Leu-M1 Antigen Expression in Advanced (tumor)
Stage Mycosis Fungoides
ROSEMARY WIECZOREK, M.D., MARK SUHRLAND, M.D., DAVID RAMSAY, M.D.,
MICHAEL L. REED, M.D., AND DANIEL M. KNOWLES II, M.D.
The authors describe two patients with clinically and histopathologically documented advanced (tumor) stage mycosis fungoides.
In each case the large, pleomorphic neoplastic cells lacked the
monoclonal antibody-defined cell surface antigens commonly associated with immature and mature T-cells, i.e., Til, Leu-1, T3,
T4, T6, T8, and T10, but expressed various T-cell-associated
activation antigens, such as HLA-DR, Tac, and T21. Leu-Ml,
a monocyte-associated antigen, was not expressed by the small,
cerebriform neoplastic cells in the plaque stage lesions of either
patient. However, Leu-Ml was expressed by most of the large,
pleomorphic neoplastic cells present in the nodular lesions of
both patients. The pattern of Leu-Ml antigen expression was
identical to that previously reported in the Reed-Sternberg cells
of Hodgkin's disease. Identification of these two patients suggests
using caution in the interpretation of the results of immunophenotypic analysis of cutaneous lymphoid neoplasms and that LeuMl should not be used as a diagnostic indicator of Hodgkin's
disease or a histiocytic-derived neoplasm. These studies also
suggest that Leu-Ml may be preferentially expressed on a subpopulation of activated, rapidly proliferating, and/or dedifferentiated neoplastic T-cells that proliferate in the advanced (tumor) stages of mycosis fungoides. (Key words: Mycosis fungoides; T-cell lymphoma; Cell markers; Leu-Ml) Am J Clin
Pathol 1986; 86: 25-32
MOST T-CELL MALIGNANCIES express phenotypes
that correspond to those normally expressed during Tcell ontogeny and by functionally distinct T-cell subsets. 1719 Mycosis fungoides (MF) and the Sezary syndrome (SS) are T-cell malignancies2'4,5,9'22'23 that represent one aspect of the spectrum of cutaneous T-cell
lymphoma (CTCL).23 The neoplastic cells of MF, SS,
and other forms of CTCL commonly express the E-ro-
Immunopathology Laboratory, Department of Pathology, The
Kaplan Cancer Center, and the Department of Dermatology,
New York University School of Medicine,
New York, New York
We describe two cases of advanced (tumor) stage MF
in which the neoplastic cells lacked the T-cell lineage
marker T11 (the E-rosette receptor), the mature peripheral
T-cell markers Leu-1 and T3, and the helper T-cell-subset-associated marker T4. In both cases the neoplastic
cells expressed various T-cell-associated activation antigens and strongly expressed Leu-M 1, a monocyte-associated antigen. Leu-Ml is expressed by peripheral blood
and tissue monocytes,7,11 granulocytes,7 the Reed-Sternberg cells of Hodgkin's disease,1213'27,28 and in vitro mitogen-activated T4 + cells. 7 " These findings suggest using
caution in the interpretation of the results of immunophenotypic analysis of cutaneous lymphoid neoplasms,
especially with respect to Leu-M 1 positivity.
Patients and Methods
Patient 1
A 60-year-old white man presented seven years earlier
with a red, scaly rash on his right arm that was interpreted
as psoriasis and treated without improvement. A subsequent
skin biopsy (biopsy 1) was diagnosed as MF. The
sette receptor Til; the pan-peripheral T-cell marker
cutaneous
lesions resolved with topical nitrogen mustard
Leu-l/Tl; and the mature, peripheral helper T-cell
+
+
5910 22
treatments,
and subsequent cutaneous lesions (biopsy 2)
phenotype T3 T4 T8"
- ; and they exhibit in vitro
2,4
were
similarly
controlled. An eyelid nodule developed four
helper function.
