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Pancreatic Ductal Adenocarcinoma

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A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (30 April 2020) | Viewed by 35360

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Dr. Alessandro Cucchetti

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Guest Editor

Department of Medical and Surgical Sciences (DIMEC), Alma Mater Studiorum-University of Bologna, 40126 Bologna, Italy
Interests: liver surgery; liver transplantation; hepatocellular carcinoma; liver metastases; cholangiocarcinoma; pancreatic surgery; pancreatic ductal adenocarcinoma; ultrasonography; statistical analysis

Dr. Carlo Alberto Pacilio

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Co-Guest Editor

Unit of General Surgery and Advanced Oncological Therapies, Morgagni-Pierantoni Hospital, 47121 Forlì, Italy
Interests: pancreatic ductal adenocarcinoma; pancreatic neuroendocrine tumors; pancreatic cystic neoplasms; intraductal papillary mucinous neoplasm; HPB surgery

Special Issue Information

Dear Colleagues,

Exocrine pancreatic cancer brings a particularly poor prognosis, and by 2030, it will probably become the second cause of cancer-related death in developed countries. Surgery remains the only potentially curative treatment, but due to the late presentation, only a minority of patients are candidates for pancreatectomy.

Most ductal adenocarcinomas are generally considered to arise from PanIN, developing as a result of a series of genetic events. Moreover, research on hereditary risk factors for pancreatic cancer (hereditary breast ovarian cancer syndrome, lynch syndrome, Peutz–Jeghers syndrome, familial pancreatic cancer, hereditary pancreatitis) has helped us to understand some of its specific molecular basis. Currently, we know that pancreatic cancer is a genetic disease that is caused by inherited and acquired mutations in specific cancer-associated genes. The main key signaling pathways dysregulated in pancreatic tumorigenesis are now understood (KRAS, TP53, p16/CDKN2A, SMAD4, MLH1, MSH2). Particularly important is the role of the KRAS oncogene, an early mutation occurring in more than 90% of pancreatic cancers. This gene can be one reliable biomarker that molecular genetics might offer to clinicians for early detection (as well as microRNAs). Furthermore, the SMAD4 gene status could also become a useful tool for prognostic stratification and therapeutic decision making. Indeed, the recognition of germline mutations in pancreatic cancer genes implies the possibility of genetic testing in order to provide clinical benefits to the patients. In addition, one of the main present challenges in this field is to identify cancer susceptibility mutations that might be therapeutically targetable (oxaliplatin in BRCA mutations or nab-paclitaxel in presence of SPARC overexpression). In the next few decades, it will be important to create an algorithm that includes biological and molecular therapies, as already happens for colorectal or breast cancer. The improvement in chemotherapeutic regimens will lead to new clinical possibilities such as considering combined resections of primary pancreatic cancer and liver metastases in highly selected patients. However, predictors of outcome are not yet identified; similarly, the oncological advantage of such procedures is still under debate and requires further investigations.

This Special Issue will highlight the role of molecular genetics in pancreatic cancer and its possible implications in early diagnosis as well as development of future target therapies. It will also focus on the growing feeling of a potential benefit of extended surgery in identified patients with oligometastatic pancreatic cancer, trying to fill the lack of evidence.

Dr. Alessandro Cucchetti
Dr. Carlo Alberto Pacilio
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

Pancreatic ductal adenocarcinoma
Pancreatic intraepithelial neoplasia
Familial pancreatic cancer
KRAS
SMAD4
MicroRNAs
Targeted therapy
Neoadjuvant therapies
Liver metastasis

Published Papers (10 papers)

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Research

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23 pages, 5386 KiB

Open AccessArticle

Profound Reprogramming towards Stemness in Pancreatic Cancer Cells as Adaptation to AKT Inhibition

by Hugo Arasanz, Carlos Hernández, Ana Bocanegra, Luisa Chocarro, Miren Zuazo, Maria Gato, Karina Ausin, Enrique Santamaría, Joaquín Fernández-Irigoyen, Gonzalo Fernandez, Eva Santamaria, Carlos Rodríguez, Idoia Blanco-Luquin, Ruth Vera, David Escors and Grazyna Kochan

