GESTATIONAL TROPHOBLASTIC

NEOPLASMS: M O R P H O L O G I C
CONSIDERATIONS
Shirley G. Driscoll, M.D.*

Abstract
Abnormal trophoblastic proliferation is the hallmark of a spectrum of
lesions constituting the gestational trophoblastic neoplasms. Rapid proliferation,
infiltration, vascular invasion, hen]atogenot~s dissemination, and spontaneous
regression are features of both normal and neoplastic trophoblast. Troplmblas-
tic hyperplasia without hydrops, hydatidiform mole, invasive mole, and gesta-
tional choriocarcinoma are related lesions, characterized by increasingly
aberrant trophoblastic growth and worsening prognosis, if untreated. Difli-
ctflties in diagnosis may arise with respect to the normal early implantation site,
the hydropic abortus, and postgestational, involuting, residual trophoblast.
Histologic grading of hydatidiform moles is relevant to their prognosis and
biologic behavior. Trophoblastic neoplasia may begin at any stage of preg-
nancy or puerperally with immediate or late and local or distant manifestations
in the mother or the child. Cognizance of the capricious potential behavior of
trophoblast permits successfifl management of its proliferative lesions, moni-
tored by serial measurement of gonadotropin secretion.

Gestational trophoblastic neoplasms untreated. They are linked pathogenetic-

include three categories of disease charac-
terized by abnormal proliferation of troph-
oblast: hydatidiform mole, invasive mole,
and choriocarcinoma. These lesions mimic
the behavior of normal gestational tropho-
blast. They arise from a tissue genetically
dissimilar from the host, invade her tis-
sues, may be disseminated in her blood
from the site of in]plantation, and often
regress spontaneously after the termina- r
tion of pregnancy. They secrete chorlomc
gonadotropin, which is useful as a tumor
marker. By and large, they conform to dis-
crete morphologic entities with predict-
able biologic behavior and outcome, if
ally and epidemiologically and are the first
solid tumors to have responded complete-
ly to chemotherapy in the majority of
cases, even when metastasis has preceded
the initiation of treatment. Early and
atypical proliferative lesions of tropho-
blast, not readily accommodated by con-
ventional taxonomy, share these features
of hydatidiform moles and choriocarci-
. .
nomas. Recognition of such lesions lends
credence to a tmitary view of tropho-
blastic overgrowth as a continnum of
hyl~erplastic and neoplastic phenomena,
most notoriously exemplified by, but not
limited to, molar pregnancy and gesta-