However, several investigators have
years
later,
which
did not respond to topical therapy, but
shown that one or more of the mature, peripheral T-cell
which
was
successfully
treated with local irradiation. Submarkers may be lost in some cases of MF, SS, and other
sequent
cutaneous
nodules
were radiation resistant but
forms of CTCL, especially in advanced stages of the dis5 20,25 36 37,39
improved
clinically
with
Accutane®.
Systemic evaluation
ease, ' '
as well as in peripheral T-cell lympho20,35
at
that
time
failed
to
demonstrate
visceral
involvement,
mas.
however, a mass in the left neck was noted six months
later. The mass was biopsied (biopsy 3) and interpreted
Received August 5, 1985; received revised manuscript and accepted
for publication November 20, 1985.
as a diffuse, aggressive, non-Hodgkin's lymphoma of large
Address reprint requests to Dr. ICnowles: New York University Medical
Center, University Hospital, Department of Pathology, 550 First Avenue, cell type. The patient responded poorly to systemic multidrug chemotherapy and spot radiation therapy.
New York, New York 10016.
25
26
WIECZOREK ET AL.
Patient 2
An 89-year-old white woman presented with a severalmonth history of erythematous scaly patches on her left
leg. Biopsies (biopsies 1 and 2) were interpreted as MF.
The cutaneous lesions were treated with topical nitrogen
mustard with limited success. The patient returned with
a supraorbital plaque, a large ulcerating nodule on the
right thigh, and a left chest wall mass six months later.
Biopsy of the chest wall mass (biopsy 3) was interpreted
as nodular stage MF. The lesions regressed following radiation therapy, and the patient was discharged.
Patient Specimens
A representative portion of the most recent biopsy (biopsy 3) from each patient was fixed in 10% buffered formalin and processed for histopathology. Another representative portion was embedded in OCT (Miles Scientific,
Naperville, IL), snap-frozen in isopentane and dry ice,
and stored at - 8 0 °C. A portion of biopsy 3 from patient
1 also was processed for cell suspension analysis. Formalin-fixed, paraffin-embedded tissue blocks representing
the prior two cutaneous biopsies from each patient were
obtained from the files of the New York University Medical Center.
Heteroanti-Sera and Monoclonal Antibodies
The heteroanti-sera and monoclonal antibodies used
in this study have been characterized previously and have
been extensively used in our laboratory. We employed
heterologous anti-sera that detect human lysozyme,24 alpha- 1 -anti-chymotrypsin,26 and S-100 protein6 (Dako,
Denmark). We also used rabbit anti-human kappa and
lambda light chains (Meloy Laboratories, Springfield, VA)
and murine monoclonal antibodies T200, BA1 (Hybritech, San Diego, CA), B1 (Coulter Immunology, Hialeah,
FL), HLA-DR, Leu-1 (Dr. Chang Yi Wang), OKB2,
OKM1, OKM5, OKT3, OKT4, OKT4A, OKT4B,
OKT4C, OKT4D, OKT4E, OKT6, OKT8, OKT9,
OKT10, O K T l l a , OKT14, OKT16, OKT19, OKT21
(Ortho Pharmaceutical, Raritan, NJ), Tac (Dr. Thomas
Waldmann), Leu-7, Leu-Ml (Becton-Dickenson, Sunnyvale, CA).1-7-8-17'19'30-32
Cell Suspension Lymphoid Marker Analysis
A portion of biopsy 3 from patient 1 was processed for
cell suspension lymphoid marker analysis.16 Lymphoid
cell surface antigen expression was determined by indirect
immunofluorescence.38
Immunohistochemical
Staining
Cryostat sections were cut from each snap-frozen tissue
block, fixed, and prepared for immunohistochemical
A.J.C.P. . J u l y 1986
staining.18 The presence of common leukocyte and Bcell-, T-cell-, and monocyte-associated antigens was determined using a panel of monoclonal antibodies and a
two-step indirect immunoperoxidase technic. Briefly, the
cryostat sections were incubated with 40-90 nL of each
of the primary antibodies of previously determined appropriate dilutions in a moist chamber for 60 minutes at
room temperature. The second step was a 30-minute
room-temperature incubation with a peroxidase-labeled
goat anti-mouse IgG and IgM diluted 1:40 (Kirkegaard
Perry Laboratories, Gaithersburg, MD). Negative controls
included sections incubated with phosphate buffered saline (PBS) alone, secondary antibody alone, and ascites
obtained from mice injected with nonsecretory hybridoma
cells. The inal brown reaction product was produced by
incubation with 3,3'-diaminobenzidine (Sigma Chemical,
St. Louis, MO) and H 2 0 2 . 1 8 All steps were separated by
5-minute, room-temperature washes in PBS. The slides
were counterstained with hematoxylin, dehydrated,
mounted in Permount®, and examined with an American
Optical® microscope.