Cancers 2020, 12(8), 2181; https://doi.org/10.3390/cancers12082181 - 05 Aug 2020

Cited by 7 | Viewed by 3018

Abstract

Cancer cells acquire resistance to cytotoxic therapies targeting major survival pathways by adapting their metabolism. The AKT pathway is a major regulator of human pancreatic adenocarcinoma progression and a key pharmacological target. The mechanisms of adaptation to long-term silencing of AKT isoforms of human and mouse pancreatic adenocarcinoma cancer cells were studied. Following silencing, cancer cells remained quiescent for long periods of time, after which they recovered proliferative capacities. Adaptation caused profound proteomic changes largely affecting mitochondrial biogenesis, energy metabolism and acquisition of a number of distinct cancer stem cell (CSC) characteristics depending on the AKT isoform that was silenced. The adaptation to AKT1 silencing drove most de-differentiation and acquisition of stemness through C-MYC down-modulation and NANOG upregulation, which were required for survival of adapted CSCs. The changes associated to adaptation sensitized cancer cells to inhibitors targeting regulators of oxidative respiration and mitochondrial biogenesis. In vivo pharmacological co-inhibition of AKT and mitochondrial metabolism effectively controlled pancreatic adenocarcinoma growth in pre-clinical models. Full article

(This article belongs to the Special Issue Pancreatic Ductal Adenocarcinoma)

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10 pages, 582 KiB

Open AccessArticle

The Lipase/Amylase Ratio (LAR) in Peripheral Blood Might Represent a Novel Prognostic Marker in Patients with Surgically Resectable Pancreatic Cancer

by Michael Stotz, Dominik A. Barth, Jakob M. Riedl, Eva Asamer, Eva V. Klocker, Peter Kornprat, Georg C. Hutterer, Felix Prinz, Karoline Lackner, Herbert Stöger, Armin Gerger and Martin Pichler

Cancers 2020, 12(7), 1798; https://doi.org/10.3390/cancers12071798 - 05 Jul 2020

Cited by 9 | Viewed by 4148

Abstract

Pancreatic enzymes might play a pivotal role in the pathophysiology and prognosis of pancreatic cancer. The aim of this study is to investigate the lipase/amylase ratio (LAR), representing a marker previously used in the differentiation of pancreatitis, as a potential prognostic marker in pancreatic cancer. Data from 157 surgically treated patients with ductal pancreatic adenocarcinoma and 351 patients with metastatic disease were evaluated retrospectively. Cancer-specific survival (CSS) was considered the endpoint of the study. After applying Kaplan–Meier curve analysis, uni- and multivariate Cox regression models were calculated to evaluate the prognostic relevance of LAR. An elevated LAR at diagnosis of localized pancreatic cancer was significantly associated with higher CA19-9 levels (p < 0.05). In univariate analysis, we observed an increased LAR as a significant factor for lower CSS in localized pancreatic cancer patients (HR = 1.63; 95% CI = 1.12–2.36; p = 0.01), but not in metastatic patients (HR = 1.12; 95% CI = 0.87–1.43; p = 0.363). In multivariate analysis, including age, gender, tumor stage, Karnofsky Performance Status, tumor grade, administration of chemotherapy and the LAR, an increased LAR was confirmed to represent an independent prognostic factor regarding CSS (HR = 1.81; 95% CI = 1.17–2.77; p = 0.007) in localized pancreatic cancer patients. In conclusion, our study identified the LAR as an independent prognostic factor in surgically treated pancreatic cancer patients. Full article

(This article belongs to the Special Issue Pancreatic Ductal Adenocarcinoma)