*Professor of l'athology at Boston Hospital for Women: ttarvard Medical School. Pathologist,
Boston ttospital for "Women,Boston, Massachusetts. 529
 HUMAN PATHOLOGY--VOLUME 8, NUMBER 5 September 1977
tional choriocarcinoma. Abnornml troph-
oblastic proliferation is the sine qtm non
of this spectrum of lesions and the deter-
minant of their biologic behavior.
Morphologic interpretation of tropho-
blastic growths is complicated by the
unusual predilection of normal tropho-
blast for rapid proliferation, infihration,
vascular invasion, and deportation.
Awareness of aberrant trophoblastic
growth raises the possibility of hormonal
ntonitoring and cllemotlterapy to avert
catastrophic local or systenfic complica-
tions. Tire response to therapy of neo-
plastic trophoblast is generally correlated
with its degree of proliferation and atypia
as compared to tlmt of its normal counter-
part.
M O R B I D A N A T O M Y OF
GESTATIONAL TROPHOBLASTIC
NEOPLASMS
In its configuration and relation to the
site of implantation, the hydatidiform
mole is a caricature of a normal immature
placenta (Fig. 1). Usually a bulky and
fragile mass of vesicles produced by the
"ltydropic" swelling of chorionic villi, the
mole is unlikely to be accompanied by an
intact embryo or fetus. Diligent search
Figure 1. Hydatidifornl mole. Vesicular strt,ctures bulge from incised uterus. Note bilateral ovarian en-
530 largement, an effect of gonadotropin secretion.
often reveals tile cltorionic cavity, derived
from the segmentation cavity of the orig-
inal blastocyst. Each bulla or vesicle is a
cystic villus, lacking intrinsic vessels, with
its stroma replaced by thin, clear or turbid
fluid; adjacent vesicles are strung togetlter,
beadlike, along strands of delicate connec-
tive tissue. Trophoblastic proliferation
xnay tlticken the walls of the swollen villi.
The degree and extent of villous fiydrops
vary fi'om one mole to another and within
a single specimen; a myxoid stroma or
normal villous mesencfiyme may be seen.
The quantity of trophoblast, its patterns
of growth, and its maturation also vary to
considerable degrees. Necrosis of entire
villi and within islands of trophoblast is
comnaon. In situ the hydatidiform mole is
often covered by a film of decidua, filling
and expanding but not obliterating the
endometrial cavity. A plane of cleavage,
similar to tlmt seen in normal gestation,
may be identified at tire base of the mole
in the decidua. Of course, these relations
are distorted or destroyed as the lesion
enlarges, partial infarction occurs, and
expulsion or mantml extraction super-
venes.
At the interface of molar and uterine
tissues, tropltoblast mingles with decidua,
invades vessels, and penetrates tire myo-
metritun. Tire histologic features of this
 GESTATIONAL TROPHOBLASTIC NEOPLASMS-- DRISCOLL
zone vary from case to case. In general,
the quantity of trophoblast infiltrating the
uterus at the molar implantation site ex-
ceeds that in normal gestation. Discrete
trophoblastic cells are intimately inter-
mixed with uterine tissues, but solid masses
of cytotrophoblast are unustml. Eosino-
philic amorphous debris and fibrin-like
deposits are sometimes abundant at this
site. The endometrium tends to be decidu-
alized, congruent with the gestational
status of the host. Decidual necrosis is
uncommon and is usually not extensive.
Endometrial, endosalpingeal, and endo-
cervical epithelia occasionally exlfibit
nuclear enlargement and hyperchro-
matism. Polymorphonuclear leukocytes
signify the presence of necrosis. Only oc-
casionally is a zone of mononuclear inflam-
matory cells encountered in the host
tissue adjacent to the lesion.
Rarely trophoblastic hyperplasia and
villous hydrops affect only a portion of
the chorionic villi of an otherwise normal
placenta. This condition has been termed
"focal" or "partial hydatidiform mole,"
usually depending on the extent of the
gross vesicular change.
Diffnse villous enlargement, without
trophoblastic hyperplasia, characterizes
many products of spontaneous abortion.
Figure 2. Chorionic villi of "blighted ovum," aborted spontaneousl) ill first trimester. Note avascular
hydropic villi without trophoblastic proliferation. (Hematoxylin and eosin stain, x50.)
In such cases the villi tend to be avascular,
with theil- trophoblast attenuated and their
stroma nearly structureless. Overall, the
conceptus retains a modicum of the gen-
eral conformation of a chorionic vesicle,
often containing an amnion, a body stalk,
and an embryo, which is rarely well formed
and preserved. This constellation of mor-
phologic features has been dubbed a
"blighted ovum" (Fig. 2). When the asso-
ciated villous swelling reaches macroscopic
proportions, a diagnosis of "transitional
mole" may have been offered (Fig. 3). In
cases o f this type, ahhough the villous
hydrops suggests a hydatidiform mole,
there is no trophoblastic overgrowth. Such
lesions should be distinguished from the
proliferative disorders of gestational
trophoblast. To maintain distinctions and
avoid ambigttity, it seems appropriate to
limit the term "mole" in gestational path-
ology to hydropic lesions within the spec-
trum of trophoblastic neoplasia. The
anachronism "Breus' mole" should also
be replaced by an appropriately precise
term, avoiding confilsion with the hydati-
diform mole.
T h e invasive, or destructive, mole is
one that has invaded the myometrium,
penetrated the adnexa, or spread to dis-
tant sites. The archaic term, "chorioade-
531
 Figure 3. l'roducts aborted spon-
taneously in second trimester. General
configuration of chorionic structures is
preserved, but villi are swollen to macro-
scopic degree.

Figure 4. ,4, Invasive mole. ttemor-

rhagic necrotic tumor has replaced much
of the myonletriunl and perforated the
serosa. B, Invasive mole, metastatic to
hmg. (Hematoxylin and eosin stain.

