Open Access

Intraductal papillary‑mucinous carcinoma with portal vein tumor thrombus and multifocal liver metastasis: An autopsy case

  • Authors:
    • Naohiro Matsushita
    • Akitoshi Douhara
    • Hirotsugu Ueno
    • Shohei Asada
    • Koji Murata
    • Koji Yanase
    • Masahiro Tsutsumi
  • View Affiliations

  • Published online on: March 13, 2021     https://doi.org/10.3892/mco.2021.2263
  • Article Number: 101
  • Copyright : © Matsushita et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The prognosis of intraductal papillary‑mucinous neoplasm is superior to that of conventional pancreatic ductal adenocarcinoma. Only a few advanced cases of intraductal papillary‑mucinous carcinoma (IPMC) have been reported to date. We herein report the case of a 78‑year‑old male patient with advanced pancreatobiliary type IPMC with portal vein invasion and liver metastasis. The IPMC invaded the portal vein to form a tumor thrombus and it also metastasized to the liver via the portal vein. After receiving best supportive care, the patient succumbed to the disease following an exacerbation of IPMC 90 days after the initial presentation. On autopsy, a very long tumor thrombus was identified, along with liver metastatic lesions, which had retained the structure of the primary IPMC on histological examination.

Introduction

Intraductal papillary-mucinous neoplasm (IPMN) of the pancreas is a cystic tumor arising from the cells lining the pancreatic ducts. IPMN is divided into main-duct, branch-duct and mxixed-type lesions, depending on the site of origin (1). The disease spectrum ranges from low-grade dysplasia to invasive intraductal papillary-mucinous carcinoma (IPMC) (2). Moreover, IPMN may occasionally be associated with pancreatic carcinoma at a site distant from IPMN (1). Histologically, IPMNs are subdivided into intestinal, pancreatobiliary, gastric and oncocytic types based on the expression of immunohistochemical markers, such as mucin core protein (MUC)1, MUC2 and CDX2(3). Generally, the prognosis following surgical resection of IPMN with an associated invasive carcinoma has been reported to be superior to that of pancreatic ductal adenocarcinoma (PDAC) (4). However, the prognosis of the pancreatobiliary type IPMN is worse compared with that of the other subtypes (5). We herein report a case of a pancreatobiliary type IPMC with formation of a portal vein tumor thrombus and multifocal liver metastasis.

Case report

A 78-year-old man visited a regional hospital with complaints of fever and vomiting. An abdominal plain computed tomography (CT) scan at the hospital revealed dilatation of the bile ducts and the presence of cystic lesions in the pancreatic head and liver, and the patient was referred to Saiseikai Chuwa Hospital (Sakurai, Japan) for further examination and treatment.

The patient had a history of hypertension and benign prostatic hyperplasia and received regular treatment with nifedipine and tamsulosin hydrochloride. There was no history of liver dysfunction or a specific family history. The patient reported no allergies, cigarette smoking, or alcohol consumption.

When the patient first visited our hospital in March 2018, his vital signs were stable, with a body temperature of 36.3˚C, heart rate of 56 bpm, blood pressure of 120/66 mmHg, respiratory rate of 16 breaths/min and SpO2 of 96% in room air. The conjunctivas were slightly anemic. There were no murmurs or rales on chest auscultation, and the abdomen was soft and flat with no tenderness on palpation. The laboratory tests (Table I) revealed mild normocytic anemia, reduced levels of albumin and increased levels of hepatic and biliary enzymes, including aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, γ-glutamyl transpeptidase and pancreatic amylase. The levels of tumor markers, including carbohydrate antigen (CA)19-9, DUPAN-2, carcinoembryonic antigen and α-fetoprotein were measured, and the CA19-9 level was found to be increased. To evaluate the pancreatic and liver masses, an abdominal contrast-enhanced CT scan was performed (Fig. 1). A polycystic low-density area was identified in the pancreatic head, with a width of 46 mm, and the wall of this polycystic area was partially well-enhanced. The common bile duct was obstructed due to the polycystic tumor in the pancreatic head and was dilated to 20 mm. Multiple polycystic low-density areas were identified in the liver, with a morphology similar to that of the cystic lesion in the pancreatic head. Moreover, a 10-mm filling defect was observed in the superior mesenteric vein (SMV). The magnetic resonance cholangiopancreatography signals from a T2-weighted image revealed that the pancreatic head tumor exhibited low intensity, with a small high-intensity area (Fig. 2). Similarly, on the CT scan, the common bile duct was obstructed by the polycystic tumor in the pancreatic head and was dilated to a width of 20 mm. In order to drain the bile duct and perform diagnostic brush cytology, endoscopic retrograde cholangiopancreatography (ERCP) was performed (Fig. 3). The papilla of Vater was normal. First, contrast medium was injected into the pancreatic duct. The main pancreatic duct was dilated to a width of 4 mm. Pooling of mucus in the pancreatic duct was suspected due to the shallow filling defects. Second, contrast medium was injected into the bile duct. The proximal bile duct was markedly dilated, whereas the distal bile duct was narrowed and was 20 mm in length. Brush cytology of the narrowed bile duct was conducted, and endoscopic biliary stenting (EBS) was performed using a plastic stent in order to drain the bile duct. The brush cytology findings revealed the presence of atypical ductal cells.

