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Cancers
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How Does Obesity Cause Cancer?
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How Does Obesity Cause Cancer?

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (30 April 2020) | Viewed by 64756

Special Issue Editor

Dr. Kyle Lee Hoehn

E-Mail Website
Guest Editor
School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW 2052, Australia
Interests: metabolism; physiology; nutrition; mitochondria; bioenergetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

There is no doubt that obesity is a strong risk factor for many types of cancer. The correlation between obesity and cancer is extremely worrisome considering that the worldwide rate of obesity in adults has doubled in the past 30 years and tripled in children. Next to smoking, obesity is labelled the second-leading preventable “cause” of cancer. The lag time between the onset of obesity and the diagnosis of cancer remains unclear, but if it is like the 20 to 30-year lag time between smoking and lung cancer, then we are only at the beginning of a new age of increased cancer incidence. Factoring in that the three-fold more obese children today are five times more likely to become obese adults, the future looks bleak unless efforts are made now to better understand how to prevent and treat obesity-related cancers.

Significant research has focused on determining how obesity causes cancer, with significant attention directed at changes in inflammation, hormones, oxidative stress, the microbiome, and circulating metabolites. However, importantly, obesity can be uncoupled from tumorigenesis in many well-defined model systems by altering the diet or microbiome without affecting adiposity, so it is a worthwhile exercise to take a step backwards and reconsider the question, “does obesity cause cancer?”

This Special Issue will highlight research that focuses on the cause versus correlation relationship between obesity and cancer.

Assoc. Prof. Dr. Kyle L. Hoehn
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. 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
  • nutrition
  • microbiome
  • risk factors

Published Papers (15 papers)

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Editorial

Jump to: Research, Review

3 pages, 179 KiB  
Editorial
How Does Obesity Cause Cancer?
by Kyle Lee Hoehn
Cancers 2021, 13(21), 5330; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13215330 - 23 Oct 2021
Cited by 1 | Viewed by 1570
Abstract
This series comprises 14 articles (5 original articles and 9 reviews) that investigate connections between excess body mass and cancer risk or cancer treatment response [...] Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)