The presence or absence of Leu-Ml (1:50), S-100 protein (1:300), lysozyme (1:200), and alpha-1-anti-chymotrypsin (1:200) was determined in each of the three biopsies from each patient. The two-step indirect immunoperoxidase technic described above was performed on
deparaffinized sections prepared from the formalin-fixed,
paraffin-embedded tissue blocks.
Results
Light Microscopy
Patient 1. Cutaneous biopsy 1 (Fig. 1) showed a bandlike dermal mononuclear cell infiltrate lying immediately
subjacent to, and invading the basilar portions of, the
epidermis. Epidermal erosion was absent. The infiltrate
was primarily composed of small, atypical cerebriform
Sezary-like cells, but occasional larger, hyperconvoluted
cells also were present. Eosinophils and neutrophils were
absent. Mitotic figures were inconspicuous. Cutaneous
biopsy 2 contained an extensive mononuclear cell infiltrate involving the superficial and deep dermis with multifocal erosion of the overlying epidermis. The neoplastic
cell population consisted of a mixture of small and intermediate-sized, cerebriform Sezary-like cells. Large, bizarre, pleomorphic cells were absent. Light microscopic
examination of biopsy 3 (Fig. 2) showed diffuse tissue
replacement by sheets of large, tumor cells with abundant
acidophilic cytoplasm and pleomorphic and bizarre nuclear configurations. The nuclear membranes were thin
but distinct, and the nuclei contained finely dispersed
chromatin that was focally condensed. Occasional cells
displayed prominent acidophilic nucleoli. Small, cerebri-
Vol. 86 • No. 1
27
LEU-MI POSITIVE MYCOSIS FUNGIODES
**•?&-• '
kt
• ^£'vT «'•'i* %%*«5\1 *£f F •• to €
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FIG. 1 (upper, left). Patient 1, biopsy 1. A band-like dermal mononuclear cell infiltrate extends into the epidermis to form an occasional Pautrier's
microabscess. The infiltrate is composed of predominantly small cerebriform Sezary-like cells and occasional larger cells with convoluted nuclei,
consistent with plaque stage mycosis fungoides. Hematoxylin and eosin (X40); (X100).
FIG. 2 (lower, left). Patient 1, biopsy 3. The soft tissue is diffusely infiltrated by sheets of large, neoplastic cells containing moderately abundant
acidophilic cytoplasm and large vesicular to pleomorphic nuclei with occasional prominent nucleoli. Small cerebriform cells are virtually absent.
Hematoxylin and eosin (X250).
FIG. 3 (upper, right). Patient 2, biopsy 1. A broad, band-like dermal mononuclear cell infiltrate extends into the overlying epidermis. The infiltrate
consists of a mixture of small and intermediate-sized cerebriform cells and larger cells with moderately abundant cytoplasm and convoluted nuclei,
consistent with plaque stage mycosis fungoides. Hematoxylin and eosin (X40); (X250).
