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Review Article

Review literature on uterine

carcinosarcoma
ABSTRACT

Rajendra Singh

Carcinosarcoma of the uterus is a rare gynaecological neoplasm, which is also known as malignant mixed mesodermal tumor.
Traditionally this tumour has been regarded as a subtype of uterine sarcoma, and its origin remains controversial. The exact nature
and prognosis was not clear in the past. It is believed that uterine carcinosarcoma have a Mullerian duct origin and have a capacity
to differentiate into various mesenchymal and epithelial components. Regarding the histogensis, various theories have been given;
of which conversion theory was broadly accepted. Carcinosarcoma are mostly of monoclonal origin with the carcinomatous
component being the driving force. This type of tumor is broadly divided into two groups, homologous and heterologous, depending
on the characteristics of the stroma or mesenchymal components of endometrial tissue. It is more frequent in black women and
postmenopausal women. Radiation is a possible etiological factor but the exact etiology is not known yet. However, tamoxifen may
induce carcinogenesis in some patients. Its clinical feature is very similar to endometrial carcinoma i.e. postmenopausal vaginal
bleeding, have a very aggressive behavior and a poor prognosis. This pelvic malignancy is treated by multimodality therapy including
surgery, chemotherapy and radiotherapy. Here we are reviewing old concepts about the disease and modern understandings of the
origin, classification, pathogenesis and recent advances in the treatment of the uterine carcinosarcoma.

Department of
Radiation Oncology,
Tarini Cancer Hospital
and ResearchInstitute,
Alwar, Rajasthan,
India
For correspodence:
Dr.Rajendra Singh,
C42 AmbedkarNagar,
Alwar 301001,
Rajasthan, India.
Email:drrsingh99@
rediffmail.com

KEY WORDS: Carcinosarcoma, heterologous, homologous, monoclonal, radiation

INTRODUCTION
Carcinosarcomas are most bizarre uterine
malignancy in women with diverse origin and
histopathological characteristics. It is also known
as mixed mesodermal tumor.[1] This tumor has
been extensively discussed in literature since the
time of Virchow. The exact nature and existence
has been of much controversy. It has highly
malignant in behavior and generally has a poor
prognosis.[2] It accounts for less than 3% of all uterine
malignancies. This tumor shows preponderance in
postmenopausal women;[3] however, it may occur
in premenopausal women as well.
Epidemiology and risk factors
It usually arises from the uterus but may also
rarely appear in the ovary, fallopian tube, cervix
or peritoneum.[46] Occasionally it may develop
from benign endometrial polyp. [7] The relative
incidence of carcinosarcoma is about 1.5-3% of all
uterine malignancies in various clinical series cases.
Its incidence begins to increase at approximately
50years of age and reached a maximum at the
age of 75years, and thereafter plateaus.[8] The
median age of diagnosis is 6267years.[9] The overall
incidence in black is twice as compared with white,
but with no differences in survival for women, who
received similar therapy.

The most commonly associated etiological

factors of carcinosarcoma are previous exposure
to radiation.[10] The frequency of carcinosarcoma
after radiation exposure increased from a baseline
rate as expected. It has been suggested that
postirradiation carcinosarcoma occur at a younger
age than those arising de novo. [11] Other risk
factors that are associated with the development
of carcinosarcoma are exposure to tamoxifen,
exogenous estrogen and obesity. Some authors have
also suggested that null parity may be one of the
risk factors.[12] Compared to endometrial neoplasm,
carcinosarcomas are more likely to metastasize to
the lungs and lymph nodes.[13] Surgical stage of
disease at time of diagnosis is the most important
prognostic factors that determine the prognosis of
patients of carcinosarcoma.[14]
This tumor shares the risk factors with carcinoma
of the endometrium; but the effects of these risk
factors are not much stronger than the carcinoma
endometrium.[15] However, there is great share of
epidemiological risk factor of endometrial type
endometrial carcinoma with carcinosarcoma,
such as obesity, selective estrogenreceptor
modulator.[1618] Tamoxifen is also a risk factor for
uterine carcinosarcoma but risk is lesser as compared
with uterine carcinoma. The incidence of tamoxifen
therapy related uterine carcinoma is 160 per hundred