Research

Jump to: Editorial, Review

18 pages, 2868 KiB  
Article
DPP9: Comprehensive In Silico Analyses of Loss of Function Gene Variants and Associated Gene Expression Signatures in Human Hepatocellular Carcinoma
by Jiali Carrie Huang, Abdullah Al Emran, Justine Moreno Endaya, Geoffrey W. McCaughan, Mark D. Gorrell and Hui Emma Zhang
Cancers 2021, 13(7), 1637; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13071637 - 01 Apr 2021
Cited by 8 | Viewed by 3365
Abstract
Dipeptidyl peptidase (DPP) 9, DPP8, DPP4 and fibroblast activation protein (FAP) are the four enzymatically active members of the S9b protease family. Associations of DPP9 with human liver cancer, exonic single nucleotide polymorphisms (SNPs) in DPP9 and loss of function (LoF) variants have [...] Read more.
Dipeptidyl peptidase (DPP) 9, DPP8, DPP4 and fibroblast activation protein (FAP) are the four enzymatically active members of the S9b protease family. Associations of DPP9 with human liver cancer, exonic single nucleotide polymorphisms (SNPs) in DPP9 and loss of function (LoF) variants have not been explored. Human genomic databases, including The Cancer Genome Atlas (TCGA), were interrogated to identify DPP9 LoF variants and associated cancers. Survival and gene signature analyses were performed on hepatocellular carcinoma (HCC) data. We found that DPP9 and DPP8 are intolerant to LoF variants. DPP9 exonic LoF variants were most often associated with uterine carcinoma and lung carcinoma. All four DPP4-like genes were overexpressed in liver tumors and their joint high expression was associated with poor survival in HCC. Increased DPP9 expression was associated with obesity in HCC patients. High expression of genes that positively correlated with overexpression of DPP4, DPP8, and DPP9 were associated with very poor survival in HCC. Enriched pathways analysis of these positively correlated genes featured Toll-like receptor and SUMOylation pathways. This comprehensive data mining suggests that DPP9 is important for survival and that the DPP4 protease family, particularly DPP9, is important in the pathogenesis of human HCC. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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17 pages, 781 KiB  
Article
Lifestyle Intervention on Body Weight and Physical Activity in Patients with Breast Cancer Can Reduce the Risk of Death in Obese Women: The EMILI Study
by Laura Cortesi, Federica Sebastiani, Anna Iannone, Luigi Marcheselli, Marta Venturelli, Claudia Piombino, Angela Toss and Massimo Federico
Cancers 2020, 12(7), 1709; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12071709 - 27 Jun 2020
Cited by 12 | Viewed by 2624
Abstract
Background obesity and sedentary lifestyle have been shown to negatively affect survival in breast cancer (BC). The purpose of this study was to test the efficacy of a lifestyle intervention on body mass index (BMI) and physical activity (PA) levels among BC survivors [...] Read more.
Background obesity and sedentary lifestyle have been shown to negatively affect survival in breast cancer (BC). The purpose of this study was to test the efficacy of a lifestyle intervention on body mass index (BMI) and physical activity (PA) levels among BC survivors in Modena, Italy, in order to show an outcome improvement in obese and overweight patients. Methods: This study is a single-arm experimental design, conducted between November 2009 and May 2016 on 430 women affected by BC. Weight, BMI, and PA were assessed at baseline, at 12 months, and at the end of the study. Survival curves were estimated among normal, overweight, and obese patients. Results: Mean BMI decreased from baseline to the end of the study was equal to 2.9% (p = 0.065) in overweight patients and 3.3% in obese patients (p = 0.048). Mean PA increase from baseline to the end of the study was equal to 125% (p < 0.001) in normal patients, 