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  Table of Contents    
CASE REPORT  
Year : 2021  |  Volume : 64  |  Issue : 5  |  Page : 172-174
Pancreatic collision tumor of ductal adenocarcinoma and neuroendocrine tumor—A rare case report


1 Department of Pathology, Kalinga Institute of Medical Sciences, Bhubaneswar, Odisha, India
2 Department of Surgical Gastroenterology, Kalinga Institute of Medical Sciences, Bhubaneswar, Odisha, India

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Date of Submission21-Sep-2019
Date of Decision22-Dec-2019
Date of Acceptance29-Dec-2019
Date of Web Publication7-Jun-2021
 

   Abstract 


A collision tumor is composed of two adjacent histological distinct neoplasms without the histological admixture of cell types in the same organ or tissue. It is rare in pancreas. Herein we report an unusual case of a mixed malignant neuroendocrine tumor (NET) and ductal adenocarcinoma of pancreas in a 24 year old male who presented with history abdomen pain. A clinicoradiological diagnosis of chronic calcific pancreatitis with carcinoma body of pancreas was made. Distal pancreaticosplenectomy specimen showed a grey white, nodular growth measuring 2 x 2 x 1.2 cm on the cut surface of pancreas. Histopathology revealed a composite tumor consisting of ductal and neuroendocrine origin. Immunohistochemistry showed complementary staining for CK7 in adenocarcinoma and chromogranin A in NET areas confirming a collision tumor. Accurate evaluation of the radiologic pointers, histomorphologic evaluation to recognize and quantitate the individual components, appropriate immunohistochemical evaluation and correlation is essential for diagnosis.

Keywords: Collision tumor, ductal adenocarcinoma, neuroendocrine tumor, IHC

How to cite this article:
Das P, Panigrahi R, Pradhan P, Senapati U, Mohapatra MK. Pancreatic collision tumor of ductal adenocarcinoma and neuroendocrine tumor—A rare case report. Indian J Pathol Microbiol 2021;64:172-4

How to cite this URL:
Das P, Panigrahi R, Pradhan P, Senapati U, Mohapatra MK. Pancreatic collision tumor of ductal adenocarcinoma and neuroendocrine tumor—A rare case report. Indian J Pathol Microbiol [serial online] 2021 [cited 2021 Jun 13];64:172-4. Available from: https://www.ijpmonline.org/text.asp?2021/64/5/172/317922





   Introduction Top


Pancreatic neuroendocrine tumors (NET) are relatively uncommon. With an annual incidence of 2.5–5 per 100,000 population worldwide, its coexistence with pancreatic duct adenocarcinoma has been rarely described in the literature.[1] The management of such mixed tumors is challenging mainly because of the significant differences in the natural course and responsiveness to chemotherapy of each histological type.[2] Herein we report an unusual case of a mixed malignant NET and ductal adenocarcinoma of pancreas.


   Case Report Top


A 24-year-old male, a known case of type 2 diabetes mellitus on insulin therapy and chronic alcoholism presented with history of dull aching pain in upper abdomen for 10 years. The pain was radiating to back and was associated with bilious vomiting and significant weight loss. There was no history of fever, gastrointestinal bleed, jaundice, abdominal distention, or steatorrhoea. The bowel and bladder habits were normal. Investigations revealed random blood sugar of 286 mg/dl (HbA1c 10.4%). Renal and liver function tests, serum lipid profile, amylase and lipase levels were within normal limits. Serum CA-19.9 levels was markedly elevated (954.9 u/ml). Ultrasonography abdomen showed multiple calcifications in the pancreas. CECT abdomen showed a radioenhancing mass in body of pancreas measuring 13 × 10 mm. A clinicoradiological diagnosis of chronic calcific pancreatitis with carcinoma body of pancreas was made. Radical distal pancreaticosplenectomy with end to side pancreaticojejunostomy was done.