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Singh: Review of literature on uterine carcinosarcoma

thousand per year for endometrial cancer and only 0.5 per lakh
per year for uterine sarcoma.[19,20] The relationship of developing
uterine sarcoma due to exposure of tamoxifen has been described
in many series but data is limited. However, the period between
the exposure of tamoxifen to the patients and development of
uterine sarcoma is ranged between 1 years to 20years.[21,22] The
endometrial carcinogenesis induced by tamoxifen is assumed to
be due to higher concentration of tamoxifen metabolites in the
endometrium as compared with serum.[23]
Classification
The classification of this uterine carcinosarcoma has
been controversial since Kheres proposed the term mixed
mesodermal tumor 1906. By 1935, Mcforland had collected
119 names representing to attempt designation of the gross
or microscopic features in individual cases.[24] The basic
neoplastic component is mesenchymal sarcoma often called
undifferentiated cellular sarcoma, endometrial sarcoma or
fibrosarcoma. Carcinomatous elements are also frequent, out
of which the most common is endometrial carcinoma.
Zenker in 1864 classified mesenchymal sarcomas in two groups
based on types of cells present in the tissue of neoplasm, one as
pure that contains the single cell type and other as mixed that
contains more than one cell type. He also divided mesenchymal
sarcoma as homologous, those made up of tissue elements
indigenous to the uterus and heterologous, those containing
tissue elements normally foreign to the uterus.
Ober in 1956 proposed an elaborate classification of
mesenchymal sarcoma that is primarily based on Zenker
classification. According to that classification any tumor of
the corpus uteri that contains stromal sarcoma plus one or
more heterologous elements or that contains two or more
heterologous elements should be coded as mixed mesodermal
tumor.[25] The World Health organization(WHO) classified
these uterine neoplasms as carcinosarcomas, an alternative
designation is a malignant mixed Mullerian tumor.
Development
How does the tumor develope from different sites of the
urogenital system? To understand their origin, first let us
consider the embryonic development of the urogenital system.
The primitive paramesonephric(Mullerian) duct developed
from the mesenchyme of the urogenital ridge and the lining of
celomic epithelium. This primitive duct ultimately undergoes
differentiation into the body of the uterus, fallopian tubes,
cervix and the upper part of vagina. This analog gives rise
to all the uterine elements like myometrial smooth muscles,
endometrial stroma and endometrial glands. Hence, the term
mixed Mullerian tumor is applicable to all uterine tumors that
are formed from both mesenchymal and epithelial elements.
All these components are derived from Mullerian duct. These
tumors are more common in uterus as compared to other sites
most probably because the epithelial and mesenchymal cells
at this site share a common embryonic origin.
462

The uterus is the most common site of gynecologic sarcoma.

Uterine sarcoma can be divided into two general groups with
an origin from either the endometrial or the mesenchymal
compartment. Endometrial stromal sarcomas are derived only
from the endometrial compartment; whereas, leiomyosarcoma
is derived solely from the myometrial compartment and the
mixed Mullerian malignant tumors have contributed from
both compartments.[26]
Pathology
Uterine carcinosarcomas can be divided into homologous and
heterologous subtypes depending on the characteristics of
the stroma or mesenchymal component of the endometrial
tissue. Earlier studies have shown that this has a prognostic
importance but recent studies show histological features
of stromal component that have no prognostic value.[27,28]
Grossly, the endometrial carcinosarcomas show sessile or
polypoid, bulky often hemorrhagic mass usually filling the
endometrial cavity or may protrude through the cervical os
and fills the vaginal vault.[29] In some instances the tumor
infiltrates deeply to myometrium of the uterus that leads to
expansion of the walls. Less frequently, it may develop into
a large pelvic mass in which uterus cannot be identified. In
most cases myometrial invasion is obvious microscopic. The
cut surface of this tumor is usually soft and moist and shows
extensive necrosis, hemorrhage, grayish whitish or pinkish or
purplish in appearance. Occasionally there are gritty or hard
areas corresponding to bone and cartilage, and tumor surface
is smooth. The size of tumor shows variation range from
less than 2.0cm to over20cm in diameter. Microscopically,
carcinosarcoma has both the epithelial and mesenchymal
elements. The malignant epithelial elements are typically an
adenocarcinoma of endometriod type but serous, mucinous,
clear cell, squamous cell and differentiated carcinomas are
not infrequent. The mesenchymal elements are usually high
grade and may be homologous or heterologous. In homologous
tumors, it resembles endometrial stromal sarcoma or fibro
sarcoma. Alternatively in heterologous tumor, mesenchymal
differentiation can be found in association with areas of
endometrial, stromal or undifferentiated sarcomas. The
most common heterologous sarcoma is rhabdomyosarcoma,
chondrosarcoma, osteosarcoma, and liposarcoma in decreasing
order of frequency. The pattern of histology of high grade
sarcoma is without specific differentiation, which is commonly
found.
The carcinomatous components correspond to any Mullerian
type. Commonly there is a sharp demarcation between the
epithelial and mesenchymal components. The epithelial
proportion in tumors varies from less to more and in some
instances the sarcomatous components are predominant
to such an extent that carcinoma may be difficult to
identify. In such condition, extensive sampling is required
to demonstrate the carcinoma. However, in some cases the
carcinoma is predominant. The most common heterologous
elements present in striated muscles, is identifiable, if the