200% (p < 0.001) in overweight patients and 100% (p < 0.001) in obese patients. After 70 months of follow-up, the 5-year overall survival (OS) rate was 96%, 96%, and 93%, respectively in normal, obese, and overweight patients. Overweight patients had significantly worse OS than normal ones (HR = 3.69, 95%CI = 1.82–4.53 p = 0.027) whereas no statistically significant differences were seen between obese and normal patients (HR 2.45, 95%CI = 0.68–8.78, p = 0.169). Conclusions: A lifestyle intervention can lead to clinically meaningful weight loss and increase PA in patients with BC. These results could contribute to improving the OS in obese patients compared to overweight ones. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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19 pages, 1651 KiB  
Article
Assessment of Periprostatic and Subcutaneous Adipose Tissue Lipolysis and Adipocyte Size from Men with Localized Prostate Cancer
by Dushan Miladinovic, Thomas Cusick, Kate L. Mahon, Anne-Maree Haynes, Colin H. Cortie, Barbara J. Meyer, Phillip D. Stricker, Gary A. Wittert, Lisa M. Butler, Lisa G. Horvath and Andrew J. Hoy
Cancers 2020, 12(6), 1385; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12061385 - 28 May 2020
Cited by 10 | Viewed by 4888
Abstract
The prostate is surrounded by periprostatic adipose tissue (PPAT), the thickness of which has been associated with more aggressive prostate cancer (PCa). There are limited data regarding the functional characteristics of PPAT, how it compares to subcutaneous adipose tissue (SAT), and whether in [...] Read more.
The prostate is surrounded by periprostatic adipose tissue (PPAT), the thickness of which has been associated with more aggressive prostate cancer (PCa). There are limited data regarding the functional characteristics of PPAT, how it compares to subcutaneous adipose tissue (SAT), and whether in a setting of localized PCa, these traits are altered by obesity or disease aggressiveness. PPAT and SAT were collected from 60 men (age: 42–78 years, BMI: 21.3–35.6 kg/m2) undergoing total prostatectomy for PCa. Compared to SAT, adipocytes in PPAT were smaller, had the same basal rates of fatty acid release (lipolysis) yet released less polyunsaturated fatty acid species, and were more sensitive to isoproterenol-stimulated lipolysis. Basal lipolysis of PPAT was increased in men diagnosed with less aggressive PCa (Gleason score (GS) ≤ 3 + 4) compared to men with more aggressive PCa (GS ≥ 4 + 3) but no other measured adipocyte parameters related to PCa aggressiveness. Likewise, there was no difference in PPAT lipid biology between lean and obese men. In conclusion, lipid biological features of PPAT do differ from SAT; however, we did not observe any meaningful difference in ex vivo PPAT biology that is associated with PCa aggressiveness or obesity. As such, our findings do not support a relationship between altered PCa behavior in obese men and the metabolic reprogramming of PPAT. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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11 pages, 1353 KiB  
Article
Association between Abdominal Obesity and Incident Colorectal Cancer: A Nationwide Cohort Study in Korea
by Ga Eun Nam, Se-Jin Baek, Hong Bae Choi, Kyungdo Han, Jung-Myun Kwak, Jin Kim and Seon-Hahn Kim
Cancers 2020, 12(6), 1368; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12061368 - 26 May 2020
Cited by 12 | Viewed by 2415
Abstract
Background: We investigated the association of w May aist circumference (WC) and abdominal obesity with the incident colorectal cancer risk in Korean adults. Methods: This nationwide population-based cohort study was based on health insurance claims data. We analyzed data from 9,959,605 participants acquired [...] Read more.
