkin–Reed–Sternberg (HRS) cells.
In our studies on cell death in HD,2,3 we have reached
conclusions about mummy cells which are similar to
those of the authors. We found that mummy cells did
not show DNA fragmentation (by the ApopTag assay).
However, although the electron microscopic (EM) features of these cells were similar to those found by
Lorenzen et al.,1 we were impressed by the swollen
mitochondria which imparted to these cells the appearance of ‘dark cells’. Nonetheless, we agree with the
authors on the significance of this phenomenon. We are
dealing with irreversibly damaged cells, probably
showing an atypical form of apoptosis, perhaps
para-apoptosis.
On the other hand, we were able to demonstrate
apoptotic cells which were strongly reactive by in situ
end labelling of DNA fragments. These cells were interpreted as apoptotic HRS cells, based on their size, on
their positivity by CD15 immunostaining, and most
importantly, on their EM features.
The discrepancy noted may be due to the different
methods used, including fixation. In our hands, DNA is
less well preserved in picric acid-based fixatives.
D B1, P B2,
J G1  J G3
1
Department of Pathology
Soroka Medical Center, Beer-Sheva, Israel
2
Laboratory of Pathology, Hopital Purpan, Toulouse, France
3
Department of Oncology
Soroka Medical Center, Beer-Sheva, Israel
REFERENCES
1.
2.
3.
Lorenzen J, Thiele J, Fischer R. The mummified Hodgkin cell: cell death in
Hodgkin’s disease. J Pathol 1997; 182: 288–298.
Benharroch D, Prinsloo I, Goldstein J, et al. A comparison of distinct
modes of tumor cell death in Hodgkin’s disease using morphology and in
situ DNA fragmentation. Ultrastruct Pathol 1996; 20: 497–505.
Brousset P, Benharroch D, Krajewski S, et al. Frequent expression of the
cell death-inducing gene Bax in Reed–Sternberg cells of Hodgkin’s disease.
Blood 1996; 87: 2470–2475.
AUTHORS’ REPLY
We should like to thank D. Benharroch et al. for their
comments on our paper and for drawing our attention
to their publication in Ultrastructural Pathology.1 It was
reassuring to find similar conclusions being drawn from
the ultrastructure and the absence of an ISEL reaction
of mummified Hodgkin- and Reed–Sternberg (HRS)
cells by an independent research group.
As pointed out in our manuscript,2 we have also
noticed a few larger cells that displayed a weak and more
diffuse in situ end-labelling reaction in nuclei that had
lost chromatin detail. These cells were occasionally
found within the cytoplasm of macrophages reacting
with the monoclonal antibody PG-M1. Although the
size of this cell population suggests that it is derived
from the HRS cells, we found no hard evidence for this
assumption, as cytological features were lost and no
immunoreaction for CD15 or CD30 could be observed
in our hands. This discrepancy may indeed be due to
different immunohistochemical methods applied, even
though no picric acid-based fixatives are used in our
laboratory. Furthermore, we are not convinced that
these mysterious cells are truly apoptotic, because they
do not display the typical crescent-shaped chromatin
condensation on electron microscopic examination or in
semi-thin sections. Whereas we do not dispute that
DNA degradation will take place at some stage during
the removal of mummified HRS cells from the tissue,
and hence might be detected by the in situ end-labelling
techniques, we have reservations about the internucleosomal nature of the ensuing DNS strand breaks.
In contrast to apoptotic bystander cells, the cell popu 1998 John Wiley & Sons, Ltd.
lation in question displays a weaker and more diffuse
nuclear ISEL reaction. Considering our experimental
findings, we thus cannot prove that the larger cells
labelled in the ISEL reaction are derived from HRS cells
and that they fulfill all of the criteria required for
classical apoptosis.
It might well be the case that differences in the
laboratory protocols for the detection of DNA strand
breaks have led us to different conclusions. In this
context, two articles by Spina and co-workers are worth
mentioning, as this group describes the presence of
DNA strand breaks in the majority of HRS cells.3,4
Hence, the books on cell death in Hodgkin’s disease are
not yet closed.
J L, J T
 R F
Department of Pathology
University of Cologne
Joseph-Stelzmann-Strasse 9
50931 Koeln, Germany
REFERENCES
1.
2.
3.
4.
Benharroch D, Prinsloo I, Goldstein J, Brousset P, Kachko L, Gopas J. A
comparison of distinct modes of tumor cell death in Hodgkin’s disease using
morphology and in situ DNA fragmentation. Ultrastruct Pathol 1996; 20:
497–505.
Lorenzen J, Thiele J, Fischer R. The mummified Hodgkin cell: cell death in
Hodgkin’s disease. J Pathol 1997; 182: 288–298.
Spina D, Leoncini L, Close P, et al. Growth vs. DNA strand breaks
in Hodgkin’s disease: impaired proliferative ability of Hodgkin and
Reed–Sternberg cells. Int J Cancer 1996; 66: 179–183.
Leoncini L, Spina D, Close P, et al. Abortive mitoses and nuclear DNA
fragmentation in CD30+ large cells of Hodgkin’s disease. Leuk Lymphoma
1996; 22: 119–124.
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