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Singh: Review of literature on uterine carcinosarcoma

rhabdoblast has well differentiated and cross striated cells. For

the staining and recognition of crossstriation, hematoxylin
and eosin(HandE) and phosphotingstic acid hematoxylin
or immunohistochemistry are required, respectively. The
rhabdoblast appear as large cells with strap like, round or
oval atypical nuclei and granular eosinophilc cytoplasm
(racket cells). They are more difficult to recognize if single and
sparse. Their presence is confirmed by immunohistochemistry
using antibody against myoglobin, desmin, sarcomin and
cactin. Other rare elements are neuroectodermal tissue,
melanoid and neuroendocrine elements.[30,31] Whenever, serum
fetoprotein is elevated, it is usually associated with yolk
sac components or elements.[32,33] Carcinomatous cells usually
show a marked degree of anaplasia with variable size and
shape of the nucleus, bizarre mitotic figure often giant cells
i.e. pleomorphic cells.
Metastasis
The pattern of metastasis in carcinosarcoma depends on
dominancy of the type of elements. Most studies suggest that the
behavior of carcinosarcomas is governed by the carcinomatous
element. Carcinoma typically spread through the lymphatic
channels to nearby lymph nodes, while sarcoma frequently
metastasize to the peritoneal cavity or hematogenously to the
lungs. In sarcoma, lymph node metastasis is very uncommon.
Astudy conducted by a Gynecologic oncology group(GOG)
has shown that when extra uterine metastasis is found, only
the epithelial component of the tumor is present.[34] Another
study analyzed 22cases of uterine carcinosarcoma where it
was found that carcinosarcoma metastasize mainly to lymph
nodes, ovaries, fallopian tubes and omentum and uncommonly
to parametrium, bowels, liver and tonsils. All metastatic foci
have only carcinomatous component.[35] This shows that the
carcinomatous component has predominantly responsible for
most metastasis and sarcomatous component has only a minor
role. This view is supported by a number of studies conducted
by different groups.[36,37]
The patients of carcinosarcomas behave much like as high grade
endometrial adenosarcoma and commonly metastasize to pelvic
or par aortic lymph nodes. Leiomyosarcoma rarely involves
nodal sites. When metastatic foci analyzed histologically, most
often neoplastic nests in lymph vascular spaces were present
and this mimics the epithelial component of neoplasm.[38,39]
One of the recent study(Ferguson etal.) have concluded
that most carcinosarcoma have myometrial invasion(85%)
mostly in less than half of the wall, lymhovascular invasion
present in(60%) and carcinomatous component mostly
invading the myometrium and lymhovascular spaces.[40] While
studying the histological feature of 62 metastasis of uterine
carcinosarcomas, Sreeman and Hart observed carcinoma only in
43, both carcinoma and sarcoma in 15 and 4 had only sarcoma.
Based on these finding, authors speculated that the potential
for sarcomatous in metastatic lesion is enhanced in anatomic
sites with hollow space that allow polypoid growth such as
peritoneal cavity and vagina. In view of this observation, we

