The research, led by the UN World Health Organization’s centre for cancer research, pooled data from nearly 2.5 million people across Asia, Australia, Europe, and North America.
It revealed a “modest but significant” association between alcohol consumption and the risk of developing pancreatic cancer, regardless of sex or smoking status.
“Alcohol consumption is a known carcinogen, but until now, the evidence linking it specifically to pancreatic cancer has been considered inconclusive,” said Pietro Ferrari, senior author of the study at the international cancer research agency and Head of Nutrition and Metabolism Branch at the WHO International Agency for Research on Cancer (IARC).
The pancreas is a vital organ that produces enzymes for digestion and hormones that regulate blood sugar. Pancreatic cancer is among the most lethal cancers, largely due to late diagnosis.
All drinkers are at risk
The IARC study found that each additional 10 grams of alcohol consumed per day was associated with a 3 per cent increase in pancreatic cancer risk.
For women consuming 15 to 30 grams of alcohol daily – about one to two drinks – the risk rose by 12 per cent compared to light drinkers. Among men, those who drank 30 to 60 grams daily faced a 15 per cent increased risk, while men drinking more than 60 grams daily saw a 36 per cent higher risk.
“Alcohol is often consumed in combination with tobacco, which has led to questions about whether smoking might confound the relationship,” Mr. Ferrari said.
“However, our analysis showed that the association between alcohol and pancreatic cancer risk holds even for non-smokers, indicating that alcohol itself is an independent risk factor.”
Further research is needed, he added, to better understand the impact of lifetime alcohol consumption, including patterns such as binge drinking and early-life exposure.
A growing global challenge
Pancreatic cancer is the twelfth most common cancer globally, but it accounts for 5 per cent of cancer-related deaths due to its high fatality rate.
In 2022, incidence and mortality rates were up to five times higher in Europe, North America, Australia and New Zealand, and Eastern Asia than in other regions.
The Royal Swedish Academy of Sciences has awarded the 2022 Nobel Prize in Chemistry to Carolyn Bertozzi, Morten Meldal, and K. Barry Sharpless “for the development of click chemistry and bioorthogonal chemistry.”
Bertozzi, a professor of chemistry at Stanford University, is the eighth woman to be awarded the prize. From 1996 to 2015, before joining Stanford, she was a faculty scientist at the Department of Energy’s Lawrence Berkeley National Laboratory and a UC Berkeley professor. She also served as the director of the Molecular Foundry, a DOE Office of Science nanoscience user facility located at Berkeley Lab, from 2006 to 2010.
The award to Bertozzi brings the number of Nobel Prizes associated with Berkeley Lab scientists to sixteen. (Earlier this week, on Tuesday, Oct. 4, former Lab postdoc John Clauser’s 2022 Nobel Prize in Physics brought the Lab’s tally to fifteen.)
According to today’s Nobel Prize announcement, “The Nobel Prize in Chemistry 2022 is about making difficult processes easier. Barry Sharpless and Morten Meldal have laid the foundation for a functional form of chemistry – click chemistry – in which molecular building blocks snap together quickly and efficiently. Carolyn Bertozzi has taken click chemistry to a new dimension and started utilising it in living organisms.”
Carolyn Bertozzi/CREDIT:Jenny Nuss/Berkeley Lab
“Carolyn Bertozzi had a profound impact at Berkeley Lab, not only through her brilliant science, but as someone who created new institutions that encouraged team science,” said Berkeley Lab Director Mike Witherell.
By pioneering a method for mapping biomolecules on the surface of cells, Bertozzi helped create a suite of techniques comprising “bioorthogonal chemistry,” a term Bertozzi coined, which means “not interacting with biology.” The method describes chemical reactions that allow scientists to explore cells and track biological processes without disrupting the normal chemistry of the cell.
Bertozzi’s lab first developed the method in the late 1990s and early 2000s. During that time, she was one of the six scientists who helped establish the Molecular Foundry, a nanoscience research facility that provides scientists from around the world access to cutting-edge expertise and instrumentation. She served as the Molecular Foundry’s director when the facility first opened its doors to the research community in 2006, and she founded the Foundry’s Biological Nanostructures Facility, where scientists study the synthesis, analysis and mimicry of biological nanostructures.
