Objectives Information of the clinicopathological characteristics and outcome data of patients with adenosquamous carcinoma of the pancreas (ASCAP) remains limited. This study's aim is to describe the clinical, pathological, and molecular characteristics of 25 resected ASCAPs. Methods Of all 25 cases, patient characteristics, follow-up data, and pathological/immunohistological features were reviewed and analyzed. Results In this 3-institutional retrospective analysis of 562 pancreatic cancer patients, we identified 25 cases with histologically confirmed ASCAP (4.4%). Follow-up was available in 21 ASCAP and 50 pancreatic ductal adenocarcinoma control patients with a median overall survival of 8.2 and 21 months, respectively. Age, tumor size, localization in the tail, lymph node status, and resection margin seem to be the most significant factors of survival in our ASCAP cohort. In contrast to pancreatic ductal adenocarcinoma, positive expression of p63, keratins K5/14, and the epidermal growth factor receptor are a robust marker profile of these tumors. Conclusions Adenosquamous carcinoma of the pancreas comprises a group of neoplasms in which stage and adverse morphological features contribute to its bad prognosis. Further work must be pursued to improve detection and treatment options to reduce mortality. Specifically, differences in biology might become a target for the development of possible therapies.

Adenosquamous carcinoma

10.1097/mpa.0000000000001548

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Citations (17)

Platelet counts as predictors of short- and long-term outcomes in liver transplantation: cassandras or just rats on a sinking ship?

HPB (2018)

Iakovos Amygdalos Zoltán Czigány J. Böcker F. Meister Daniel Antonio Morales Santana

Youden's J statistic

Univariate analysis

10.1016/j.hpb.2018.06.2371

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The prognostic role of tumor-associated unilateral portal vein occlusion in perihilar cholangiocarcinoma

HPB (2021)

Jan Bednarsch Zoltán Czigány Lara R. Heij Tom Luedde Georg Wiltberger

10.1016/j.hpb.2021.03.012

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Laparotomy closure using an elastic suture: A promising approach

Journal of Biomedical Materials Research Part B Applied Biomaterials (2014)

Andreas Lambertz Ruben R. M. Vogels Daniel A. Busch P. Schuster Stefan Jockenhövel

Abstract Background: Midline laparotomy wound failure like burst abdomen remains one of the major complications after abdominal surgery. The use of sutures with a closer resemblance to abdominal wall physiology, like elastic threads, could decrease the risk of these complications occurring. Thus, we evaluated the possibility of using a new elastic thread composed of thermoplastic polyurethane (TPU) as a suture for the closure of midline laparotomies compared to conventionally used polypropylene (PP) in a rabbit model. Methods: The elastic TPU thread was processed and tensile tests were performed. Twenty female chinchilla rabbits underwent midline laparotomy. They were randomized to a TPU and a PP group depending on the suture used for fascia closure. After 7 or 21 days, the abdominal walls were assessed macroscopically for wound healing complications and were explanted for histopathological investigation. Results: Tensile tests showed a mean elastic elongation of 55.5% and a sufficient material strength of the TPU thread. In animal experiments, there was no difference between the groups at 7 days; however, the TPU suture showed significantly less CD68 positive cells ( p < 0.001) and a higher collagen I/III ratio ( p = 0.011) than PP did after 21 days. The amount of apoptotic cells was significantly elevated in the TPU group ( p = 0.007) after 21 days. No differences were found concerning granuloma size and number of Ki67‐positive cells. Conclusions: The newly developed TPU thread shows promising tensile characteristics. Midline laparotomy closure is feasible and safe in a rabbit model. Immunohistochemistry indicates similar biocompatibility and wound healing after implantation compared to PP after 21 days. To confirm these findings and to proof long‐term capability further studies need to be conducted. © 2014 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 103B: 417–423, 2015.

10.1002/jbm.b.33222

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Citations (15)

Postoperative outcome in premature infants with open abdomen

Hernia (2014)

Andreas Lambertz Marcel Binnebösel A Röth T Orlikowsky Ulf P. Neumann

Necrotizing Enterocolitis

Ileus

10.1007/s10029-014-1226-8

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Citations (4)

Flow Relevant Stenosis of the Celiac Artery Is an Independent Risk Factor for Postoperative Pancreatic Fistula: A Retrospective, Multicentre, International Cohort Study

HPB (2021)

Marcel den Dulk Federico Pedersoli Christiaan van der Leij Mariëlle M.E. Coolsen Anne Andert

Pancreatic fistula

Celiac artery

10.1016/j.hpb.2021.08.058

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Influence of cholestasis on portal vein embolization-induced hypertrophy of the future liver remnant

Langenbeck s Archives of Surgery (2023)

Xinwei Chang Remon Korenblik Bram Olij Robrecht R M M Knapen Christiaan van der Leij