Intraoperatively, a 2 × 2 cm mass in body of pancreas just to left of splenoportal confluence. Grossly a distal pancreaticosplenectomy specimen was received with spleen measuring 12 × 6.5 × 4.5 cm and part of pancreas measuring 7.5 × 4 × 2 cm [Figure 1]. On cut surface of pancreas, there is grey white, firm, solid nodular growth measuring 2 × 2 × 1.2 cm. The adjacent areas shows dilated duct. The nodule is 0.2 cm away from the closest cut margin. Cut section of the spleen was unremarkable.
Figure 1: (a) Distal pancreaticosplenectomy specimen; (b) Cut surface of the pancreas showing grey white, firm, solid nodular growth measuring 2 × 2 × 1.2 cm

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Multiple sections were studied from the tumor. Sections reveal tumors with two different histomorphology in adjacent areas [Figure 2]. A collision tumor comprising of ductal adenocarcinoma with mucinous differentiation and neuroendocrine carcinoma. One composed of duct lining showing dysplasia along with infiltration. The tumor cells of ductal carcinoma were arranged in acinar and cribriform pattern with surrounding desmoplastic stroma and focal mucin pools. There was moderate degree of pleomorphism. The neuroendocrine component was more than 30% of the whole tumor. The neuroendocrine component showed cells arranged in nests having mild pleomorphism and characteristic salt and pepper chromatin. Mitotic figures were also present. The tumor had infiltrated the peripancreatic fat. Extensive perineural invasion was present. There was no lymphovascular invasion or lymph node metastasis.
Figure 2: (a) Sections from adenocarcinomatous areas showing malignant cells arranged in acinar and cribriform pattern with surrounding desmoplastic stroma and focal mucin pools. (H and E, 100×). (b) Adjacent ductal lining epithelium showing dysplasia (H and E, 100×). (c and d) Sections from the neuroendocine component show cells arranged in nests having mild pleomorphism and characteristic salt and pepper chromatin. Extensive perineural invasion was present. (d) (c: 100×, d: 400×)

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Immunohistochemistry showed positivity for Pancytokeratin (PanCK) in the adenocarcinomatous areas with high Ki67 labelling index [Figure 3]. The tumor cells showing neuroendocrine differentiation were positive for synaptophysin and low Ki-67 (<2%) [Figure 4]. So, a collision tumor was confirmed.
Figure 3: Diffuse strong cytoplasmic positivity of PanCK in the adenocarcinomatous foci (400×)

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Figure 4: (a) Diffuse positivity for Chromogranin A in neuroendocrine areas. (400×); (b) Ki67 labelling index less than 2% (400×)

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   Discussion Top


According to the WHO histological classification, collision tumors are composed of at least 2 different malignant components, separated by stroma without histological admixture. They can occur in any organ of the body, but most common site is stomach and oesophagus.[3] Diagnosis of a collision tumor is usually a postoperative based on the pathological examination of the surgical specimen, as there may be no specific symptoms or radiological features before surgery.[4]

Pancreatic collision tutors are very rare, and the literature is therefore limited. Little is known about the mechanism of carcinogenesis of collision cancers. There are, however, several proposed theories in the literature. One hypothesis is that there may be a dysfunction of multiple tumour-suppressor genes that causes inadequate repair of genes, resulting in multiple types of malignancies.[4] Other theories postulate that different tumors can originate from totipotent endodermal or intermediate cells, which are able to differentiate into both endocrine and ductular structures as demonstrated in experimental carcinogenesis of rodents.[5] The concept of epigenetic alterations, somatic mutations induced by carcinogens, as well as heritable mutations in cancer susceptibility genes has become a well-accepted theory of carcinogenesis in any part of the body. The hypothesis of field carcinogenesis could be a possible explanation for synchronous and metachronous lesions in the pancreas and throughout the gastrointestinal tract.[6]