“Carolyn Bertozzi’s impact on nanoscience is huge,” said Jeff Neaton, associate laboratory director of Berkeley Lab’s Energy Sciences Area. “The chemistry she developed paved the way for the science and engineering of living-nonliving interfaces, a frontier of nanoscience which also became a major theme of the Foundry.”
Under Bertozzi’s leadership, the Foundry grew immensely, bringing in scientists from across the disciplines. This multidisciplinary approach inspired collaborations with visiting scientists, including longtime Foundry user K. Barry Sharpless, co-recipient of the Nobel Prize in Chemistry with Bertozzi and Morten Meldal.
“Carolyn put the Foundry on the map,” said Bruce Cohen, a staff scientist in the Foundry’s Biological Nanostructures facility since 2006. “She oversaw the opening of the facility, which is a major administrative and scientific feat.” He added that Bertozzi’s “science is so creative and original, as well as technically on point, and it’s opened up entire new areas of study. This is a well-deserved Nobel Prize. I couldn’t be happier for her.”
Cohen said that Bertozzi is also “a great mentor to all of the scientists around her, and has always been an inspirational role model for both women and LGBTQ people in science.”
Bertozzi and others have used her methods to answer fundamental questions about the role of sugars in biology, to study how cells build proteins and other molecules, to develop new cancer medicines, and to produce new materials for energy storage, among many other applications.
The Nobel committee said in a statement that “click chemistry and bio-orthogonal reactions have taken chemistry into the era of functionalism,” adding that “this is bringing the greatest benefit to humankind.”
Among her many awards, Bertozzi is a recipient of the 2014 Ernest Orlando Lawrence Award, the Department of Energy’s highest scientific honor. She was named a MacArthur Fellow in 1999. She won the Wolf Prize in Chemistry in 2022.
Bertozzi completed her undergraduate degree in chemistry at Harvard University and her Ph.D. at UC Berkeley. She has been a Howard Hughes Medical Institute Investigator since 2000. She joined Stanford in 2015.
Scientists have identified immune cell types that could be targeted to develop specific immunotherapies in chemotherapy-resistant breast cancers.
Researchers from King’s College London and The Institute of Cancer Research, London, with support from Breast Cancer Now, have performed a deep dive into the different immune markers within tumour tissues and blood samples of early breast cancer patients whose cancer failed to respond to chemotherapy given to them prior to surgery.
The research, published today in Clinical Cancer Research, a journal of the American Association for Cancer Research, gives insight into the function of immune cells in patients with chemotherapy-resistant breast cancers. While chemotherapy may not kill cancer cells in these high-risk patients, immunotherapy, a type of treatment that helps the immune system to attack cancer cells, may provide a benefit.
To investigate the immune environment that surrounds these chemotherapy resistant tumours, researchers employed multiple and novel complementary technologies looking at proteins and genes on both pre-treatment and post-treatment breast cancer tissue. They also measured how 1,330 cancer and immune-related genes within cancer tissues were affected by chemotherapy.
Flax seeds help women combat menstrual complications and fight post-menopausal risk of breast cancer, say studies
They found that chemotherapy resistant cancer cells had very few immune cells around them, but chemotherapy did induce changes in several immune cell types. Specifically, they found increases in the number of “innate” (first responder) cells such as neutrophils and natural killer (NK) cells. NK cells help the body to fight infection and cancer. But analysis found the increased NK cells in patients with chemotherapy resistant disease lacked cytotoxic activity – the ‘killing instinct’.
Researchers also found immune-related genes associated with NK cells were those associated with cell inhibition or exhaustion, which meant NK cells were unable to fight cancer cells. This new insight into the behaviour of NK cells could be used to develop specific immunotherapies for these high-risk patients. This would need to be investigated in future clinical trials.
These findings also show that blood monitoring during chemotherapy may help predict chemotherapy response early, potentially allow for tailoring of treatment prior to surgery.
Lead author Dr Sheeba Irshad, Cancer Research UK Clinician Scientist at King’s College London said: “Chemotherapy resistance in aggressive early breast cancers is a major reason why cancer regrows after treatment, contributing significantly to people not surviving their disease. In order to find the right targets for drug developments, it’s important to have a deep understanding of the complex mechanisms that allow some cancer cells to resist treatment, then hide from our immune system to only re-emerge later when they’re harder to eradicate.
