scholarly journals Pulses and carcinogenesis: potential for the prevention of colon, breast and other cancers

2002 ◽  
Vol 88 (S3) ◽  
pp. 273-279 ◽  
Author(s):  
John C. Mathers
Keyword(s):  
Cancer Risk ◽  
Evidence Base ◽  
Mechanisms Of Action ◽  
Gene Interactions ◽  
Non Communicable Diseases ◽  
Biological Basis ◽  
Rich Variety ◽  
Healthy Diets ◽  
Quantitative Contribution

Consumption of pulses as components of healthy diets is encouraged because it is believed that this is likely to help in reducing the risk of common non-communicable diseases, including cancers. However, the evidence base for the role of pulses in prevention of cancers is unconvincing because of the difficulties, using conventional epidemiological tools, in ascertaining the quantitative contribution made by pulses to cancer risk. Advances in understanding of the biological basis of cancer and of the mechanisms of action of cancer-preventing compounds offer new insights into the role of food-derived substances and of diet—gene interactions in modulating cancer risk. Pulses contain a rich variety of compounds which, if consumed in sufficient quantities, may help to reduce tumour risk.

scholarly journals The Role of Diet in Cancer Prevention and Chemotherapy Efficacy

2020 ◽  
Vol 40 (1) ◽  
pp. 273-297 ◽  
Author(s):  
Steven D. Mittelman
Keyword(s):  
Cancer Risk ◽  
Disease Prevention ◽  
Cancer Treatment ◽  
Cancer Patients ◽  
Healthy Diets ◽  
Diet And Cancer ◽  
Obesity And Cancer ◽  
Chemotherapy Efficacy

Despite great advances in treatment, cancer remains a leading cause of death worldwide. Diet can greatly impact health, while caloric restriction and fasting have putative benefits for disease prevention and longevity. Strong epidemiological associations exist between obesity and cancer, whereas healthy diets can reduce cancer risk. However, less is known about how diet might impact cancer once it has been diagnosed and particularly how diet can impact cancer treatment. In the present review, we discuss the links between obesity, diet, and cancer. We explore potential mechanisms by which diet can improve cancer outcomes, including through hormonal, metabolic, and immune/inflammatory effects, and present the limited clinical research that has been published in this arena. Though data are sparse, diet intervention may reduce toxicity, improve chemotherapy efficacy, and lower the risk of long-term complications in cancer patients. Thus, it is important that we understand and expand the science of this important but complex adjunctive cancer treatment strategy.

Autophagy Modulators and Neuroinflammation

2020 ◽  
Vol 27 (6) ◽  
pp. 955-982 ◽  
Author(s):  
Kyoung Sang Cho ◽  
Jang Ho Lee ◽  
Jeiwon Cho ◽  
Guang-Ho Cha ◽  
Gyun Jee Song
Keyword(s):  
Neurodegenerative Disorders ◽  
Neurological Disorders ◽  
Mammalian Cells ◽  
Critical Role ◽  
Therapeutic Agents ◽  
Mechanisms Of Action ◽  
Scientific Interest ◽  
Therapeutic Tools ◽  
Underlying Mechanisms

Background: Neuroinflammation plays a critical role in the development and progression of various neurological disorders. Therefore, various studies have focused on the development of neuroinflammation inhibitors as potential therapeutic tools. Recently, the involvement of autophagy in the regulation of neuroinflammation has drawn substantial scientific interest, and a growing number of studies support the role of impaired autophagy in the pathogenesis of common neurodegenerative disorders. Objective: The purpose of this article is to review recent research on the role of autophagy in controlling neuroinflammation. We focus on studies employing both mammalian cells and animal models to evaluate the ability of different autophagic modulators to regulate neuroinflammation. Methods: We have mostly reviewed recent studies reporting anti-neuroinflammatory properties of autophagy. We also briefly discussed a few studies showing that autophagy modulators activate neuroinflammation in certain conditions. Results: Recent studies report neuroprotective as well as anti-neuroinflammatory effects of autophagic modulators. We discuss the possible underlying mechanisms of action of these drugs and their potential limitations as therapeutic agents against neurological disorders. Conclusion: Autophagy activators are promising compounds for the treatment of neurological disorders involving neuroinflammation.