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14 pages, 2891 KiB

Open AccessArticle

Systemic Proteome Alterations Linked to Early Stage Pancreatic Cancer in Diabetic Patients

by Hong Peng, Sheng Pan, Yuanqing Yan, Randall E. Brand, Gloria M. Petersen, Suresh T. Chari, Lisa A. Lai, Jimmy K. Eng, Teresa A. Brentnall and Ru Chen

Cancers 2020, 12(6), 1534; https://doi.org/10.3390/cancers12061534 - 11 Jun 2020

Cited by 19 | Viewed by 3302

Abstract

Background: Diabetes is a risk factor associated with pancreatic ductal adenocarcinoma (PDAC), and new adult-onset diabetes can be an early sign of pancreatic malignancy. Development of blood-based biomarkers to identify diabetic patients who warrant imaging tests for cancer detection may represent a realistic approach to facilitate earlier diagnosis of PDAC in a risk population. Methods: A spectral library-based proteomic platform was applied to interrogate biomarker candidates in plasma samples from clinically well-defined diabetic cohorts with and without PDAC. Random forest algorithm was used for prediction model building and receiver operating characteristic (ROC) curve analysis was applied to evaluate the prediction probability of potential biomarker panels. Results: Several biomarker panels were cross-validated in the context of detection of PDAC within a diabetic background. In combination with carbohydrate antigen 19-9 (CA19-9), the panel, which consisted of apolipoprotein A-IV (APOA4), monocyte differentiation antigen CD14 (CD14), tetranectin (CLEC3B), gelsolin (GSN), histidine-rich glycoprotein (HRG), inter-alpha-trypsin inhibitor heavy chain H3 (ITIH3), plasma kallikrein (KLKB1), leucine-rich alpha-2-glycoprotein (LRG1), pigment epithelium-derived factor (SERPINF1), plasma protease C1 inhibitor (SERPING1), and metalloproteinase inhibitor 1 (TIMP1), demonstrated an area under curve (AUC) of 0.85 and a two-fold increase in detection accuracy compared to CA19-9 alone. The study further evaluated the correlations of protein candidates and their influences on the performance of biomarker panels. Conclusions: Proteomics-based multiplex biomarker panels improved the detection accuracy for diagnosis of early stage PDAC in diabetic patients. Full article

(This article belongs to the Special Issue Pancreatic Ductal Adenocarcinoma)

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22 pages, 4149 KiB

Open AccessArticle

Glutathione S-Transferase pi-1 Knockdown Reduces Pancreatic Ductal Adenocarcinoma Growth by Activating Oxidative Stress Response Pathways

by Rahul R. Singh, Jiyan Mohammad, Megan Orr and Katie M. Reindl

Cancers 2020, 12(6), 1501; https://doi.org/10.3390/cancers12061501 - 09 Jun 2020

Cited by 17 | Viewed by 4498

Abstract

Glutathione S-transferase pi-1 (GSTP1) plays an important role in regulating oxidative stress by conjugating glutathione to electrophiles. GSTP1 is overexpressed in breast, colon, lung, and prostate tumors, where it contributes to tumor progression and drug resistance; however, the role of GSTP1 in pancreatic ductal adenocarcinoma (PDAC) is not well understood. Using shRNA, we knocked down GSTP1 expression in three different PDAC cell lines and determined the effect on cell proliferation, cell cycle progression, and reactive oxygen species (ROS) levels. Our results show GSTP1 knockdown reduces PDAC cell growth, prolongs the G₀/G₁ phase, and elevates ROS in PDAC cells. Furthermore, GSTP1 knockdown results in the increased phosphorylation of c-Jun N-terminal kinase (JNK) and c-Jun and the decreased phosphorylation of extracellular signal-regulated kinase (ERK), p65, the reduced expression of specificity protein 1 (Sp1), and the increased expression of apoptosis-promoting genes. The addition of the antioxidant glutathione restored cell viability and returned protein expression levels to those found in control cells. Collectively, these data support the working hypothesis that the loss of GSTP1 elevates oxidative stress, which alters mitogen-activated protein (MAP) kinases and NF-κB signaling, and induces apoptosis. In support of these in vitro data, nude mice bearing orthotopically implanted GSTP1-knockdown PDAC cells showed an impressive reduction in the size and weight of tumors compared to the controls. Additionally, we observed reduced levels of Ki-67 and increased expression of cleaved caspase-3 in GSTP1-knockdown tumors, suggesting GSTP1 knockdown impedes proliferation and upregulates apoptosis in PDAC cells. Together, these results indicate that GSTP1 plays a significant role in PDAC cell growth and provides support for the pursuit of GSTP1 inhibitors as therapeutic agents for PDAC. Full article