Table I

Laboratory data at the patient's first visit.

Table I

Laboratory data at the patient's first visit.

Laboratory parameters (normal range)ValueUnit
Hematology  
     White blood cell count (3,300-8,600)4,600/µl
     Red blood cell count (435-555x104) 351x104/µl
     Hematocrit (40.7-50.1)32.1%
     Hemoglobin (13.7-16.8)10.6g/dl
     Mean corpuscular volume (83.6-98.2)91.5fl
     Platelet count (15.8-34.8x104) 16.1x104/µl
Coagulation  
     Prothrombin time-INR (0.85-1.15)1.03INR
     Activated partial thromboplastin time (25-40)31.9sec
     Fibrinogen (150-400)491mg/dl
     Fibrin degradation products (0-10)3.4µg/ml
     D-dimer (0-1)1.0µg/ml
Chemistry  
     Albumin (4.1-5.1)3.2g/dl
     Aspartate transaminase (13-30)41IU/l
     Alanine transaminase (10-42)66IU/l
     Lactate dehydrogenase (124-222)86IU/l
     Alkaline phosphatase (106-322)788IU/l
     γ-Glutamyl transpeptidase (13-64)160IU/l
     Amylase (44-132)357IU/l
     P-amylase (16-52)282IU/l
     Total bilirubin (0.4-1.5)0.5mg/dl
     Blood urea nitrogen (8-20)16.5mg/dl
     Creatinine (0.65-1.07)0.75mg/dl
     Na (138-145)134mEq/l
     K (3.6-4.8)4.2mEq/l
     C-reactive protein (0-0.29)5.165mg/dl
     Procalcitonin (0-0.4)0.39ng/ml
     Brain natriuretic peptide (0-18.4)19.6pg/ml
     Hemoglobin A1c (4.7-6.2)8.7%
Tumor markers  
     Carbohydrate antigen 19-9 (0-37)84.6U/ml
     DUPAN-2 (0-150)46U/ml
     Carcinoembryonic antigen (0-5)3.5ng/ml
     α-Fetoprotein (0-15)2.0ng/ml
     Protein induced by vitamin K absence-II (0-39)25.45mAU/ml

[i] INR, international normalized ratio.

The comprehensive diagnosis was advanced IPMC with invasion of the bile duct and liver metastasis. The clinical stage was stage IV (T3N0M1) according to the Union for International Cancer Control TNM classification (6). As regards treatment, systemic chemotherapy was recommended; however, the patient and his family opted for best supportive care due to his declining performance status (performance status score: 4). Thus, EBS was performed to drain the bile duct on the 2nd day of hospitalization and the plastic stent was exchanged for a metallic stent on the 8th day to prolong stent patency. Subsequently, the patient developed cholangitis and aspiration pneumonia, and he eventually succumbed to IPMC 90 days after the initial admission.

After obtaining informed consent from the patient's daughter, an autopsy was performed to examine the tumor. Macroscopically, the polycystic tumor in the pancreatic head was sized 5x4.5 cm and the cysts contained mucus. Moreover, the tumor had invaded the portal vein and formed an elongated tumor thrombus, extending from the SMV to the hilar portal vein. Polycystic tumor lesions were also identified in the liver, and the structure of these metastatic lesions was identical to that of the primary pancreatic head tumor (Fig. 4).