“Our work has identified several cell types that would be worth investigating further to understand how they are interacting with the resistant cancer cell and how we can tweak that for our benefit. I am excited to continue to investigate these findings further.”
chemotherapy
Professor Andrew Tutt, Director of the Breast Cancer Now Toby Robins Research Centre at The Institute of Cancer Research, London, and of the Breast Cancer Now Research Unit at King’s College London, said: “Great strides have been made in harnessing immunotherapies to treat several types of cancer, but we need to do better to realise their potential for patients with breast cancer.
“This exciting work advances our understanding of the interaction between cancer cells and the immune system during treatment, and why existing treatments work well for some patients, but not others. I hope this research will help us to enhance the anti-cancer immune response in breast cancer, particularly for patients whose cancer has not responded well to chemotherapy.”
Dr Kotryna Temcinaite, Senior Research Communications Manager at Breast Cancer Now, said: “With an estimated 35,000 people living with incurable secondary (metastatic) breast cancer in the UK, it’s vital we develop smarter, more effective treatments to ensure fewer people hear the devastating news the disease has returned and spread to other parts of the body. This exciting early-stage research, which has been part-funded by Breast Cancer Now, helps to lay the groundwork for discovering a way to target breast cancer cells that resist chemotherapy treatment. We hope by building on these findings, scientists will ultimately be able to develop immunotherapy treatments that may help more people survive breast cancer.”
One approach to treating cancer is photodynamic therapy using photo-uncaging systems, in which light is used to activate a cancer-fighting agent in situ at the tumor. However, suitable agents must be stable under visible light, have an anti-tumor effect in low-oxygen environments, and have the ability to be activated by low-energy tissue-penetrative red light – a combination of properties that is difficult to achieve. Now, a team from The Institute of Industrial Science at The University of Tokyo has developed a new platform that uses, for the first time, organorhodium(III) phthalocyanine complexes to achieve this combination of traits.
Conventional photodynamic techniques depend on the formation of reactive oxygen species to destroy tumor cells, but many tumors contain environments that lack oxygen. Photo-uncaging systems, where the agent is administered in an inactive form and then activated, or “uncaged”, in the location of the tumor, address this issue. They uncage alkyl radicals, which are known to be capable of inducing cell death both with and without the presence of oxygen. Alkyl radicals are converted into terminal aldehydes in the presence of oxygen, and these terminal aldehydes can also induce cell death. The team used molecules called “organorhodium(III) phthalocyanine (Pc) complexes” to develop, for the first time, a novel platform for photo-uncaging therapy.
Researchers from The Institute of Industrial Science, The University of Tokyo have developed a streamlined photo-uncaging system for photodynamic cancer therapy, using a pulse of light for tumor-specific activation of a cancer-fighting agent/CREDIT Institute of Industrial Science, The University of Tokyo
“The organorhodium(III) phthalocyanine (Pc) complexes we developed are highly stable under ambient light during the processes of synthesis, purification, and measurement, but can be activated by a laser that gives out nanosecond pulses of red light,” explains lead author Kei Murata. These nanosecond-pulsing lasers (pulsing for a billionth of a second) are relatively easy for medical staff to handle.
They went on to show that the compounds that were released after the organorhodium(III) phthalocyanine (Pc) complexes were activated showed toxicity to HeLa cells, a cell line developed from cancer, indicating that these compounds would have the ability to fight cancer if released inside a tumor.
“Our new technology could allow the photochemical generation of a wide variety of alkyl radicals and aldehydes, making possible the site-selective release of various bioactive molecules,” says senior author Kazuyuki Ishii. As an improvement on other photo-uncaging systems, it opens an exciting new avenue for the treatment of cancer by phototherapy.
Engineers at the Georgia Institute of Technology and Stanford University have created a small, autonomous device with a stretchable/flexible sensor that can be adhered to the skin to measure the changing size of tumors below. The non-invasive, battery-operated device is sensitive to one-hundredth of a millimeter (10 micrometers) and can beam results to a smartphone app wirelessly in real-time with the press of a button.
In practical terms, the researchers say, their device—dubbed FAST for “Flexible Autonomous Sensor measuring Tumors”—represents a wholly new, fast, inexpensive, hands-free, and accurate way to test the efficacy of cancer drugs. On a grander scale, it could lead to promising new directions in cancer treatment.
