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Cancers
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Obesity: Current Insights into Its Role in Pancreatic Cancer
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Obesity: Current Insights into Its Role in Pancreatic Cancer

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

Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 13154

Special Issue Editor

Prof. Dr. Guido Eibl

E-Mail Website
Guest Editor
Departments of Surgery, David Geffen School of Medicine at UCLA, 675 Charles E Young Drive South Campus-733022, Los Angeles, CA 90095, USA
Interests: pancreatic cancer; obesity; inflammation; animal models; signaling pathways; prevention

Special Issue Information

Dear Colleagues,

Obesity is an enormous health care problem worldwide and a known risk factor for several types of cancers, including pancreatic cancer. In fact, the expected increase in mortality from pancreatic cancer may be related to the high prevalence of obesity.

Several potential mechanisms by which obesity may accelerate pancreatic cancer formation and growth have been postulated such as chronic systemic and local tissue inflammation, hyperinsulinemia and hyperglycemia, changes in adipokine production, alterations in sex and other hormones, and gut dysbiosis.

This Special Issue “Obesity: Current Insights into its Role in Pancreatic Cancer” will discuss our current understanding of obesity as a risk factor for pancreatic and its underlying mechanisms as well as the impact of obesity on advanced pancreatic cancer and response to therapy.  

Prof. Dr. Guido Eibl
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 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

  • obesity
  • pancreatic cancer
  • prevention
  • inflammation
  • mechanisms
  • animal models

Published Papers (4 papers)

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Research

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10 pages, 237 KiB  
Article
Traditional and Novel Adiposity Indicators and Pancreatic Cancer Risk: Findings from the UK Women’s Cohort Study
by Sangeetha Shyam, Darren Greenwood, Chun-Wai Mai, Seok Shin Tan, Barakatun Nisak Mohd Yusof, Foong Ming Moy and Janet Cade
Cancers 2021, 13(5), 1036; https://doi.org/10.3390/cancers13051036 - 2 Mar 2021
Cited by 4 | Viewed by 1902
Abstract
(1) Background: We studied the association of both conventional (BMI, waist and hip circumference and waist–hip ratio) and novel (UK clothing sizes) obesity indices with pancreatic cancer risk in the UK women’s cohort study (UKWCS). (2) Methods: The UKWCS recruited 35,792 women from [...] Read more.
(1) Background: We studied the association of both conventional (BMI, waist and hip circumference and waist–hip ratio) and novel (UK clothing sizes) obesity indices with pancreatic cancer risk in the UK women’s cohort study (UKWCS). (2) Methods: The UKWCS recruited 35,792 women from England, Wales and Scotland from 1995 to 1998. Cancer diagnosis and death information were obtained from the National Health Service (NHS) Central Register. Cox’s proportional hazards regression was used to evaluate the association between baseline obesity indicators and pancreatic cancer risk. (3) Results: This analysis included 35,364 participants with a median follow-up of 19.3 years. During the 654,566 person-years follow up, there were 136 incident pancreatic cancer cases. After adjustments for age, smoking, education and physical activity, each centimetre increase in hip circumference (HR: 1.03, 95% CI: 1.01–1.05, p = 0.009) and each size increase in skirt size (HR: 1.12, 95% CI: 1.02–1.23, p = 0.041) at baseline increased pancreatic cancer risk. Baseline BMI became a significant predictor of pancreatic cancer risk (HR: 1.04, 95% CI: 1.00–1.08, p = 0.050) when latent pancreatic cancer cases were removed. Only baseline hip circumference was associated with pancreatic cancer risk (HR: 1.03, 95% CI: 1.00–1.05, p = 0.017) when participants with diabetes at baseline were excluded to control for reverse causality. (4) Conclusion: Hip circumference and skirt size were significant predictors of pancreatic cancer risk in the primary analysis. Thus, hip circumference is useful to assess body shape relationships. Additionally, standard skirt sizes offer an economical and objective alternative to conventional obesity indices for evaluating pancreatic cancer risk in women. Full article
(This article belongs to the Special Issue Obesity: Current Insights into Its Role in Pancreatic Cancer)

