Role In Incidence Of Cancer Research Articles

Abstract 4123540: Cardiovascular Health and Cancer Incidence and Mortality: NHANES-III and -Continuous study

Background: Cancer and cardiovascular disease (CVD) are the leading causes of death worldwide. Limited evidence is available regarding the relationship between CVD, cardiovascular risk factors (CVRF), and cancer mortality; and how CVRF further modify that relationship. Methods: The first part included 438 and 2100 CVD patients aged 65+ from NHANES-III and Continuous (1999-2016) datasets, respectively. Competing risk models with subdistribution hazards ratio (aHR) were used to identify risk factors for cancer incidence. The second part included 44,591 adult individuals from NHANES-Continuous merged with Medicare and National Death Index mortality data until the end of 2018. We included individuals with no history of cancer at baseline. We used competing risk modeling to test the relationship between CVD at baseline and cancer mortality. We also conducted a comprehensive risk factor analysis. Results: In the first part (Figure), females in NHANES-III had lower cancer risk (aHR 0.39, P=0.001) compared to males. Poor physical activity was associated with increased cancer risk in both datasets (aHR 2.59 in NHANES-III, aHR 1.59 in Continuous). In NHANES-Continuous, age (aHR 1.07, P<0.001) and current smoking (aHR 2.55, P=0.001) showed a significant association with developing cancer. No other factors investigated showed significant associations. In the second analysis (Table), the included sample size represented 1,738,423,317 individuals (52% females, 67% non-Hispanic Whites, and 9% Hispanics). Competing risk modeling showed a significantly higher risk of cancer mortality in individuals with CVD (aHR 1.37, 95% CI 1.07-1.76, P=0.01) after adjusting for age, sex, and race/ethnicity. Notably, cancer mortality increased with aging (aHR 1.08, 95%CI 1.05-1.11, P<0.0001), current smoking status (aHR 6.78, 95%CI 3.43-13.42, P<0.0001), and obesity (aHR 2.32, 95%CI 1.13-4.79, P=0.02). Finally, a significant interaction (P=0.034) was found where those with CVD and obesity showed higher cancer mortality than those with normal BMI (aHR, 95%CI 1.03-2.91, P=0.04). Conclusions: Our study highlights the close relationship between cardiovascular health and cancer, including among CVD patients. Our findings suggest that physical activity and obesity may play a significant role in cancer incidence and mortality among the general population and CVD patients. These findings emphasize the need for more proactive approach in the management of shared risk factors for CVD and cancer.

NCCN Policy Summit: Reducing the Cancer Burden Through Prevention and Early Detection.

Cancer prevention, screening, and early detection play an integral role in cancer incidence and outcomes. It is estimated that 30% to 50% of cancers worldwide are preventable, and it is well established that early detection of many cancers is associated with improved treatment outcomes. A recent NCCN Policy Summit: Reducing the Cancer Burden Through Prevention and Early Detection brought together healthcare providers, payers, policymakers, patient advocates, industry representatives, and technology representatives to explore challenges, triumphs, and outstanding questions surrounding current practices. Keynotes were delivered by Dr. Lisa Richardson, Director of the Division of Cancer Prevention and Control within the CDC, and Dr. Danielle Carnival, White House Cancer Moonshot Coordinator. Dr. Richardson focused on the field of public health, translating its utility in preventing and diagnosing cancer in the United States, while Dr. Carnival discussed ambitious goals by the Cancer Moonshot in reducing the cancer burden. Panelists highlighted characteristics of high-impact prevention and early detection programs, including how genetic testing has impacted this space. Existing programs are often challenged due to limitations in data, as well as financial, structural, and social barriers to motivating individuals to act on recommendations. Despite these barriers, we can learn from highly successful programs and should apply proven attributes, such as community engagement, more broadly.

Potential application of Helicobacter pylori against cancer: carcinogenic pathogen or therapeutic agent?

