scholarly journals Molecular Mechanisms Leading from Periodontal Disease to Cancer

2022 ◽  
Vol 23 (2) ◽  
pp. 970
Author(s):  
Bartosz Kamil Sobocki ◽  
Charbel A. Basset ◽  
Bożena Bruhn-Olszewska ◽  
Paweł Olszewski ◽  
Olga Szot ◽  
...  

Periodontitis is prevalent in half of the adult population and raises critical health concerns as it has been recently associated with an increased risk of cancer. While information about the topic remains somewhat scarce, a deeper understanding of the underlying mechanistic pathways promoting neoplasia in periodontitis patients is of fundamental importance. This manuscript presents the literature as well as a panel of tables and figures on the molecular mechanisms of Porphyromonas gingivalis and Fusobacterium nucleatum, two main oral pathogens in periodontitis pathology, involved in instigating tumorigenesis. We also present evidence for potential links between the RANKL–RANK signaling axis as well as circulating cytokines/leukocytes and carcinogenesis. Due to the nonconclusive data associating periodontitis and cancer reported in the case and cohort studies, we examine clinical trials relevant to the topic and summarize their outcome.

Author(s):  
Declan Timothy Waugh

In this study, several lines of evidence are provided to show that Na + , K + -ATPase activity exerts vital roles in normal brain development and function and that loss of enzyme activity is implicated in neurodevelopmental, neuropsychiatric and neurodegenerative disorders, as well as increased risk of cancer, metabolic, pulmonary and cardiovascular disease. Evidence is presented to show that fluoride (F) inhibits Na + , K + -ATPase activity by altering biological pathways through modifying the expression of genes and the activity of glycolytic enzymes, metalloenzymes, hormones, proteins, neuropeptides and cytokines, as well as biological interface interactions that rely on the bioavailability of chemical elements magnesium and manganese to modulate ATP and Na + , K + -ATPase enzyme activity. Taken together, the findings of this study provide unprecedented insights into the molecular mechanisms and biological pathways by which F inhibits Na + , K + -ATPase activity and contributes to the etiology and pathophysiology of diseases associated with impairment of this essential enzyme. Moreover, the findings of this study further suggest that there are windows of susceptibility over the life course where chronic F exposure in pregnancy and early infancy may impair Na + , K + -ATPase activity with both short- and long-term implications for disease and inequalities in health. These findings would warrant considerable attention and potential intervention, not to mention additional research on the potential effects of F intake in contributing to chronic disease.


2017 ◽  
Vol 32 (1-2) ◽  
pp. 45-54 ◽  
Author(s):  
Nina Holland

Abstract Environmental research and public health in the 21st century face serious challenges such as increased air pollution and global warming, widespread use of potentially harmful chemicals including pesticides, plasticizers, and other endocrine disruptors, and radical changes in nutrition and lifestyle typical of modern societies. In particular, exposure to environmental and occupational toxicants may contribute to the occurrence of adverse birth outcomes, neurodevelopmental deficits, and increased risk of cancer and other multifactorial diseases such as diabetes and asthma. Rapidly evolving methodologies of exposure assessment and the conceptual framework of the Exposome, first introduced in 2005, are new frontiers of environmental research. Metabolomics and adductomics provide remarkable opportunities for a better understanding of exposure and prediction of potential adverse health outcomes. Metabolomics, the study of metabolism at whole-body level, involves assessment of the total repertoire of small molecules present in a biological sample, shedding light on interactions between gene expression, protein expression, and the environment. Advances in genomics, transcriptomics, and epigenomics are generating multidimensional structures of biomarkers of effect and susceptibility, increasingly important for the understanding of molecular mechanisms and the emergence of personalized medicine. Epigenetic mechanisms, particularly DNA methylation and miRNA expression, attract increasing attention as potential links between the genetic and environmental determinants of health and disease. Unlike genetics, epigenetic mechanisms could be reversible and an understanding of their role may lead to better protection of susceptible populations and improved public health.


2020 ◽  
Vol 8 ◽  
Author(s):  
Joshua Manor ◽  
Seema R. Lalani

Abnormally excessive growth results from perturbation of a complex interplay of genetic, epigenetic, and hormonal factors that orchestrate human growth. Overgrowth syndromes generally present with inherent health concerns and, in some instances, an increased risk of tumor predisposition that necessitate prompt diagnosis and appropriate referral. In this review, we introduce some of the more common overgrowth syndromes, along with their molecular mechanisms, diagnostics, and medical complications for improved recognition and management of patients affected with these disorders.


