Myogenin is a Specific Marker for Rhabdomyosarcoma:
An Immunohistochemical Study in Paraffin-Embedded
S. Kumar, M.D., E. Perlman, M.D., C.A. Harris, B.Sc., M. Raffeld, M.D., M. Tsokos, M.D.
Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda Maryland (SK,
CAH, MR, MT), and Johns Hopkins Hospital, Baltimore, Maryland (EP)
Myogenin belongs to a group of myogenic regula-
tory proteins whose expression determines com-
mitment and differentiation of primitive mesenchy-
mal cells into skeletal muscle. The expression of
myogenin has been demonstrated to be extremely
specific for rhabdomyoblastic differentiation, which
makes it a useful marker in the differential diagno-
sis of rhabdomyosarcomas (RMS) from other malig-
nant small round cell tumors of childhood. Com-
mercially available antibodies capable of detecting
myogenin in routinely processed formalin-fixed
paraffin-embedded (FFPE) tissue are now available.
In this study, we evaluated myogenin expression
using the monoclonal myf-4 antibody (Novocastra
Labs) on FFPE in a large number of pediatric tu-
mors in order to define the clinical utility of this
marker. A total of 119 tumors were studied. These
included 48 alveolar RMS (ARMS), 20 embryonal
RMS (ERMS), one spindle cell RMS, 16 Ewing’s sar-
comas (ES), six nephroblastomas, two ectomesen-
chymomas, seven precursor hematopoietic neo-
neuroblastomas, six desmoplastic small round cell
tumors, and five rhabdoid tumors. Distinct nuclear
staining for myogenin was noted in all 69 RMS.
Notably, the number of positive tumor cells differed
between the ARMS and ERMS. In ARMS, the major-
ity of tumor cells (75 to 100%) were positive, in
contrast to ERMS, in which the positivity ranged
from rare ? to 25% in all but three tumors. Addi-
tionally, myogenin positivity was seen in two of two
ectomesenchymomas and in two nephroblastomas
with myogenous differentiation. All other tumors
were clearly negative. Our results indicate that
staining for myogenin is an extremely reliable and
specific marker for rhabdomyoblastic differentia-
tion. It gives consistent and easily interpretable re-
sults in routinely fixed tissues.
Paraffin-embedded tissue, Immunohistochemistry.
Mod Pathol 2000;13(9):988–993
WORDS: Myogenin, Rhabdomyosarcoma,
The differential diagnosis of rhabdomyosarcomas
(RMS) from other poorly differentiated pediatric
round cell tumors, including the Ewing’s sarcoma
family of tumors (ESFT), neuroblastomas, and hema-
topoietic neoplasms can be difficult on histologic
grounds alone, although the use of an antibody panel
including mic-2, desmin, and hematopoietic lineage-
specific antibodies now allows an accurate diagnosis
in the majority of cases. The expression of markers
ularly useful in defining lineage in some poorly differ-
entiated/undifferentiated tumors and antibodies to
MyoD1 and myogenin proteins have been found to
be of most use in this regard (1–5). Although staining
for MyoD1 was the first to be used in the diagnostic
setting, nonspecific cytoplasmic staining often makes
interpretation of results problematic when fixed tis-
human homologue of myogenin, are also available
and have been evaluated in a few studies (3, 6–8).
However, these studies have included relatively few
cases of RMS, particularly of alveolar subtype (3, 6, 8)
or are reported only in abstract form (6). In addition,
some have been performed only on frozen sections
(9). In this study, we report our findings with a new,
commercially available anti-myogenin antibody in a
large series of RMS and other pediatric sarcomas to
define the utility of this marker in the routine diag-
MATERIALS AND METHODS
Cases were retrieved from the files of the Labora-
tory of Pathology, National Cancer Institute, National
Copyright © 2000 by The United States and Canadian Academy of
VOL. 13, NO. 9, P. 988, 2000 Printed in the U.S.A.
Date of acceptance: April 6, 2000.
Address reprint requests to: Shimareet Kumar, M.D., Anatomic Pathology,
Children’s National Medical Center, 111 Michigan Avenue, NW, Washing-
ton, DC 20010-2970; fax: 202-884-4030.