Background: We investigated the association of w May aist circumference (WC) and abdominal obesity with the incident colorectal cancer risk in Korean adults. Methods: This nationwide population-based cohort study was based on health insurance claims data. We analyzed data from 9,959,605 participants acquired through health check-ups of the Korean National Health Insurance Service in 2009 who were followed up until the end of 2017. We performed multivariable Cox proportional hazards regression analysis. Results: During 8.3 years of follow up, 101,197 cases (1.0%) of colorectal cancer were recorded. After adjusting for potential confounders, there was a positive association between WC and colorectal cancer risk (p for trend <0.001). Abdominal obesity was associated with an increased risk of colorectal (hazard ratio: 1.10, (95% confidence interval: 1.08–1.12)), colon (1.11, 1.09–1.13), and rectal cancer (1.08, 1.05–1.10). These associations were independent of body mass index and were more pronounced in men and elderly individuals. Conclusion: We revealed that higher WC is related to colorectal cancer risk, thus suggesting that abdominal obesity may be a risk factor for colorectal cancer in this East Asian population. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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18 pages, 3410 KiB  
Article
Visfatin Mediates Malignant Behaviors through Adipose-Derived Stem Cells Intermediary in Breast Cancer
by Jyun-Yuan Huang, Yen-Yun Wang, Steven Lo, Ling-Ming Tseng, Dar-Ren Chen, Yi-Chia Wu, Ming-Feng Hou and Shyng-Shiou F. Yuan
Cancers 2020, 12(1), 29; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12010029 - 20 Dec 2019
Cited by 25 | Viewed by 3991
Abstract
Adipose-derived stem cells (ADSCs) have been implicated in tumor growth and metastasis in breast cancer. ADSCs exhibit tumor tropism, and are of increasing clinical relevance due to the autologous fat grafting for breast reconstruction. Although we have previously shown that a high level [...] Read more.
Adipose-derived stem cells (ADSCs) have been implicated in tumor growth and metastasis in breast cancer. ADSCs exhibit tumor tropism, and are of increasing clinical relevance due to the autologous fat grafting for breast reconstruction. Although we have previously shown that a high level of the adipocytokine visfatin in human breast cancer tissues correlated with tumor progression mediated by cAbl and STAT3, the effects of visfatin in the tumor microenvironment are unclear. To understand how visfatin modulates breast cancer within the tumor-stromal environment, we examined determinants of breast cancer progression using a visfatin-primed ADSCs-tumor co-culture model. ADSCs were isolated from tumor-free adipose tissue adjacent to breast tumors. ADSCs were treated with or without visfatin for 48 h and then collected for co-culture with breast cancer cell line MDA-MB-231 for 72 h in a transwell system. We found that the MDA-MB-231 cells co-cultured with visfatin-treated ADSCs (vADSCs) had higher levels of cell viability, anchorage independent growth, migration, invasion, and tumorsphere formation than that co-cultured with untreated ADSCs (uADSCs). Growth differentiation factor 15 (GDF15) upregulation was found in the co-culture conditioned medium, with GDF15 neutralizing antibody blocking the promoting effect on MDA-MB-231 in co-culture. In addition, a GDF15-induced AKT pathway was found in MDA-MB-231 and treatment with PI3K/AKT inhibitor also reversed the promoting effect. In an orthotopic xenograft mouse model, MDA-MB-231 co-injected with vADSCs formed a larger tumor mass than with uADSCs. Positive correlations were noted between visfatin, GDF15, and phosphor-AKT expressions in human breast cancer specimens. In conclusion, visfatin activated GDF15-AKT pathway mediated via ADSCs to facilitate breast cancer progression. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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Review