FIG. 4 (lower, right). Patient 2, biopsy 3. The dermal nodule is almost entirely composed of large neoplastic cells containing abundant acidophilic
cytoplasm and large round to spheric nuclei with bizarre lobated and convoluted contours with prominent nucleoli. Small cerebriform Sezary-like
cells are rarely identified. Hematoxylin and eosin (X500).
form Sezary-like cells were absent. Abundant karyorrhetic
debris was present, and mitoticfigureswere numerous.
Patient 2. Thefirsttwo cutaneous biopsies from patient
2 (Fig. 3) were histopathologically similar. Each biopsy
contained a broad dermal mononuclear cell infiltrate that
extended into and eroded the overlying epidermis. In each
instance, the infiltrate consisted of predominantly, small,
atypical cerebriform Sezary-like cells and occasional,
WIECZOREK ET AL.
28
AJ.C.P. • July 1986
Table 1. Results of Immunohistochemical Staining of Paraffin Tissue Sections
Cell Marker
Patient
1
Biopsy
Site
Histologic
Diagnosis
Leu-Ml
1
2*
3
Skin
Skin
Neck mass
MF, plaque
MF, nodular
Large cell lymphoma
—
+++
++
1
2
3
Skin
Skin
Skin
MF, plaque
MF, plaque
MF, nodular
+ = <25% positive cells; + + = 25-50% positive cells; + + + = 50-75% positive cells; + + + +
>75% positive cells.
larger hyperconvoluted cells. Some of the latter cells exhibited nuclear pleomorphism. Mitotic figures were
present.
Light microscopic examination of biopsy 3 (Fig. 4)
showed a dermal nodule that was predominantly composed of large, bizarre, pleomorphic tumor cells. Small,
cerebriform cells were almost totally absent. The large
neoplastic cells possessed abundant acidophilic cytoplasm
and round-to-spheric nuclei that often exhibited lobated
and hyperconvoluted configurations. The cells possessed
thin but distinct nuclear membranes that enclosed finely
dispersed chromatin and one to several nucleoli. Mitotic
figures were abundant.
Electron Microscopy
Electron microscopic examination of biopsy 3 from
each patient demonstrated similar findings (Fig. 5). The
tumor cells were large and round to oval in shape. They
possessed moderate amounts of cytoplasm, which contained numerous mitochondria, free nbosomes, and scattered smooth and rough endoplasmic reticulum. The nuclei were large and centrally placed and displayed highly
irregular contours and deep clefts. The chromatin was
condensed along the nuclear membrane. Nucleoli were
readily identified. Phagolysosomes, melanosomes, and
intercellular junctions were absent. The cells were believed
to be lymphoid in origin and not of histiocytic, melanocyte, or epithelial derivation.
S-100
al-Antichymotrypsin
Lysozyme
++
++
++
* All cells displayed a prominent solitary paranuclear cytoplasmic focus of positivity with absent
membranous staining. The remaining cases displayed both membranous and cytoplasmic positivity.
Immunohistochemistry
Patient 1. Immunohistochemical staining of the paraffin
tissue sections from biopsies 1, 2, and 3 demonstrated
that the infiltrating mononuclear cells were S-100 protein,
alpha-1-anti-chymotrypsin, and lysozyme negative (Table
1). S-100 protein-positive Langerhans' cells in the dermis
and epidermis and rare alpha-1 -anti-chymotrypsin- and/
or lysozyme-positive dermal macrophages were identified.