Microscopically, on hematoxylin and eosin staining, the pancreatic head tumor exhibited a papilliform structure consisting of small tumor cells and the tumor cysts were filled with mucus. On immunostaining, MUC1 and MUC5AC were positive (Fig. 5), but MUC2 was negative (data not shown). Therefore, the histological diagnosis was pancreatobiliary type IPMC, and the morphological diagnosis, which was based on the dilation of both the main pancreatic duct as well as its branches, was mixed-type IPMC. The polycystic liver tumors and SMV tumor thrombus had the same morphology as the pancreatic tumors on pathological examination, with pooling of mucus in the cysts of the liver metastatic lesions (Fig. 6). The pancreatic head tumor had not metastasized to the regional lymph nodes, but rather directly metastasized to the liver via the portal vein, retaining the IPMC structure and mucus production.

Discussion

There were two clinical issues with the present case: First, the pancreatic tumor directly invaded the portal vein and caused tumor thrombosis. Second, the pancreatic tumor metastasized to the liver via the portal vein, retained the IPMC structure and produced mucus. Currently, invasive IPMN is considered to have a better prognosis compared with conventional PDAC (7,8). Ueda et al (9) reported the case of a female patient with IPMN with metastases to the lymph nodes, liver and lung, who achieved long-term survival (5 years and 2 months), as she responded to chemotherapy following pancreaticoduodenectomy. However, in the present case, the patient's survival duration after diagnosis was very short due to the widespread local invasion, distant metastases and lack of anticancer treatment, such as systemic chemotherapy or radiotherapy.

IPMN and other cystic pancreatic tumors may be accurately and timely diagnosed due to the advances in imaging techniques, including MRI and ERCP (10). On occasion, these tumors are incidentally found on abdominal CT in asymptomatic patients. Other patients may present with variable symptoms, such as abdominal pain, obstructive jaundice and vomiting, as in the present case. The progression of obstructive jaundice with IPMN has been previously reported, as mucus produced from IPMN may obstruct the common bile duct (11). However, in the present case, the common bile duct was directly invaded and obstructed by the tumor.

Serum CA19-9 level is a well-known predictor of PDAC and poor survival. Elevated serum CA19-9 levels were found to be associated with mixed invasive IPMC, which is consistent with several previous reports (12,13), and this finding may indicate that invasive IPMC shares similar characteristics with PDAC. Hirono et al (14) evaluated the diagnostic value of the factors associated with invasive IPMC identified in their study, and branch-duct IPMN with elevated serum CA19-9 levels was associated with invasive IPMC, with a sensitivity of 86.4%, specificity of 96.6%, positive predictive value of 86.4%, negative predictive value of 96.6% and accuracy of 94.5%.

IPMNs are classified into four subtypes (intestinal, pancreatobiliary, gastric and oncocytic) based on their histomorphology and mucin phenotype (15). The subtype of the present case was pancreatobiliary, as determined based on the positive expression of MUC1 and MUC5AC and negative expression of MUC2. The pancreatobiliary type is the most malignant among the four subtypes (5). Moreover, the main-duct or mixed-type morphological classifications of IPMN are associated with a higher risk of evolving into invasive IPMC compared with the branch-duct type (16). Mixed-type IPMN includes various histological types. Masuda et al (17) previously reported that mixed IPMN with positive MUC2 expression had a significantly higher prevalence of high-grade dysplasia and invasive IPMC compared with MUC2-negative IPMN. However, the tumor in the present case was classified as invasive IPMC, despite the negative MUC2 expression. It was previously reported that the mixed type of IPMN rarely includes the pancreatobiliary type (17). The pancreatobiliary type is MUC2-negative, as are the gastric and oncocytic types. Thus, this contradiction regarding whether mixed-type IPMN is invasive may be attributed to selection bias in the report.

It was reported that 19-45% of IPMNs are accompanied by invasive carcinomas (8). However, the presence of portal vein invasion was significantly lower among patients with invasive IPMC compared with those with PDAC (8). Invasive IPMCs with portal vein invasion and tumor thrombosis, such as in the present case, have rarely been reported (16,18). Moreover, our patient had a long tumor thrombus and liver metastases. When an abdominal contrast-enhanced CT was first performed, the tumor thrombus was only 10 mm. However, when the autopsy was performed after 90 days, the tumor thrombus had grown and extended from the SMV to the hilar portal vein. The rapid growth of the portal thrombosis indicated a highly malignant tumor. In addition, invasion into the vasculature is a significant predictor of poor outcome (19). Moreover, in the present case, the structure of the polycystic liver tumors was identical to that of the pancreatic tumors on pathological examination. The SMV tumor thrombosis metastasized to the liver, maintaining its polycystic structure and mucus production. As the pancreatic head tumor had not metastasized to the regional lymph nodes, it was inferred that part of the SMV tumor thrombus, with a polycystic structure and mucus content, was detached and reached the liver via the portal vein.