Institutes of Health, Bethesda, Maryland and The
Johns Hopkins Hospital, Baltimore, Maryland. A total
of 119 tumors were evaluated, as summarized in Ta-
ble 1. These included 69 cases of RMS (48 alveolar
subtype/ARMS; 20 embryonal subtype/ERMS; one
spindle cell RMS) and 50 other tumors, consisting of
16 ESFT, two ectomesenchymomas, six nephroblas-
cluding four lymphoblastic lymphomas), six desmo-
plastic small round cell tumors (DSRCT), five
olfactory neuroblastomas (ONB), three neuroblasto-
mas/ganglioneuroblastomas (NB/GNB), and five rh-
abdoid tumors. Formalin-fixed paraffin-embedded
(FFPE) blocks or unstained sections were available for
all of the cases. Routine morphologic and immuno-
phenotypic studies were performed on 4-?m thick
hematoxylin- and eosin-stained sections. Staining for
myogenin was also evaluated in a variety of fetal and
adult tissues (including skeletal muscle, heart, liver,
lung, kidney, gastrointestinal tract, spleen, lymph
nodes, and brain).
Immunoperoxidase staining for myogenin was
performed using the myf-4 antibody (L026, 1:10,
mouse monoclonal, Novocastra Labs, Burlingame,
CA), according to the manufacturer’s recom-
mended protocol. Antigen retrieval was done in a
pressure cooker for 40 min in 10 mM citrate buffer
with 0.1% Tween 20 at pH 6.0. Slides were incu-
bated overnight with the primary antibody, fol-
lowed by detection using standard protocol on an
automated immunostainer (Ventana Medical Sys-
tems, Tuscon, AZ), according to the manufacturer’s
instructions. Other immunoperoxidase stains in-
cluded actin (HHF35, ENZO, Farmingdale, NY),
desmin (D33), Der 11, NSE, 12E7 (p30/32mic2) (all
from DAKO, Carpinteria, CA), AE1/3 (Boehringer
Mannheim, Indianapolis, IN), and S100 (Biogenex,
San Ramon, CA).
Staining for myogenin was graded from 1? to 4?
as follows, based on the percentage of tumor cell
nuclei staining positive: rare positive to 25%, 1?; 25
to 50%, 2?; 50 to 75%, 3?; and 75 to 100%, 4?.
Diagnosis was based on a combination of routine
histologic and immunophenotypic criteria as well
as, in some cases, correlation with ultrastructural
and molecular findings. The alveolar RMS were
composed of nests of undifferentiated primitive-
appearing small round blue cells in solid nests or
with a focal alveolar pattern. In some cases, cells
with more abundant eosinophilic cytoplasm or
multinucleated giant cell forms were evident. The
PAX3/FKHR fusion transcript was detected in 16 of
22 cases evaluated by RT-PCR. The embryonal RMS
were composed of round to spindled cells, often
with eosinophilic cytoplasm, arranged in compactly
cellular to more loose areas with a myxoid stroma.
The results of staining for myogenin are summa-
rized in Table 1. Nuclear staining for myogenin was
seen in all 48 ARMS (Fig. 1, 2, 3), 20 ERMS (Fig. 4),
as well as in the spindle cell RMS. The results of
grading in the RMS cases are summarized in Table
2. Grade 4? staining with 75 to 100% of nuclei
staining positive was present in 44 ARMS, two cases
showed 3? staining and in another two cases only
20% of nuclei stained, consistent with 1? staining.
In contrast, in the ERMS group, 17 of 20 cases
showed 1? staining, with the number of positive
staining nuclei ranging from rare positive to 25%. In
three ERMS, staining was graded as 2?, with 25 to
50% nuclei positive. None of the ERMS showed
Grade 3? or 4? staining. The single case classified
as spindle cell RMS showed 3? staining. In 66 of the
69 RMS, desmin-stained slides were available for
review and all cases stained desmin-positive. In
some of the more primitive appearing ARMS, how-
ever, the number of myogenin-positive cells clearly
exceeded the desmin positivity (Fig. 5).
TABLE 1. Results of Immunostaining with myf-4 in
Various Pediatric Tumors
Diagnosis (# of Cases)myf-4
Spindle cell (1)
Other pediatric sarcomas (50)
Precursor hematopoeitic neoplasms (7)
Olfactory neuroblastoma (5)
ESFT, Ewing’s sarcoma family of tumors; DSRCT, desmoplastic small
round cell tumor; NB/GNB, neuroblastoma/ganglioneuroblastoma.
aThese two nephroblastomas had myogenous differentiation.
FIGURE 1. Tumor cells with intense nuclear positivity infiltrate in
solid nests as well as line spaces in an alveolar rhabdomyosarcoma.