All of the infiltrating mononuclear cells in biopsy 1 and
the small cerebriform cells present in biopsy 2 were LeuM1 negative. However, most of the intermediate-sized
cells present in biopsy 2 exhibited focal, paranuclear cytoplasmic Leu-M 1 positivity. A proportion of the large
pleomorphic tumor cells in biopsy 3 displayed diffuse,
membranous, and cytoplasmic Leu-M 1 positivity, similar
to that reported for the Reed-Sternberg cells of Hodgkin's
disease12'3'27,28 and the large atypical cells of lymphomatoid papulosis.15
Combined immunoperoxidase staining of cryostat sections and immunofluorescent staining of suspended cells
from biopsy 3 demonstrated that most of the infiltrating
mononuclear cells weakly expressed the common leukocyte antigen T200 and strongly expressed the pan-Tcell marker T16, T-cell activation associated antigen T21,
and monocyte-associated antigen Leu-Ml (Fig. 6). The
neoplastic cells did not exhibit any of the markers commonly expressed by immature and mature T-cells, B-cells,
and monocytes (Table 2).
FIG. 5 (upper). Patient 1, biopsy 3: The neoplastic cells in biopsy 3 obtained from each patient exhibited similar ultrastructural appearances. They
possessed moderately abundant cytoplasm, containing numerous mitochondria, free ribosomes, and scattered smooth and rough endoplasmic reticulum
and large nuclei with highly irregular contours and deep clefts. These features, combined with the lack of intercellular functions, phagolysosomes,
and melanosomes, strongly suggest a lymphoid origin (X 10,000).
FIG. 6 (lower, left). Patient 1, biopsy 3. Cryostat section stained by immunoperoxidase to demonstrate Leu-Ml. Most of the cells exhibit dark
brown membranous and cytoplasmic reaction product indicative of Leu-M 1 antigen expression (X250).
FIG. 7 (lower, right). Patient 2, biopsy 3. Paraffin section stained by immunoperoxidase to demonstrate Leu-Ml. Many of the large atypical tumor
cells display focal Golgi, cytoplasmic and membranous dark brown reaction product indicative of Leu-M 1 antigen expression (X250).
Vol. 86 • No. I
29
LEU-Ml POSITIVE MYCOSIS FUNGIODES
3f$ '
tMt *4t*t
30
WIECZOREK ET AL.
Table 2. Results of Immunophenotypic Analyses
Performed on Cryostat Sections and/or
Cell Suspensions from Biopsy #3
Cell Marker
Patient 1
T200
Tll/E
Leu-1
T3
T4*
T6
T8
T9
T10
T14
T16
T18
T19
T21
Tac
HLA-DR
Leu-7
BA1
Bl
SIg
OKB2
Leu-Ml
Leu-M3
OKM1
OK.M5
+++ (weak)
++++
+++
ND
ND
++++
-
+ = <25% positive cells; + + = 25-50% positive cells; + + + = 50-75% positive cells; + + + +
= >75% positive cells. ND = not done.
• Staining was performed with OKT4, OKT4A, OKT4B, OKT4C, OKT4D, OKT4E, and
various combinations of these antibodies in an attempt to demonstrate T4+ cells.
Patient 2. Increasingly greater numbers of large, atypical, and pleomorphic tumor cells were present in each
succeeding cutaneous biopsy obtained from Patient 2.
Immunoperoxidase staining of paraffin tissue sections
demonstrated that the large, atypical, pleomorphic tumor
cells exhibited strong diffuse membranous and/or cytoplasmic staining for Leu-Ml (Fig. 7) and were S-100 protein-, alpha- 1-anti-chymotrypsin-, and lysozyme-negative
(Table 1). S-100 protein-positive Langerhans' cells and
rare alpha-1-anti-chymotrypsin- and/or lysozyme-positive dermal macrophages were present in each of the three
biopsies.
Immunoperoxidase staining of cryostat sections of biopsy 3 demonstrated that most of both the small cerebriform and the large pleomorphic neoplastic cells strongly
expressed the common leukocyte antigen T200; three
markers associated with T-cell activation, Tac, HLA-DR,
T21; and monocyte-associated antigen Leu-Ml. Occasional small cerebriform, but not the large pleomorphic,
neoplastic cells also expressed the E-rosette receptor T11
and the helper T-cell subset-associated antigen T4.