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22 pages, 757 KiB  
Review
Is There a Causal Relationship between Childhood Obesity and Acute Lymphoblastic Leukemia? A Review
by Molly J. Dushnicky, Samina Nazarali, Adhora Mir, Carol Portwine and Muder Constantine Samaan
Cancers 2020, 12(11), 3082; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12113082 - 22 Oct 2020
Cited by 13 | Viewed by 3670
Abstract
Childhood obesity is a growing epidemic with numerous global health implications. Over the past few years, novel insights have emerged about the contribution of adult obesity to cancer risk, but the evidence base is far more limited in children. While pediatric patients with [...] Read more.
Childhood obesity is a growing epidemic with numerous global health implications. Over the past few years, novel insights have emerged about the contribution of adult obesity to cancer risk, but the evidence base is far more limited in children. While pediatric patients with acute lymphoblastic leukemia (ALL) are at risk of obesity, it is unclear if there are potential causal mechanisms by which obesity leads to ALL development. This review explores the endocrine, metabolic and immune dysregulation triggered by obesity and its potential role in pediatric ALL’s genesis. We describe possible mechanisms, including adipose tissue attraction and protection of lymphoblasts, and their impact on ALL chemotherapies’ pharmacokinetics. We also explore the potential contribution of cytokines, growth factors, natural killer cells and adipose stem cells to ALL initiation and propagation. While there are no current definite causal links between obesity and ALL, critical questions persist as to whether the adipose tissue microenvironment and endocrine actions can play a causal role in childhood ALL, and there is a need for more research to address these questions. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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20 pages, 1038 KiB  
Review
Is Host Metabolism the Missing Link to Improving Cancer Outcomes?
by Christopher M. Wright, Anuradha A. Shastri, Emily Bongiorno, Ajay Palagani, Ulrich Rodeck and Nicole L. Simone
Cancers 2020, 12(9), 2338; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12092338 - 19 Aug 2020
Cited by 3 | Viewed by 2970
Abstract
For the past 100 years, oncologists have relentlessly pursued the destruction of tumor cells by surgical, chemotherapeutic or radiation oncological means. Consistent with this focus, treatment plans are typically based on key characteristics of the tumor itself such as disease site, histology and [...] Read more.
For the past 100 years, oncologists have relentlessly pursued the destruction of tumor cells by surgical, chemotherapeutic or radiation oncological means. Consistent with this focus, treatment plans are typically based on key characteristics of the tumor itself such as disease site, histology and staging based on local, regional and systemic dissemination. Precision medicine is similarly built on the premise that detailed knowledge of molecular alterations of tumor cells themselves enables better and more effective tumor cell destruction. Recently, host factors within the tumor microenvironment including the vasculature and immune systems have been recognized as modifiers of disease progression and are being targeted for therapeutic gain. In this review, we argue that—to optimize the impact of old and new treatment options—we need to take account of an epidemic that occurs independently of—but has major impact on—the development and treatment of malignant diseases. This is the rapidly increasing number of patients with excess weight and its’ attendant metabolic consequences, commonly described as metabolic syndrome. It is well established that patients with altered metabolism manifesting as obesity, metabolic syndrome and chronic inflammation have an increased incidence of cancer. Here, we focus on evidence that these patients also respond differently to cancer therapy including radiation and provide a perspective how exercise, diet or pharmacological agents may be harnessed to improve therapeutic responses in this patient population. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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26 pages, 1960 KiB  
Review
The Role of Dysfunctional Adipose Tissue in Pancreatic Cancer: A Molecular Perspective
by Davide Brocco, Rosalba Florio, Laura De Lellis, Serena Veschi, Antonino Grassadonia, Nicola Tinari and Alessandro Cama
Cancers 2020, 12(7), 1849; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12071849 - 09 Jul 2020
Cited by 20 | Viewed by 3859
Abstract
Pancreatic cancer (PC) is a lethal malignancy with rising incidence and limited therapeutic options. Obesity is a well-established risk factor for PC development. Moreover, it negatively affects outcome in PC patients. Excessive fat accumulation in obese, over- and normal-weight individuals induces metabolic and [...] Read more.
Pancreatic cancer (PC) is a lethal malignancy with rising incidence and limited therapeutic options. Obesity is a well-established risk factor for PC development. Moreover, it negatively affects outcome in PC patients. Excessive fat accumulation in obese, over- and normal-weight individuals induces metabolic and inflammatory changes of adipose tissue microenvironment leading to a dysfunctional adipose “organ”. This may drive the association between abnormal fat accumulation and pancreatic cancer. In this review, we describe several molecular mechanisms that underpin this association at both local and systemic levels. We focus on the role of adipose tissue-derived circulating factors including adipokines, hormones and pro-inflammatory cytokines, as well as on the impact of the local adipose tissue in promoting PC. A discussion on potential therapeutic interventions, interfering with pro-tumorigenic effects of dysfunctional adipose tissue in PC, is included. Considering the raise of global obesity, research efforts to uncover the molecular basis of the relationship between pancreatic cancer and adipose tissue dysfunction may provide novel insights for the prevention of this deadly disease. In addition, these efforts may uncover novel targets for personalized interventional strategies aimed at improving the currently unsatisfactory PC therapeutic options. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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23 pages, 1020 KiB  