Each year researchers test thousands of potential cancer drugs on mice with subcutaneous tumors. Few make it to human patients, and the process for finding new therapies is slow because technologies for measuring tumor regression from drug treatment take weeks to read out a response. The inherent biological variation of tumors, the shortcomings of existing measuring approaches, and the relatively small sample sizes make drug screenings difficult and labor-intensive.
“FAST” sensor/Photo:Stanford University
“In some cases, the tumors under observation must be measured by hand with calipers,” says Alex Abramson, first author of the study and a recent post-doc in the lab of Zhenan Bao at the Stanford School of Engineering and now an assistant professor at Georgia Tech. The use of metal pincer-like calipers to measure soft tissues is not ideal, and radiological approaches cannot deliver the sort of continuous data needed for real-time assessment. FAST can detect changes in tumor volume on the minute-timescale, while caliper and bioluminescence measurements often require weeks-long observation periods to read out changes in tumor size.
FAST’s sensor is composed of a flexible and stretchable skin-like polymer that includes an embedded layer of gold circuitry. This sensor is connected to a small electronic backpack designed by former post-docs and co-authors Yasser Khan and Naoji Matsuhisa. The device measures the strain on the membrane—how much it stretches or shrinks—and transmits that data to a smartphone. Using the FAST backpack, potential therapies that are linked to tumor size regression can quickly and confidently be excluded as ineffective or fast-tracked for further study.
The researchers say that the new device offers few significant advances.
It provides continuous monitoring, as the sensor is physically connected to the mouse/human patients and remains in place over the entire experimental period.
FAST can detect changes in tumor volume on the minute-timescale, while caliper and bioluminescence measurements often require weeks-long observation periods to read out changes in tumor size.
FAST is both autonomous and non-invasive. It is connected to the skin, not unlike a band-aid, battery operated and connected wirelessly. The mouse/human patients are free to move unencumbered by the device or wires, and scientists do not need to actively handle the mice following sensor placement.
FAST packs are also reusable, cost just $60 or so to assemble and can be attached to the mouse/human patients in minutes.
FAST could significantly expedite, automate and lower the cost of the process of screening cancer therapies.
FAST’s sensor is composed of a flexible and stretchable skin-like polymer that includes an embedded layer of gold circuitry.\/Photo:Alex Abramson, Bao Group, Stanford University
The breakthrough is in FAST’s flexible electronic material. Coated on top of the skin-like polymer is a layer of gold, which, when stretched, develops small cracks that change the electrical conductivity of the material. Stretch the material and number of cracks increases, causing the electronic resistance in the sensor to increase as well. When the material contracts, the cracks come back into contact and conductivity improves.
Both Abramson and co-author Naoji Matsuhisa, an associate professor at the University of Tokyo, characterized how these crack propagation and exponential changes in conductivity can be mathematically equated with changes in dimension and volume.
One hurdle the researchers had to overcome was the concern that the sensor itself might compromise measurements by applying undue pressure to the tumor, effectively squeezing it. To circumvent that risk, they carefully matched the mechanical properties of the flexible material to skin itself to make the sensor as pliant and as supple as real skin.
“It is a deceptively simple design,” Abramson says, “But these inherent advantages should be very interesting to the pharmaceutical and oncological communities. FAST could significantly expedite, automate and lower the cost of the process of screening cancer therapies.”
New York, Sep 12 (IANS) The risk of type 2 diabetes is more than halved by weekly injections of the new obesity drug semaglutide, which was recently approved in the US and has been provisionally approved in England, says a new study.
The researchers of the study, to be presented at the annual meeting of the European Association for the Study of Diabetes (EASD), said semaglutide reduces the future risk of diabetes by over 60 per cent in patients with obesity.
“Semaglutide appears to be the most effective medication to date for treating obesity and is beginning to close the gap with the amount of weight loss following bariatric surgery,” said researcher W. Timothy Garvey from the University of Alabama at Birmingham in the US.
diabetes
Obesity is known to increase the risk of type 2 diabetes at least six-fold and the team was interested in understanding whether semaglutide could reduce this risk. To learn more, they conducted a new analysis of the data from two trials of semaglutide.
In STEP 1, 1,961 overweight or obese participants received an injection of 2.4 mg of semaglutide or a placebo weekly, for 68 weeks.
STEP 4 involved 803 participants with overweight or obesity. All received weekly injections of 2.4 mg semaglutide for 20 weeks. They then either remained on semaglutide or were switched to placebo for the next 48 weeks.
