Cancer

Posted on Cancer

A new study finds 40 per cent of cancer cases and almost half of all deaths in the US are linked to lifestyle factors.

A new study led by researchers at the American Cancer Society (ACS) finds four in 10 cancer cases and about one-half of all cancer deaths in adults 30 years old and older in the United States (or 713,340 cancer cases and 262,120 cancer deaths in 2019) could be attributed to modifiable risk factors, including cigarette smoking, excess body weight, alcohol consumption, physical inactivity, diet, and infections. Cigarette smoking was by far the leading risk factor, contributing to nearly 20% of all cancer cases and 30% of all cancer deaths. The findings are published today in CA: A Cancer Journal for Clinicians.

“Despite considerable declines in smoking prevalence during the past few decades, the number of lung cancer deaths attributable to cigarette smoking in the United States is alarming. This finding underscores the importance of implementing comprehensive tobacco control policies in each state to promote smoking cessation, as well as heightened efforts to increase screening for early detection of lung cancer when treatment could be more effective,” said Dr Farhad Islami, senior scientific director, cancer disparity research at the American Cancer Society and lead author of the report. “Interventions to help maintain healthy body weight and diet can also substantially reduce the number of cancer cases and deaths in the country, especially given the increasing incidence of several cancer types associated with excess body weight, particularly in younger individuals.”

In this study, researchers used nationally representative data on cancer incidence and mortality and risk factor prevalence to estimate the proportion and number of cancer cases and deaths attributable to potentially modifiable risk factors (excluding non-melanoma skin cancers) for 30 cancer types. These risk factors included cigarette smoking (current and former smoking); secondhand smoke; excess body weight; alcohol consumption; consumption of red and processed meat; low consumption of fruits and vegetables, dietary fibre, and dietary calcium; physical inactivity; ultraviolet (UV) radiation; and infection with Epstein-Barr virus (EBV), Helicobacter pylori, hepatitis B virus (HBV), hepatitis C virus (HCV), human herpes virus-8 (HHV-8; also called Kaposi sarcoma herpesvirus), human immunodeficiency virus (HIV), and human papillomavirus (HPV).

The results showed cigarette smoking had the most considerable population-attributable fraction (PAF) or proportion of cancer cases attributable to risk factors in the population (344,070 cases; 19.3% of all cases), contributing to 56.0% of all potentially preventable cancers in men (206,550 of 368,600) and 39.9% in women (137,520 of 344,740). Excess body weight had the second largest PAF (7.6%), followed by alcohol consumption (5.4%), UV radiation exposure (4.6%), and physical inactivity (3.1%).

By cancer type, the proportion of cases caused by potentially modifiable risk factors ranged from 100% for cervical cancer and Kaposi sarcoma to 4.9% for ovarian cancer. It exceeded 50% for 19 of 30 evaluated cancer types. In addition to cervical cancer and Kaposi sarcoma, more than 80% of all melanomas of the skin (92.2%) and cancers of the anus (94.2%), larynx (89.9%), lung and bronchus (lung; 88.2%), pharynx (87.4%), trachea (85.6%), oesophagus (85.4%), and oral cavity (83.7%) were attributable to evaluated risk factors. Lung cancer had the most significant number of cases attributable to evaluated risk factors in both men (104,410 cases) and women (97,250), followed by skin melanoma (50,570), colorectal cancer (44,310), and urinary bladder cancer (32,000) in men and by breast (83,840), corpus uteri (35,790), and colorectal (34,130) cancer in women.

“These findings show a continued need to increase equitable access to preventive health care and awareness about preventive measures. Effective vaccines are available for hepatitis B virus, which causes liver cancer and HPV, which can cause several cancer types, including cervical, other anogenital, and oropharyngeal cancers,” added Dr Ahmedin Jemal, senior vice president of surveillance and health equity science at the American Cancer Society and senior author of the study. “Vaccination at the recommended time can substantially reduce the risk of chronic infection and, consequently, cancers associated with these viruses. HPV vaccination uptake in the United States is suboptimal.”

Posted on A to Z of Medical Conditions, Cancer, Diabetes

Researchers develop a painless, wearable patch for continuous monitoring of important health data

Patch and quarter

The monitoring patch is compared to a 25-cent coin. CREDIT University of Waterloo Patch reads and sends data on blood glucose, lactates and other critical biomarkers, including indicators of acute cardiac disease

Researchers at two Ontario universities have developed a pain-free, wearable sensor that can continuously monitor blood sugar levels, lactates and other critical health indicators for weeks, sending results to a smartphone or other device.

The Wearable Aptalyzer, created by a team featuring researchers from McMaster University and the University of Waterloo, uses an array of tiny hydrogel needles that penetrate just deeply enough to reach the interstitial fluid beneath the skin but not far enough to reach the blood vessels or nerves.

