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Nutrients
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Nutrition and Cancer: From Prevention to After-Care
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Nutrition and Cancer: From Prevention to After-Care

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Public Health".

Deadline for manuscript submissions: 25 March 2025 | Viewed by 5731

Special Issue Editor

Prof. Dr. Zhenhua Liu

E-Mail Website
Guest Editor
1. Department of Nutrition, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA 01003, USA
2. UMass Cancer Center, Chan Medical School, University of Massachusetts, Worcester, MA 01655, USA
Interests: micronutrients; dietary bioactive components; traditional chinese medicine; nutritional epigenetics; obesity and inflammation; gastrointestinal health; cancer prevention

Special Issue Information

Dear Colleagues,

The prevalence of cancer is anticipated to steadily increase in the upcoming years, paralleled by a notable rise in the number of cancer survivors, owing to improved survival rates in recent decades. Cancer development is intricately influenced by a range of genetic, environmental and lifestyle factors. Notably, nutrition emerges as a malleable and impactful component, serving as both a protective barrier against the initiation of cancer and a complementary therapeutic tool in its management. This in-depth exploration into the intersection of nutrition and cancer will cover the entire spectrum, from pre-diagnosis to survivorship.

We invite contributions from various research domains, including laboratory studies, epidemiological investigations and comprehensive reviews, delving into the roles played by diet, nutrition, bioactive components in foods and lifestyle factors. These studies aim to elucidate how these elements can prevent the onset of cancer, aid individuals in overcoming treatment-related side effects and enhance the overall quality of life for cancer survivors. We welcome you to join us on this journey as we navigate the evolving terrain of nutrition and cancer, seeking insights that empower individuals to make informed dietary choices regarding the prevention treatment and optimal care post-cancer.

Prof. Dr. Zhenhua Liu
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 short 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. Nutrients 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

  • cancer prevention, treatment and post-care
  • diet and nutrition
  • foods and dietary bioactive components
  • traditional Chinese medicine
  • obesity

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Published Papers (4 papers)