532
 GESTATIONAL TROPHOBLASTIC NEOPLASMS--DRISCOLL
noma destruens," is inaccurate as well as
stq)erfluous. Hydropic villi are found in
the uterine wall, the broad ligament, the
vagina, the lungs, or the brain (Fig. 4).
Uterine perforation, vaginal bleeding,
pulmonary infarction, and cerebral lle-
morrhage signal the occurrence of these
complications. As a group, invasive moles
are clmracterized by a greater abundance
and atypia of trophoblast than moles not
exhibiting a similarly aggressive belmvior
(Fig. 5).
Gestational choriocarcinoma (former-
ly designated "claorioepittaelioma") is the
malignant neoplasm of gestational tropho-
blast. It may originate during pregnancy,
although the first signs of disease may ap-
pear at a considerable interval thereafter,
and at an anatomic site remote from the
uterus. Choriocarcinomas have been re-
ported to "follow" a hydatidiform mole, a
spontaneous abortion, a normal gestation,
and, rarely, an ectopic pregnancy. Clearly
such tumors arise fi'om the trophoblast of
the relevant conceptus either during ges-
tation or from remnants of the tropho-
blast retained in the uterus or at sites of
deportation, having failed to involute
normally after the termination of preg-
nancy. Continued growth, with or without
Figure 5. Invasive mole within myonletrium. Note abundance of trophoblast, fi~rming solid masses at-
tached to hydropic villus. (ltematoxylin and eosin stain, x40.)
spread to other organs, gives rise to the
clinical manifestations of the tumor.
Choriocarcinomas are composed of masses
of proliferating trophoblast, often exten-
sively hemorrlmgic and necrotic, filling
and distending blood vessels and dissem-
inating widely through the blood. Invasion
and destruction of the uterus and metas-
tases to the lungs, vagina, liver, and brain
are common; lymph node metastases are
very infrequent. T h e constituent tropho-
blast may be composed of a solid growth
of cytotrophoblast with little pleomor-
phism and nfinimai maturation at the
periphery to form a syncytium (Fig. 6). In
other instances, the tumor is extremely
pleomorphic, with karyomegaly, numer-
ous and atypical mitotic figures, lobated
nuclei, multiple and giant nucleoli, and a
variable formation of syncytiotropho-
blast (Fig. 7). The tumor does not contain
intrinsic stronm or blood vessels.
Occasionally chorionic tissues tlmt are
recovered as products of elective or spont-
aneous abortions are characterized by
hyperplasia of trophoblast, with little or
no associated villous hydrops (Fig. 8). The
degree of hyperplasia and maturation into
syncytium varies. These hyperplastic le-
sions of trophoblast probably represent
533
 HUMAN PATHOLOGY-VOLUME 8, NUMBER 5 September 1977

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Figure 6. Gestational choriocarcinoma infihrating myometrium. Solid mass of fairly uniform, proliferating
cytotrophoblast. (tlematoxylin and eosin stain.

incipient neoplasms, including the pre- designate postgestational lesions clmrac-

hydropic stages of hydatidiform moles. terized by prolonged persistence of
Similarly the postgestational involution of trophoblast.'-' T o minimize ambiguity and
the implantation site is sometimes delayed, clarify the nosology of trophoblastic le-
especially after a molar pregnancy (Fig. 9). sions, a simpler descriptive terminology is
These phenomena reflect the diversity of recommended, incorporating valid infer-
trophoblastic growths, variously recapitu- ences as to the biologic behavior of the le-
lating the behavior of normal gestational sion in question. Familiarity with the
trophoblast yet expressing many features infiltrative habits of nornmi gestational
of other neoplasms. T h e terms "syncytial trophoblast serves to discriminate involut-
endometritis," "syncytioma," and "tropho- ing residna from significant trophoblastic
blastic pseudotunior" lmve been nsed to disease.

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Figure 7. (,estatkmal choriocarcinon~a metaslatic to lung. Undifferentiated and atypical trophoblast with
534 prominent nucleoli. (tlematoxylin and eosin stain, x160.)
 GESTATIONAL TROPHOBLASTIC NEOPLASMS=-- DRISCOLL

', '";51,., .. ::.::i .

Figure 8. Chorionictissue from electiveabortion at eight weeks of gestation. Note hyperplasia of tropho-
blast, without villous hydrops. (Hcmatoxylin and eosin stain, x40.)