While the patient and his family opted for best supportive care in the present case, several therapies for invasive IPMC have been reported. Pancreatectomy with lymph node dissection are recommended for invasive IPMC and PDAC, if the tumor is resectable (20), whereas the efficacy of postoperative adjuvant therapy for invasive IPMC remains controversial. McMillan et al (21) reported that postoperative adjuvant therapy may improve the survival of patients with advanced-stage invasive IPMC or lymph node metastases. However, another study reported that postoperative adjuvant therapy does not affect the survival of patients with invasive IPMC (22). Moreover, it is unclear whether systemic chemotherapy improves the survival of patients with unresectable invasive IPMN. Chemoradiotherapy has been demonstrated to prolong the survival of patients with PDAC (23). Regarding chemotherapy for PDAC, gemcitabine or S-1 (tegafur, gimeracil, oteracil potassium) as systemic chemotherapy for unresectable invasive IPMC is clinically considered (24).

To date, there have been reports of IPMC with portal invasion or liver metastasis (25,26). However, to the best of our knowledge, this is the first report of a IPMC metastasizing to the liver while maintaining its IPMC structure.

As regards the limitations of the present study, the expression of proliferating cell nuclear antigen, tumor protein p53, vascular endothelial growth factor and the KRAS mutation status were not determined due to health insurance-related restrictions. From an academic perspective, however, immunohistochemical examination must be performed to evaluate the status of carcinogenesis.

In conclusion, we herein present our experience with an autopsy case of IPMC accompanied by a long tumor thrombus in the portal vein and multifocal liver metastasis that maintained the structure of the primary pancreatic head tumor.

Acknowledgements

Not applicable.

Availability of data and materials

All data generated or analyzed during this study are included in this published article.

Authors' contributions

NM wrote the report. NM and AD were the attending physicians for the patient. NM, AD, HU, SA, KM and KY conducted the ERCP. MT made the pathological diagnosis. AD supervised the report. All the authors have read and approved the final version of the manuscript.

Ethics approval and consent to participate

Not applicable.

Patient consent for publication

The family of the patient consented to the publication of the case details and associated images.

Competing interests

The authors declare that they have no competing interests.

References

1 

Tanaka M, Fernández-Del Castillo C, Kamisawa T, Jang JY, Levy P, Ohtsuka T, Salvia R, Shimizu Y, Tada M and Wolfgang CL: Revision of international consensus Fukuoka guidelines for the management of IPMN of the pancreas. Pancreatology. 17:738–753. 2017.PubMed/NCBI View Article : Google Scholar

2 

Adsay V, Mino-Kenudson M, Furukawa T, Basturk O, Zamboni G, Marchegiani G, Bassi C, Salvia R, Malleo G, Paiella S, et al: Pathologic evaluation and reporting of intraductal papillary mucinous neoplasms of the pancreas and other tumoral intraepithelial neoplasms of pancreatobiliary tract: Recommendations of verona consensus meeting. Ann Surg. 263:162–177. 2016.PubMed/NCBI View Article : Google Scholar

3 

Adsay NV, Merati K, Basturk O, Iacobuzio-Donahue C, Levi E, Cheng JD, Sarkar FH, Hruban RH and Klimstra DS: Pathologically and biologically distinct types of epithelium in intraductal papillary mucinous neoplasms: Delineation of an ‘intestinal’ pathway of carcinogenesis in the pancreas. Am J Surg Pathol. 28:839–848. 2004.PubMed/NCBI View Article : Google Scholar

4 

Aronsson L, Andersson R and Ansari D: Intraductal papillary mucinous neoplasm of the pancreas-epidemiology, risk factors, diagnosis, and management. Scand J Gastroenterol. 52:803–815. 2017.PubMed/NCBI View Article : Google Scholar

5 

Kim J, Jang KT, Mo Park S, Lim SW, Kim JH, Lee KH, Lee JK, Heo JS, Choi SH, Choi DW, et al: Prognostic relevance of pathologic subtypes and minimal invasion in intraductal papillary mucinous neoplasms of the pancreas. Tumour Biol. 32:535–542. 2011.PubMed/NCBI View Article : Google Scholar

6 

James D: Brierley and Marry K: Gospodarowicz, Christian Wittekind. TMN Classification of Malignant Tumors, 8th ed. New York, Wiley-Blackwell, 2016.

