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Advances in the Molecular Diagnosis and Treatment of Pancreatic Cancer
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Advances in the Molecular Diagnosis and Treatment of Pancreatic Cancer

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

Deadline for manuscript submissions: 20 March 2025 | Viewed by 7849

Special Issue Editors

Dr. Steven T. Brower

E-Mail Website
Guest Editor
Department of Surgical Oncology and HPB Surgery, Englewood Hospital and Medical Center, Englewood, NJ 07631, USA
Interests: pancreatic cancer; cancer prevention; bloodless medicine
Dr. Robert Pergolizzi

E-Mail Website
Guest Editor
Englewood Hospital and Medical Center, Englewood, NJ 07631, USA
Interests: genomics; mechanisms of cancer; gene therapy; vascular biology

Special Issue Information

Dear Colleagues,

Pancreatic cancer represents a formidable health challenge, characterized by its aggressive nature, late-stage diagnosis, and limited treatment options. Despite advancements in cancer research and treatment modalities, the prognosis for pancreatic cancer remains bleak, with a five-year survival rate of only about 10%. The development and implementation of molecular diagnostics and targeted therapies have emerged as promising strategies to improve outcomes for patients with pancreatic cancer.

Molecular diagnostics play a pivotal role in the accurate and early detection of pancreatic cancer. By analyzing genetic alterations, epigenetic changes, and biomarker expression profiles, molecular tests can aid in the identification of high-risk individuals, enable early-stage diagnosis, and inform personalized treatment decisions. Furthermore, molecular profiling of pancreatic tumors has led to the identification of distinct molecular subtypes, each with unique biological characteristics and potential therapeutic vulnerabilities.

Targeted therapies represent a paradigm shift in the treatment of pancreatic cancer, moving away from traditional cytotoxic chemotherapy towards more precise and effective treatment approaches. By targeting specific molecular aberrations, such as mutations in oncogenes or dysregulation of signaling pathways, targeted therapies offer the potential for enhanced efficacy and reduced toxicity compared to conventional chemotherapy. Additionally, targeted therapies can help overcome the inherent heterogeneity of pancreatic tumors, which contributes to treatment resistance and disease progression.

In this Special Issue, we examine the current landscape of molecular diagnosis and targeted treatment strategies for pancreatic cancer, highlighting the utility of precision medicine for increased understanding of cancer mechanisms. We highlight recent advancements in molecular profiling technologies, the identification of novel biomarkers, and the development of innovative, targeted therapies. These studies have led to the emergence of newer types of clinical trials, such as the “basket” trial, which have shown promise in the more rapid acquisition of data on the effectiveness of treatment modalities. Furthermore, we address the challenges and limitations associated with molecular diagnostics and targeted therapies in pancreatic cancer, as well as future directions for research and clinical practice.

Dr. Steven T. Brower
Dr. Robert G. Pergolizzi
Guest Editors

Manuscript Submission Information

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Keywords

  • pancreatic cancer
  • molecular diagnostics
  • biomarkers
  • oncogenes
  • epigenetics
  • genomic profiling
  • next-generation sequencing
  • liquid biopsy
  • precision medicine

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Published Papers (5 papers)

