Das A, Bararia A, Mukherjee S, Sikdar N. Chronic pancreatitis as a driving factor for pancreatic cancer: An epidemiological understanding. World J Clin Oncol 2024; 15(12): 1459-1462 [DOI: 10.5306/wjco.v15.i12.1459]
Corresponding Author of This Article
Nilabja Sikdar, PhD, Research Scientist, Human Genetics Unit, Indian Statistical Institute, No. 203 Plot, Barrackpore Trunk Road, Dunlop, Bonhooghly Government Colony, Kolkata 700108, India. snilabja@gmail.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Amlan Das, Department of Biochemistry, Royal Global University, Guwahati 781035, India
Akash Bararia, Nilabja Sikdar, Human Genetics Unit, Indian Statistical Institute, Kolkata 700108, India
Sanghamitra Mukherjee, Department of Pathology, R. G. Kar Medical College and Hospital, Kolkata 700004, India
Nilabja Sikdar, Scientist G, Estaurine and Costal Studies Foundation, Howrah 711101, India
Author contributions: Das A and Bararia A wrote the manuscript; Mukherjee S did the clinical evaluation of the study; Sikdar N conceptualized, edited, proofread, and corresponded the manuscript; all of the authors read and approved the final version of the manuscript to be published.
Supported byThe Department of Biotechnology, Government of India Grant Sanction, No. RLS/BT/Re-entry/05/2012.
Conflict-of-interest statement: The authors don’t have any competing interests to disclose.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Nilabja Sikdar, PhD, Research Scientist, Human Genetics Unit, Indian Statistical Institute, No. 203 Plot, Barrackpore Trunk Road, Dunlop, Bonhooghly Government Colony, Kolkata 700108, India. snilabja@gmail.com
Received: May 21, 2024 Revised: September 21, 2024 Accepted: October 8, 2024 Published online: December 24, 2024 Processing time: 153 Days and 22.8 Hours
Abstract
The retrospective study by Lew et al (2022) examined the rising hospitalization rates for chronic pancreatitis (CP) and its association with pancreatic ductal adenocarcinoma (PDAC), revealing significant ethno-racial disparities and risk factors. Overweight black men aged 40-59 years and white men over 40 years with higher incomes showed an elevated risk of PDAC among CP patients. The study, which included 14.2 million admissions from 2016-2017, found that 2.6% of adult patients were diagnosed with CP, with white males being the majority. Multivariate regression analysis identified men, black individuals, those aged 40-59 years, and individuals with a body mass index (BMI) between 25 and 29.9 as having an increased risk for CP. Moreover, 0.78% of CP patients also had PDAC, with older age and BMI being significant risk factors for developing PDAC in CP patients. The study also highlighted disparities in healthcare access and utilization among different socioeconomic and ethno-racial groups, which may impact the risk and outcomes of CP and PDAC.
Core Tip: The United States has a high incidence of pancreatic cancer (PanCa) cases that result from chronic pancreatitis (CP). This link between diseases is well-established in many scientific studies and clinical practices. In CP, the chronic inflammation of the pancreas causes DNA mutations and cellular changes that may make one prone to cancerous tumors. The CP is responsible for the persistent damage and fibrosis as a consequence of continuous inflammation of the organ over time. Such chronic inflammation promotes DNA mutations and oxidative stress, and damages cells thus leading to an increased risk of carcinogenesis. On a long-term basis, these alterations can cause the development of pancreatic intraepithelial neoplasia, a precancerous stage prior to pancreatic ductal adenocarcinoma (PDAC), which is another name for PDAC; it’s also regarded as the most prevalent type of this ailment. An example is that hereditary pancreatitis patients have up to 40% lifetime risk by age 70 years. Non-genetic CP also increases risks, although not very greatly. Development of PanCa is partly associated with CP risk factors like genetic mutations such as protease serine 1, serine protease inhibitor kazal type 1, cystic fibrosis transmembrane conductance regulator, heavy alcohol use, and smoking.