The repeated exposure of normal cells to carcinogenic agents may lead to mutations in their genetic material, changing them into cancerous cells. In this case, the structure and function of these cells would alter, and they would not behave like a normal cell. Treatment of cancer by bacteria is a promising and new strategy. Recently, scientists demonstrated that bacteria could induce apoptosis in cancerous cells. Cell death was identified by cellular cytotoxicity assays when bacterial structures were utilized, and these observations proved bacterial capability for apoptosis induction. Helicobacter pylori (or H. pylori) is known as a pathogenic and carcinogenic bacterium that can cause various problems. Recently, practical therapeutic applications of this bacterium has drawn attention. Here, we analyzed the advantages and merits of bacterial compounds of H. pylori as active remedial agents for cancer treatment. Besides describing H. pylori virulent factors and their role in cancer incidence, we also discuss how their potentials can significantly be strengthened and used for cancer treatment. This review results suggest that some factors of H. pylori can be exploited as therapeutic agents for cancer therapy in future (Tab. 1, Fig. 3, Ref. 77). Keywords: apoptosis induction, bacteriotherapy, cancer treatment, Helicobacter pylori.

Evaluation of serotonin receptors (5HTR2A and 5HTR3A) mRNA expression changes in tumor of breast cancer patients

Background: Several studies have proven the pattern of neurotransmitters, especially serotonin, in carcinogenesis and tumor development. Several studies have also shown that changes in serotonin receptors, especially 5HTR2A and 5HTR3A, can play an important role in incidence of cancers. This study was conducted to investigate changes in mRNA expression of 5HTR2A and 5HTR3A receptors in the breast tumor tissue compared to their marginal zone. Methods: In this study, tissue samples were obtained from 40 female patients with breast cancer. Entire RNA was obtained from the tissues and cDNA synthesis was performed. Finally, real ime PCR technique was performed to investigate the gene expression variation of both 5HTR2A and 5HTR3A. To analyze the results of real time PCR, both ΔΔCt and 2-ΔΔCt equations were used. All statistical analyses were performed using the SPSS 18 software and R-Studio 1.0.136. P values less than 0.05 (p<0.05) and 0.001 (p<0.001) were considered statistically significant. Results: The results showed increased expression of 5HTR2A and 5HTR3A genes in tumoral tissues of patients with breast cancer compared to their marginal tissues, where the 5HTR2A and 5HTR3A genes expression in tumor tissue was 3.12 and 3.24 times more than that of the marginal zone, respectively. Conclusion: The results indicated an increase in the mRNA expression of serotonin receptors (5HTR2A and 5HTR3A) in the tumor tissue compared to the marginal zone, which due to the mitogenic nature of these receptors, is likely to induce more proliferation of cancer cells.

Dismantling Fixations on Failed Fictions: A-Bomb Survivor Study Denies The Low-Dose Radiogenic Cancer Narrative

The linear no-threshold (LNT) model of low dose ionizing radiation's (LDIR) role in radiogenic cancer incidence has long served as a pseudo-scientific belief arising from evidence that has never been proven, but has been contested. One source of current evidence that favors the LNT model is the Radiation Effects Research Foundation’s (RERF) Life Span Study (LSS) cohort of Japanese atomic bomb survivors. The RERF has managed the input data, model development, and data analyses for the LSS cohort for 45 years, publishing research papers and reports updating the RERF’s progress. In recent years, the RERF has attempted to identify other cancer risk factors that may have played a role in the cancer incidence of cohort survivors, and this effort has drawn attention to the fact that many earlier years of papers and reports from the RERF have never considered these risk factors, making such publications of questionable merit. This investigation examines two recent papers from the RERF that denominate how the RERF now analyzes specific cancer incidence for cohort members, how it treats lifestyle and other risk factors for various cancers that have arisen in the cohort, and how it continues to find and assert that bomb-blast LDIR remains a distinguishable source of radiogenic cancer in the cohort. The investigation observes that the cohort input data and modeling have extensive deficiencies and defects, many having been identified by RERF authors themselves, that substantially compromise the findings of these two papers, and offers concluding evidence that the LDIR radiogenic cancer model is highly implausible if not impossible. From such evidence, a final conclusion must arise that supports a threshold model for the dose–response relationship between LDIR exposure and radiogenic cancer.

Phytochemicals as Modulators of Long Non-Coding RNAs and Inhibitors of Cancer-Related Carbonic Anhydrases.