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Research

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23 pages, 3285 KiB  
Article
Metagenomic Study Reveals Phage–Bacterial Interactome Dynamics in Gut and Oral Microbiota in Pancreatic Diseases
by Laura Vilà-Quintana, Esther Fort, Laura Pardo, Maria T. Albiol-Quer, Maria Rosa Ortiz, Montserrat Capdevila, Anna Feliu, Anna Bahí, Marc Llirós, Adelaida García-Velasco, Mireia Morell Ginestà, Berta Laquente, Débora Pozas, Victor Moreno, Librado Jesús Garcia-Gil, Eric Jeffrey Duell, Ville Nikolai Pimenoff, Robert Carreras-Torres and Xavier Aldeguer
Int. J. Mol. Sci. 2024, 25(20), 10988; https://doi.org/10.3390/ijms252010988 - 12 Oct 2024
Viewed by 779
Abstract
Individuals with pancreatic-related health conditions usually show lower diversity and different composition of bacterial and viral species between the gut and oral microbiomes compared to healthy individuals. We performed a thorough microbiome analysis, using deep shotgun sequencing of stool and saliva samples obtained [...] Read more.
Individuals with pancreatic-related health conditions usually show lower diversity and different composition of bacterial and viral species between the gut and oral microbiomes compared to healthy individuals. We performed a thorough microbiome analysis, using deep shotgun sequencing of stool and saliva samples obtained from patients with chronic pancreatitis (CP), pancreatic ductal adenocarcinoma (PDAC), and healthy controls (HCs).We observed similar microbiota composition at the species level in both the gut and oral samples in PDAC patients compared to HCs, among which the most distinctive finding was that the abundance of oral-originated Fusobacterium nucleatum species did not differ between the oral and the gut samples. Moreover, comparing PDAC patients with HCs, Klebsiella oxytoca was significantly more abundant in the stool samples of PDAC patients, while Streptococcus spp. showed higher abundance in both the oral and stool samples of PDAC patients. Finally, the most important finding was the distinctive gut phage–bacterial interactome pattern among PDAC patients. CrAssphages, particularly Blohavirus, showed mutual exclusion with K. oxytoca species, while Burzaovirus showed co-occurrence with Enterobacteriaceae spp., which have been shown to be capable of inducing DNA damage in human pancreatic cells ex vivo. The interactome findings warrant further mechanistic studies, as our findings may provide new insights into developing microbiota-based diagnostic and therapeutic methods for pancreatic diseases. Full article
(This article belongs to the Special Issue Advances in the Molecular Diagnosis and Treatment of Pancreatic Cancer)
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20 pages, 1459 KiB  
Article
Cytokines and Pancreatic Ductal Adenocarcinoma: Exploring Their Relationship with Molecular Subtypes and Prognosis
by Laura Gutierrez-Sainz, Victoria Heredia-Soto, Ana Margarita Rodríguez-García, María Gema Crespo Sánchez, María Gemma Serrano-Olmedo, Marta Molero-Luis, Itsaso Losantos-García, Ismael Ghanem, Pablo Pérez-Wert, Ana Custodio, Marta Mendiola and Jaime Feliu
Int. J. Mol. Sci. 2024, 25(17), 9368; https://doi.org/10.3390/ijms25179368 - 29 Aug 2024
Viewed by 582
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is characterized by its poor prognosis. The current challenge remains the absence of predictive biomarkers. Cytokines are crucial factors in the pathogenesis and prognosis of PDAC. Furthermore, there is growing interest in differentiating between molecular subtypes of PDAC. The [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is characterized by its poor prognosis. The current challenge remains the absence of predictive biomarkers. Cytokines are crucial factors in the pathogenesis and prognosis of PDAC. Furthermore, there is growing interest in differentiating between molecular subtypes of PDAC. The aim of our study is to evaluate the association between the analyzed cytokines and the molecular subtypes of PDAC and to determine their prognostic value. Cytokine levels were measured in 73 patients, and molecular subtypes were analyzed in 34 of these patients. Transforming Growth Factor Beta 2 (TGF-β2) levels were independently associated with the basal-like and null subtypes. In patients with locally advanced and metastatic PDAC, elevated levels of interleukin (IL)-1α, IL-1β, IL-6, IL-8, IL-9, and IL-15 were associated with a higher risk of progression during first-line treatment, and increased levels of IL-1β, IL-6, IL-8, IL-9, and IL-15 were related to increased mortality. Furthermore, a significant association was observed between higher percentiles of IL-6 and IL-8 and shorter progression-free survival (PFS) during first-line treatment, and between higher percentiles of IL-8 and shorter overall survival (OS). In the multivariate analysis, only elevated levels of IL-8 were independently associated with a higher risk of progression during first-line treatment and mortality. In conclusion, the results of our study suggest that cytokine expression varies according to the molecular subtype of PDAC and that cytokines also play a relevant role in patient prognosis. Full article
(This article belongs to the Special Issue Advances in the Molecular Diagnosis and Treatment of Pancreatic Cancer)
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18 pages, 6042 KiB  
Article
The Wdr5-H3K4me3 Epigenetic Axis Regulates Pancreatic Tumor Immunogenicity and Immune Suppression
by Kaidi Deng, Liyan Liang, Yingcui Yang, Yanmin Wu, Yan Li, Rongrong Zhang, Yulin Tian and Chunwan Lu
Int. J. Mol. Sci. 2024, 25(16), 8773; https://doi.org/10.3390/ijms25168773 - 12 Aug 2024
Viewed by 912
Abstract
The WDR5/MLL1-H3K4me3 epigenetic axis is often activated in both tumor cells and tumor-infiltrating immune cells to drive various cellular responses in the tumor microenvironment and has been extensively studied in hematopoietic cancer, but its respective functions in tumor cells and immune cells in [...] Read more.
