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Cancers
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Histology and Pathology of Pancreatic Cancer
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Histology and Pathology of Pancreatic Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Pathophysiology".

Deadline for manuscript submissions: closed (30 September 2024) | Viewed by 6235

Special Issue Editors

Dr. Jiaqi Shi

E-Mail Website
Guest Editor
Department of Pathology & Clinical Labs, School of Medicine, University of Michigan, Ann Arbor, MI 48109, USA
Interests: pancreas pathology; pancreatic cancer biology; tumor microenvironment; epigenetic regulation
Dr. Olca Basturk

E-Mail Website
Guest Editor
Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
Interests: pancreaticobiliary diseases; pancreas and gallbladder neoplasms

Special Issue Information

Dear Colleagues,

Pancreatic cancer is a heterogeneous group of malignant epithelial neoplasms arising from the pancreas. Pancreatic ductal adenocarcinoma (PDA) is the most common type of pancreatic cancer and is the third leading cause of cancer death in the U.S., with a dismal 12% five-year survival rate. There are many recent developments in molecular classifications, candidate targetable molecular alterations, and the important role of tumor microenvironment in pancreatic cancer. Specifically, we learn that PDAs can be molecularly classified into classical and basal subtypes, with the latter subtype carrying a much worse prognosis and less treatment response. Identifying mismatch repair protein deficient PDAs, BRCA1/2 or PALB2-mutated PDAs, and PDAs with NTRK fusion provided new biomarkers to guide therapy. Additionally, classifications of pancreatic neuroendocrine neoplasms and cystic intraductal neoplasms have been recently updated due to new molecular and clinical findings.

It is crucial to understand the interaction between PDA cells and their surroundings. Increasing evidence supports the importance of the tumor microenvironment in PDA progression and immune evasion. PDA cells interact with heterogenous cancer-associated fibroblasts, immune cells, adipocytes, endothelial, dendritic, and other cells in the tumor microenvironment to facilitate tumor growth. Cytokines, metabolites, and other signaling molecules in the tumor microenvironment also promote tumor development and maintenance.

This Special Issue will spotlight the latest advances in the histology and pathology of pancreatic cancer, focusing on the new classifications, prognosis and treatment biomarkers, and the role of the tumor microenvironment

Dr. Jiaqi Shi
Dr. Olca Basturk
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 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 cancer
  • pathology
  • classification
  • molecular mechanisms
  • tumor microenvironment

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Published Papers (3 papers)

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Research

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12 pages, 1865 KiB  
Article
The Association between Sampling and Survival in Patients with Pancreatic Ductal Adenocarcinoma Who Received Neoadjuvant Therapy and Pancreaticoduodenectomy
by Mehran Taherian, Matthew H. G. Katz, Laura R. Prakash, Dongguang Wei, Yi Tat Tong, Zongshan Lai, Deyali Chatterjee, Hua Wang, Michael Kim, Ching-Wei D. Tzeng, Naruhiko Ikoma, Robert A. Wolff, Dan Zhao, Eugene J. Koay, Anirban Maitra and Huamin Wang
Cancers 2024, 16(19), 3312; https://doi.org/10.3390/cancers16193312 - 27 Sep 2024
Viewed by 626
Abstract
Adequate sampling is essential to an accurate pathologic evaluation of pancreatectomy specimens resected for pancreatic ductal adenocarcinoma (PDAC) after neoadjuvant therapy (NAT). However, limited data are available for the association between the sampling and survival in these patients. We examined the association of [...] Read more.
Adequate sampling is essential to an accurate pathologic evaluation of pancreatectomy specimens resected for pancreatic ductal adenocarcinoma (PDAC) after neoadjuvant therapy (NAT). However, limited data are available for the association between the sampling and survival in these patients. We examined the association of the entire submission of the tumor (ESOT) and the entire submission of the pancreas (ESOP) with disease-free survival (DFS) and overall survival (OS), as well as their correlations with clinicopathologic features, for 627 patients with PDAC who received NAT and pancreaticoduodenectomy. We demonstrated that both ESOT and ESOP were associated with lower ypT, less frequent perineural invasion, and better tumor response (p < 0.05). ESOP was also associated with a smaller tumor size (p < 0.001), more lymph nodes (p < 0.001), a lower ypN stage (p < 0.001), better differentiation (p = 0.02), and less frequent lymphovascular invasion (p = 0.009). However, since ESOP and ESOT were primarily conducted for cases with no grossly identifiable tumor or minimal residual carcinoma in initial sections, potential bias cannot be excluded. Both ESOT and ESOP were associated with less frequent recurrence/metastasis and better DFS and OS (p < 0.05) in the overall study population. ESOP was associated with better DFS and better OS in patients with ypT0/ypT1 or ypN0 tumors and better OS in patients with complete or near-complete response (p < 0.05). ESOT was associated with better OS in patients with ypT0/ypT1 or ypN0 tumors (p < 0.05). Both ESOT and ESOP were independent prognostic factors for OS according to multivariate survival analyses. Therefore, accurate pathologic evaluation using ESOP and ESOT is associated with the prognosis in PDAC patients with complete or near-complete pathologic response and ypT0/ypT1 tumor after NAT. Full article
(This article belongs to the Special Issue Histology and Pathology of Pancreatic Cancer)
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Review