Myogenin Expression in RMS (S. Kumar, et al.)989
Myogenin-positive cells were identified in the
two ectomesenchymomas, correlating with the
desmin positive areas. In one case, the majority of
the tumor was composed of undifferentiated cells
that expressed only mic-2, whereas, in focal areas,
the mic-2 positive cells also co-expressed myoge-
nin, desmin and actin, as illustrated in Figure 6,
A-C. Staining for myogenin (as well as desmin) was
also noted in two of six nephroblastomas, and cor-
related with areas of myogenous differentiation
(not shown). Staining for myogenin was absent in
all other tumors studied (Table 1). Among the nor-
mal tissues evaluated for myogenin, positive stain-
ing was seen only in fetal striated muscle, as ex-
pected. All other tissues (adult and fetal) were
The process of myogenesis involves the commit-
ment and differentiation of pluripotent primitive
mesodermal cells into skeletal muscle and is regu-
lated by members of the MyoD family of genes. This
family includes the MyoD1/myf-3, myogenin/myf4,
myf-5, and MRF-4 genes that encode for DNA bind-
ing proteins that act as transcription factors and
bind to enhancer regions on muscle specific genes
to induce their expression (10–16). Because the ex-
pression of these genes has been shown to be re-
stricted to skeletal muscle, antibodies to MyoD1
and myogenin have been used to define lineage and
confirm diagnosis of RMS in otherwise poorly dif-
FIGURE 2. A case of solid alveolar rhabdomyosarcoma with the
majority of cells showing nuclear staining (4? staining).
FIGURE 3. Staining for myf-4 in an alveolar rhabdomyosarcoma
metastatic to the lymph node. Distinct nuclear positivity is seen in
tumor cells within the subcapsular sinus whereas adjacent small
lymphocytes are negative.
FIGURE 4. Scattered but distinctly myogenin-positive cells in an
embryonal rhabdomyosarcoma. Nuclei in some of the multinucleated
rhabdomyoblasts are also positive.
TABLE 2. Grading of Myogenin Expression in ARMS &
Staining for myf-4
Grade 1Grade 2 Grade 3 Grade 4
RMS, rhabdomyosarcoma; ARMS, alveolar RMS; ERMS, embryonal
FIGURE 5. The number of tumor cells staining for myogenin (A) are
more numerous than those marking with desmin (B) in a solid alveolar
990 Modern Pathology
ferentiated sarcomas. Earlier studies required fro-
zen tissue sections for evaluation of expression (1,
2, 4, 5), but staining is now also possible on fixed
tissue sections, and antibodies have recently be-
come commercially available, allowing for wider
use in the routine diagnostic setting (6, 8) Staining
of fixed tissue sections with antibodies to MyoD1,
however, often shows non-specific cytoplasmic
staining, making interpretation of results difficult.
This problem has been commented upon by several
investigators (6, 7, 8) and has also been our obser-
vation, particularly with the commercially available
antibody, and tends to limit the clinical utility of
this marker. This does not appear to be a problem
with staining for myogenin, but, overall, relatively
few cases of RMS have been analyzed for the ex-
pression of this protein. Moreover, the correlation
of myogenin expression with different histologic
subtypes of RMS has recently been suggested (9)
but has not been further evaluated.
Our study included 69 cases of RMS and staining
for myogenin was observed in all of these tumors.
In prior studies, myogenin positivity has ranged
from 71 to 91% of RMS, which is somewhat lower
than what we observed. In the studies by Cui et al.
(8) and Wang et al. (3), 16/20 (80%) and 31/33 (91%)
RMS, respectively, were myogenin positive. The
possibility that this slight difference could be attrib-
utable to the antibody used cannot be completely
excluded because these two studies used an anti-
body different from ours: the clone 5FD antibody.
However, in a third study, which included only
seven RMS and was reported only in abstract form,
Berezowski et al. (6) used the same antibody as ours
but found only five of seven (71%) cases to stain.