The WDR5/MLL1-H3K4me3 epigenetic axis is often activated in both tumor cells and tumor-infiltrating immune cells to drive various cellular responses in the tumor microenvironment and has been extensively studied in hematopoietic cancer, but its respective functions in tumor cells and immune cells in the context of tumor growth regulation of solid tumor is still incompletely understood. We report here that WDR5 exhibits a higher expression level in human pancreatic tumor tissues compared with adjacent normal pancreas. Moreover, WDR5 expression is negatively correlated with patients’ response to chemotherapy or immunotherapy in human colon cancer and melanoma. However, WDR5 expression is positively correlated with the HLA level in human cancer cells, and H3K4me3 enrichment is observed at the promoter region of the HLA-A, HLA-B, and HLA-C genes in pancreatic cancer cells. Using mouse tumor cell lines and in vivo tumor models, we determined that WDR5 deficiency or inhibition significantly represses MHC I expression in vitro and in vivo in pancreatic tumor cells. Mechanistically, we determine that WDR5 deficiency inhibits H3K4me3 deposition at the MHC I (H2K) promoter region to repress MHC I (H2K) transcription. On the other hand, WDR5 depletion leads to the effective downregulation of immune checkpoints and immunosuppressive cytokines, including TGFβ and IL6, in the pancreatic tumor microenvironments. Our data determine that WDR5 not only regulates tumor cell immunogenicity to suppress tumor growth but also activates immune suppressive pathways to promote tumor immune evasion. Selective activation of the WDR5-MHC I pathway and/or selective inhibition of the WDR5–immune checkpoint and WDR5–cytokine pathways should be considered in WDR5-based epigenetic cancer immunotherapy. Full article
(This article belongs to the Special Issue Advances in the Molecular Diagnosis and Treatment of Pancreatic Cancer)
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16 pages, 1372 KiB  
Article
Functional Copy-Number Alterations as Diagnostic and Prognostic Biomarkers in Neuroendocrine Tumors
by Hayley Vaughn, Heather Major, Evangeline Kadera, Kendall Keck, Timothy Dunham, Qining Qian, Bartley Brown, Aaron Scott, Andrew M. Bellizzi, Terry Braun, Patrick Breheny, Dawn E. Quelle, James R. Howe and Benjamin Darbro
Int. J. Mol. Sci. 2024, 25(14), 7532; https://doi.org/10.3390/ijms25147532 - 9 Jul 2024
Cited by 1 | Viewed by 3528
Abstract
Functional copy-number alterations (fCNAs) are DNA copy-number changes with concordant differential gene expression. These are less likely to be bystander genetic lesions and could serve as robust and reproducible tumor biomarkers. To identify candidate fCNAs in neuroendocrine tumors (NETs), we integrated chromosomal microarray [...] Read more.
Functional copy-number alterations (fCNAs) are DNA copy-number changes with concordant differential gene expression. These are less likely to be bystander genetic lesions and could serve as robust and reproducible tumor biomarkers. To identify candidate fCNAs in neuroendocrine tumors (NETs), we integrated chromosomal microarray (CMA) and RNA-seq differential gene-expression data from 31 pancreatic (pNETs) and 33 small-bowel neuroendocrine tumors (sbNETs). Tumors were resected from 47 early-disease-progression (<24 months) and 17 late-disease-progression (>24 months) patients. Candidate fCNAs that accurately differentiated these groups in this discovery cohort were then replicated using fluorescence in situ hybridization (FISH) on formalin-fixed, paraffin-embedded (FFPE) tissues in a larger validation cohort of 60 pNETs and 82 sbNETs (52 early- and 65 late-disease-progression samples). Logistic regression analysis revealed the predictive ability of these biomarkers, as well as the assay-performance metrics of sensitivity, specificity, and area under the curve. Our results indicate that copy-number changes at chromosomal loci 4p16.3, 7q31.2, 9p21.3, 17q12, 18q21.2, and 19q12 may be used as diagnostic and prognostic NET biomarkers. This involves a rapid, cost-effective approach to determine the primary tumor site for patients with metastatic liver NETs and to guide risk-stratified therapeutic decisions. Full article
(This article belongs to the Special Issue Advances in the Molecular Diagnosis and Treatment of Pancreatic Cancer)
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Review

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14 pages, 599 KiB  
Review
Molecular Targets for the Diagnosis and Treatment of Pancreatic Cancer
by Robert G. Pergolizzi and Steven T. Brower
Int. J. Mol. Sci. 2024, 25(19), 10843; https://doi.org/10.3390/ijms251910843 - 9 Oct 2024
Viewed by 1436
Abstract
Pancreatic cancer is one of the most aggressive and lethal forms of cancer, with a five-year survival rate of less than 10%. Despite advances in treatment modalities, the prognosis for pancreatic cancer patients remains poor, highlighting the urgent need for innovative approaches for [...] Read more.
Pancreatic cancer is one of the most aggressive and lethal forms of cancer, with a five-year survival rate of less than 10%. Despite advances in treatment modalities, the prognosis for pancreatic cancer patients remains poor, highlighting the urgent need for innovative approaches for early diagnosis and targeted therapies. In recent years, there has been significant progress in understanding the molecular mechanisms underlying pancreatic cancer development and progression. This paper reviews the current knowledge of molecular targets for the diagnosis and treatment of pancreatic cancer. Full article
(This article belongs to the Special Issue Advances in the Molecular Diagnosis and Treatment of Pancreatic Cancer)
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