2022 ◽  
Vol 12 ◽  
Author(s):  
A Losada-García ◽  
SA Cortés-Ramírez ◽  
M Cruz-Burgos ◽  
M Morales-Pacheco ◽  
Carlos D Cruz-Hernández ◽  
...  

Neoplasic transformation is a continuous process that occurs in the body. Even before clinical signs, the immune system is capable of recognizing these aberrant cells and reacting to suppress them. However, transformed cells acquire the ability to evade innate and adaptive immune defenses through the secretion of molecules that inhibit immune effector functions, resulting in tumor progression. Hormones have the ability to modulate the immune system and are involved in the pathogenesis of autoimmune diseases, and cancer. Hormones can control both the innate and adaptive immune systems in men and women. For example androgens reduce immunity through modulating the production of pro-inflammatory and anti-inflammatory mediators. Women are more prone than men to suffer from autoimmune diseases such as systemic lupus erythematosus, psoriasis and others. This is linked to female hormones modulating the immune system. Patients with autoimmune diseases consistently have an increased risk of cancer, either as a result of underlying immune system dysregulation or as a side effect of pharmaceutical treatments. Epidemiological data on cancer incidence emphasize the link between the immune system and cancer. We outline and illustrate the occurrence of hormone-related cancer and its relationship to the immune system or autoimmune diseases in this review. It is obvious that some observations are contentious and require explanation of molecular mechanisms and validation. As a result, future research should clarify the molecular pathways involved, including any causal relationships, in order to eventually allocate information that will aid in the treatment of hormone-sensitive cancer and autoimmune illness.


2021 ◽  
Vol 12 ◽  
Author(s):  
Tímea Pócza ◽  
Vince Kornél Grolmusz ◽  
János Papp ◽  
Henriett Butz ◽  
Attila Patócs ◽  
...  

In addition to single nucleotide variations and small-scale indels, structural variations (SVs) also contribute to the genetic diversity of the genome. SVs, such as deletions, duplications, amplifications, or inversions may also affect coding regions of cancer-predisposing genes. These rearrangements may abrogate the open reading frame of these genes or adversely affect their expression and may thus act as germline mutations in hereditary cancer syndromes. With the capacity of disrupting the function of tumor suppressors, structural variations confer an increased risk of cancer and account for a remarkable fraction of heritability. The development of sequencing techniques enables the discovery of a constantly growing number of SVs of various types in cancer predisposition genes (CPGs). Here, we provide a comprehensive review of the landscape of germline SV types, detection methods, pathomechanisms, and frequency in CPGs, focusing on the two most common cancer syndromes: hereditary breast- and ovarian cancer and gastrointestinal cancers. Current knowledge about the possible molecular mechanisms driving to SVs is also summarized.


2020 ◽  
Vol 65 (4) ◽  
pp. 5-11
Author(s):  
D. Kalinkin ◽  
T. Takhauova ◽  
A. Karpov ◽  
Yu. Samoilova ◽  
M. Plaksin ◽  
...  

Purpose: Development of the basic directions of a modern strategy for protecting the health of the adult population living in the activity zone of nuclear industry enterprises (using the example of the Seversk population). Material and methods: The object of the study was the population of the city of Seversk, formed around the Siberian Group of Chemical Enterprises. The subject of the study was demographic indicators; disability; incidence of malignant neoplasms, diseases of the circulatory system, injuries and accidents); socio-economic, behavioral and technological risk factors affecting the occurrence of major diseases. Results: It was established that by the end of the study period (1970–2017), the studied population was in a state of natural population decline due to a decrease in the birth rate and an increase in mortality, while the mortality rate exceeded the birth rate. During the period under review, the primary incidence of malignant neoplasia significantly increased; at the same time, the incidence of cardiovascular diseases, as well as the frequency of injuries and poisoning, decreased. Among the adult population of Seversk, behavioral factors (the habit of smoking, regular use of alcohol, a sedentary lifestyle, lack of regular physical activity) are more common than socio-economic (living conditions, financial situation) risk factors. Important risk factors are incorrect assessment by citizens of their own health and the reasons for its violation. Among Siberian Group of Chemical Enterprises workers exposed to tekhnogenic risk factor (long-term occupational exposure), there is an increased risk of cancer death of all localizations taken together, respiratory and digestive organs; bones, joints, mesothelium, soft tissues and genitals. At the same time, the risk of oncological mortality during irradiation was not exceeded in the range of small doses of (up to 100 mSv), and for any of the localization of malignant neoplasms this effect is not dose-dependent. Conclusion: The data obtained made it possible to specify and substantiate the basic directions of the modern strategy for protecting the health of the adult population living in the activity zone of nuclear industry enterprises (using the example of the Seversk population).


