risk of cancer
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2022 ◽  
Vol 76 ◽  
pp. 102057
Arthur Sillah ◽  
Nathaniel F. Watson ◽  
Ulrike Peters ◽  
Mary L. Biggs ◽  
F. Javier Nieto ◽  

2022 ◽  
Vol 12 ◽  
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.

2022 ◽  
Vol 12 ◽  
Xianjun Feng ◽  
Jiajun Ma ◽  
Zhiqian Liu ◽  
Xuan Li ◽  
Yinghua Wu ◽  

Glucosinolates (GSLs) are important secondary metabolites that play important defensive roles in cruciferous plants. Chinese flowering cabbage, one of the most common vegetable crops, is rich in GSLs and thus has the potential to reduce the risk of cancer in humans. Many genes that are involved in GSL biosynthesis and metabolism have been identified in the model plant Arabidopsis thaliana; however, few studies investigated the genes related to GSL biosynthesis and metabolism in Chinese flowering cabbage. In the present study, the GSL composition and content in three different organs of Chinese flowering cabbage (leaf, stalk, and flower bud) were determined. Our results showed that the total GSL content in flower buds was significantly higher than in stalks and leaves, and aliphatic GSLs were the most abundant GSL type. To understand the molecular mechanisms underlying the variations of GSL content, we analyzed the expression of genes encoding enzymes involved in GSL biosynthesis and transport in different tissues of Chinese flowering cabbage using RNA sequencing; the expression levels of most genes were found to be consistent with the pattern of total GSL content. Correlation and consistency analysis of differentially expressed genes from different organs with the GSL content revealed that seven genes (Bra029966, Bra012640, Bra016787, Bra011761, Bra006830, Bra011759, and Bra029248) were positively correlated with GSL content. These findings provide a molecular basis for further elucidating GSL biosynthesis and transport in Chinese flowering cabbage.

Cancers ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 437
Valentin Suteau ◽  
John Bukasa-Kakamba ◽  
Beatrice Virjogh-Cenciu ◽  
Antoine Adenis ◽  
Nadia Sabbah ◽  

The prevalence of obesity and type 2 diabetes is higher in French Guiana compared to mainland France. These metabolic disorders are associated with an increased risk of cancer. One of the factors involved is hyperinsulinemia that promotes the action of glucose transporter 1 (GLUT-1). The objective of this study is to characterize the expression of GLUT-1 in breast cancers cells in diabetic and obese patients compared to those who are not and to describe the clinical and histological prognostic factors of breast cancer in this population. We conducted a monocentric study including patients with breast cancer diagnosed between 2014 and 2020. Patients were classified into three groups: diabetes, obesity, and control group. The GLUT-1 expression was assessed by immunohistochemistry. In total, 199 patients were included in this study. The median age was 53.5 years, and the median tumor size was 2.8 cm. Luminal A was the most frequent molecular type (58.1%), followed by the triple-negative type (19.9%). The breast cancer in our population was characterized by a younger age at diagnosis, more aggressive molecular types, and larger tumor size. Thus, we suggest the advancement of the age of breast cancer screening in this territory. A total of 144 patients (31 diabetes, 22 obese, and 91 control group) were included for the study of GLUT-1 expression. Overexpression of GLUT-1 was observed in 60.4% of cases and in all carcinoma in situ lesions. GLUT-1 overexpression was associated with more aggressive cancers. This overexpression is correlated with high histological grade, high proliferation index, and aggressive molecular types. Our study found no difference in GLUT-1 expression between the diabetic or obese patients and the control group. These results highlight the potential role of GLUT-1 as a tumor metabolic prognostic marker and also as an interesting target therapy, independently of patient metabolic disorder.

BMC Cancer ◽  
2022 ◽  
Vol 22 (1) ◽  
Linda Rainey ◽  
Daniëlle van der Waal ◽  
Louise S. Donnelly ◽  
Jake Southworth ◽  
David P. French ◽  