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Research

18 pages, 5783 KiB  
Article
The Impact of a Ketogenic Diet on Late-Stage Pancreatic Carcinogenesis in Mice: Efficacy and Safety Studies
by Natalia E. Cortez, Tarek A. Bacha, Aya Samir Ead, Cecilia Rodriguez Lanzi, Cassandra Lacroix, Anais Franceschetti, Brian V. Hong, Karen Matsukuma and Gerardo G. Mackenzie
Nutrients 2024, 16(22), 3919; https://doi.org/10.3390/nu16223919 (registering DOI) - 16 Nov 2024
Viewed by 483
Abstract
Background: High-fat diets (HFDs) have been associated with an increased risk of pancreatic cancer. In contrast, ketogenic diets (KDs) have been shown to display anti-tumor characteristics. The objective of this work was to evaluate the efficacy of a KD on late-stage pancreatic carcinogenesis [...] Read more.
Background: High-fat diets (HFDs) have been associated with an increased risk of pancreatic cancer. In contrast, ketogenic diets (KDs) have been shown to display anti-tumor characteristics. The objective of this work was to evaluate the efficacy of a KD on late-stage pancreatic carcinogenesis in a genetically modified mouse model of pancreatic cancer [LSL-KrasG12D/+; Ptf1-Cre (KC) mice], as well as its liver safety, and to compare it to that of an HFD. Methods: Six-month-old female and male KC mice were randomly allocated to either a control diet (CD) (%kcal: 20% fat, 15% protein, 65% carbohydrates), an HFD (%kcal: 40% fat, 15% protein, 45% carbohydrate) or a KD (%kcal: 84% fat, 15% protein, 1% carbohydrate) and fed these diets for 6 months. Results: HFD-fed, but not KD-fed, mice showed a 15% increase in body weight, plus elevated serum insulin (2.4-fold increase) and leptin (2.9-fold increase) levels, compared to CD-fed mice. At the pancreas level, no differences in pancreatic cancer incidence rates were observed among the diet groups. Regarding the liver safety profile, the HFD-fed mice had higher serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP), when compared to the CD and KD groups. In addition, upon histologic examination, an HFD, but not a KD, showed a ~2-fold increase in both macro- and microsteatosis, as well as 35% and 32% higher levels of TLR4 and NF-κB activation, respectively, compared to CD-fed mice. Conclusions: In summary, although a KD intervention alone did not prevent pancreatic carcinogenesis, our data suggests that a KD modulates insulin signaling and hepatic lipid metabolism, highlighting its beneficial effects on healthspan and liver function when compared to an HFD. Full article
(This article belongs to the Special Issue Nutrition and Cancer: From Prevention to After-Care)
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12 pages, 2627 KiB  
Article
Efficacy of 1-Kestose Supplementation in Patients with Pancreatic Ductal Adenocarcinoma: A Randomized Controlled Pilot Study
by Kazunori Nakaoka, Eizaburo Ohno, Kento Kuramitsu, Teiji Kuzuya, Kohei Funasaka, Takumi Tochio, Tadashi Fujii, Hideaki Takahashi, Nobuhiro Kondo, Ryoji Miyahara, Senju Hashimoto and Yoshiki Hirooka
Nutrients 2024, 16(17), 2889; https://doi.org/10.3390/nu16172889 - 29 Aug 2024
Viewed by 1585
Abstract
Less than half of all patients diagnosed with pancreatic ductal adenocarcinoma (PDAC) respond to chemotherapy, and the prognosis of PDAC is poor, which may be mediated by the gut microbiota. We investigated the clinical improvement effects of 1-kestose, a fructooligosaccharide, on PDAC chemotherapy [...] Read more.
Less than half of all patients diagnosed with pancreatic ductal adenocarcinoma (PDAC) respond to chemotherapy, and the prognosis of PDAC is poor, which may be mediated by the gut microbiota. We investigated the clinical improvement effects of 1-kestose, a fructooligosaccharide, on PDAC chemotherapy in this single-center, randomized, controlled pilot trial conducted at Fujita Health University Hospital, which enrolled patients with PDAC. The trial included 1-kestose administration and non-administration groups. The 1-kestose group received 9 g of 1-kestose daily for 12 weeks, and their blood markers, imaging studies, physical findings, and gut microbiota were evaluated. In the 1-kestose administration group, the cancer marker CA19-9 significantly decreased, and there was a reduction in the neutrophil-to-lymphocyte ratio (NLR). There was also suppression of the reduction of albumin levels and of an increase in C-reactive protein. Additionally, Escherichia coli, which typically increases in PDAC, significantly decreased in the 1-kestose group. Thus, 1-kestose altered the gut microbiota and improved the prognostic factors for PDAC. Large-scale, long-term trials of 1-kestose interventions for PDAC are thus warranted to improve the prognosis of PDAC. Full article
(This article belongs to the Special Issue Nutrition and Cancer: From Prevention to After-Care)
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20 pages, 5729 KiB  
Article
Antrodia camphorata Supplementation during Early Life Alters Gut Microbiota and Inhibits Young-Onset Intestinal Tumorigenesis in APC1638N Mice Later in Life
by Tingchun Lin, Lauren Daddi, Ying Tang, Yanjiao Zhou, Buping Liu, Matthew D. Moore and Zhenhua Liu