Most of these tumors do not show any specific symptoms or any particular radiologic findings and are detected only on resected specimens postoperatively. These entities are identified by their distinct histologic features as is shown in the present case. The neuroendocrine component shows cells arranged in nests with distinct organoid pattern with thin vascular septae which on immunohistochemistry is positive for the neuroendocrine markers like Neuron Specific Enolase (NSE), CD56, synaptophysin, and chromogranin. The adenocarcinoma was readily recognized by the characteristic features of dysplastic lining and invasive glands, immunohistochemically confirmed by PanCK and high Ki-67. Differential diagnosis between mixed exocrine–endocrine and collision tumors may arise. However, in the mixed type, the exocrine–endocrine cells are closely combined while the collision type shows separate endocrine and exocrine components without an intermixed central zone, as in our case.[7] Also the presence of >30% of neuroendocrine islands rules out the possibility of hyperplasia of the neuroendocrine elements.

From the small number of reported cases, collision tumors appear to have a poor prognosis. Preoperative diagnosis can be nearly impossible to make, and are typically diagnosed postoperatively.[8] Surgical resection appears to be a rational method of treatment. It has been suggested in the literature that special attention should be paid to atypical radiologic features such as heterogeneity on CT imaging, presence of surrounding low-density areas.[9] As highlighted in this case, a multidisciplinary approach involving clinicoradiological inputs, histomorphological, and immunohistochemical assessment is very important for diagnosis.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
La Rosa S, Marando A, Sessa F, Capella C. Mixed adenoneuroendocrine carcinomas (MANECs) of the gastrointestinal tract: An update. Cancers 2012;4:11-30.  Back to cited text no. 1
    
2.
Ehehalt F, Saeger HD, Schmidt CM, Grutzmann R. Neuroendocrine tumors of the pancreas. Oncologist 2009;14:456-67.  Back to cited text no. 2
    
3.
Liu SW, Chen GH, Hsieh PP. Collision tumour of the stomach: A case report of mixed gastrointestinal stromal tumour and adenocarcinoma. J Clin Gastroenterol 2002;35:332-4.  Back to cited text no. 3
    
4.
Niu GM, Jin DY, Ji Y, Hou J, Wang DS, Lou WH. Survival analysis of pancreatic and periampullary collision cancers. J Dig Dis 2010;11:231-6.  Back to cited text no. 4
    
5.
Stukavec J, Jirasek T, Mandys V, Denemark L, Havluj L, Sosna B, et al. Poorly differentiated endocrine carcinoma and intraductal papillary – Mucinous neoplasm of the pancreas: Description of an unusual case. Pathol Res Pract 2007;203:879-84.  Back to cited text no. 5
    
6.
Wang Y, Gandhi S, Basu A, Ijeli A, Kovarik P, Sekosan M, et al. Pancreatic collision tumor of ductal adenocarcinoma and neuroendocrine tumor. ACG Case Rep J 2018;5:e39.  Back to cited text no. 6
    
7.
Chang SM, Yan ST, Wei CK, Lin CW, Tseng CE. Solitary concomitant endocrine tumor and ductal adenocarcinoma of pancreas. World J Gastroenterol 2010;16:2692-7.  Back to cited text no. 7
    
8.
Kim HJ, Choi BG, Kim CY, Cho CK, Kim JW, Lee JH, et al. Collision tumor of the ampulla of Vater: Coexistence of neuroendocrine carcinoma and adenocarcinoma: Report of a case. Korean J Hepatobiliary Pancreat Surg 2013;17:186-90.  Back to cited text no. 8
    
9.
Araki K, Shimura T, Kobayashi T, Saito K, Wada W, Sasaki S, et al. Mixed ductal-endocrine carcinoma of the pancreas occurring as a double cancer: Report of a case. Int Surg 2011;96:153-8.  Back to cited text no. 9
    

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Correspondence Address:
Prita Pradhan
Department of Pathology, Kalinga Institute of Medical Sciences, Bhubaneswar - 751 024, Odisha
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IJPM.IJPM_735_19

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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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