(This article belongs to the Special Issue Pancreatic Ductal Adenocarcinoma)

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17 pages, 1681 KiB

Open AccessArticle

Metabolic Profiling of Early and Late Recurrent Pancreatic Ductal Adenocarcinoma Using Patient-Derived Organoid Cultures

by Lukas M. Braun, Simon Lagies, Rhena F. U. Klar, Saskia Hussung, Ralph M. Fritsch, Bernd Kammerer and Uwe A. Wittel

Cancers 2020, 12(6), 1440; https://doi.org/10.3390/cancers12061440 - 01 Jun 2020

Cited by 16 | Viewed by 3359

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is associated with high mortality and will become the second most common cause of cancer-associated mortality by 2030. The poor prognosis arises from a lack of sensitive biomarkers, limited therapeutic options, and the astonishingly high recurrence rate after surgery of 60–80%. The factors driving this recurrence, however, remain enigmatic. Therefore, we generated patient-derived organoids (PDOs) from early- and late-recurrent PDAC patients. Cellular identity of PDOs was confirmed by qPCR, ddPCR, and IHC analyses. This is the first study investigating the metabolism in PDOs of different, clinically significant PDAC entities by untargeted GC/MS profiling. Partial least square discriminant analysis unveiled global alterations between the two sample groups. We identified nine metabolites to be increased in early recurrent PDOs in comparison to late recurrent PDOs. More than four-times increased were fumarate, malate, glutamate, aspartate, and glutamine. Hence, α-keto acids were elevated in PDO-conditioned medium derived from early recurrent patients. We therefore speculate that an increased anaplerotic metabolism fuels the Krebs-cycle and a corresponding higher accessibility to energy fastens the recurrence in PDAC patients. Therein, a therapeutic intervention could delay PDAC recurrence and prolong survival of affected patients or could serve as biomarker to predict recurrence in the future. Full article

(This article belongs to the Special Issue Pancreatic Ductal Adenocarcinoma)

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9 pages, 390 KiB

Open AccessArticle

Decreased Activity of Circulating Butyrylcholinesterase in Blood Is an Independent Prognostic Marker in Pancreatic Cancer Patients

by Eva Valentina Klocker, Dominik Andreas Barth, Jakob Michael Riedl, Felix Prinz, Joanna Szkandera, Konstantin Schlick, Peter Kornprat, Karoline Lackner, Jörg Lindenmann, Herbert Stöger, Michael Stotz, Armin Gerger and Martin Pichler

Cancers 2020, 12(5), 1154; https://doi.org/10.3390/cancers12051154 - 04 May 2020

Cited by 9 | Viewed by 2985

Abstract

Introduction: The activity of butyrylcholinesterase (BChE) in blood reflects liver function and has recently been associated with systemic inflammatory response and tumor cachexia. As these conditions have been previously linked with pancreatic cancer (PC), the purpose of the present study was to evaluate the prognostic impact of plasma BChE in PC. Methods: Data from 574 consecutive PC patients, treated between 2004 and 2018 at a single academic center, was evaluated. The primary endpoint was cancer-specific survival (CSS), analyzed by Kaplan–Meier curve, and both univariate and multivariate Cox proportional models. Results: BChE activity negatively correlated with other liver parameters (bilirubin, gamma-glutamyl transferase (GGT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and C-reactive protein (CRP)), and positively correlated with albumin levels, respectively (p < 0.01). In univariate analysis, a low plasma BChE activity was a factor of poor CSS (hazard ratio: 1.4, 95% confidence interval: 1.129–1.754, p = 0.002). In multivariate analysis, tumor stage, tumor grade, administration of chemotherapy, bilirubin levels and a low BChE activity (hazard ratio: 1.42, 95% confidence interval: 1.10–1.82; p = 0.006) were identified as independent prognostic factors. Conclusion: Decreased activity of BChE in blood plasma predicts shorter survival time in PC patients. Therefore, BChE might be helpful in additional stratification of patients into different prognostic risk groups. Full article