Abstract Purpose In the pre-clinical setting, hepatocellular bile salt accumulation impairs liver regeneration following partial hepatectomy. Here, we study the impact of cholestasis on portal vein embolization (PVE)-induced hypertrophy of the future liver remnant (FLR). Methods Patients were enrolled with perihilar cholangiocarcinoma (pCCA) or colorectal liver metastases (CRLM) undergoing PVE before a (extended) right hemihepatectomy. Volume of segments II/III was considered FLR and assessed on pre-embolization and post-embolization CT scans. The degree of hypertrophy (DH, percentual increase) and kinetic growth rate (KGR, percentage/week) were used to assess PVE-induced hypertrophy. Results A total of 50 patients (31 CRLM, 19 pCCA) were included. After PVE, the DH and KGR were similar in patients with CRLM and pCCA (5.2 [3.3–6.9] versus 5.7 [3.2–7.4] %, respectively, p = 0.960 for DH; 1.4 [0.9–2.5] versus 1.9 [1.0–2.4] %/week, respectively, p = 0.742 for KGR). Moreover, pCCA patients with or without hyperbilirubinemia had comparable DH (5.6 [3.0–7.5] versus 5.7 [2.4–7.0] %, respectively, p = 0.806) and KGR (1.7 [1.0–2.4] versus 1.9 [0.8–2.4] %/week, respectively, p = 1.000). For patients with pCCA, unilateral drainage in FLR induced a higher DH than bilateral drainage (6.7 [4.9–7.9] versus 2.7 [1.5–4.2] %, p = 0.012). C-reactive protein before PVE was negatively correlated with DH ( ρ = − 0.539, p = 0.038) and KGR ( ρ = − 0.532, p = 0.041) in patients with pCCA. Conclusions There was no influence of cholestasis on FLR hypertrophy in patients undergoing PVE. Bilateral drainage and inflammation appeared to be negatively associated with FLR hypertrophy. Further prospective studies with larger and more homogenous patient cohorts are desirable.

Portal vein embolization

10.1007/s00423-023-02784-w

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Citations (1)

Hepatobiliäre Anastomosentechniken

Der Chirurg (2010)

Christoph Heidenhain R. Rösch Ulf P. Neumann

Common hepatic duct

10.1007/s00104-010-1902-x

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Citations (16)

IκB kinaseα/β control biliary homeostasis and hepatocarcinogenesis in mice by phosphorylating the cell‐death mediator receptor‐interacting protein kinase 1

Hepatology (2016)

Christiane Koppe Patricia Verheugd Jérémie Gautheron Florian Reisinger Karina Kreggenwinkel

The IκB‐Kinase (IKK) complex—consisting of the catalytic subunits, IKKα and IKKβ, as well as the regulatory subunit, NEMO—mediates activation of the nuclear factor κB (NF‐κB) pathway, but previous studies suggested the existence of NF‐κB‐independent functions of IKK subunits with potential impact on liver physiology and disease. Programmed cell death is a crucial factor in the progression of liver diseases, and receptor‐interacting kinases (RIPKs) exerts strategic control over multiple pathways involved in regulating novel programmed cell‐death pathways and inflammation. We hypothesized that RIPKs might be unrecognized targets of the catalytic IKK‐complex subunits, thereby regulating hepatocarcinogenesis and cholestasis. In this present study, mice with specific genetic inhibition of catalytic IKK activity in liver parenchymal cells (LPCs; IKKα/β LPC‐KO ) were intercrossed with RIPK1 LPC‐KO or RIPK3 −/− mice to examine whether RIPK1 or RIPK3 might be downstream targets of IKKs. Moreover, we performed in vivo phospho‐proteome analyses and in vitro kinase assays, mass spectrometry, and mutagenesis experiments. These analyses revealed that IKKα and IKKβ—in addition to their known function in NF‐κB activation—directly phosphorylate RIPK1 at distinct regions of the protein, thereby regulating cell viability. Loss of this IKKα/β‐dependent RIPK1 phosphorylation in LPCs inhibits compensatory proliferation of hepatocytes and intrahepatic biliary cells, thus impeding HCC development, but promoting biliary cell paucity and lethal cholestasis. Conclusions: IKK‐complex subunits transmit a previously unrecognized signal through RIPK1, which is fundamental for the long‐term consequences of chronic hepatic inflammation and might have potential implications for future pharmacological strategies against cholestatic liver disease and cancer. (H epatology 2016;64:1217‐1231)

IκB kinase

10.1002/hep.28723

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Citations (52)

Diagnostic Accuracy of Cross-sectional and Endoscopic Imaging in Malignant and Benign Ampullary Tumours – A Systematic Review

HPB (2023)

Anouk J. de Wilde Evelien J.M. de Jong Kurinchi Selvan Gurusamy Mohammed Abu Hilal Marc G. Besselink

Cross-sectional study

10.1016/j.hpb.2023.07.586

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