Long non-coding RNAs (lncRNAs) are classified as a group of transcripts which regulate various biological processes, such as RNA processing, epigenetic control, and signaling pathways. According to recent studies, lncRNAs are dysregulated in cancer and play an important role in cancer incidence and spreading. There is also an association between lncRNAs and the overexpression of some tumor-associated proteins, including carbonic anhydrases II, IX, and XII (CA II, CA IX, and CA XII). Therefore, not only CA inhibition, but also lncRNA modulation, could represent an attractive strategy for cancer prevention and therapy. Experimental studies have suggested that herbal compounds regulate the expression of many lncRNAs involved in cancer, such as HOTAIR (HOX transcript antisense RNA), H19, MALAT1 (metastasis-associated lung adenocarcinoma transcript 1), PCGEM1 (Prostate cancer gene expression marker 1), PVT1, etc. These plant-derived drugs or phytochemicals include resveratrol, curcumin, genistein, quercetin, epigallocatechin-3-galate, camptothcin, and 3,3′-diindolylmethane. More comprehensive information about lncRNA modulation via phytochemicals would be helpful for the administration of new herbal derivatives in cancer therapy. In this review, we describe the state-of-the-art and potential of phytochemicals as modulators of lncRNAs in different types of cancers.

Monocytes inhibit NK activity via TGF-β in patients with obstructive sleep apnoea.

Obstructive sleep apnoea (OSA) is associated with cancer incidence and mortality. The contribution of the immune system appears to be crucial; however, the potential role of monocytes and natural killer (NK) cells remains unclear.Quantitative reverse transcriptase PCR, flow cytometry and in vitro assays were used to analyse the phenotype and immune response activity in 92 patients with OSA (60 recently diagnosed untreated patients and 32 patients after 6 months of treatment with continuous positive airway pressure (CPAP)) and 29 healthy volunteers (HV).We determined that monocytes in patients with OSA exhibit an immunosuppressive phenotype, including surface expression of glycoprotein-A repetitions predominant protein (GARP) and transforming growth factor-β (TGF-β), in contrast to those from the HV and CPAP groups. High levels of TGF-β were detected in OSA sera. TGF-β release by GARP+ monocytes impaired NK cytotoxicity and maturation. This altered phenotype correlated with the hypoxic severity clinical score (CT90). Reoxygenation eventually restored the altered phenotypes and cytotoxicity.This study demonstrates that GARP+ monocytes from untreated patients with OSA have an NK-suppressing role through their release of TGF-β. Our findings show that monocyte plasticity immunomodulates NK activity in this pathology, suggesting a potential role in cancer incidence.

Olive leaf extract containing oleuropein modulates the cytotoxic effect of epirubicin on breast cancer cells depending on the cell line

Abstract Objective Epidemiologic studies showed that nutrition plays a role in incidence of cancer. However, little is known if nutrition also modulates the effect of chemotherapeutics. For this purpose, the present study investigates the cytotoxic effect of olive leaf extract and its combination with epirubicin. Method Cell viability was measured via ATP assay on MDA-MB-231 and MCF-7 cell lines. Apoptosis was detected by poly(ADP-ribose) polymerase (PARP) cleavage, and the expression of apoptosis-related genes. A single extract was used throughout the study. Results Both olive leaf extract and epirubicin resulted in cytotoxic effect in a dose-dependent manner in both cell lines. The extract further increased the cytotoxic effect of epirubicin in MDA-MB-231 cell line. However, in contrast, it abolished the cytotoxic effect of epirubicin in MCF-7 cell line. As a confirmative result, the increased expressions of FASLG and HRK following epirubicin treatment were down-regulated when epirubicin was used in combination with the extract in MCF-7 cells. Conclusion Olive leaf extract modulates the cytotoxic effect of epirubicin when it is in combination depending on the type of cell line. This warrants further in vivo experiments for better understanding of this intriguing result.

Vitamin D and Colorectal, Breast, and Prostate Cancers: A Review of the Epidemiological Evidence.