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18 pages, 598 KiB  
Review
Molecular Pathology of Pancreatic Cystic Lesions with a Focus on Malignant Progression
by Yan Hu, Dan Jones, Ashwini K. Esnakula, Somashekar G. Krishna and Wei Chen
Cancers 2024, 16(6), 1183; https://doi.org/10.3390/cancers16061183 - 18 Mar 2024
Viewed by 2126
Abstract
The malignant progression of pancreatic cystic lesions (PCLs) remains understudied with a knowledge gap, yet its exploration is pivotal for effectively stratifying patient risk and detecting cancer at its earliest stages. Within this review, we delve into the latest discoveries on the molecular [...] Read more.
The malignant progression of pancreatic cystic lesions (PCLs) remains understudied with a knowledge gap, yet its exploration is pivotal for effectively stratifying patient risk and detecting cancer at its earliest stages. Within this review, we delve into the latest discoveries on the molecular level, revealing insights into the IPMN molecular landscape and revised progression model, associated histologic subtypes, and the role of inflammation in the pathogenesis and malignant progression of IPMN. Low-grade PCLs, particularly IPMNs, can develop into high-grade lesions or invasive carcinoma, underscoring the need for long-term surveillance of these lesions if they are not resected. Although KRAS and GNAS remain the primary oncogenic drivers of neoplastic development in IPMNs, additional genes that are important in tumorigenesis have been recently identified by whole exome sequencing. A more complete understanding of the genes involved in the molecular progression of IPMN is critical for effective monitoring to minimize the risk of malignant progression. Complicating these strategies, IPMNs are also frequently multifocal and multiclonal, as demonstrated by comparative molecular analysis. Algorithms for preoperative cyst sampling and improved radiomic techniques are emerging to model this spatial and temporal genetic heterogeneity better. Here, we review the molecular pathology of PCLs, focusing on changes associated with malignant progression. Developing models of molecular risk stratification in PCLs which can complement radiologic and clinical features, facilitate the early detection of pancreatic cancer, and enable the development of more personalized surveillance and management strategies are summarized. Full article
(This article belongs to the Special Issue Histology and Pathology of Pancreatic Cancer)
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30 pages, 2183 KiB  
Review
Clinical Evaluation of the Pancreatic Cancer Microenvironment: Opportunities and Challenges
by Julianne M. Szczepanski, Mark A. Rudolf and Jiaqi Shi
Cancers 2024, 16(4), 794; https://doi.org/10.3390/cancers16040794 - 15 Feb 2024
Viewed by 2805
Abstract
Advances in our understanding of pancreatic ductal adenocarcinoma (PDAC) and its tumor microenvironment (TME) have the potential to transform treatment for the hundreds of thousands of patients who are diagnosed each year. Whereas the clinical assessment of cancer cell genetics has grown increasingly [...] Read more.
Advances in our understanding of pancreatic ductal adenocarcinoma (PDAC) and its tumor microenvironment (TME) have the potential to transform treatment for the hundreds of thousands of patients who are diagnosed each year. Whereas the clinical assessment of cancer cell genetics has grown increasingly sophisticated and personalized, current protocols to evaluate the TME have lagged, despite evidence that the TME can be heterogeneous within and between patients. Here, we outline current protocols for PDAC diagnosis and management, review novel biomarkers, and highlight potential opportunities and challenges when evaluating the PDAC TME as we prepare to translate emerging TME-directed therapies to the clinic. Full article
(This article belongs to the Special Issue Histology and Pathology of Pancreatic Cancer)
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