scholarly journals 466 Resection or Enucleation for Extremely Giant Hepatic Haemangiomata? A Case Report and Review of The Literature

2021 ◽  
Vol 108 (Supplement_2) ◽  
Author(s):  
R E Fraser ◽  
G R Layton ◽  
L L Kuan ◽  
A R Dennison
Keyword(s):  
Expectant Management ◽  
Evidence Base ◽  
Primary Treatment ◽  
Cavernous Haemangioma ◽  
Liver Tumours ◽  
Case Presentation ◽  
Best Management ◽  
Anatomical Liver Resection ◽  
Benign Liver

Abstract Background Cavernous hepatic haemangiomas are benign liver tumours and although common when small, giant haemangiomas (usually accepted as being greater than 10cm) are infrequent. Treatment is indicated in patients who are symptomatic or if diagnosis is unclear, although with giant haemangiomas, many support expectant management of asymptomatic lesions due to the risk of major complications. Traditionally hepatic resection has been the primary treatment option for these lesions, but a variety of other techniques, including enucleation, have been described as safe and effective alternatives. There remains equipoise in respect of the best management of giant haemangiomas above 10cm. Cases of such size are rare and so there is a paucity of data available. Case presentation We present a case of a 65-year-old male who underwent successful anatomical liver resection for a 5kg giant cavernous haemangioma of 26cm diameter following its incidental identification during an ultrasound scan. We also discuss and compare the role of resection and enucleation for the treatment of haemangiomata greater than 20cm in diameter. Conclusions This case demonstrates successful resection of an unusually giant haemangioma which, in contrast to the majority of literature, provides a valuable addition to the limited evidence base for management of this condition by anatomical resection.

scholarly journals DIAPH2, PTPRD and HIC1 Gene Polymorphisms and Laryngeal Cancer Risk

2021 ◽  
Vol 18 (14) ◽  
pp. 7486
Author(s):  
Mirosław Śnit ◽  
Maciej Misiołek ◽  
Wojciech Ścierski ◽  
Anna Koniewska ◽  
Grażyna Stryjewska-Makuch ◽  
...  
Keyword(s):  
Cancer Risk ◽  
Laryngeal Cancer ◽  
Basic Research ◽  
Control Groups ◽  
Allele Distribution ◽  
Study Results ◽  
Risk Patients ◽  
And Control ◽  
The Relationship

AIM, DIAPH2, PTPRD and HIC1 are the cell glycoprotein, which play an important role in the occurrence and development of tumors. This study was designed to assess the association between DIAPH2, PTPRD and HIC1 SNPs and laryngeal cancer risk. PATIENTS AND METHODS: This study including 267 patients with histologically confirmed laryngeal cancer and 157 controls. The relationship between genetic variations DIAPH2 (rs6620138), PTPRD (rs3765142) and HIC1 (rs9901806) and the onset of laryngeal cancer were investigated. Statistical analysis to calculate the relationship between DIAPH2, PTPRD and HIC1 genes polymorphism and pathogenesis of laryngeal cancer. RESULTS: The results showed that rs6620138 DIAPH2 polymorphism could increase the onset risk of laryngeal cancer. Statistically significant differences in allele distribution of rs6620138 DIAPH2 and rs9901806 HIC1 in the case and control groups subgroups. CONCLUSIONS: This study results suggested that genetic variation of rs6620138 DIAPH2 polymorphism is related to the susceptibility to laryngeal cancer. Our results provide a basis to begin basic research on the role of DIAPH2 gene in the pathogenesis of laryngeal cancer.

scholarly journals Gut microbiota influence in type 2 diabetes mellitus (T2DM)

Gut Pathogens ◽  
2021 ◽  
Vol 13 (1) ◽  
Author(s):  
A. L. Cunningham ◽  
J. W. Stephens ◽  
D. A. Harris
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Gut Microbiota ◽  
Potential Role ◽  
Evidence Base ◽  
Human Metabolism ◽  
Altered Glucose