Over the past two decades, the question of whether vitamin D has a role in cancer incidence, progression, and mortality has been studied in detail. Colorectal, breast, and prostate cancers have been a particular area of focus; together, these three malignancies account for approximately 35% of cancer cases and 20% of cancer deaths in the United States, and as such are a major public health concern. Herein, we review and synthesize the epidemiological research regarding vitamin D, as measured by the biomarker 25-hydroxycholecalciferol [25(OH)D], and the incidence, progression, and mortality of these cancers. Overall, the results of observational studies of the relationship between 25(OH)D and colorectal cancer have revealed a consistent inverse association for incidence and mortality; while for breast cancer, results have generally demonstrated a relationship between higher 25(OH)D and lower risk for progression and mortality. In contrast, randomized, double-blind clinical trials conducted to date have generally failed to support these findings. For prostate cancer, there is no convincing evidence of an association between 25(OH)D and incidence, and inconsistent data for progression and mortality, though results of one open label clinical trial suggest that supplementation with 4000 IU/d of vitamin D3 may inhibit progression of the disease. Nonetheless, until the results of additional ongoing randomized, double-blind clinical trials are reported, it will be difficult to ascertain if vitamin D itself is related to a reduction in risk for some cancer endpoints, or whether high concentrations of the vitamin D biomarker 25(OH)D may instead serve as a marker for an overall beneficial risk factor profile.

Commentary: eight ways to prevent cancer: a framework for effective prevention messages for the public.

Research over the past 40 years has convincingly shown that lifestyle factors play a huge role in cancer incidence and mortality. The public, though, can often discount the preventability of cancer. That health information on the Internet is a vast and often scientifically suspect commodity makes promoting important and sound cancer prevention messages to the public even more difficult. To help address these issues and improve the public's knowledge of, and attitudes toward, cancer prevention, there need to be concerted efforts to create evidence-based, user-friendly information about behaviors that could greatly reduce overall cancer risk. Toward this end, we condensed the current scientific evidence on the topic into eight key behaviors. While not an end in themselves, "Eight Ways to Stay Healthy and Prevent Cancer" forms an evidence-based and targeted framework that supports broader cancer prevention efforts.

The Role of Overweight and Obesity in Perceived Risk Factors for Cancer: Implications for Education

Epidemiological evidence indicates that obesity plays an important role in cancer incidence. A telephone survey of 1,433 adults, aged 18+ years who reported their knowledge and beliefs regarding behavioral risk factors for cancer, was conducted. Most respondents believed that people can take steps to reduce cancer risk; however, many, particularly obese respondents, did not rate being overweight as a very important risk factor. A dedicated public education campaign focused on overweight and cancer is needed to address the significant gap in knowledge about the role of weight control in preventing cancer, particularly among those most afflicted.

The Social Determinants of Cancer

It is clear that social factors play a role in cancer incidence and mortality. Increased risk of cancer is associated with tobacco use, diet and alcohol, reduced physical activity, exposure to the sun and to environmental toxins. These relationships are relatively well established and quantified and there is broad understanding of their pathophysiological role in the etiology of cancer. All these factors are influenced by social, cultural, and environmental factors. The growing field of social epidemiology, however, is drawing attention to the role of more 'upstream' factors in health and disease [1]. Examples might include the influence of commercial marketing activities, relative social status, levels of income and education, access to the health care system system and the strength or absence of social networks. There is increasing evidence that such social level factors have an important etiologic role in cancer, but this role is far more difficult to study. This challenge has stimulated research that seeks to clarify the relationship of social factors and cancer and this issue of the journal presents two examples. In the first, Ocafia-Riola et al., studied the relationship between the incidence of cancers, socioeconomic levels and exposure to environmental toxins in defined geographic regions of Southern Spain [2]. They hypothesized that cancer may be associated with differential exposure to environmental toxins as reflected by areal measures. They found associations for most cancers with a measure of urbanization and for some cancer sites with measures of unemployment, illiteracy, and area under cultivation. Unfortunately, even though these association may suggest topics for further exploration, there seemed to be no commonality between the cancer sites associated with various factors. The authors did not offer any conjectures about biologic mechanisms. Jansson et al., in Sweden, looked at the possible impact of psychologically demanding work on the incidence of esophageal adenocarcinoma, squamouscell carcinoma, and adenocarcinoma of the gastric cardia [3]. They used data from individuals asked to recall conditions from 20-years earlier on job strain and work place satisfaction. The study demonstrated a modest relationship of new cases of these cancers with coping styles, not the job stress itself and a rather strong relationship with satisfaction regarding the pace of work. The authors speculate that the mechanism might be due either to the effect of inadequate coping with psychological stress on relaxing lower esophageal sphincter pressure, or perhaps to impaired immune function. The results of these two studies are of interest independently, but also illustrate the need for a broader approach if epidemiologists hope to elucidate the role of social determinants of cancer. Far more detailed