Review

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19 pages, 963 KiB  
Review
From Liver Fat to Cancer: Perils of the Western Diet
by Ju Youn Kim, Feng He and Michael Karin
Cancers 2021, 13(5), 1095; https://doi.org/10.3390/cancers13051095 - 4 Mar 2021
Cited by 22 | Viewed by 3884
Abstract
Hepatocellular carcinoma (HCC), the most common type of primary liver cancer provides the prototypical example of an obesity-related cancer. The obesity epidemic gave rise to an enormous increase in the incidence of non-alcoholic fatty liver disease (NAFLD), a condition that affects one third [...] Read more.
Hepatocellular carcinoma (HCC), the most common type of primary liver cancer provides the prototypical example of an obesity-related cancer. The obesity epidemic gave rise to an enormous increase in the incidence of non-alcoholic fatty liver disease (NAFLD), a condition that affects one third of American adults. In about 20% of these individuals, simple liver steatosis (hepatosteatosis) progresses to non-alcoholic steatohepatitis (NASH) characterized by chronic liver injury, inflammation, and fibrosis. In addition to liver failure, NASH greatly increases the risk of HCC. Here we discuss the metabolic processes that control the progression from NAFLD to NASH and from NASH to HCC, with a special emphasis on the role of free-non-esterified cholesterol in the process. Full article
(This article belongs to the Special Issue Obesity: Current Insights into Its Role in Pancreatic Cancer)
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19 pages, 1083 KiB  
Review
Pancreatic Tumorigenesis: Oncogenic KRAS and the Vulnerability of the Pancreas to Obesity
by Yongde Luo, Xiaokun Li, Jianjia Ma, James L. Abbruzzese and Weiqin Lu
Cancers 2021, 13(4), 778; https://doi.org/10.3390/cancers13040778 - 13 Feb 2021
Cited by 9 | Viewed by 3220
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies and KRAS (Kirsten rat sarcoma 2 viral oncogene homolog) mutations have been considered a critical driver of PDAC initiation and progression. However, the effects of mutant KRAS alone do not recapitulate the [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies and KRAS (Kirsten rat sarcoma 2 viral oncogene homolog) mutations have been considered a critical driver of PDAC initiation and progression. However, the effects of mutant KRAS alone do not recapitulate the full spectrum of pancreatic pathologies associated with PDAC development in adults. Historically, mutant KRAS was regarded as constitutively active; however, recent studies have shown that endogenous levels of mutant KRAS are not constitutively fully active and its activity is still subject to up-regulation by upstream stimuli. Obesity is a metabolic disease that induces a chronic, low-grade inflammation called meta-inflammation and has long been recognized clinically as a major modifiable risk factor for pancreatic cancer. It has been shown in different animal models that obesogenic high-fat diet (HFD) and pancreatic inflammation promote the rapid development of mutant KRAS-mediated PDAC with high penetrance. However, it is not clear why the pancreas with endogenous levels of mutant KRAS is vulnerable to chronic HFD and inflammatory challenges. Recently, the discovery of fibroblast growth factor 21 (FGF21) as a novel anti-obesity and anti-inflammatory factor and as a downstream target of mutant KRAS has shed new light on this problem. This review is intended to provide an update on our knowledge of the vulnerability of the pancreas to KRAS-mediated invasive PDAC in the context of challenges engendered by obesity and associated inflammation. Full article
(This article belongs to the Special Issue Obesity: Current Insights into Its Role in Pancreatic Cancer)
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16 pages, 1673 KiB  
Review
Pancreatic Macrophages: Critical Players in Obesity-Promoted Pancreatic Cancer
by Yaroslav Teper and Guido Eibl
Cancers 2020, 12(7), 1946; https://doi.org/10.3390/cancers12071946 - 17 Jul 2020
Cited by 10 | Viewed by 3464
Abstract
Obesity is a known risk factor for the development of pancreatic cancer, one of the deadliest types of malignancies. In recent years it has become clear that the pancreatic microenvironment is critically involved and a contributing factor in accelerating pancreatic neoplasia. In this [...] Read more.
Obesity is a known risk factor for the development of pancreatic cancer, one of the deadliest types of malignancies. In recent years it has become clear that the pancreatic microenvironment is critically involved and a contributing factor in accelerating pancreatic neoplasia. In this context obesity-associated chronic inflammation plays an important role. Among several immune cells, macrophages have been shown to contribute to obesity-induced tissue inflammation. This review article summarizes the current knowledge about the role of pancreatic macrophages in early pancreatic cancer development. It describes the heterogenous origin and mixture of pancreatic macrophages, their role in pancreatic endocrine and exocrine pathology, and the impact of obesity on islet and stromal macrophages. A model is postulated, by which during obesity monocytes are recruited into the pancreas, where they are polarized into pro-inflammatory macrophages that drive early pancreatic neoplasia. This occurs in the presence of local inflammatory, metabolic, and endocrine signals. A stronger appreciation and more detailed knowledge about the role of macrophages in early pancreatic cancer development will lead to innovative preventive or interceptive strategies. Full article
(This article belongs to the Special Issue Obesity: Current Insights into Its Role in Pancreatic Cancer)
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