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A novel classification of portal venous tumor invasion to predict residual tumor status after surgery in patients with pancreatic neuroendocrine neoplasms

  • Original Article – Clinical Oncology
  • Published:
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Abstract

Purpose

To elucidate whether portal venous tumor invasion (PVTI) is a prognostic factor for patients with pancreatic neuroendocrine neoplasms (Pan-NENs).

Methods

From 2002 to 2019, 240 patients with Pan-NEN were included to examine prognostic factors. PVTI based on computed tomography (CT) images are classified into four types: no PVTI (Vp0/1), PVTI not invading the superior mesenteric vein (Vp2), PVTI invading the superior mesenteric vein or portal vein (Vp3), and PVTI invading the portal bifurcation (Vp4).

Results

Simultaneous liver metastases (SLM) determined the overall survival (OS) in 240 patients. The 5-year OS rates with and without SLM were 46% and 92%, respectively (P < 0.001). PVTIs were observed in 56 of the 240 patients (23%). Among such patients, 39, 11, and 6 had Vp2, Vp3, and Vp4, respectively. The 5-year OS rates with and without PVTI were 62% and 82%, respectively (P < 0.001). Severity of PVTI did not decide PFS and OS after R0/1 resection. There was significant difference in the prognoses between Vp0/1 and Vp2–4. In 161 patients without SLM, 21 had PVTI (13%). According to a multivariate analysis, PVTI and Ki-67 index were independent prognostic factors for progression-free survival (PFS) in patients without SLM. The 5-year PFS rates with and without PVTI were 18% and 77%, respectively (P < 0.001). The 5-year OS rates with and without PVTI were 76% and 95%, respectively (P = 0.02). PVTI was associated with tumor functionality, high serum NSE, and high Ki-67 index.

Conclusions

PVTI may be a predictor for postoperative recurrence.

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Availability of data and material

The data sets analyzed during the current study are available from the corresponding author on reasonable request.

Code availability

Not applicable.

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Acknowledgements

This work was supported by Grant-in-Aid for Scientific Research (C) 19K09041.

Funding

This work was supported by Grant-in-Aid for Scientific Research (C) (Grant Number: 19K09041).

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Authors

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The authors’ contributions are described in the separate sheet “Authorship Contribution”.

Corresponding author

Correspondence to Atsushi Kudo.

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Conflict of interest

There are no conflicts of interests for any of the authors.

Ethical approval

This study was approved by the ethics committees of the faculty of Tokyo Medical and Dental University (permission no. M2000-1080, G2017-018).

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All patients provided written informed consent for inclusion in the study.

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Supplementary Information

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432_2021_3660_MOESM1_ESM.tif

Supplementary file1 Supplemental Figure 1 The prognoses of Pan-NEN patients in the presence or absence of radiologic PVTI. a Progression-free survival. b Overall survival. Pan-NENs, pancreatic neuroendocrine neoplasms; PVTI, portal venous tumor invasion. (TIF 2390 KB)

432_2021_3660_MOESM2_ESM.tif

Supplementary file2 Supplemental Figure 2 Relationship between radiologic classification of PVTI and tumor status. a Percentage of each category. b Percentage of each category according to the primary tumor size. c Percentage of each category according to the tumor grade. NEC, neuroendocrine carcinoma; NET, neuroendocrine tumor; Pan-NENs, pancreatic neuroendocrine neoplasms; PVTI, portal venous tumor invasion. (TIF 2390 KB)

432_2021_3660_MOESM3_ESM.tif

Supplementary file3 Supplemental Figure 3 The prognoses of Pan-NEN patients according to the novel radiologic classification of PVTI. a Progression-free survival. b Overall survival. Pan-NENs, pancreatic neuroendocrine neoplasms; PVTI, portal venous tumor invasion. (TIF 2390 KB)

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Kato, T., Kudo, A., Kinowaki, Y. et al. A novel classification of portal venous tumor invasion to predict residual tumor status after surgery in patients with pancreatic neuroendocrine neoplasms. J Cancer Res Clin Oncol 148, 931–941 (2022). https://doi.org/10.1007/s00432-021-03660-0

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  • DOI: https://doi.org/10.1007/s00432-021-03660-0

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