AbstractA strong and expanding evidence base supports the influence of gut microbiota in human metabolism. Altered glucose homeostasis is associated with altered gut microbiota, and is clearly associated with the development of type 2 diabetes mellitus (T2DM) and associated complications. Understanding the causal association between gut microbiota and metabolic risk has the potential role of identifying susceptible individuals to allow early targeted intervention.

scholarly journals Metabolic Surgery and Cancer Risk: An Opportunity for Mechanistic Research

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3183
Author(s):  
Edward R. Sauter ◽  
Brandy Heckman-Stoddard
Keyword(s):  
Weight Loss ◽  
Cancer Risk ◽  
Risk Reduction ◽  
Dramatic Improvement ◽  
Role Of Government ◽  
Sustained Weight Loss ◽  
Historical Role ◽  
Cancer Risk Reduction

Metabolic (bariatric) surgery (MBS) is recommended for individuals with a BMI > 40 kg/m2 or those with a BMI 35–40 kg/m2 who have one or more obesity related comorbidities. MBS leads to greater initial and sustained weight loss than nonsurgical weight loss approaches. MBS provides dramatic improvement in metabolic function, associated with a reduction in type 2 diabetes mellitus and cardiovascular risk. While the number of MBS procedures performed in the U.S. and worldwide continues to increase, they are still only performed on one percent of the affected population. MBS also appears to reduce the risk of certain obesity related cancers, although which cancers are favorably impacted vary by study, who benefits most is uncertain, and the mechanism(s) driving this risk reduction are mostly speculative. The goal of this manuscript is to highlight 1) emerging evidence that MBS influences cancer risk, and that the potential benefit appears to vary based on cancer, gender, surgical procedure, and likely other variables; 2) the role of the NIH in MBS research in T2DM and CV risk for many years, and more recently in cancer; and 3) the opportunity for research to understand the mechanism(s) by which MBS influences cancer. There is evidence that women benefit more from MBS than men, that MBS may actually increase the risk of colorectal cancer in both women and men, and there is speculation that the benefit in cancer risk reduction may vary according to which MBS procedure an individual undergoes. Herein, we review what is currently known, the historical role of government, especially the National Institutes of Health (NIH), in driving this research, and provide suggestions that we believe could lead to a better understanding of whether and how MBS impacts cancer risk, which cancers are impacted either favorably or unfavorably, the role of the NIH and other research agencies, and key questions to address that will help us to move the science forward.

scholarly journals The Role of Oxidative Stress in NAFLD–NASH–HCC Transition—Focus on NADPH Oxidases

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 687
Author(s):  
Daniela Gabbia ◽  
Luana Cannella ◽  
Sara De De Martin
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Current Knowledge ◽  
Mechanisms Of Action ◽  
Nadph Oxidases ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

A peculiar role for oxidative stress in non-alcoholic fatty liver disease (NAFLD) and its transition to the inflammatory complication non-alcoholic steatohepatitis (NASH), as well as in its threatening evolution to hepatocellular carcinoma (HCC), is supported by numerous experimental and clinical studies. NADPH oxidases (NOXs) are enzymes producing reactive oxygen species (ROS), whose abundance in liver cells is closely related to inflammation and immune responses. Here, we reviewed recent findings regarding this topic, focusing on the role of NOXs in the different stages of fatty liver disease and describing the current knowledge about their mechanisms of action. We conclude that, although there is a consensus that NOX-produced ROS are toxic in non-neoplastic conditions due to their role in the inflammatory vicious cycle sustaining the transition of NAFLD to NASH, their effect is controversial in the neoplastic transition towards HCC. In this regard, there are indications of a differential effect of NOX isoforms, since NOX1 and NOX2 play a detrimental role, whereas increased NOX4 expression appears to be correlated with better HCC prognosis in some studies. Further studies are needed to fully unravel the mechanisms of action of NOXs and their relationships with the signaling pathways modulating steatosis and liver cancer development.

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