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Pancreatic Disease: From Molecular Basis to Novel Therapies
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Pancreatic Disease: From Molecular Basis to Novel Therapies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (20 April 2024) | Viewed by 4338

Special Issue Editor

Dr. Agnieszka B. Bialkowska

E-Mail Website
Guest Editor
Department of Medicine, Renaissance School of Medicine at Stony Brook University, 101 Nicolls Road, Stony Brook, NY 11794, USA
Interests: transcription factors; Krüppel-like factor 4 (KLF4); Krüppel-Like Factor 5 (KLF5); intestinal biology; injury; inflammation; pancreatic neoplasia; pancreatic cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The pancreas, with its exocrine and endocrine functions, sits at the intersection of the body’s digestive and endocrine systems. Pancreatic acinar and ductal cells act accordantly to synthesize, store, and release digestive enzymes into pancreatic ducts, which drain into the duodenum. Pancreatic endocrine glands, called islets of Langerhans, regulate blood sugar levels by secreting two hormones into the blood: insulin and glucagon. The physiology of the pancreas is very tightly controlled, and disruptions result in pancreatitis (acute and chronic), pancreatic cancer, and Diabetes Mellitus (type 1 and 2). Several known perturbations induce acute pancreatitis, including the overactivation of trypsinogen, increased inflammatory cell infiltration, and the destruction of secretory cells. Recently, mitochondrial, lysosomal, and autophagic dysfunction, as well as calcium overload and increased endoplasmic reticulum stress, have been identified as drivers of pancreatitis progression. Chronic injury is characterized by fibro-inflammatory pathophysiology leading to the destruction of the pancreatic parenchyma. It is caused by genetic and environmental factors that are exacerbated by alcohol, nicotine, nutritional, and metabolic factors, to name a few. It has been shown that obesity, smoking, chronic pancreatitis, bacterial infections, and diabetes are primary risk factors for pancreatic cancer development. Diabetes Mellitus is characterized by impaired sugar, protein, and fat metabolism resulting from insulin deficiency. Managing pancreatic diseases has yet to be very successful. Thus, novel interventions are required that can necessitate a better understanding of the mechanisms underlying the development of pancreatic pathologies. This Special Issue highlights recent progress in understanding the physiology and pathophysiology of the pancreas and therapeutic developments.

Dr. Agnieszka B. Bialkowska
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • pancreatitis
  • acinar-to-ductal neoplasia
  • early pancreatic neoplasia
  • fibroinflammatory disease
  • pancreatic cancer
  • Diabetes Mellitus

Published Papers (4 papers)

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Research

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11 pages, 820 KiB  
Communication
Mutation Analysis of Pancreatic Juice and Plasma for the Detection of Pancreatic Cancer
by Iris J. M. Levink, Maurice P. H. M. Jansen, Zakia Azmani, Wilfred van IJcken, Ronald van Marion, Maikel P. Peppelenbosch, Djuna L. Cahen, Gwenny M. Fuhler and Marco J. Bruno
Int. J. Mol. Sci. 2023, 24(17), 13116; https://doi.org/10.3390/ijms241713116 - 23 Aug 2023
Cited by 1 | Viewed by 1142
Abstract
Molecular profiling may enable earlier detection of pancreatic cancer (PC) in high-risk individuals undergoing surveillance and allow for personalization of treatment. We hypothesized that the detection rate of DNA mutations is higher in pancreatic juice (PJ) than in plasma due to its closer [...] Read more.
Molecular profiling may enable earlier detection of pancreatic cancer (PC) in high-risk individuals undergoing surveillance and allow for personalization of treatment. We hypothesized that the detection rate of DNA mutations is higher in pancreatic juice (PJ) than in plasma due to its closer contact with the pancreatic ductal system, from which pancreatic cancer cells originate, and higher overall cell-free DNA (cfDNA) concentrations. In this study, we included patients with pathology-proven PC or intraductal papillary mucinous neoplasm (IPMN) with high-grade dysplasia (HGD) from two prospective clinical trials (KRASPanc and PACYFIC) for whom both PJ and plasma were available. We performed next-generation sequencing on PJ, plasma, and tissue samples and described the presence (and concordance) of mutations in these biomaterials. This study included 26 patients (25 PC and 1 IPMN with HGD), of which 7 were women (27%), with a median age of 71 years (IQR 12) and a median BMI of 23 kg/m2 (IQR 4). Ten patients with PC (40%) were (borderline) resectable at baseline. Tissue was available from six patients (resection n = 5, biopsy n = 1). A median volume of 2.9 mL plasma (IQR 1.0 mL) and 0.7 mL PJ (IQR 0.1 mL, p < 0.001) was used for DNA isolation. PJ had a higher median cfDNA concentration (2.6 ng/μL (IQR 4.2)) than plasma (0.29 ng/μL (IQR 0.40)). A total of 41 unique somatic mutations were detected: 24 mutations in plasma (2 KRAS, 15 TP53, 2 SMAD4, 3 CDKN2A 1 CTNNB1, and 1 PIK3CA), 19 in PJ (3 KRAS, 15 TP53, and 1 SMAD4), and 8 in tissue (2 KRAS, 2 CDKN2A, and 4 TP53). The mutation detection rate (and the concordance with tissue) did not differ between plasma and PJ. In conclusion, while the concentration of cfDNA was indeed higher in PJ than in plasma, the mutation detection rate was not different. A few cancer-associated genetic variants were detected in both biomaterials. Further research is needed to increase the detection rate and assess the performance and suitability of plasma and PJ for PC (early) detection. Full article
(This article belongs to the Special Issue Pancreatic Disease: From Molecular Basis to Novel Therapies)
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Review