Review
Current and Future Treatments in the Fight against Non-Alcoholic Fatty Liver Disease
by Benoit Smeuninx, Ebru Boslem and Mark A. Febbraio
Cancers 2020, 12(7), 1714; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12071714 - 28 Jun 2020
Cited by 28 | Viewed by 5640
Abstract
Obesity is recognised as a risk factor for many types of cancers, in particular hepatocellular carcinoma (HCC). A critical factor in the development of HCC from non-alcoholic fatty liver disease (NAFLD) is the presence of non-alcoholic steatohepatitis (NASH). Therapies aimed at NASH to [...] Read more.
Obesity is recognised as a risk factor for many types of cancers, in particular hepatocellular carcinoma (HCC). A critical factor in the development of HCC from non-alcoholic fatty liver disease (NAFLD) is the presence of non-alcoholic steatohepatitis (NASH). Therapies aimed at NASH to reduce the risk of HCC are sparse and largely unsuccessful. Lifestyle modifications such as diet and regular exercise have poor adherence. Moreover, current pharmacological treatments such as pioglitazone and vitamin E have limited effects on fibrosis, a key risk factor in HCC progression. As NAFLD is becoming more prevalent in developed countries due to rising rates of obesity, a need for directed treatment is imperative. Numerous novel therapies including PPAR agonists, anti-fibrotic therapies and agents targeting inflammation, oxidative stress and the gut-liver axis are currently in development, with the aim of targeting key processes in the progression of NASH and HCC. Here, we critically evaluate literature on the aetiology of NAFLD-related HCC, and explore the potential treatment options for NASH and HCC. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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18 pages, 940 KiB  
Review
Obesity and Breast Cancer: A Case of Inflamed Adipose Tissue
by Ryan Kolb and Weizhou Zhang
Cancers 2020, 12(6), 1686; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12061686 - 25 Jun 2020
Cited by 48 | Viewed by 6173
Abstract
Obesity is associated with an increased risk of estrogen receptor-positive breast cancer in postmenopausal women and a worse prognosis for all major breast cancer subtypes regardless of menopausal status. While the link between obesity and the pathogenesis of breast cancer is clear, the [...] Read more.
Obesity is associated with an increased risk of estrogen receptor-positive breast cancer in postmenopausal women and a worse prognosis for all major breast cancer subtypes regardless of menopausal status. While the link between obesity and the pathogenesis of breast cancer is clear, the molecular mechanism of this association is not completely understood due to the complexity of both obesity and breast cancer. The aim of this review is to highlight the association between obesity and breast cancer and discuss the literature, which indicates that this association is due to chronic adipose tissue inflammation. We will discuss the epidemiological data for the association between breast cancer incidence and progression as well as the potential molecular mechanisms for this association. We will focus on the role of inflammation within the adipose tissue during the pathogenesis of breast cancer. A better understanding of how obesity and adipose tissue inflammation affects the pathogenesis of breast cancer will lead to new strategies to reduce breast cancer risk and improve patient outcomes for obese patients. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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17 pages, 834 KiB  
Review
Obesity and the Impact on Cutaneous Melanoma: Friend or Foe?
by Lorey K. Smith, Shaghayegh Arabi, Emily J. Lelliott, Grant A. McArthur and Karen E. Sheppard
Cancers 2020, 12(6), 1583; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12061583 - 15 Jun 2020
Cited by 28 | Viewed by 3709
Abstract
Excess body weight has been identified as a risk factor for many types of cancers, and for the majority of cancers, it is associated with poor outcomes. In contrast, there are cancers in which obesity is associated with favorable outcomes and this has [...] Read more.
Excess body weight has been identified as a risk factor for many types of cancers, and for the majority of cancers, it is associated with poor outcomes. In contrast, there are cancers in which obesity is associated with favorable outcomes and this has been termed the “obesity paradox”. In melanoma, the connection between obesity and the increased incidence is not as strong as for other cancer types with some but not all studies showing an association. However, several recent studies have indicated that increased body mass index (BMI) improves survival outcomes in targeted and immune therapy treated melanoma patients. The mechanisms underlying how obesity leads to changes in therapeutic outcomes are not completely understood. This review discusses the current evidence implicating obesity in melanoma progression and patient response to targeted and immunotherapy, and discusses potential mechanisms underpinning these associations. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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20 pages, 2899 KiB  