can say that primary carcinosarcoma in the genital tract and

nongenital tract areas(for e.g. as an esophagus) are usually
have polypoid neoplasm that tend to grow intraluminally in
organ with hollow space. Finally, we conclude that sarcomatoid
differentiation may be a marker of more aggressive behavior
and of regression to more primitive stem cell like phenotype
with the ability to give rise to epithelial or stromal progenitor
cells. Usually the epithelial is the main component driving
metastasis.
Traditionally carcinosarcoma considered as a subtypes of
uterine sarcoma and oncological treatment have often been
similar to those used for high grade uterine sarcoma, but
patients failed to respond such treatment. This occurred
due to different histology and the origin of tumors than the
counterpart high grade uterine sarcoma. Therefore, four main
theories regarding the histogensis of uterine carcinosarcoma
are put forward, namely:
The collision theory suggests that the epithelial and
mesenchymal elements have arisen independently and
collided to give the impression of single mixed tumor
The combination theory suggests that both the
components are derived from a single stem cell that has
undergone diverge differentiation in the early evolution
of tumors
The conversion theory suggests that the sarcomatous
element is derived from carcinoma during the evolution
of the tumor
Composition tumor is an endometrial carcinoma with
reactive, atypical stroma.
The composition theory can be easily excluded because in these
neoplasms, the sarcomatous component shows malignant
histological feature. At present, there has been ample evidence
that most but not all carcinosarcomas are of monoclonal origin
i.e.being derived from single stem cell and the carcinomatous
component is the driving force.[41,42]
However, collision tumors rarely occur, but these are easily
identified in the hysterectomy specimen where separate
areas of carcinoma and sarcoma are present. Rarely
carcinoma arises from preexisting adenosrcoma.[4345] The
combination and conversion theory are not mutually exclusive
in the prime nodes of histogensis of these neoplasms. To
date, the conversion theory is broadly accepted, in which the
sarcomatous component is derived from carcinoma.
Clinical characteristics
The carcinosarcoma arise mostly in the uterus and the
majority of patients are presented with postmenopausal
vaginal bleeding, and in some patient it is associated
with a protuberant fleshy mass from the cervix.[28,46] The
presentation of uterine carcinosarcoma is based on the
site of origin. Most patients present with irregular vaginal
bleeding that may be slight or profuse.[47] The discharge may
be bloody or watery. The patient could also complain gradual

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Singh: Review of literature on uterine carcinosarcoma

weakness, abdominal swelling, pain or abdominal mass and

sometime increased abdominal girth. In advanced stages, the
patient could complain of urinary tract or gastrointestinal
symptoms.

for abdominal dissemination. But patients may need adjuvant

radiotherapy and chemotherapy. While in advanced stages
(III, IV) tumors are treated by debulking surgery, chemotherapy,
and adjuvant radiation.

Prognosis
Uterine carcinoma has a poor prognosis despite different
treatment modalities used. It is usually worse than the
corresponding set of high grade endometrial carcinoma,
mainly in typeI carcinoma with median survival of 1836months. For women with carcinosarcoma, their prognosis
vary inversely with the initial stage at presentation, which
include tumor size, lymph node metastasis, adenexal spread,
lymphovascular invasion, histological grade, cell type and
depth of myometrial invasion. Other factors also influence the
prognosis of carcinosarcoma patients, like types of surgery,
chemotherapy doses and regimens, adjuvant radiotherapy and
patients characteristics. Gloria etal., studied the serum CA125
levels in patients of carcinosarcoma and has shown that the
preoperative elevation is a marker of extra uterine disease and
deep myometrial invasion.[48] Postoperative CA125 elevation is
an independent prognostic factor for poor survival.

In the past treatment approach for patients of uterine

sarcoma was surgery and adjuvant radiation. At that time,
chemotherapy was not used but adjuvant radiation was given
infrequently both in pre and post operative stages. Controversy
exsits regarding the effectiveness of radiation for improvement
of survival. Some authors had reported that some patients
showed improvement but others did not.[52] Carcinosarcoma
staging to be performed in the same manner as endometrial
carcinoma. One study has established that very good survival
can be achieved in patients with carcinosarcoma, if they
undergo surgical staging and postoperative radiation therapy,
based on surgical finding followed by adjuvant chemotherapy
with cisplatin and epirubicin.[53]