(This article belongs to the Special Issue Pancreatic Ductal Adenocarcinoma)

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19 pages, 1564 KiB

Open AccessArticle

Comparison of Minimally Invasive versus Open Pancreatoduodenectomy for Pancreatic Ductal Adenocarcinoma: A Propensity Score Matching Analysis

by Jaewoo Kwon, Ki Byung Song, Seo Young Park, Dakyum Shin, Sarang Hong, Yejong Park, Woohyung Lee, Jae Hoon Lee, Dae Wook Hwang and Song Cheol Kim

Cancers 2020, 12(4), 982; https://doi.org/10.3390/cancers12040982 - 15 Apr 2020

Cited by 12 | Viewed by 2282

Abstract

Background: Few studies have compared perioperative and oncological outcomes between minimally invasive pancreatoduodenectomy (MIPD) and open pancreatoduodenectomy (OPD) for pancreatic ductal adenocarcinoma (PDAC). Methods: A retrospective review of patients undergoing MIPD and OPD for PDAC from January 2011 to December 2017 was performed. Perioperative, oncological, and survival outcomes were analyzed before and after propensity score matching (PSM). Results: Data from 1048 patients were evaluated (76 MIPD, 972 OPD). After PSM, 73 patients undergoing MIPD were matched with 219 patients undergoing OPD. Operation times were longer for MIPD than OPD (392 vs. 327 min, p < 0.001). Postoperative hospital stays were shorter for MIPD patients than OPD patients (12.4 vs. 14.2 days, p = 0.040). The rate of overall complications and postoperative pancreatic fistula did not differ between the two groups. Adjuvant treatment rates were higher following MIPD (80.8% vs. 59.8%, p = 0.002). With the exception of perineural invasion, no differences were seen between the two groups in pathological outcomes. The median overall survival and disease-free survival rates did not differ between the groups. Conclusions: MIPD showed shorter postoperative hospital stays and comparable perioperative and oncological outcomes to OPD for selected PDAC patients. Future randomized studies will be required to validate these findings. Full article

(This article belongs to the Special Issue Pancreatic Ductal Adenocarcinoma)

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16 pages, 1410 KiB

Open AccessArticle

Potential of Exosomal microRNA-200b as Liquid Biopsy Marker in Pancreatic Ductal Adenocarcinoma

