Synchronous Gastric Gastrointestinal Stromal Tumor and Colon Adenocarcinoma: A Case Report

Abstract

Gastrointestinal stromal tumors (GISTs) represent the majority of primary mesenchymal tumors of the gastrointestinal tract. They are generally considered to be solitary tumors and therefore the synchronous occurrence with other primary malignancies of gastrointestinal track is considered a rare event. Here we present the case of a 75-year-old man admitted to our hospital with a 10-day history of gastrointestinal bleeding. Colonoscopy revealed an ulcerative mass of 4 cm in diameter in the ascending colon. Gastroscopy revealed a bulge in the gastric body measuring 1 cm in diameter with normal overlying mucosa. Surgical intervention was suggested and ileohemicolectomy with regional lymph node resection along with gastric wedge resection was performed. Pathologic examination of the ascending colon mass showed an invasive moderately differentiated adenocarcinoma stage III B (T3N1M0). Grossly resected wedge of stomach showed a well circumscribed intramural tumor which microscopically was consistent with essentially benign gastrointestinal stromal tumor (according to Miettinen criteria). The patient did not receive additional treatment. Two years later the patient showed no evidence of recurrence or metastasis.

Full text

Case Report
Synchronous Gastric Gastrointestinal Stromal Tumor
and Colon Adenocarcinoma: A Case Report
Thivi Vasilakaki,1Kalliroi Koulia,1Aikaterini Tsavari,1Elissavet Arkoumani,1
Efstratios Kouroumpas,2Anargiros Pavlis,2Georgios Christopoulos,2
Konstantinos Stamatiou,2Kassiani Manoloudaki,1and Dimitrios Zisis3
1Department of Pathology, “Tzaneion” General Hospital of Piraeus, 1 Afendouli Avenue, 18536 Piraeus, Greece
2Department of Surgery, “Tzaneion” General Hospital of Piraeus, 1 Afendouli Avenue, 18536 Piraeus, Greece
3Department of Gastroenterology, “Tzaneion” General Hospital of Piraeus, 1 Afendouli Avenue, 18536 Piraeus, Greece
Correspondence should be addressed to Konstantinos Stamatiou; stamatiouk@gmail.com
Received  June ; Revised  July ; Accepted  July ; Published  August 
Academic Editor: Raaele Palmirotta
Copyright ©  ivi Vasilakaki et al. is is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Gastrointestinal stromal tumors (GISTs) represent the majority of primary mesenchymal tumors of the gastrointestinal tract. ey
are generally considered to be solitary tumors and therefore the synchronous occurrence with other primary malignancies of
gastrointestinal track is considered a rare event. Here we present the case of a -year-old man admitted to our hospital with a
-day history of gastrointestinal bleeding. Colonoscopy revealed an ulcerative mass of  cm in diameter in the ascending colon.
Gastroscopyrevealedabulgeinthegastricbodymeasuringcmindiameterwithnormaloverlyingmucosa.Surgicalintervention
was suggested and ileohemicolectomy with regional lymph node resection along with gastric wedge resection was performed.
Pathologic examination of the ascending colon mass showed an invasive moderately dierentiated adenocarcinoma stage III B
(TNM). Grossly resected wedge of stomachshowed a well circumscribed intramural tumor which microscopically was consistent
with essentially benign gastrointestinal stromal tumor (according to Miettinen criteria). e patient did not receive additional
treatment. Two years later the patient showed no evidence of recurrence or metastasis.
1. Introduction
Gastrointestinal stromal tumors (GISTs) are the most com-
mon primary mesenchymal neoplasms of the gastrointestinal
track and they account for .% of all malignant gastric
tumors. GISTs can occur anywhere along the GI tract but
aremostcommoninthestomach(–%)andsmall
bowel (–%). Colon (%), omentum/mesentery (%),
and esophagus (%) are less common primary sites [–].
Most GISTs arise from interstitial cells of Cajal. ese cells
are present inside and around the myenteric plexus and show
both myogenic and neural dierentiation, a fact that explains
the immunohistochemical heterogeneity of the tumors that
derive from them [,,]. e spectrum of GIST includes
neoplasms with both benign and malignant behaviour. e
last has been associated with size, location, and mitotic count
of the tumor. In fact, GISTs that are  cm or less in size can