Nutrients 2024, 16(15), 2408; https://doi.org/10.3390/nu16152408 - 25 Jul 2024
Viewed by 1196
Abstract
Young-onset colorectal cancer is an increasing concern worldwide due to the growing prevalence of Westernized lifestyles in childhood and adolescence. Environmental factors during early life, particularly early-life nutrition, significantly contribute to the increasing incidence. Recently, there have been reports of beneficial effects, including [...] Read more.
Young-onset colorectal cancer is an increasing concern worldwide due to the growing prevalence of Westernized lifestyles in childhood and adolescence. Environmental factors during early life, particularly early-life nutrition, significantly contribute to the increasing incidence. Recently, there have been reports of beneficial effects, including anti-inflammation and anti-cancer, of a unique fungus (Antrodia camphorate, AC) native to Taiwan. The objective of this study is to investigate the impact of AC supplementation in early life on the development of young-onset intestinal tumorigenesis. APC1638N mice were fed with a high-fat diet (HF) at 4–12 weeks of age, which is equivalent to human childhood/adolescence, before switching to a normal maintenance diet for an additional 12 weeks up to 24 weeks of age, which is equivalent to young to middle adulthood in humans. Our results showed that the body weight in the HF groups significantly increased after 8 weeks of feeding (p < 0.05). Following a switch to a normal maintenance diet, the change in body weight persisted. AC supplementation significantly suppressed tumor incidence and multiplicity in females (p < 0.05) and reduced IGF-1 and Wnt/β-catenin signaling (p < 0.05). Moreover, it altered the gut microbiota, suppressed inflammatory responses, and created a microenvironment towards suppressing tumorigenesis later in life. Full article
(This article belongs to the Special Issue Nutrition and Cancer: From Prevention to After-Care)
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25 pages, 11130 KiB  
Article
Modeling of Intracellular Taurine Levels Associated with Ovarian Cancer Reveals Activation of p53, ERK, mTOR and DNA-Damage-Sensing-Dependent Cell Protection
by Daniel Centeno, Sadaf Farsinejad, Elena Kochetkova, Tatiana Volpari, Aleksandra Gladych-Macioszek, Agnieszka Klupczynska-Gabryszak, Teagan Polotaye, Michael Greenberg, Douglas Kung, Emily Hyde, Sarah Alshehri, Tonja Pavlovic, William Sullivan, Szymon Plewa, Helin Vakifahmetoglu-Norberg, Frederick J. Monsma, Jr., Patricia A. J. Muller, Jan Matysiak, Mikołaj Piotr Zaborowski, Analisa DiFeo, Erik Norberg, Laura A. Martin and Marcin Iwanickiadd Show full author list remove Hide full author list
Nutrients 2024, 16(12), 1816; https://doi.org/10.3390/nu16121816 - 9 Jun 2024
Viewed by 1907
Abstract
Taurine, a non-proteogenic amino acid and commonly used nutritional supplement, can protect various tissues from degeneration associated with the action of the DNA-damaging chemotherapeutic agent cisplatin. Whether and how taurine protects human ovarian cancer (OC) cells from DNA damage caused by cisplatin is [...] Read more.
Taurine, a non-proteogenic amino acid and commonly used nutritional supplement, can protect various tissues from degeneration associated with the action of the DNA-damaging chemotherapeutic agent cisplatin. Whether and how taurine protects human ovarian cancer (OC) cells from DNA damage caused by cisplatin is not well understood. We found that OC ascites-derived cells contained significantly more intracellular taurine than cell culture-modeled OC. In culture, elevation of intracellular taurine concentration to OC ascites-cell-associated levels suppressed proliferation of various OC cell lines and patient-derived organoids, reduced glycolysis, and induced cell protection from cisplatin. Taurine cell protection was associated with decreased DNA damage in response to cisplatin. A combination of RNA sequencing, reverse-phase protein arrays, live-cell microscopy, flow cytometry, and biochemical validation experiments provided evidence for taurine-mediated induction of mutant or wild-type p53 binding to DNA, activation of p53 effectors involved in negative regulation of the cell cycle (p21), and glycolysis (TIGAR). Paradoxically, taurine’s suppression of cell proliferation was associated with activation of pro-mitogenic signal transduction including ERK, mTOR, and increased mRNA expression of major DNA damage-sensing molecules such as DNAPK, ATM and ATR. While inhibition of ERK or p53 did not interfere with taurine’s ability to protect cells from cisplatin, suppression of mTOR with Torin2, a clinically relevant inhibitor that also targets DNAPK and ATM/ATR, broke taurine’s cell protection. Our studies implicate that elevation of intracellular taurine could suppress cell growth and metabolism, and activate cell protective mechanisms involving mTOR and DNA damage-sensing signal transduction. Full article
(This article belongs to the Special Issue Nutrition and Cancer: From Prevention to After-Care)
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