The patch gathers and sends information about markers in the fluid to an electronic device such as a smart phone, creating an ongoing record of patterns in the rise and fall of critical biomarkers.

Once developed for clinical use, it will allow health professionals to access current medical information available only retrospectively after blood tests and lab work.

The new technology could make monitoring the markers of specific diseases and conditions as simple as tracking pulse, blood pressure and other vital signs.

“This technology can provide real-time information about chronic and acute health conditions, allowing caregivers to act more quickly and with greater certainty when they see trouble,” says one of the paper’s two corresponding authors, McMaster’s Leyla Soleymani.

“The Wearable Aptalyzer is a general platform, meaning it can measure any biomarkers of interest, ranging from diabetes to cardiac biomarkers,” says corresponding author Mahla Poudineh, an assistant professor and director of the IDEATION Lab in the Department of Electrical and Computer Engineering at Waterloo. “Continuous health monitoring doesn’t just help catch diseases early and track how treatments work. It also helps us understand how diseases happen, filling in important gaps in our knowledge that need attention.”

A user would apply and remove the patch like a small bandage held in place with barely visible, soft hooks. The convenience is likely to appeal to diabetics and others who test themselves by drawing samples of blood or by using solid monitoring patches with metal needles that penetrate deeper and rely on less specific electrodes.

The greatest promise of the technology, though, may lie in its ability to produce weeks’ worth of meaningful results at a time, and to transmit data to electronic devices experts can read without sophisticated equipment.


Among the other potential applications, the Wearable Aptalyzer can make it possible to read and send data that signals cardiac events in real time, making it a potentially valuable tool for monitoring patients in ambulances and emergency rooms, and during treatment. The same technology can readily be adapted to monitor the progress and treatment of many chronic illnesses, including cancers, the researchers say.

Posted on Cancer, Rheumatoid arthritis

Socioeconomic status influences genetic risk for many complex diseases, including RA

Differences in socioeconomic status (SES) are known to be linked to differences in the risk of developing disease. While people with lower SES are more likely to develop complex diseases such as diabetes and cardiovascular disease, those with a higher SES are at increased risk of developing certain types of cancer. Using biobank and national register data, researchers from Finland have now found that people with lower SES (educational achievement and occupation) have a greater genetic susceptibility to develop many other complex diseases such as rheumatoid arthritis, lung cancer, depression, and alcohol use disorder, as well as Type 2 diabetes, whereas those with a higher SES are more at risk of developing breast, prostate, and all cancers.

Dr Fiona Hagenbeek, a postdoctoral researcher at the Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Finland, who will present her group‘s work at the annual conference of the European Society of Human Genetics today (Sunday), says that these promising initial results mean that it is likely that polygenic risk scores, which measure an individual‘s risk of a particular disease based on genetic information, could be added to the screening protocols for multiple diseases and in several countries. “Understanding that the impact of polygenic scores on disease risk is context-dependent may lead to further stratified screening protocols,“ she says. “For example, in the future, screening protocols for breast cancer may be adapted so that females with a high genetic risk and who are highly educated receive earlier or more frequent screening than females with lower genetic risk or less education.”

The researchers used genomics, SES, and health data from approximately 280,000 Finnish individuals in the FinnGen study, a research project in genomics and personalised medicine that aims to understand the genetic basis of diseases. The participants were aged 35 – 80 at the time of entry into the study. The study aimed to systematically assess the evidence of gene-environment interaction (GxE) through the differing genetic susceptibility to disease in diverse socioeconomic groups. While previous studies have shown the presence of such a difference in risk, this is the first to systematically assess GxE for SES in 19 complex diseases that have a high burden in high-income countries.

“Most clinical risk prediction models include basic demographic information such as biological sex and age, recognising that disease incidence differs between males and females, and is age-dependent,“ says Dr Hagenbeek. “Acknowledging that such context also matters when incorporating genetic information into healthcare is an important first step. But now, we can show that the genetic prediction of disease risk also depends on an individual’s socioeconomic background. So while our genetic information does not change throughout our lifetime, the impact of genetics on disease risk changes as we age or change our circumstances.“

The researchers hope that the study will be followed up to see whether further differences can be identified when looking at more specific aspects of educational and professional achievement. While their current results for profession generally mirror those for education, they do not match completely, indicating that each can provide unique information on the interplay of socioeconomic status and genetics on disease risk. Expanding the list of socioeconomic indices to be studied may bring about new insights into how the overlapping aspects of a person’s socioeconomic environment may, together with genetic information, influence their disease risk.