7 

Sohn TA, Yeo CJ, Cameron JL, Hruban RH, Fukushima N, Campbell KA and Lillemoe KD: Intraductal papillary mucinous neoplasms of the pancreas an updated experience. Ann Surg. 239:788–797; discussion 797-9. 2004.PubMed/NCBI View Article : Google Scholar

8 

Murakami Y, Uemura K, Sudo T, Hayashidani Y, Hashimoto Y, Nakashima A and Sueda T: Invasive intraductal papillary-mucinous neoplasm of the pancreas: Comparison with pancreatic ductal adenocarcinoma. J Surg Oncol. 100:13–18. 2009.PubMed/NCBI View Article : Google Scholar

9 

Ueda N, Kaida D, Tomita Y, Ohnishi T, Funaki H, Fujita H, Kinami S, Nakano Y and Kosaka T: A patient with lnvasive carcinoma derived from IPMN who achieved long-term survival despite lymph node metastasis. Gan To Kagaku Ryoho. 41:2202–2204. 2014.PubMed/NCBI(In Japanese).

10 

Aşkan G, Bağci P, Memiş B and Baştürk O: Intraductal neoplasms of the pancreas: An update. Turk Patoloji Derg. 33:87–102. 2017.PubMed/NCBI View Article : Google Scholar

11 

Patel A, Lambiase L, Decarli A and Fazel A: Management of the mucin filled bile duct. A complication of intraductal papillary mucinous tumor of the pancreas. JOP. 6:255–259. 2005.PubMed/NCBI

12 

Fritz S, Hackert T, Hinz U, Hartwig W, Büchler MW and Werner J: Role of serum carbohydrate antigen 19-9 and carcinoembryonic antigen in distinguishing between benign and invasive intraductal papillary mucinous neoplasm of the pancreas. Br J Surg. 98:104–110. 2011.PubMed/NCBI View Article : Google Scholar

13 

Kim JR, Jang JY, Kang MJ, Park T, Lee SY, Jung W, Chang J, Shin Y, Han Y and Kim SW: Clinical implication of serum carcinoembryonic antigen and carbohydrate antigen 19-9 for the prediction of malignancy in intraductal papillary mucinous neoplasm of pancreas. J Hepatobiliary Pancreat Sci. 22:699–707. 2015.PubMed/NCBI View Article : Google Scholar

14 

Hirono S, Kawai M, Okada KI, Miyazawa M, Shimizu A, Kitahata Y, Ueno M, Yanagisawa A and Yamaue H: Factors associated with invasive intraductal papillary mucinous carcinoma of the pancreas. JAMA Surg. 152(e165054)2017.PubMed/NCBI View Article : Google Scholar

15 

Furukawa T: Subtyping of IPMN. Methods Mol Biol. 1882:1–8. 2019.PubMed/NCBI View Article : Google Scholar

16 

Castellano-Megías VM, Andrés CI, López-Alonso G and Colina-Ruizdelgado F: Pathological features and diagnosis of intraductal papillary mucinous neoplasm of the pancreas. World J Gastrointest Oncol. 6:311–324. 2014.PubMed/NCBI View Article : Google Scholar

17 

Masuda A, Arisaka Y, Hara S, Matsumoto I, Takenaka M, Sakai A, Shiomi H, Matsuki N, Sugimoto M, Fujita T, et al: MUC2 expression and prevalence of high-grade dysplasia and invasive carcinoma in mixed-type intraductal papillary mucinous neoplasm of the pancreas. Pancreatology. 13:583–588. 2013.PubMed/NCBI View Article : Google Scholar

18 

Tomimaru Y, Ishikawa O, Ohigashi H, Eguchi H, Yamada T, Sasaki Y, Kishi K, Takachi K, Noura S, Miyashiro I, et al: Intraductal papillary-mucinous carcinoma of the pancreas with tumor thrombus in the portal vein: A report of two cases. Hepatogastroenterology. 54:1585–1588. 2007.PubMed/NCBI