MORPHOLOGIC DIAGNOSIS OF t h o r o u g h sampling of the lesion provides

GESTATIONAL T R O P H O B L A S T I C
NEOPLASMS
Pitfalls in the diagnosis o f gestational
trophoblastic neoplasms can be attributed
to the histologic vagaries o f trophoblast
itself, the variety of chorionic lesions that
may be associated with spontaneous abor-
tion, and the morphologic diversity of the
proliferative lesions as a group. Unless a
evidence of abnormal trophoblastic pro-
liferation, it is tmwise to make the diag-
nosis o f hydatidiform mole or gestational
choriocarcinonm. Fortunately the avail-
ability o f gonadotropin assays, notabl)' the
radioimmunoassay of the beta subunit of
chorionic gonadotropin, offers the means
o f monitoring the postgestational behavior
of questionable lesions. Alerted by the
histopathologic interpretation, the clin-

Figure 9. Residualtrophublast at molar iml)lantatiol~site. Note discrete trophoblastic cells and l)'ml)hO- 5 3 5
cytes intermixed in eladometrium. (ttematox)lin and eosin stain, x250.)
 HUMAN PATHOLOGY-VOLUME 8, NUMBER 5 September1977
ician can base treatment on the temporal
pattern of gonadotropin secretion by
residual, persistent, or neoplastic tropho-
blast. Of course, supervening pregnancy,
conceived during the interval of endocrine
surveillance, may subvert the clinical
follow-up of an antecedent trophoblastic
lesion.
GRADING HYDATIDIFORM MOLES
Hertig and Iris coworkers 3"4 proposed
a system for the histopathologic subclassi-
fication of hydatidiform moles tlmt has
proved generally predictive of their clini-
cal course. This system evaluates the de-
gree of aberrancy of the trophoblast as
compared with its normal counterpart. On
the basis of the quantity of trophoblast
present, its patterns of growth, mitotic
activity, and cytologic atypia, moles that
appear only to exaggerate norlnal chorion-
ic structure can be separated from others
characterized by exuberant hyperplasia
and minimal differentiation. Intermediate
lesions of varying degrees of differentia-
tion can also be recognized. Thorougli
sampling of molar specimens permits one
to evaluate them according to traditional
morphologic criteria, often to assess local
invasive belmvior, and to identify host
reactions that may be relevant to prog-
nosis.
In practice, hydatidiform moles are
" k a~
J ei "~ t ~
!::;:
Figure 10. Hydatidiform mole, grade 1. Trophoblast is focallyhyperplastic, but well differentiated. Note
536 villous hydrops. (Hematoxylinand eosin stain.
reproducibly subdivided into three grades
of increasing atypia, decreasing differen-
tiation, and generally worsening prog-
nosis. On the basis of the original scheme
of Hertig and Sheldon, 3 which assigned
these lesions to six numbered groups
(benign, probably benign, possibly be-
nign, possibly malignant, probably
nmlignant, malignant), this modification
focuses on the characteristics of the pro-
liferating trophoblast:
Grade 1: Minimal hyperplasia, well dif-
ferentiated trophoblast (Fig. 10).
Grade 2: Moderate to marked hyper-
plasia, well differentiated
trophoblast (Fig. 11).
Grade 3: Marked hyperplasia, undiffer-
entiated trophoblast (Fig. 12).
In each instance villous hydrops is con-
sidered an intrinsic feature of the lesion,
a result of trophoblastic dysfunction. The
villi of the mole are not regarded as simply
the scaffolding upon which the aberrant
trophoblast grows. Gestational chorio-
carcinonm, lacking villous hydrops, is the
least differentiated of the trophoblastic
lesions.
This simple system of grading is
analogous to that of other neoplasms,
associating morpbologic attributes with
prognosis. In combination with histologic
indicators of the host response to the
tumor, grading can be correlated with
' o,t
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_'..:.;7, _ .... ,. ]/'_ _ :.:_
 GESTATIONAL TROPHOBLASTIC NEOI'LASMS-- DRISCOLL

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- ..,:, 9 ;~... -...:.'~ ~., :: ~.~" .