In STEP 1 participants receiving semaglutide, 10-year risk scores for type 2 diabetes decreased by 61 per cent (from 18.2 per cent at week 0 to 7.1 per cent at week 68). This compares to a 13 per cent reduction in risk score for those given the placebo (17.8 per cent at week +0 to 15.6 per cent at week 68).
In the STEP 4 participants, the largest decreases in risk scores were seen in the first 20 weeks (from 20.6 per cent at week 0 to 11.4 per cent at week 20). In those who continued receiving semaglutide, the risk score decreased further to 7.7 per cent but in those who were switched to placebo, it rose to 15.4 per cent.
Boosting physical activity levels and curbing sitting time are highly likely to lower breast cancer risk, finds research designed to strengthen proof of causation and published online in the British Journal of Sports Medicine.
The findings were generally consistent across all types and stages of the disease, reveals the Mendelian randomisation study, prompting the researchers to recommend a stronger focus on exercise as a way of warding off breast cancer.
Mendelian randomisation is a technique that uses genetic variants as proxies for a particular risk factor—in this case lifelong physical activity levels/sedentary behaviour—to obtain genetic evidence in support of a causal relationship.
Exercise/Photo:en.wikipedia.org
Observational studies show that physical inactivity and sedentary behaviour are linked to higher breast cancer risk, but proving they cause breast cancer is another matter.
The researchers therefore used Mendelian randomisation to assess whether lifelong physical activity and sitting time might be causally related to breast cancer risk in general, and specifically to different types of tumour.
They included data from 130,957 women of European ancestry: 69, 838 of them had tumours that had spread locally (invasive); 6667 had tumours that hadn’t yet done so (in situ); and a comparison group of 54,452 women who didn’t have breast cancer.
Exercise-Yoga/Photo:en.wikipedia.org
The researchers then drew on previously published studies that had used the vast repository of UK Biobank data on potential genetic explanations for overall predisposition to physical activity, vigorous physical activity, or sitting time—as measured by wrist-worn activity trackers—to genetically predict how physically active or inactive their own study participants were.
Next, the researchers estimated overall breast cancer risk, according to whether the women had or hadn’t gone through the menopause; and by cancer type,stage (size and extent of tumour spread), and grade (degree of tumour cell abnormality).
Analysis of the data showed that a higher overall level of genetically predicted physical activity was associated with a 41% lower risk of invasive breast cancer, and this was largely irrespective of menopausal status, tumour type, stage, or grade.
Similarly, genetically predicted vigorous physical activity on 3 or more days of the week was associated with a 38% lower risk of breast cancer, compared with no self-reported vigorous activity. These findings were consistent across most of the case groups.
cancer cells/photo:en.wikipedia.org
Finally, a greater level of genetically predicted sitting time was associated with a 104% higher risk of triple negative breast cancer. These findings were consistent across hormone-negative tumour types.
The findings were unchanged after factoring in the production by a single gene of two or more apparently unrelated effects (pleiotropy), such as smoking and overweight, for example.
There are plausible biological explanations for their findings, say the researchers, who point to a reasonable body of evidence indicating numerous causal pathways between physical activity and breast cancer risk, such as overweight/obesity, disordered metabolism, sex hormones, and inflammation.
“Mechanisms linking sedentary time and cancer are likely to at least partially overlap with those underpinning the physical activity relationship,” suggest the researchers.
Their findings provide “strong evidence” that more overall physical activity and less sitting time are likely to reduce breast cancer risk, they say.
And they conclude: “Increasing physical activity and reducing sedentary time are already recommended for cancer prevention. Our study adds further evidence that such behavioural changes are likely to lower the incidence of future breast cancer rates.
“A stronger cancer-control focus on physical activity and sedentary time as modifiable cancer risk factors is warranted, given the heavy burden of disease attributed to the most common cancer in women.”
Young Australians can now access a free DNA saliva test to learn whether they face increased risk of some cancers and heart disease, which can be prevented or treated early if detected, in a world-first DNA screening study.
The nationally collaborative project, led by Monash University and supported by researchers and clinicians across Australia, will screen at least 10,000 people aged 18-40 for genes that increase risk of certain types of cancers and heart disease that often go undetected.