Some studies have shown that hormonal receptor status

may have prognostic value and help in determining the
treatment modalities. One of the studies that was performed
by Ansink etal., investigated the role of estrogen receptor(ER)
and progesterone receptor(PR) receptor status in uterine
carcinosarcomas and they concluded that the hormone
receptor positivity may have associated with clinical outcome.
They also drawn the conclusion, on the basis of receptor
positivity in four patients out of 11patients, three out of
11patients were alive, and two of these had hormone receptor
positivity in the epithelial sarcoma patients.[49] George etal.,
has shown that the prognosis is correlated with the type and
degree of differentiation of the epithelial component of uterine
carcinosarcoma.[50] Michel etal., study has shown the women
who were postmenopausal or had a history of prior pelvic
radiation, pain at presentation, clinical stage(IIIII disease),
uterine enlargement(>12weeks) or an abnormal papnicolaou
finding had a significant poor prognosis that those without
these factors.[51]
Management
Surgery is often the principal means of diagnosis and is the
primary treatment for all patients with uterine sarcoma.
Uterine carcinosarcoma required combined modality
approach which includes surgery, chemotherapy, radiotherapy
and sometimes hormonal therapy. However, standard
treatment is surgery which includes hysterectomy, bilateral
salpingoophrectomy, lymph node dissection and resection
of all gross disease. The stage of disease is important for the
selection of type of treatment modality to be used. For e.g.if
patients are in stage I and II, they are usually treated by total
abdominal hysterectomy, and the bilateral salpingoophrectomy
and omentectomy are also performed due to the propensity
464

The role of radiation therapy as an adjuvant for the treatment

of carcinosarcoma depends on postoperative residual
disease or surgical inaccessible sites as well as lymph node
status. Most of the studies have shown that radiotherapy
reduces local recurrence.[54,55] Callister etal., reported that
radiotherapy reduced risk of local recurrence from 48%
to 28% and prolonged the time to distant relapse but did
not improve overall survival. One of the retrospective
review was carried out in Canada, in patients of early stage
uterine carcinosarcoma and their analysis report have
suggestedthat the patient with poor histological prognostic
factor may be benefited with adjuvant radiation therapy,
which consequently improve in progression free and overall
survival.[56] Piver etal., reported that only an estimated
five year survival rate of 36% in surgically treated patients
in early stage uterine carcinosarcoma. [57] While Gadduci
etal., obtained a five year survival rate of 33% in early
stage patients with uterine carcinosarcoma treated with
a combination of radiotherapy and surgery.[58] The role of
radiotherapy is controversial as different conclusions were
reached by different small series.[5961]
Radiation therapy has been most commonly used as an
treatment effort to reduce pelvic failure. It has been advocated
that radiation therapy to be given in doses of 5000-6000 cGy
to the pelvis. Some authors also recommend intravaginal
brachytherapy to deliver a boost to the vaginal cuff.
Preoperative radiation is infrequently used and typically given
in patients with bulky cervical involvement or parametrial
extension. One of the recent data has reported that there has
been a significant improvement in survival of the patients
of uterine carcinosarcoma, who had received radiation.[62]
Though the above study suggested benefit of pelvic radiation
but it is limited to stage II, III, IV. While on stage I there was
no statistically significant difference in survival between
surgeryalone and in combination of surgery plus adjuvant
radiation.[63]

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The adjuvant radiation reduced chances of local recurrences as

depicted by the number of trials like Major etal.,[64] has found
that pelvic radiation reduced recurrence rate in patients as
compared with those who had not received radiation. It appears
that patients treated with radiation have a greater degree of
local tumor control, i.e.pelvic control, than without radiation.
The majority of patients treated with radiation had recurrences
or failure in site distant from the pelvis. This indicates patients
require a systemic agent, which will reduce distant site of
failure. Several published retrospective reports suggesting
that combined adjuvant radiation and chemotherapy may
impart an even longer survival mainly in stages I and II of
the disease.[54,65,66] Uterine sarcoma has a high rate of distant
metastasis even in the absence of intraperitonial or lymph
node metastasis. It has been concluded that this is due to the
high rate of hematogenous and lymphatic dissemination.[67]
Even for surgical stage I disease, the recurrence rate is high.[34]
A number of drugs have been tried but only three
chemotherapeutic agents have demonstrated effectiveness
against the disease. These are ifosfamide, cisplatin and
paclitaxel.[6873] Out of the three drugs, ifosfamide is the
most active agent studied to date. It produced 25 complete
responses and 12 partial responses(overall responses 36%)
among 102patients with no prior chemotherapy. Several
reports have demonstrated the combination chemotherapy
usually results in a higher response rate than single agent
treatment.[74,75] However, all combination regimens have had
an impact upon survival.[76] A phase III trial carried out by
GOG has shown greater response in patients who received a
combination regimen(paclitaxel plus ifosfamide) than single
drug chemotherapy. This also demonstrated that the addition of
paclitaxel significantly improved overall survival and response
rate.[69] One of the studies performed by GOG in patients of
carcinosarcomas was to compare the effects of whole abdominal
irradiation and cisplatinifosfamide based chemotherapy
between two groups and to see the pattern of failure. On
analysis it was found that only vaginal recurrence appeared
to be increased in the chemotherapy cohort vs radiotherapy
cohort. Other sites of relapse were similar except for a notable
reduction in abdominal failure in the chemotherapy treated
group as compared with radiotherapy treated group. Based
on these patterns of recurrences the vaginal brachytherapy
may be required for chemotherapy treated patients.[77] Recent
studies have shown that ifosfamide based combination
chemotherapy significantly improved progressionfree survival
and overall survival over ifosfamide alone in advanced
persistent or recurrent uterine carcinosarcomas.[70] But this
drug also gives better response in the early stage of disease.
Several drugs have been tried in patients who have relapsed or
persisting disease. These are cisplatin, doxorubicin, paclitaxel,
ifosfamide, cyclophosphamide, liposomal doxorubicin,
docetexel, gemcitabine, imitinib mesylate etc. All these
drugs are usually given in various combinations and show
a variable rate of response. Two recent phase II trials have
been performed, that shows not much activity against the