Review
Linking Obesity with Colorectal Cancer: Epidemiology and Mechanistic Insights
by Pengfei Ye, Yue Xi, Zhiying Huang and Pengfei Xu
Cancers 2020, 12(6), 1408; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12061408 - 29 May 2020
Cited by 64 | Viewed by 7658
Abstract
The incidence of obesity and colorectal cancer (CRC) has risen rapidly in recent decades. More than 650 million obese and 2 billion overweight individuals are currently living in the world. CRC is the third most common cancer. Obesity is regarded as one of [...] Read more.
The incidence of obesity and colorectal cancer (CRC) has risen rapidly in recent decades. More than 650 million obese and 2 billion overweight individuals are currently living in the world. CRC is the third most common cancer. Obesity is regarded as one of the key environmental risk factors for the pathogenesis of CRC. In the present review, we mainly focus on the epidemiology of obesity and CRC in the world, the United States, and China. We also summarize the molecular mechanisms linking obesity to CRC in different aspects, including nutriology, adipokines and hormones, inflammation, gut microbiota, and bile acids. The unmet medical needs for obesity-related CRC are still remarkable. Understanding the molecular basis of these associations will help develop novel therapeutic targets and approaches for the treatment of obesity-related CRC. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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29 pages, 1903 KiB  
Review
Molecular Mechanisms Regulating Obesity-Associated Hepatocellular Carcinoma
by Yetirajam Rajesh and Devanand Sarkar
Cancers 2020, 12(5), 1290; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12051290 - 20 May 2020
Cited by 23 | Viewed by 5366
Abstract
Obesity is a global, intractable issue, altering inflammatory and stress response pathways, and promoting tissue adiposity and tumorigenesis. Visceral fat accumulation is correlated with primary tumor recurrence, poor prognosis and chemotherapeutic resistance. Accumulating evidence highlights a close association between obesity and an increased [...] Read more.
Obesity is a global, intractable issue, altering inflammatory and stress response pathways, and promoting tissue adiposity and tumorigenesis. Visceral fat accumulation is correlated with primary tumor recurrence, poor prognosis and chemotherapeutic resistance. Accumulating evidence highlights a close association between obesity and an increased incidence of hepatocellular carcinoma (HCC). Obesity drives HCC, and obesity-associated tumorigenesis develops via nonalcoholic fatty liver (NAFL), progressing to nonalcoholic steatohepatitis (NASH) and ultimately to HCC. The better molecular elucidation and proteogenomic characterization of obesity-associated HCC might eventually open up potential therapeutic avenues. The mechanisms relating obesity and HCC are correlated with adipose tissue remodeling, alteration in the gut microbiome, genetic factors, ER stress, oxidative stress and epigenetic changes. During obesity-related hepatocarcinogenesis, adipokine secretion is dysregulated and the nuclear factor erythroid 2 related factor 1 (Nrf-1), nuclear factor kappa B (NF-κB), mammalian target of rapamycin (mTOR), phosphatidylinositol-3-kinase (PI3K)/phosphatase and tensin homolog (PTEN)/Akt, and Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathways are activated. This review captures the present trends allied with the molecular mechanisms involved in obesity-associated hepatic tumorigenesis, showcasing next generation molecular therapeutic strategies and their mechanisms for the successful treatment of HCC. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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20 pages, 1309 KiB  
Review
The Role of Hyperglycemia in Endometrial Cancer Pathogenesis
by Frances L. Byrne, Amy R. Martin, Melidya Kosasih, Beth T. Caruana and Rhonda Farrell
Cancers 2020, 12(5), 1191; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12051191 - 08 May 2020
Cited by 34 | Viewed by 5381
Abstract
Endometrial cancer is one of the most common cancers in women worldwide and its incidence is increasing. Epidemiological evidence shows a strong association between endometrial cancer and obesity, and multiple mechanisms linking obesity and cancer progression have been described. However, it remains unclear [...] Read more.
Endometrial cancer is one of the most common cancers in women worldwide and its incidence is increasing. Epidemiological evidence shows a strong association between endometrial cancer and obesity, and multiple mechanisms linking obesity and cancer progression have been described. However, it remains unclear which factors are the main drivers of endometrial cancer development. Hyperglycemia and type 2 diabetes mellitus are common co-morbidities of obesity, and there is evidence that hyperglycemia is a risk factor for endometrial cancer independent of obesity. This review aims to explore the association between hyperglycemia and endometrial cancer, and discuss the evidence supporting a role for increased glucose metabolism in endometrial cancer and how this phenotype may contribute to endometrial cancer growth and progression. Finally, the potential role of blood glucose lowering strategies, including drugs and bariatric surgery, for the treatment of this malignancy will be discussed. Full article
(This article belongs to the Special Issue How Does Obesity Cause Cancer?)
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