It is also possible that this apparent difference
may relate to the subtypes of RMS evaluated in
these prior studies and ours because a recent study
has suggested that myogenin expression may cor-
relate specifically with the alveolar subtype (9). Be-
cause ARMS is less common than the embryonal
type, the majority of tumors evaluated in prior stud-
ies have been of embryonal type. In fact, only 4/33
and 6/20 RMS studied by Wang et al. (3) and Cui et
al. (8), respectively, were of the alveolar subtype,
whereas Berezowski et al. (6) did not specify sub-
type in their seven cases. Our study, in contrast,
included a very large number of ARMS (48 cases)
because our primary aim was to evaluate myogenin
in the differential diagnosis of primitive round cell
tumors of childhood, and it is the alveolar subtype
that is often a differential diagnostic problem. In
addition, given this recent observation by Palmer et
al. (9) regarding strong myogenin expression spe-
cifically in ARMS, we wished to address this partic-
ular issue in a large number of cases. In their study,
which was reported in an abstract, Palmer and col-
leagues evaluated 11 ARMS and 19 ERMS using a
recombinant fusion protein from rat myogenin on
cryostat sections. They found that all 11 ARMS
showed strong myogenin expression, whereas the
ERMS stained only weakly positive or were nega-
tive. Only 3/19 ERMS showed staining of a degree
comparable to the ARMS cases (9). Our study es-
sentially confirmed their observations in that we
found consistent and strong expression of myoge-
nin in virtually all our ARMS cases, with 46/48 cases
showing 3? to 4? staining and the two remaining
cases showing 1? staining. Among our ERMS cases,
only 3/20 showed 2? staining, similar to the obser-
vations of Palmer et al. However, it should be em-
phasized that the 17 remaining ERMS in our study
also showed distinct myogenin positivity, with in-
tense individual nuclear staining, although the
number of positive nuclei was clearly lower and
ranged from a few to 25%. This latter observation
differs somewhat from that of Palmer et al. (9), who
stated that their remaining ERMS cases were only
weakly myogenin-positive or were negative, but did
not elaborate further or specify the number of
ERMS that were completely negative. Therefore, it
is quite possible that the lower rate of myogenin-
positive RMS reported in the earlier studies (3, 8)
might be accounted for by the predominance of
ERMS in these studies. Although this may suggest
that staining for myogenin may not be as useful a
marker for the ERMS group, our observations indi-
cate that this is not necessarily true. Our study
included cases where only one small tissue frag-
ment among multiple contained tumor (ERMS),
and distinctly positive cells, although few in num-
ber, could readily be identified in such fragments.
Moreover, the myogenin positivity in these cases
paralleled or exceeded the desmin positivity and
was therefore quite helpful in confirming diagnosis.
It has been proposed that this strong correlation
of myogenin expression with alveolar histology may
relate to the stage of differentiation of the tumor
FIGURE 6. Composite figure of serial sections of an
ectomesenchymoma showing co-expression of myogenin/myf-4 (A),
desmin (B), and mic-2 (C) by the malignant cells. In most other areas
(not shown in this figure), the tumor cells stained only for mic-2.
Myogenin Expression in RMS (S. Kumar, et al.) 991
cells. During the process of myogenesis, MyoD1
expression correlates with the initial stage of com-
mitment to myogenesis: it is present in more un-
differentiated cells, but becomes down regulated as
differentiation proceeds. Myogenin expression, on
the other hand, correlates with the stage of onset of
differentiation as well as with maintenance of the
differentiated state, and is therefore present in
more differentiated cells (14, 15). Studies have com-
pared muscle-specific gene expression profiles in
RMS to the stages of normal fetal skeletal muscle
development to investigate if phenotypic variations
between RMS (embryonal versus alveolar) reflect
malignant transformation of cells at specific stages
of the myogenic pathway (11). Detection of myoge-
nin transcripts in all ARMS (eight of eight) and the
majority but not all ERMS (five of eight) in this
study indicate that RMS resemble a relatively re-
stricted segment of skeletal muscle development,
limited at one end by the stage of commitment to
myogenesis and, at the other, by the earliest overt
stages of myogenesis. Within this scheme, the alve-
olar subtype phenotypically represents a restricted
group, whereas the embryonal subtype encom-
passes a broader range of phenotypes and may
show considerable overlap with the alveolar sub-
type. The two subtypes, however, may not neces-
sarily represent malignant transformation of nor-
mal cells at different positions of myogenesis (11).