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31 pages, 4651 KiB  
Review
The Importance of Intra-Islet Communication in the Function and Plasticity of the Islets of Langerhans during Health and Diabetes
by Thomas G. Hill and David J. Hill
Int. J. Mol. Sci. 2024, 25(7), 4070; https://doi.org/10.3390/ijms25074070 - 06 Apr 2024
Viewed by 595
Abstract
Islets of Langerhans are anatomically dispersed within the pancreas and exhibit regulatory coordination between islets in response to nutritional and inflammatory stimuli. However, within individual islets, there is also multi-faceted coordination of function between individual beta-cells, and between beta-cells and other endocrine and [...] Read more.
Islets of Langerhans are anatomically dispersed within the pancreas and exhibit regulatory coordination between islets in response to nutritional and inflammatory stimuli. However, within individual islets, there is also multi-faceted coordination of function between individual beta-cells, and between beta-cells and other endocrine and vascular cell types. This is mediated partly through circulatory feedback of the major secreted hormones, insulin and glucagon, but also by autocrine and paracrine actions within the islet by a range of other secreted products, including somatostatin, urocortin 3, serotonin, glucagon-like peptide-1, acetylcholine, and ghrelin. Their availability can be modulated within the islet by pericyte-mediated regulation of microvascular blood flow. Within the islet, both endocrine progenitor cells and the ability of endocrine cells to trans-differentiate between phenotypes can alter endocrine cell mass to adapt to changed metabolic circumstances, regulated by the within-islet trophic environment. Optimal islet function is precariously balanced due to the high metabolic rate required by beta-cells to synthesize and secrete insulin, and they are susceptible to oxidative and endoplasmic reticular stress in the face of high metabolic demand. Resulting changes in paracrine dynamics within the islets can contribute to the emergence of Types 1, 2 and gestational diabetes. Full article
(This article belongs to the Special Issue Pancreatic Disease: From Molecular Basis to Novel Therapies)
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20 pages, 887 KiB  
Review
Functional and Potential Therapeutic Implication of MicroRNAs in Pancreatic Cancer
by Amartya Pal, Anushka Ojha and Jingfang Ju
Int. J. Mol. Sci. 2023, 24(24), 17523; https://doi.org/10.3390/ijms242417523 - 15 Dec 2023
Cited by 2 | Viewed by 1124
Abstract
The alarmingly low five-year survival rate for pancreatic cancer presents a global health challenge, contributing to about 7% of all cancer-related deaths. Late-stage diagnosis and high heterogeneity are the biggest hurdles in treating pancreatic cancer. Thus, there is a pressing need to discover [...] Read more.
The alarmingly low five-year survival rate for pancreatic cancer presents a global health challenge, contributing to about 7% of all cancer-related deaths. Late-stage diagnosis and high heterogeneity are the biggest hurdles in treating pancreatic cancer. Thus, there is a pressing need to discover novel biomarkers that could help in early detection as well as improve therapeutic strategies. MicroRNAs (miRNAs), a class of short non-coding RNA, have emerged as promising candidates with regard to both diagnostics and therapeutics. Dysregulated miRNAs play pivotal roles in accelerating tumor growth and metastasis, orchestrating tumor microenvironment, and conferring chemoresistance in pancreatic cancer. The differential expression profiles of miRNAs in pancreatic cancer could be utilized to explore novel therapeutic strategies. In this review, we also covered studies on recent advancements in various miRNA-based therapeutics such as restoring miRNAs with a tumor-suppressive function, suppressing miRNA with an oncogenic function, and combination with chemotherapeutic drugs. Despite several challenges in terms of specificity and targeted delivery, miRNA-based therapies hold the potential to revolutionize the treatment of pancreatic cancer by simultaneously targeting multiple signaling pathways. Full article
(This article belongs to the Special Issue Pancreatic Disease: From Molecular Basis to Novel Therapies)
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Other

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11 pages, 4237 KiB  
Brief Report
Undifferentiated Carcinoma with Osteoclast-like Giant Cells of the Pancreas: Molecular Genetic Analysis of 13 Cases
by Jan Hrudka, Markéta Kalinová, Vanda Ciprová, Jana Moravcová, Radim Dvořák and Radoslav Matěj
Int. J. Mol. Sci. 2024, 25(6), 3285; https://doi.org/10.3390/ijms25063285 - 14 Mar 2024
Viewed by 623
Abstract
Undifferentiated carcinoma with osteoclast-like giant cells (UCOGC) of the pancreas is a rare malignancy regarded as a subvariant of pancreatic ductal carcinoma (PDAC) characterized by variable prognosis. UCOGC shows a strikingly similar spectrum of oncogenic DNA mutations to PDAC. In the current work, [...] Read more.
Undifferentiated carcinoma with osteoclast-like giant cells (UCOGC) of the pancreas is a rare malignancy regarded as a subvariant of pancreatic ductal carcinoma (PDAC) characterized by variable prognosis. UCOGC shows a strikingly similar spectrum of oncogenic DNA mutations to PDAC. In the current work, we analyzed the landscape of somatic mutations in a set of 13 UCOGC cases via next-generation sequencing (NGS). We detected a spectrum of pathogenic or likely pathogenic mutations similar to those observed in PDAC following previously published results (10 KRAS, 9 TP53, 4 CDKN2A, and 1 SMAD4, CIC, GNAS, APC, ATM, NF1, FBXW7, ATR, and FGFR3). Our results support the theory that UCOGC is a variant of PDAC, despite its unique morphology; however, a UCOGC-specific genomic signature as well as predictive markers remain mainly unknown. Programmed death ligand 1 (PD-L1) status remains an important predictive marker based on previous studies. Full article
(This article belongs to the Special Issue Pancreatic Disease: From Molecular Basis to Novel Therapies)
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