2018 ◽  
Vol 19 (12) ◽  
pp. 4110 ◽  
Author(s):  
Coral Warr ◽  
Katherine Shaw ◽  
Arani Azim ◽  
Matthew Piper ◽  
Linda Parsons

Many of the links between diet and cancer are controversial and over simplified. To date, human epidemiological studies consistently reveal that patients who suffer diet-related obesity and/or type II diabetes have an increased risk of cancer, suffer more aggressive cancers, and respond poorly to current therapies. However, the underlying molecular mechanisms that increase cancer risk and decrease the response to cancer therapies in these patients remain largely unknown. Here, we review studies in mouse cancer models in which either dietary or genetic manipulation has been used to model obesity and/or type II diabetes. These studies demonstrate an emerging role for the conserved insulin and insulin-like growth factor signaling pathways as links between diet and cancer progression. However, these models are time consuming to develop and expensive to maintain. As the world faces an epidemic of obesity and type II diabetes we argue that the development of novel animal models is urgently required. We make the case for Drosophila as providing an unparalleled opportunity to combine dietary manipulation with models of human metabolic disease and cancer. Thus, combining diet and cancer models in Drosophila can rapidly and significantly advance our understanding of the conserved molecular mechanisms that link diet and diet-related metabolic disorders to poor cancer patient prognosis.


2013 ◽  
Vol 1 (1) ◽  
pp. 12-18 ◽  
Author(s):  
Daniela Araújo Veloso Popoff ◽  
Mateus Prates Coelho ◽  
Daniella Reis Barbosa Martelli ◽  
Rajiv Saini ◽  
Ricardo Della Coletta ◽  
...  

Objective: To discuss the risk of cancer among relatives of individuals with cleft lip and palate (CL/P), as well as the risk of CL/P among relatives of individuals with cancer, since studies published currently have suggested  an increased risk of cancer among relatives of cleft individuals. Design: A systematic literature review was carried out in accordance with the Cochrane Collaboration Group protocol, including literature search strategy, selection of papers through the inclusion and exclusion criteria, data extraction and quality assessment. PubMed, Scopus and ISI - Web of Science databases were systematically searched using the fallowing search strings: “cleft lip and palate” AND “cancer”, “oral clefts” AND “cancer” and “orofacial clefts” AND “cancer”. Results: From 653 studies accessed, 8 comprised the final sample: 6 investigating CL/P index cases and their family history of cancer and 2 investigating individuals with cancer and their family history for CL/P. The sample sizes were not homogeneous. Oral clefts, the type of cancer and the degree of kinship family were not categorized in all studies. Leukemia, breast cancer and colon cancer were the most cited types, even as first-and-second degree relatives. Conclusions: An increased risk of cancer among relatives of cleft individuals could not be entirely confirmed. However, studies with this specific purpose suggest that first-and-second degrees relatives of cleft individuals have some types of cancer more often than unexposed families, highlighting that future studies should expand their samples to investigate possible common molecular mechanisms that allow relating oral clefts and cancer.


Neurographics ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 228-235
Author(s):  
S. Naganawa ◽  
T. Donohue ◽  
A. Capizzano ◽  
Y. Ota ◽  
J. Kim ◽  
...  

Li-Fraumeni syndrome is a familial cancer predisposition syndrome associated with germline mutation of the tumor suppressor gene 53, which encodes the tumor suppressor p53 protein. Affected patients are predisposed to an increased risk of cancer development, including soft-tissue sarcomas, breast cancer, brain tumors, and adrenocortical carcinoma, among other malignancies. The tumor suppressor gene TP53 plays an important, complex role in regulating the cell cycle, collaborating with transcription factors and other proteins. The disruption of appropriate cell cycle regulation by mutated TP53 is considered to be the cause of tumorigenesis in Li-Fraumeni syndrome. Appropriate surveillance, predominantly by using MR imaging, is used for early malignancy screening in an effort to improve the survival rate among individuals who are affected. Patients with Li-Fraumeni syndrome are also at increased risk for neoplasm development after radiation exposure, and, therefore, avoiding unnecessary radiation in both the diagnostic and therapeutic settings is paramount. Here, we review the epidemiology, genetics, imaging findings, and the current standard surveillance protocol for Li-Fraumeni syndrome from the National Comprehensive Cancer Network as well as potential treatment options.Learning Objective: Describe the cause of second primary malignancy among patients with Li-Fraumeni syndrome.


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