19 

D'Angelica M, Brennan MF, Suriawinata AA, Klimstra D and Conlon KC: Intraductal papillary mucinous neoplasms of the pancreas: An analysis of clinicopathologic features and outcome. Ann Surg. 239:400–408. 2004.PubMed/NCBI View Article : Google Scholar

20 

Hirono S and Yamaue H: Surgical strategy for intraductal papillary mucinous neoplasms of the pancreas. Surg today. 50:50–55. 2020.PubMed/NCBI View Article : Google Scholar

21 

McMillan MT, Lewis RS, Drebin JA, Teitelbaum UR, Lee MK, Roses RE, Fraker DL and Vollmer CM: The efficacy of adjuvant therapy for pancreatic invasive intraductal papillary mucinous neoplasm (IPMN). Cancer. 122:521–533. 2016.PubMed/NCBI View Article : Google Scholar

22 

Hirono S, Shimizu Y, Ohtsuka T, Kin T, Hara K, Kanno A, Koshita S, Hanada K, Kitano M, Inoue H, et al: Recurrence patterns after surgical resection of intraductal papillary mucinous neoplasm (IPMN) of the pancreas; a multicenter, retrospective study of 1074 IPMN patients by the Japan Pancreas Society. J Gastroentrol. 55:86–99. 2020.PubMed/NCBI View Article : Google Scholar

23 

Ochiai T, Igari K, Furuyama T, Ito H, Mitsunori Y, Aihara A, Kumagai Y, Iida M, Odajima H, Tanaka S, et al: Favorable response after Gemcitabine-Radiotherapy for invasive pancreatic intraductal papillary mucinous neoplasm: A case report. Int Surg. 98:340–345. 2013.PubMed/NCBI View Article : Google Scholar

24 

Kameyama S, Motonari H, Ishimine T and Isa T: Successful treatment with conversion surgery following chemoradiotherapy for unresectable invasive intraductal papillary mucinous neoplasm. Clin J Gastroenterol. 13:579–584. 2020.PubMed/NCBI View Article : Google Scholar

25 

Marsoner K, Haybaeck J, Csengeri D, Waha JE, Schagerl J, Langeder R, Mischinger HJ and Kornprat P: Pancreatic resection for intraductal papillary mucinous neoplasm- a thirteen-year single center experience. BMC Cancer. 16(844)2016.PubMed/NCBI View Article : Google Scholar

26 

Matsuda Y, Hagio M, Naito Z and Ishiwata T: Clinicopathological features of 30 autopsy cases of pancreatic carcinoma. J Nippon Med Sch. 79:459–467. 2012.PubMed/NCBI View Article : Google Scholar

Related Articles

Journal Cover

May-2021
Volume 14 Issue 5

Print ISSN: 2049-9450
Online ISSN:2049-9469

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Matsushita N, Douhara A, Ueno H, Asada S, Murata K, Yanase K and Tsutsumi M: Intraductal papillary‑mucinous carcinoma with portal vein tumor thrombus and multifocal liver metastasis: An autopsy case. Mol Clin Oncol 14: 101, 2021
APA
Matsushita, N., Douhara, A., Ueno, H., Asada, S., Murata, K., Yanase, K., & Tsutsumi, M. (2021). Intraductal papillary‑mucinous carcinoma with portal vein tumor thrombus and multifocal liver metastasis: An autopsy case. Molecular and Clinical Oncology, 14, 101. https://doi.org/10.3892/mco.2021.2263
MLA
Matsushita, N., Douhara, A., Ueno, H., Asada, S., Murata, K., Yanase, K., Tsutsumi, M."Intraductal papillary‑mucinous carcinoma with portal vein tumor thrombus and multifocal liver metastasis: An autopsy case". Molecular and Clinical Oncology 14.5 (2021): 101.
Chicago
Matsushita, N., Douhara, A., Ueno, H., Asada, S., Murata, K., Yanase, K., Tsutsumi, M."Intraductal papillary‑mucinous carcinoma with portal vein tumor thrombus and multifocal liver metastasis: An autopsy case". Molecular and Clinical Oncology 14, no. 5 (2021): 101. https://doi.org/10.3892/mco.2021.2263