Discussion
We have described two patients with clinically and histopathologically documented advanced (tumor) stage MF
A.J.C.P. • July 1986
in which the large, pleomorphic neoplastic cells fail to
express the monoclonal antibody-defined cell surface antigens commonly associated with immature and mature
T-cells, i.e., Tl 1, Leu-1, T3, T4, T6, T8, or T10. Nonetheless, the T-cell derivation of these two neoplasms could
be inferred. In each case the neoplastic cells expressed the
common leukocyte antigen, thereby demonstrating their
hematopoietic derivation and excluding an epithelial origin. Most of the neoplastic cells in case 1 reacted strongly
with OKT16, a monoclonal antibody with 3A1 or Leu9-like reactivity and distribution, i.e., present on most
normal immature and mature T-cells, most cases of Tacute lymphoblastic leukemia,8 and a small proportion
of cases of mature, peripheral T-cell lymphoma.3 These
neoplastic cells also expressed T21, a T-cell-associated
activation antigen that is absent from resting T-cells but
that is expressed by allogeneic and phytohemagglutininstimulated T-cells in vitro}x Most of the neoplastic cells
in case 2 expressed three T-cell-associated activation antigens, T21, Tac, and HLA-DR. Tac, the Interleukin-2
receptor, is most frequently expressed in cases of human
T leukemia virus (HTLV)-positive T-cell leukemia/lymphoma but is expressed in some cases of HTLV-negative
CTCL as well.33 Serum from our two patients was not
tested for anti-HTLV antibodies. HLA-DR antigen
expression by the neoplastic T-cells of CTCL and peripheral T-cell lymphoma has been documented frequently.I0,39 The neoplastic cells did not express the Bcell-associated antigens BA-1, B1, and OKB2, which are
stably expressed in more than 90% of cases of SIg+ and
SIg- B-NHL.19 Moreover, they did not express monocyte/
histiocyte-associated markers lysozyme, alpha-anti-chymotrypsin, OKM1, OKM5, Leu-M3, or the dendritic cellassociated marker, S-100 protein. Thus, we concluded that
the large pleomorphic tumor cells are most likely of Tcell derivation. This interpretation best fits the combined
clinical, histopathologic, ultrastructural, and immunophenotypic features of these two cases.
The unifying phenotypic feature of the T-cell malignancies occurring in these two patients is the absence of
the conventional T-cell-associated antigens and the
expression of the monocyte-associated antigen Leu-M 1.
Leu-M 1 was not expressed by the small, cerebriform Sezary-like neoplastic cells of plaque stage MF in either patient. However, Leu-M 1 was present in the intermediatesized cerebriform tumor cells in the second plaque stage
biopsy of case 1, where it was expressed as focal, paranuclear cytoplasmic positivity. Leu-M 1 was demonstrable
in the majority of the large, pleomorphic and bizarre neoplastic cells in the nodular stage MF lesions of both patients, where it was expressed as diffuse, abundant membranous, and cytoplasmic positivity.
The presence of a variable proportion of Leu-Ml-positive neoplastic cells in occasional lymphoblastic, periph-
Vol. 86 • No. 1
LEU-M 1 POSITIVE MYCOSIS FUNGIODES
eral, and cutaneous T-cell lymphomas has been reported
previously.14,21,28 However, to the best of our knowledge,
cases of CTCL that lack T-cell-associated antigens but
that express Leu-M 1 have not been reported. The fact
that the large, pleomorphic tumor cells that predominate
in our two cases of advanced (tumor) stage MF were LeuM1 + suggests that this phenotype may represent a relatively common occurrence that has not been previously
appreciated. In view of the fact that in v/^o-activated T4+
cells express Leu-M 1,7 its expression by these large, pleomorphic neoplastic T-cells may simply reflect a state of
activation and/or proliferation.