Figure II. Hydatidiform mole, grade 2. Trophoblast is extensivelyh)l)erplastic, but well differentiated.
Note villous h)'drops. (Hematoxylin and eosin stain, x40.)

gonadotropin secretion and is generally tion with tile higher grades of tumor. Tile
predictive of responsiveness to chemo- atypias and polyploidy of endometrial,
therapy. 1 Lesions characterized by the endocervical, and endosalpingeal epithelia
interposition of fibrin-like material at the that often accompany gestational tropho-
tumor-host interface and by maturation blast do not seem to reflect the qtmlity or
to form syncytium tend to regress prompt- grade of trophoblastic overgrowth.
ly with therapy. Relative resistance to At sites of trophoblastic infiltration,
chemotherap), can be anticipated when the deposition of fibrin-like material is
compact growth of cytotrophoblast pre- greatest in association with well differen-
dominates and little differentiation is seen. tiated lesions and least when the lesion is
Gonadotropin levels are highest in associa- extensively invasive and histologically

Figure 12. Hydatidiform mole, grade 3. Trophoblast is extensivel)"hyperplastic and undifferentiated. (The 5 3 7
associated villous hydrops is not illustrated here.) (Hcmatoxylin and eosin stain. X100.)
 HUMAN PATHOLOGY--VOLUME 8, NUMBER 5 September1977
atypical. However, the degree and type of
cellular inflammatory response on the part
of the host are not correlated with the qual-
ity of trophoblastic growth. Plasma cells
and lymphocytes are sometimes abundant
adjacent to an invasive lesion; in other in-
stances, few if an)' inflammatory cells are
seen. Other studies have offered conflict-
ing evidence as to the implications of such
mononuclear infiltrates per se ill the over-
all prognosis of gestational trophoblastic
neoplasms? -7
Histologic grading is a useful adjunct
to the clinical classification of tropho-
blastic neoplasms promulgated by the In-
ternational Union Against Cancer. s
Standardization of the taxonomy and sys-
tematic grading of gestational tropho-
blastic tumors offer the obvious advantages
of uniform data collection now effectively
used througllout gynecologic oncology.
PATHOGENETIC INSIGHTS
Validation of a pathogenetic hypothe-
sis requires doctunentation of the early
and intermediate phases of a disease. This
is especially critical for lesions that have
been neither observed to occur spontane-
ously in species other than man nor
induced experimentally in animal models.
Authentic instances of molar pregnancy
or gestational choriocarcinoma in other
species are very rare. Analogies can be
drawn only with extreme caution and from
relatively sparse data. Experiments and
manipulations are difficult and expensive
to perform. On the other band, systematic
studies of the "experiments of nature" can
shed considerable light on human disease.
Liberalization of abortion laws has brought
normal cborionic tissues and early, pre-
symptomatic gestational trophoblastic
disease witlfin the purview of the surgical
pathologist. Preclinical lesions are re-
vealed by the character of the trophoblastic
proliferation on a continuum from that
of the normal conceptus to floridly aber-
rant overgrowth, without or with villous
hydrops. Focusing on the trophoblast to
the exclusion of other structural consti-
tuents then seems an appropriate strata-
gem, since this tissue is the locus of the
initial defect and imparts to the evolving
lesion its particular biologic attributes.
538
Absence o f villous vessels, villous hydrops,
and cavitation are sequellae of dysfunc-
tional trophoblastic growth. Hydatidiform
mole is a descriptive rubric, applicable to
gestational trophoblastic neoplasms typi-
fied by grossly vesicular villi. These phe-
nomena may be initiated ill trophoblast
at any stage of gestation, but their cause is
unknown at the present time.
Cytogenetic analyses of human abor-
tuses have disclosed an association of
triptoidy with villous hydrops, or "hydati-
diform degeneration. ''9 The phenotyl)e
includes grossly vesicular villi and villous
stromal inclusions of trophoblast, often
accompanied by an ,'inomalous fetus. No
particular predilection for trophoblastic
hyperplasia, neoplasia, or metastasis has
been reported to be associated with this
condition. On the other band, a large
number of typical hydatidiform moles
have been karyotyped; ill most instances
they have been found to have the normal
female karyotype, 46XX, whereas aminor-
it)' have been 46XY. TM Rarely tissue culture
of molar fi'agments discloses autosomal
trisomy, triploidy, or tetraploidy. The
cytogenetic features have not been evalu-
ated with reference to the overall biologic
behavior or histologic grade of the lesions
