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Proteomic and Genomic Profiling of Pancreatic Cancer

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

Deadline for manuscript submissions: closed (31 January 2025) | Viewed by 5767

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Guest Editor
Department of Immunology, Roswell Park Comprehensive Cancer Center, Elm & Carlton Sts. CGP/BLSC-L5307, Buffalo, NY 14263, USA
Interests: pancreatic cancer; Immunotherapy
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Special Issue Information

Dear Colleagues,

Pancreatic cancer is one of the deadliest forms of cancer, with a 5-year survival rate of 10%. The most common treatment for pancreatic cancer is surgery and chemotherapy; however, to date, both strategies have had limited success. To combat pancreatic cancer, in recent years, a significant amount of attention has been paid to immunotherapy and personalized medicine. PD1 therapy and presently available CART therapies are failing to treat pancreatic cancer, and there is a pressing need to collect more clinical biomarkers for the development of new therapeutic targets for personalized medicine. In the age of high-throughput techniques, genomics and proteomics in particular have had a significant impact on identifying mutations in oncogenes such as KRAS and other relevant new biomarkers for chemotherapy and immunotherapy. In addition, proteomic profiling of pancreatic cancer targeting secretomes will provide further insight into the tumor microenvironment, leading to a pivotal understanding of pancreatic cancer progression and immune response. Using the current understanding of immunotherapy, genomics and proteomics analysis of pancreatic cancer patient samples will lead to the discovery of new targets that will help in the development of novel therapeutics.

Dr. Aftab Alam
Guest Editor

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Keywords

  • pancreatic cancer
  • CART
  • chemotherapy
  • immunotherapy
  • PD1
  • biomarker
  • personalized medicine
  • secretome
  • genomics
  • proteomics
  • tumor microenvironment

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Published Papers (2 papers)

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Research

21 pages, 12068 KiB  
Article
Honey Targets Ribosome Biogenesis Components to Suppress the Growth of Human Pancreatic Cancer Cells
by Aun Ali Bangash, Sahir Sultan Alvi, Muhammad Ali Bangash, Haider Ahsan, Shiza Khan, Rida Shareef, Georgina Villanueva, Divyam Bansal, Mudassier Ahmad, Dae Joon Kim, Subhash C. Chauhan and Bilal Bin Hafeez
Cancers 2024, 16(19), 3431; https://doi.org/10.3390/cancers16193431 - 9 Oct 2024
Cited by 3 | Viewed by 2258
Abstract
Pancreatic cancer (PanCa) is one of the deadliest cancers, with limited therapeutic response. Various molecular oncogenic events, including dysregulation of ribosome biogenesis, are linked to the induction, progression, and metastasis of PanCa. Thus, the discovery of new therapies suppressing these oncogenic events and [...] Read more.
Pancreatic cancer (PanCa) is one of the deadliest cancers, with limited therapeutic response. Various molecular oncogenic events, including dysregulation of ribosome biogenesis, are linked to the induction, progression, and metastasis of PanCa. Thus, the discovery of new therapies suppressing these oncogenic events and ribosome biogenesis could be a novel therapeutic approach for the prevention and treatment of PanCa. The current study was designed to investigate the anti-cancer effect of honey against PanCa. Our results indicated that honey markedly inhibited the growth and invasive characteristics of pancreatic cancer cells by suppressing the mRNA expression and protein levels of key components of ribosome biogenesis, including RNA Pol-I subunits (RPA194 and RPA135) along with its transcriptional regulators, i.e., UBTF and c-Myc. Honey also induced nucleolar stress in PanCa cells by reducing the expression of various nucleolar proteins (NCL, FBL, and NPM). Honey-mediated regulation on ribosome biogenesis components and nucleolar organization-associated proteins significantly arrested the cell cycle in the G2M phase and induced apoptosis in PanCa cells. These results, for the first time, demonstrated that honey, being a natural remedy, has the potential to induce apoptosis and inhibit the growth and metastatic phenotypes of PanCa by targeting ribosome biogenesis. Full article
(This article belongs to the Special Issue Proteomic and Genomic Profiling of Pancreatic Cancer)
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17 pages, 7308 KiB  
Article
Molecular and Clinical Features of Pancreatic Acinar Cell Carcinoma: A Single-Institution Case Series
by Ashwathy Balachandran Pillai, Mahmoud Yousef, Abdelrahman Yousef, Kristin D. Alfaro-Munoz, Brandon G. Smaglo, Jason Willis, Robert A. Wolff, Shubham Pant, Mark W. Hurd, Anirban Maitra, Huamin Wang, Matthew Harold G. Katz, Laura R. Prakash, Ching-Wei D. Tzeng, Rebecca Snyder, Luca F. Castelnovo, Anthony Chen, Andrey Kravets, Kseniia Kudriavtseva, Artem Tarasov, Kirill Kryukov, Haoqiang Ying, John Paul Shen and Dan Zhaoadd Show full author list remove Hide full author list
Cancers 2024, 16(19), 3421; https://doi.org/10.3390/cancers16193421 - 9 Oct 2024
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Abstract
Objectives: Acinar cell carcinoma (ACC) accounts for about 1% of pancreatic cancers. The molecular and clinical features of ACC are less characterized than those of pancreatic ductal adenocarcinoma. Methods: We retrospectively evaluated the clinical and molecular features of ACC patients who underwent [...] Read more.
Objectives: Acinar cell carcinoma (ACC) accounts for about 1% of pancreatic cancers. The molecular and clinical features of ACC are less characterized than those of pancreatic ductal adenocarcinoma. Methods: We retrospectively evaluated the clinical and molecular features of ACC patients who underwent germline and/or somatic molecular testing at The University of Texas MD Anderson Cancer Center from 2008 to 2022 and two cases from 2023–2024 who underwent RNA and TME analysis by Boston Gene. Patient information was extracted from our institutional database with the approval of the Institutional Review Board. Results: We identified 16 patients with available molecular testing results. Fourteen patients had metastatic disease, one had borderline resectable disease, and one had localized resectable disease at diagnosis. Fifteen patients were wild type for KRAS (one patient had unknown KRAS status). Somatic/germline mutations of DNA damage repair genes (BRCA1/2, PALB2, and ATM) were present in 5 of 12 patients tested for these genes. One patient was found to have RET fusion and responded favorably to selpercatinib for over 42 months. The median overall survival (OS) was 24 months for patients with metastatic disease. One of the additional two cases who underwent BostonGene testing was found to have NTRK1 fusion. RNA and TME analysis by Boston Gene of the two cases reported immune desert features and relatively lower RNA levels of CEACAM5, CD47, CD74, and MMP1 and higher RNA levels of CDH6 compared with PDAC. Full article
(This article belongs to the Special Issue Proteomic and Genomic Profiling of Pancreatic Cancer)
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