The ubiquitous expression of Leu-M 1 by peripheral
blood and tissue monocytes7,11 has resulted in its widespread use as a monocyte-associated marker.11-14,21,27,28
Several investigators have described Leu-M 1 expression
in Reed-Sternberg cells and have suggested that Leu-M 1
represents an excellent marker for Hodgkin's disease.1213,21,27,28 Kadin and associates15 recently reported
that the large, atypical cells of lymphomatoid papulosis
often express Leu-M 1 and various T-cell activation antigens and, in some instances, may lack the commonly
expressed T-cell-associated antigens. The interrelationships between T-cell neoplasia, lymphomatoid papulosis,
and Hodgkin's disease have been extensively argued and
remain controversial.15,34 The two cases reported here
clearly add to that controversy by showing that some Tcell neoplasms may exhibit the Leu-M 1+ Tac+ HLA-DR+
phenotype, identical to that reported in cases of lymphomatoid papulosis15 and Hodgkin's disease.13,29 Thus,
in some instances, these entities may be indistinguishable
from one another by immunophenotypic analysis alone.
In conclusion, immunophenotypic analysis demonstrated that the large, pleomorphic tumor cells in two patients with advanced (tumor) stage MF entirely failed to
express the common T-cell-associated antigens but
strongly expressed Leu-M 1 and variably expressed certain
T-cell activation-associated antigens. We cannot prove
that the plaque stage lesions in these two patients were
T3+T4+, since we lack frozen tissue for immunophenotypic analysis. However, a small proportion of the residual
small cerebriform neoplastic cells in case 2 were Tl 1+T4+,
while the large pleomorphic neoplastic cells were
Tl 1~T4-, suggesting loss of T-cell-associated antigens by
the latter cell population. Interestingly, Leu-M 1 was not
expressed on the small, cerebriform Sezary-like neoplastic
T-cells but was a consistent marker of the large, transformed neoplastic cells seen in both plaque and nodular
stage MF. These results suggest that a phenotypic transformation, involving loss of T-cell-associated antigens and
gain of Leu-M 1, occurred in parallel with the morphologic
transformation of the neoplastic cells in these two patients.
Identification of these two patients with advanced (tumor)
stage MF, whose neoplastic cells are devoid of the classical
31
T-cell-associated markers, but that express the monocyteassociated antigen Leu-M 1, suggests caution in the interpretation of the results of immunophenotypic analysis of
cutaneous lymphoid neoplasms and reliance upon individual markers to provide an accurate immunodiagnosis.
These studies confirm previous observations that Leu-M 1
is not a monocyte-lineage restricted marker and suggest
that Leu-M 1 should not be used alone as a diagnostic
indicator of Hodgkin's disease or a histiocytic-derived
neoplasm and that Leu-M 1 may represent a marker for
a subpopulation of activated, rapidly proliferating -and/
or dedifferentiated MF cells that predominate in the advanced (tumor) stage of MF. The identification of the
presence of these Leu-M 1+ cells in the earlier plaque stage
MF lesions may have prognostic significance. Additional
studies of Leu-M 1 expression in CTCL are underway to
determine the clinical importance of this finding.
Acknowledgments. The authors thank Gideon Goldstein, Mary Ann
Talle, and Chang Yi Wang for certain monoclonal antibodies used in
these studies, Thomas Taylor for excellent technical assistance, and
Margaret Walden for help in preparing the manuscript.
Addendum. Since this manuscript was submitted, we investigated LeuM1 antigen expression in a series of 38 T-cell neoplasms. We found that
the Leu-M 1 antigen was expressed by a variable proportion of the neoplastic T-cells in 19 (50%) of these neoplasms. Leu-M 1 antigen expression
correlated with mature, postthymic stages of T-cell differentiation and
activation. (Wieczorek R, Burke JS, Knowles DM II: LeuM 1 antigen
expression in T-cell neoplasia. Am J Pathol 1985; 121:374-380).
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