studied, althougll investigation of a few
invasive moles and gestational choriocarci-
nomas has shown aneuploidy to be
associated with an aggressive behavior, n
Such observations are in accord with
the unitary concept of proliferative troph-
oblastic lesions as a spectrum of increasing
malignancy from the usual hydatidifornl
mole to the widely disseminating chorio-
carcinoma. Whether postmolar chorio-
carcinomas evolve preferentially in the
wake of moles of "male" or "female" sex
is unknown. Park, 6 who studied ante-
cedent chorionic lesions, found no rela-
tionship of the sex chromatin to the
subsequent behavior of gestational chorio-
carcinomas. Epidemiologic data demon-
strate no differences in the sex ratio of
births immediately preceding the dis-
covery of gestational cboriocarcinomas.
Cnstomarily series of ~ases of gesta-
tional choriocarcinoma are cited with ref-
erence to the course of the antecedent
pregnancy. Clinical disease is discovered
at some interval after a spontaneous or
elective abortion, an uncomplicated preg-
 GESTATIONAL
nancy and delivery, o1" the passage of a
hydatidiform mole. Infi'equently the pre-
ceding event was an ectopzc pregnancy.
Choriocarcinoma ab initio, i.e., without
apparent antecedent pregnancy, has been
described as the rarest manifestation of
gestational trophoblastic neoplasia.
In most pol)ulations hydatidiform
moles are about 100 times as common as
gestational choriocarcinomas. About one
in 4 0 moles is complicated by local de-
structive growth or distant metastasis, i.e.,
malignant belmvior. Among gestational
choriocarcinomas one third to one half
are encountered after the abortion of a
hydatidiform mole, one third to one
fourth after a "spontaneous abortion,"
and one third to one fourth after a puta-
tively normal gestation. Because of the
great variation in expression of this tumor
and its predilection for henmtogenous
spread, necrosis, and hemorrhage, the
possibility of gestational choriocareinoma
must be considered in every instance of
bizarre unexpected and tmexplained
symptoms in a nonvirginal woman of
reproductive age or recently postmeno-
pausal. That such a lesion may begin in
trophoblast at any stage of pregnancy ex-
plains the lesions arising ab initio, perhaps
from the blastocyst wall. It is also likely that
the spontaneous abortions that allegedly
precede choriocarcinomas may actually be
gestational accidents resulting fi'om aber-
rancy of the associated trophoblast. Few,
if an}', of the abortuses thought to have
preceded clinical choriocarcinonaas have
been studied with this possibility in mind.
The curious predilection of gestation-
al choriocarcinonaa to Sln'cad within the
maternal rather than the fetal host is un-
explained. In rare instances fetal anemia
or metastasis has been docnmented in
association with gestational choriocarci-
nomas. Hemorrhagic placental tumors
may permit significant transplacental,
fetonmternal hemorrhage, with grave se-
TROPHOBLASTIC NEOPLASMS--DRISGOLL
quellae for the fetus. Choriocarcinoma of
the fetus or young infant, especially when
it does not invoh'e a gonad, is likely to
lmve arisen from gestational trophoblast.
The primary lesion may be identified in
the uterus or the placenta, or overlooked
and discarded with the latter.
REFERENCES
!. Deligdisch, L., Driscoll, S. G., and Goldstein, D.
P.: Gestational trophoblastic neoplasms: mor-
phologic correlates of therapeutic response.
Am.J. Obstet. Gynecol. (In press.)
2. Kurman, R. J., Scull), R. E., and Norris, H.J.:
Trophoblastic pseudotumor of the uterus. An
exaggerated form of "syncytial endometritis"
simulating a malignant tumor. Cancer, 38:
1214, 1976.
3. ttertig, A. T., and Sheldon, W. 1t.: ilydatidi-
form m o l e - a pathologico-clinical correlation
of 200 cases. Am. J. Obstet. Gynecol., 53:1,
1947.
-4. llertig, A. T., and Mansell, tt.: Tumors of the
female sex organs. Part I. Hydatidiform mole
and choriocarcinoma. Sect. 9, Fasc. 33. Atlas
of T u m o r l'athologT. Washington, D.C.,
Armed Forces Institute of Pathology, 1956.
5. Elston, C. W.: Cellular reaction to choriocarci-
noma.J. Path. Bact., 97:261, 1969.
6. Park, W. W.: Choriocarcinoma. A Study of Its
l'athology. London, tteinemann, 1971.
7. Juniad, T. A., de V. Hendrikse, J. 1'., Williams,
A. O., and Osunkoya, B. O.: Choriocarcinoma
in lbadan: clinicopathologic studies, ttum.
l'athol., 7:215, 1976.
8. llolland, j . F.. and tlreshchyshy,~, M. M. (Edi-
tors): Choriocarcinoma. Transactions of a
Conference of the International Union Against
Cancer. Berlin, Springer Verlag, 1967.
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l)epartment of l'athology
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