be regarded as essentially benign; however, intestinal GISTs
are more aggressive than gastric GISTs of equal size, while
tumors with a KIT exon  mutation are associated with a
worse outcome than tumors with other KIT mutant isoforms
or with no detectable mutation [].
GISTs are generally considered solitary tumors and
therefore the synchronous occurrence with other primary
malignancies of gastrointestinal track is considered a rare
event. Here we report a case of small gastric GIST incidentally
detected during endoscopy that occurred synchronously with
a primary colon adenocarcinoma.
2. Case Report
A -year-old man was admitted to our hospital with a
-day history of gastrointestinal bleeding. He complained
of a bad stomach ache for about four months; however,
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Case Reports in Oncological Medicine
Volume 2014, Article ID 305848, 3 pages
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Case Reports in Oncological Medicine
F : Colon adenocarcinoma (H/E ×).
he reported no family history of gastrointestinal disease.
Computerized tomography (CT) of the pelvis showed an
obvious high-density enhancing lesion in the wall of the
ascending colon. Colonoscopy revealed an ulcerative mass
ofcmindiameterintheascendingcolon.Biopsyfrom
the mass diagnosed an invasive moderately dierentiated
adenocarcinoma. Gastroscopy revealed a bulge in the gastric
body measuring  cm in diameter with normal overlying
mucosa. Mucosal biopsies diagnosed chronic gastritis; how-
ever no evidence of Helicobacter pylori infection was found.
Endoscopic ultrasound of the gastric bulge showed a  ×cm
lesion involving the gastric wall.
Surgical intervention was suggested and ileohemicolec-
tomy with regional lymph node resection along with gastric
wedge resection was nally performed. Pathologic exami-
nationoftheascendingcolonspecimenrevealedastage
III B disease (TNM according to TNM classication)
(Figure ). Only one out of the six resected lymph nodes
showed tumor metastasis.
Grossly resected wedge of stomach showed a well cir-
cumscribed intramural tumor which microscopically was
consistent with an essentially benign gastrointestinal stromal
tumor (according to Miettinen criteria). e lesion involved
the muscularis propria with variable submucosal extension
(Figure ). e immunohistochemical study showed that the
tumor’s cells were positive for CD and CD and negative
for actin, desmin, and Sp (Figure ). e Ki labelling
index was very low. e mitotic activity was <mitosis/
highpowereld(HPF).epatientdidnotreceiveadditional
treatment and he was monitored with annual abdominal CT.
Two years later the patient showed no evidence of recurrence
or metastasis.
3. Discussion
Gastrointestinal cancer is common and is a signicant cause
of morbidity and mortality. e synchronous occurrence of
two malignancies is not uncommon, but such occurrences
oen pose diagnostic and therapeutic challenges. Moreover,
the coexistence of malignancies of dierent histological
F : Gastric GIST (H/E ×).
F : Gastric GIST, CD positive (×).
origin along the GI track, raises questions regarding the
naturalhistoryandthepathophysiologyofGIcancer.
e majority of GISTs are sporadic and tumor multiplicity
is considered an exceptional nding limited to specic condi-
tions such as hereditary GIST, paraganglioma, and Carney’s
triad syndromes []. Beyond these entities, the occurrence
of multiple distinct tumors is conventionally interpreted as
indicative of metastatic spread from a primary lesion [].
However, neoplasms with histology and immunohistochem-
istry similar to GISTs may occur outside the gastrointestinal
trackintheabdomenorintheretroperitoneum.ese
tumors must be dened as extragastrointestinal stromal
tumors since they display no connection with the gastric of
intestinal wall [,]. Actually, GISTs have a broad morpho-
logical spectrum and show positivity for CD which appear
as cytoplasmic, as membrane-associated, or sometimes as
perinuclear dots. However, a small minority (<%) especially
GISTs with mutant PDGFRA may have very limited, if
any, positivity []. On the other hand, GISTs have been
associated with synchronous primary neoplasms of dierent
histogenesis. e most common are carcinomas of gastroin-
testinal track. Other coexistent tumors include carcinomas