by Moritz Reese, Isabelle Flammang, Zixuan Yang and Sameer A. Dhayat

Cancers 2020, 12(1), 197; https://doi.org/10.3390/cancers12010197 - 13 Jan 2020

Cited by 35 | Viewed by 3456

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a highly malignant tumor entity, characterized by rapid disease progression, early metastatic dissemination, and late diagnosis at advanced tumor stages. Recently, we explored the clinical impact of several microRNAs (miR) associated with proliferation, epithelial-to-mesenchymal transition (EMT), and chemoresistance in tissue and blood serum specimens of PDAC patients. Here, we evaluated the potential of these miRs as diagnostic and prognostic biomarkers in PDAC in serum exosomes and their respective EpCAM-positive (epithelial cell adhesion molecule) subset. Expression analysis by RT-qRT-PCR (real-time quantitative reverse transcription polymerase chain reaction) revealed an overexpression of miR-200b and miR-200c in serum exosomes of PDAC patients as compared to healthy controls (p < 0.001; p = 0.024) and patients with chronic pancreatitis (p = 0.005; p = 0.19). Receiver operating characteristic (ROC) curve analysis showed that a biomarker panel consisting of miR-200b and miR-200c from total and EpCAM-positive serum exosomes enhanced the diagnostic accuracy of carbohydrate antigen 19-9 (CA.19-9) to 97% (p < 0.0001). Univariate survival analysis revealed a correlation between shorter overall survival (OS) and high expression of miR-200c in total serum exosomes (p = 0.038) and miR-200b in EpCAM-positive serum exosomes (p = 0.032), whereas EpCAM exosomal miR-200b was also indicative of shorter OS in the subgroup of patients treated with curative intent (p = 0.013). Multivariate survival analysis showed that miR-200b derived from EpCAM-positive serum exosomes might serve as an independent prognostic factor in PDAC (p = 0.044). Our findings indicate a potential role of exosomal miR-200 as diagnostic and prognostic liquid biopsy marker in PDAC and call for validation in a larger, multicenter setting. Full article

(This article belongs to the Special Issue Pancreatic Ductal Adenocarcinoma)

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11 pages, 1132 KiB

Open AccessArticle

Predictive Nomogram for Early Recurrence after Pancreatectomy in Resectable Pancreatic Cancer: Risk Classification Using Preoperative Clinicopathologic Factors

by Naru Kim, In Woong Han, Youngju Ryu, Dae Wook Hwang, Jin Seok Heo, Dong Wook Choi and Sang Hyun Shin

Cancers 2020, 12(1), 137; https://doi.org/10.3390/cancers12010137 - 06 Jan 2020

Cited by 28 | Viewed by 3287

Abstract

The survival of patients with pancreatic ductal adenocarcinoma (PDAC) is closely related to recurrence. It is necessary to classify the risk factors for early recurrence and to develop a tool for predicting the initial outcome after surgery. Among patients with resected resectable PDAC at Samsung Medical Center (Seoul, Korea) between January 2007 and December 2016, 631 patients were classified as the training set. Analyses identifying preoperative factors affecting early recurrence after surgery were performed. When the p-value estimated from univariable Cox’s proportional hazard regression analysis was <0.05, the variables were included in multivariable analysis and used for establishing the nomogram. The established nomogram predicted the probability of early recurrence within 12 months after surgery in resectable PDAC. One thousand bootstrap resamplings were used to validate the nomogram. The concordance index was 0.665 (95% confidence interval [CI], 0.637–0.695), and the incremental area under the curve was 0.655 (95% CI, 0.631–0.682). We developed a web-based calculator, and the nomogram is freely available at http://pdac.smchbp.org/. This is the first nomogram to predict early recurrence after surgery for resectable PDAC in the preoperative setting, providing a method to allow proceeding to treatment customized according to the risk of individual patients. Full article

(This article belongs to the Special Issue Pancreatic Ductal Adenocarcinoma)

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Review

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22 pages, 866 KiB

Open AccessReview

Genetic Alterations Featuring Biological Models to Tailor Clinical Management of Pancreatic Cancer Patients

by Shannon R. Nelson and Naomi Walsh

Cancers 2020, 12(5), 1233; https://doi.org/10.3390/cancers12051233 - 14 May 2020

Cited by 5 | Viewed by 4209

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer-related death worldwide. This high mortality rate is due to the disease’s lack of symptoms, resulting in a late diagnosis. Biomarkers and treatment options for pancreatic cancer are also limited. In order to overcome this, new research models and novel approaches to discovering PDAC biomarkers are required. In this review, we outline the hereditary and somatic causes of PDAC and provide an overview of the recent genome wide association studies (GWAS) and pathway analysis studies. We also provide a summary of some of the systems used to study PDAC, including established and primary cell lines, patient-derived xenografts (PDX), and newer models such as organoids and organ-on-chip. These ex vitro laboratory systems allow for critical research into the development and progression of PDAC. Full article

(This article belongs to the Special Issue Pancreatic Ductal Adenocarcinoma)

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