persistent or recurrent disease. One of them was based on

gemicitabine and docetaxel drugs, which was given weekly
in combination. The result indicated that this regimen is not
active in patients with recurrent carcinosarcoma of uterus as
secondline chemotherapy.[78]
The role of hormonal therapy has not been studied extensively
in mesenchymal uterine tumors. One trial by Wang etal.,[79]
on recurrent uterine highgrade carcinosarcomas has shown
that the dramatic response rate with letrazole therapy. For the
possible role of hormonal therapy more trial will be needed
to reach to any conclusion. Because of the aggressive nature
of this disease and poor response rate to radiotherapy and
chemotherapy biologic agents may have promising role to
overcome the problem of treatment. The recent advances
in the biology of uterine sarcoma made possible to define
the treatment target. These are tyrosine kinase receptors
and vascular endothelial growth factors. Some investigators
have studied the biologic agents. Emoto etal., demonstrated
the inhibition of vascular endothelial growth factor(VEGF)
expressing malignant mixed tumor line by TNP470(an
angiogenesis inhibitor). [80] Thalidomide was studied in
recurrent or persists mixed malignant Mullerian tumor of
the uterus by GOG, with no activity seen. Likewise, a trial
conducted by Warner etal., in 2010 to assess the efficacy
and safety of imatinib mesylate(Gleevec) in women with
recurrent or persistent carcinosarcoma of the uterus concluded
that imatinib mesylate was generally well tolerated but had
minimal activity as a single agent in unscreened patients. In
this study, sample size was very small giving the study a very
limited power. To further explore the relationship between
imitinib mesylate and clinical outcome in patients, the multi
institutional collaborative trials are required.[81]
SUMMARY
The carcinosarcomas are a biphasic malignancy consists of
malignant epithelial and mesenchymal components, which
usually appear to arise from transformation of pleuoripotent
stem cell that have the potential to produce cells with divergent
differentiation. Most but not all uterine carcinosarcomas
are monoclonal in origin, rather than true collision tumor
and should be regarded as metaplastic carcinosarcomas and
adjuvant treatment should probably be similar to that directed
against aggressive high grade endometrial sarcoma, rather
than being sarcomabased. This tumor warrants compressive
surgical staging to assess tumor dissemination followed by
systemic therapy in both early and advance stage diseases
excluding patients with noninvasive disease. Chemotherapy
is effective in advanced and metastatic stage of disease and is
ineffective as adjuvant for most early stage uterine sarcoma
and there is no proven role for chemotherapy in stage I disease
following complete surgical resection. Enough evidence is
present to support the use of pelvic radiation or vaginal
brachytherapy with or without chemotherapy for surgical I
and II stage patients of uterine carcinosarcoma.

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ACKNOWLEDGMENT
I would like to gratefully thank Dr.Shyam Singh(clinical assistant
in department of radiation oncology, Medcity, Gurgaon, Haryana) for
valuable suggestion during writing of review article.

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Cite this article as: Singh R. Review literature on uterine carcinosarcoma.
J Can Res Ther 2014;10:461-8.
Source of Support: Nil, Conflict of Interest: None declared.

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