The grade/pattern of expression of myogenin, as
detected by routine immunohistochemical staining
in our cases of ERMS and ARMS, is in keeping with
this hypothesis. Palmer et al. (9) have further pro-
posed that the strong expression of myogenin,
which appears to be an integral part of alveolar
histology, may be related to upstream activation of
the myogenesis pathway by the PAX3/FKHR fusion
protein unique to this tumor; however, this awaits
Interestingly, we observed distinct myogenin
positivity in the two ectomesenchymomas included
in our study, consistent with true rhabdomyoblastic
positive cells correlated with areas of desmin posi-
tivity (as seen in Fig. 6), although, in one case,
myogenin-expressing cells were more numerous
than those positive for desmin. Although Northern
blot analysis has demonstrated myogenin tran-
scripts in three of five cell lines derived from these
biphenotypic tumors in a prior study (17), other
studies evaluating myogenin expression have not
included examples of this rare tumor. Because
these tumors can be composed almost entirely of
undifferentiated primitive appearing cells that may
stain for mic-2 (as in the case illustrated in Fig. 6),
myogenin expression can be very helpful in distin-
guishing these from ESFT. Additionally, two Wilms’
marked positively with both myogenin and desmin,
confirming rhabdomyoblastic differentiation in
these tumors, similar to a case previously reported
by Wang et al. (3).
Desmin remains a very reliable and specific
marker for RMS in the vast majority of cases (18),
and we observed this in our study as well. However,
we found that in several cases, particularly in the
more primitive-appearing tumors, the myogenin-
positive cells exceeded those staining for desmin,
suggesting this marker may be especially useful in
such tumors. In addition, rare ESFTs may mark
with desmin. Such cases have been previously de-
scribed in the literature (3, 19) and one of the 16
ESFTs in our study also stained positive for desmin.
However, myogenin was clearly negative in this
case, and served to exclude a diagnosis of RMS.
Conversely, positivity for the mic-2 antigen may
occasionally be present in RMS, and five ARMS in
our series stained mic-2 positive. The inclusion of
myogenin in an immunohistochemical panel for
evaluating primitive round cell tumors such as
these can thus be very useful in confirming rhab-
domyoblastic lineage. Additionally, we found that
other tumors, which can express desmin (such as
DSRCT and renal/extra-renal rhabdoid tumors),
were clearly negative for myogenin, suggesting that
desmin expression is not indicative of rhabdomyo-
blastic differentiation in such cases – an observa-
tion made by others as well (3, 20). All other round
TABLE 3. Myogenin Expression in Various Tumor Types
Tumor Type, with # of Cases Positive for Myogenin
RMSESFTNBLMSMFH WilmsDSRCTASPSCa unspec RhabdoidEcto
Wang et al. (3)
Wang et al. (7)
Berezowski et al. (6)
Gomez et al. (21)
Cui et al. (8)
FFPE, formalin-fixed paraffin-embedded; ND, not done; RMS, rhabdomyosarcoma; ESFT, Ewing’s sarcoma family of tumors; NB, neuroblastoma; LMS,
leiomyosarcoma; DSRCT, desmoplastic small round cell tumor; ASPS, alveolar soft part sarcoma; MFH, malignant fibrous histiocytoma; Ca, carcinoma;
Rhabdoid, renal/extrarenal rhabdoid; Ecto, ectomesenchymoma.
aThis was a Wilms’ tumor with myogenous differentiation.
bThese two tumors had myogenous differentiation, and were positive for myogenin as well as desmin.
992 Modern Pathology
cell tumors evaluated in this study were clearly
negative for myogenin as expected.
Although our study did not include spindle cell
sarcomas or tumors such as alveolar soft part sar-
coma, recent studies have reported these tumors to
be consistently negative for myogenin (6, 7, 21). The
results of these studies are summarized in Table 3,
and, in conjunction with our large series, serve to
confirm the specificity of myogenin for rhab-
domyoblastic differentiation in the routine diag-
nostic setting. False positive results do not occur.
In conclusion, we find staining for myogenin to
be extremely sensitive and specific in defining rh-
abdomyoblastic lineage and a useful addition to the
diagnostic immunohistochemical panel for small
round blue-cell tumors. Although the literature sug-
gests that myogenin expression parallels that of
MyoD1, we believe that staining for the former is
definitely superior in terms of quality and ease of
interpretation. Furthermore, fixation does not ap-
pear to be a problem. The majority of our cases
were derived from consultation material, with an
inevitable variability in tissue fixation and process-
ing; however, good results were obtained in all
cases. Both ARMS and ERMS stain myogenin-
positive, although, clearly, the number of cells
staining in the latter subtype is fewer. This could be
a potential pitfall when only small biopsies or nee-
dle core specimens are being evaluated.
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Myogenin Expression in RMS (S. Kumar, et al.)993