Abstract Background The Predicting Risk of Cancer at Screening (PROCAS) study provided women who were eligible for breast cancer screening in Greater Manchester (United Kingdom) with their 10-year risk of breast cancer, i.e., low (≤1.5%), average (1.5–4.99%), moderate (5.-7.99%) or high (≥8%). The aim of this study is to explore which factors were associated with women’s uptake of screening and prevention recommendations. Additionally, we evaluated women’s organisational preferences regarding tailored screening. Methods A total of 325 women with a self-reported low (n = 60), average (n = 125), moderate (n = 80), or high (n = 60) risk completed a two-part web-based survey. The first part contained questions about personal characteristics. For the second part women were asked about uptake of early detection and preventive behaviours after breast cancer risk communication. Additional questions were posed to explore preferences regarding the organisation of risk-stratified screening and prevention. We performed exploratory univariable and multivariable regression analyses to assess which factors were associated with uptake of primary and secondary breast cancer preventive behaviours, stratified by breast cancer risk. Organisational preferences are presented using descriptive statistics. Results Self-reported breast cancer risk predicted uptake of (a) supplemental screening and breast self-examination, (b) risk-reducing medication and (c) preventive lifestyle behaviours. Further predictors were (a) having a first degree relative with breast cancer, (b) higher age, and (c) higher body mass index (BMI). Women’s organisational preferences for tailored screening emphasised a desire for more intensive screening for women at increased risk by further shortening the screening interval and moving the starting age forward. Conclusions Breast cancer risk communication predicts the uptake of key tailored primary and secondary preventive behaviours. Effective communication of breast cancer risk information is essential to optimise the population-wide impact of tailored screening.

2022 ◽  
Vol 23 (2) ◽  
pp. 970
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.

2022 ◽  
Vol 12 ◽  
Tannaz Moeini Shad ◽  
Reza Yazdani ◽  
Parisa Amirifar ◽  
Samaneh Delavari ◽  
Marzieh Heidarzadeh Arani ◽  

Ataxia-telangiectasia (AT) is a rare autosomal recessive neurodegenerative multisystem disorder. A minority of AT patients can present late-onset atypical presentations due to unknown mechanisms. The demographic, clinical, immunological and genetic data were collected by direct interview and examining the Iranian AT patients with late-onset manifestations. We also conducted a systematic literature review for reported atypical AT patients. We identified three Iranian AT patients (3/249, 1.2% of total registry) with later age at ataxia onset and slower neurologic progression despite elevated alpha-fetoprotein levels, history of respiratory infections, and immunological features of the syndrome. Of note, all patients developed autoimmunity in which a decrease of naïve T cells and regulatory T cells were observed. The literature searches also summarized data from 73 variant AT patients with atypical presentation indicating biallelic mild mutations mainly lead to an atypical phenotype with an increased risk of cancer. Variant AT patients present with milder phenotype or atypical form of classical symptoms causing under- or mis- diagnosis. Although missense mutations are more frequent, an atypical presentation can be associated with deleterious mutations due to unknown modifying factors.

2022 ◽  
Vol 8 (2) ◽  
Ruth Nussinov ◽  
Chung-Jung Tsai ◽  
Hyunbum Jang

This review offers why same-gene mutations can lead to cancer and neurodevelopmental disorders and why a high risk of cancer.

2022 ◽  
Sarah Jafrin ◽  
Md. Abdul Aziz ◽  
Mohammad Safiqul Islam

Review question / Objective: TP73 G4C14-A4T14 variant has been suspected of elevating the risk of cancer for many years. The available evidence was unsatisfactory and could not provide a reliable conclusion. Therefore, we performed this meta-analysis to re-evaluate the previous findings and illustrate the actual role of TP73 G4C14-A4T14 variant on cancer development. Condition being studied: The association of the G4C14-A4T14 variant with cancer risk was studied. Information sources: PubMed, Google Scholar, EMBASE, Cochrane Library, and Web of Science, CNKI.

2022 ◽  
Vol 8 ◽  
Lilite Sadovska ◽  
Jānis Auders ◽  
Laura Keiša ◽  
Nadezhda Romanchikova ◽  
Laila Silamiķele ◽  

Increasing evidence suggests that regular physical exercise not only reduces the risk of cancer but also improves functional capacity, treatment efficacy and disease outcome in cancer patients. At least partially, these effects are mediated by the secretome of the tissues responding to exercise. The secreted molecules can be released in a carrier-free form or enclosed into extracellular vesicles (EVs). Several recent studies have shown that EVs are actively released into circulation during physical exercise. Here, we for the first time investigated the effects of exercise-induced EVs on the progression of cancer in an F344 rat model of metastatic prostate cancer. Although we did not observe a consistent increase in the circulating EV levels, RNA sequencing analysis demonstrated substantial changes in the RNA content of EVs collected before and immediately after forced wheel running exercise as well as differences between EVs from runners at resting state and sedentary rats. The major RNA biotype in EVs was mRNA, followed by miRNA and rRNA. Molecular functions of differentially expressed RNAs reflected various physiological processes including protein folding, metabolism and regulation of immune responses triggered by the exercise in the parental cells. Intravenous administration of exercise-induced EVs into F344 rats with orthotopically injected syngeneic prostate cancer cells PLS10, demonstrated reduction of the primary tumor volume by 35% and possibly—attenuation of lung metastases. Hence, our data provide the first evidence that exercise-induced EVs may modulate tumor physiology and delay the progression of cancer.

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