They will also compare their results across biobank studies from Finland, UK, Norway, and Estonia through the INTERVENE* consortium, allowing them to determine whether there are country or biobank-specific issues involved. “Our study focused solely on individuals of European ancestry, and it will also be important in the future to see whether our observations concerning the interplay of socioeconomic status and genetics for disease risk are replicated in people of multiple ancestries in higher and lower-income countries,“ says Dr Hagenbeek. “As the overall aim of incorporating genetic information into healthcare is to facilitate personalised medicine, we should not treat genetic information as ‘one size fits all‘. Rather, we should investigate and then include the circumstances that modify genetic risk when carrying out disease prediction.“

Posted on Cancer, Cardiovascular disease, Diabetes, Obesity

Food’s Protective Power Against Inflammation

Inflammation can be good, signalling your body’s attempt to fight off infection or heal an injury. But when inflammatory cells soldier forth when you’re not sick or injured, chronic inflammation can ensue, contributing to obesity, cardiovascular disease, diabetes, and even autoimmune disease and cancer. The good—no, great—news is that the foods you eat can dramatically affect inflammation in your body, helping not only to prevent it but to fight it if it’s already started. Join Dr. Katsumoto as she discusses how foods can be anti-inflammatory—and how the ones you choose can also help the planet.

Posted on Cancer, Multiple Sclerosis

Multiple Sclerosis – New approach to Epstein-Barr virus and resulting diseases

The Epstein-Barr virus can cause a spectrum of diseases, including a range of cancers. Emerging data now show that inhibition of a specific metabolic pathway in infected cells can diminish latent infection and therefore the risk of downstream disease, as reported by researchers from the University of Basel and the University Hospital Basel in the journal Science.
The Epstein-Barr virus can cause a spectrum of diseases, including a range of cancers and possibly multiple sclerosis. Emerging data now show that inhibition of a specific metabolic pathway in infected cells can diminish latent infection and, therefore, the risk of downstream disease, as reported by researchers from the University of Basel and the University Hospital Basel in the journal Science.

Exactly 60 years ago, pathologist Anthony Epstein and virologist Yvonne Barr announced the discovery of a virus that has carried their names ever since. The Epstein-Barr virus (EBV) made scientific history as the first virus proven to cause cancer in humans. Epstein and Barr isolated the pathogen, which is part of the herpesvirus family, from tumour tissue and demonstrated its cancer-causing potential in subsequent experiments.

Most people are carriers of EBV: 90% of the adult population are infected with the virus, usually experiencing no symptoms and no resulting illness. Around 50% become infected before the age of five, but many people don’t catch it until adolescence. Acute infection with the virus can cause glandular fever — also known as “kissing disease” — and can put infected individuals out of action for several months. In addition to its cancerogenic properties, the pathogen is also suspected to be involved in the development of autoimmune diseases such as multiple sclerosis.

As yet, no drug or approved vaccination can specifically thwart EBV within the body. Now, a research group from the University of Basel and the University Hospital Basel has reported a promising starting point for putting the brakes on EBV. Their results have been published in the journal Science.

EBV hijacks the metabolism of infected cells

Researchers led by Professor Christoph Hess have deciphered how the immune cells infected with EBV —the so-called B cells — are reprogrammed. Known as “transformation,” this process is necessary for the infection to become chronic and cause subsequent diseases such as cancer. Specifically, the team discovered that the virus triggers the infected cell to ramp up the production of an enzyme known as IDO1. This ultimately leads to greater energy production by the power plants of infected cells: the mitochondria. In turn, this additional energy is needed for the increased metabolism and the rapid proliferation of B cells reprogrammed by EBV in this way.

Clinically, the researchers focused on a group of patients who had developed EBV-triggered blood cancer following organ transplantation. To prevent a transplanted organ from being rejected, it is necessary to weaken the immune system using medications. This, in turn, makes it easier for EBV to gain the upper hand and cause blood cancer, referred to as post-transplant lymphoma.

In the paper, which has now been published, the researchers were able to show that EBV upregulates the enzyme IDO1 already months before post-transplant lymphoma is diagnosed. This finding may help to develop biomarkers for the disease.

Second chance for a failed drug

“Previously, IDO1 inhibitors have been developed in the hope that they could help to treat established cancer — which has unfortunately turned out not to be the case. In other words, there are already clinically tested inhibitors against this enzyme,” explains Christoph Hess. Accordingly, this class of drugs might now receive a second chance in applications aimed at dampening EBV infection and thereby tackling EBV-associated diseases. Indeed, in experiments with mice, IDO1 inhibition with these drugs reduced the transformation of B cells and therefore the viral load and the development of lymphoma.

“In transplant patients, it’s standard practice to use drugs against various viruses. Until now, there’s been nothing specific for preventing or treating Epstein-Barr virus associated disease,” says Hess.