Case Reports in Oncological Medicine 
ofbreast,lung,kidney,prostate,femalegenitaltrack,so
tissue sarcomas, lymphoma, and malignant melanoma [,].
However, the etiology of synchronous occurrence of GISTs
with histologically unrelated tumors still remains unclear [].
Activation of the KIT receptor tyrosine kinase is integral
to the development of many GISTs. is activation involves
amutationwithinthec-kit gene. Most GISTs (approximately
%) harbour a mutation in exon . In about % of cases
there is a mutation in exon  of KIT, while, less commonly
(<%), mutations occur in exons  and  []. ese
mutations (including deletions and point mutations) result in
gain of function. us, KIT signalling is constitutively acti-
vated resulting in downstream phosphorylation in the signal
transduction pathway, ultimately leading to increased cel-
lular proliferation []. However, in several malignancies—
including colorectal adenocarcinomas—alterations of the
tyrosine kinase activity is associated with advanced disease.
In fact, deregulation of the TK receptor enhances the ability
of cancer cells to migrate, initiating thus the metastatic
cascade []. While it is clear that activating mutations in
KIT are an early event in GISTs, it is not known whether
they can serve as an initiating oncogenic event in colorectal
cancer [,]. e fact that in this particular case a small
GIST (with very low malignant potential) coexisted with a
large primary colon adenocarcinoma suggests an association
between adenocarcinoma and GIST; however this association
does not seem to have an impact on survival. Given the
limited number of cases further studies are required to clarify
the molecular and genetic mechanisms of carcinogenesis.
In conclusion, the patients with synchronous GIST and
other neoplasms present diagnostic diculties because it is
not always possible to recognize a coexisting tumor preoper-
atively.
Conflict of Interests
e authors declare that there is no conict of interests
regarding the publication of this paper.
References
[] R. Kaur, S. Bhalla, S. Nundy, and S. Jain, “Synchronous gastric
gastrointestinal stromal tumor (GIST) and other primary neo-
plasms of gastrointestinal track: report of two cases,” Annals of
Gastroenterology, vol. , no. , pp. –, .
[] C. Nemes, L. Rogojan, T. Surdea-Blaga, A. Seicean, D. L.
Dumitrascu, and C. Ciuce, “Gastrointestinal stromal tumor
(GIST) associated with synchronous colon adenocarcinoma—a
case report,” Journal of Gastrointestinal and Liver Diseases,vol.
,no.,pp.–,.
[] S. S. Ferreira, G. Werutsky, M. G. Toneto et al., “Synchronous
gastrointestinal stromal tumors (GIST) and other primary can-
cers: case series of a single institution experience,” International
Journal of Surgery,vol.,no.,pp.–,.
[] L.Strickland,G.D.Letson,andC.A.Muro-Cacho,“Gastroin-
testinal stromal tumors,” Cancer Control,vol.,no.,pp.–
, .
[] C. Franzini, L. Alessandri, I. Piscioli et al., “Extra-gastroin-
testinal stromal tumor of the greater omentum: report of a case
and review of the literature,” World Journal of Surgical Oncology,
vol. , article , .
[] M. Miettinen and J. Lasota, “Gastrointestinal stromal tumors:
denition, clinical, histological, immunohistochemical, and
molecular genetic features and dierential diagnosis,” Virchows
Archiv,vol.,no.,pp.–,.
[] S. Singer, B. P. Rubin, M. L. Lux et al., “Prognostic value of
KIT mutation type, mitotic activity, and histologic subtype in
gastrointestinal stromal tumors,” Journal of Clinical Oncology,
vol. , no. , pp. –, .
[] D. Gasparotto, S. Rossi, I. Bearzi et al., “Multiple primary
sporadic gastrointestinal stromal tumors in the adult: an under-
estimated entity,” Clinical Cancer Research, vol. , no. , pp.
–, .
[] M.Miettinen,J.M.Monihan,M.Sarlomo-Rikalaetal.,“Gas-
trointestinal stromal tumors/smooth muscle tumors (GISTs)
primary in the omentum and mesentery: clinicopathologic and
immunohistochemical study of  cases,” e American Journal
of Surgical Pathology, vol. , no. , pp. –, .
[] M. C. Heinrich, B. P. Rubin, B. J. Longley, and J. A. Fletcher,
“Biology and genetic aspects of gastrointestinal stromal tumors:
KIT activation and cytogenetic alterations,” Human Pathology,
vol.,no.,pp.–,.
[] G. Bellone, S. Silvestri, E. Artusio et al., “Growth stimulation of
colorectal carcinoma cells via the c-kit receptor is inhibited by
TGF-beta ,” Journal of Cellular Physiology,vol.,no.,pp.
–, .