Those found to be at high risk after DNA testing – about one in 75 or 1.3 per cent – will have their situation explained by experts and be offered genetic counselling and prevention measures, such as regular scans and check-ups.
cancer/photo:en.wikipedia.org
Until now, genetic testing for the DNA changes that increase disease risk has only been available on a small scale for those with a known family history or prior disease diagnosis. Population testing, open to everyone, has the potential to drastically improve access and maximize the preventive benefits of DNA testing.
Monash University’s Associate Professor Paul Lacaze said the project enabled a more efficient and equitable approach to genetic testing, identifying far more people at high risk than current testing methods.
“We hope to identify those at risk while they are young and healthy, not after the fact, and empower them to make more informed decisions about their health,” he said. “For some people, this could save their lives through early detection and prevention of cancer and heart disease. This will also save considerable health system costs in Australia through prevention.
“Providing genetic testing based on family history alone is not enough. Up to 90 per cent of those at high risk in the general population are not identified by current family history-based testing. Most people don’t find out about their genetic risk until it’s too late, like after an incurable cancer or heart attack is diagnosed. We want to change that.”
DNA Screen will identify people with DNA variants in the BRCA1 and BRCA2 genes that lead to an increased risk of hereditary breast and ovarian cancer in women. These genes are also linked to breast and prostate cancer in men, although not as strongly. Men and women who carry DNA variants in the BRCA1 and BRCA2 genes can also pass them onto their children.
The DNA Screen test will also focus on Lynch Syndrome – another condition that increases risk for colorectal, endometrial, and other gastrointestinal cancers. Both cancer-related conditions have effective, proven interventions available to reduce risk if identified early.
This includes attending annual check-ups and screens from age 30, and the option of risk-reducing surgery for some people. Early detection and prevention are often life-saving for cancer.
The DNA test also encompasses heart disease risk, focusing on familial hypercholesterolemia (FH) or ‘genetic high cholesterol’, which results in high risk of heart disease from a young age. Despite effective medications such as statins being available to reduce risk, an estimated 95 per cent of FH carriers are currently undiagnosed.
Associate Professor Lacaze, from the Monash University School of Public Health and Preventive Medicine, is leading a team of national collaborators who were awarded a $2.97 million Medical Research Future Fund (MRFF) grant for the project. The project is supported by the Precision Medicine laboratory at Monash University and the state-of-the-art Biobanking Victoriafacility.
The eventual goal is to develop a new population-based DNA screening program that could be offered through the Australian public healthcare system, available to everyone but targeted on certain medically-actionable conditions where early detection is key.
“We expect to identify about 1 in 75 people at high risk of these diseases. Those found to be high risk won’t necessarily get the disease, but pinpointing risk before symptoms appear enables prevention through regular check-ups, medication, or risk-reducing surgery. It could save their life.
DNA Screen, which is recruiting young people via social media, is expected to save lives and could lead to a wide scale preventive DNA testing program for cancer and heart disease risk, where early detection and prevention can be life-saving.
DNA Screen is the world’s first preventive DNA screening study designed specifically to assess population DNA screening through a national healthcare system. The test is free and involves placing a saliva sample into a small tube received by mail, and sending it back in a postage paid envelope. People can sign up online at dnascreen.monash.edu
Researchers have discovered that some immunotherapy treatments used to treat cancer can cause fertility damage.
It means these treatments could affect the future fertility and hormonal health of female cancer survivors, prompting experts to call for more research and preventative measures, such as freezing eggs.
Led by the Biomedicine Discovery Institute at Monash University and the Peter MacCallum Cancer Centre, the pre-clinical trial showed that immune checkpoint inhibitors, a common type of immunotherapy drug, resulted in permanent damage to mouse ovaries and the eggs stored inside.
cancer/photo:en.wikipedia.org
Traditional cancer therapies, such as chemotherapy and radiotherapy, are already linked to permanent, negative side effects on the ovaries. This can lead to infertility and premature menopause in young girls and women.
Researchers found that checkpoint inhibitor immunotherapy reduced the number and quality of their eggs, interfered with ovulation, and disrupted the fertility cycle.
Until now the potential fertility side effects of immunotherapy, an emerging and increasingly common cancer treatment that stimulates the immune system, have been unknown.
The study found that a type of immunotherapy called immune checkpoint inhibitors, which ‘release the brakes’ on the immune system to enhance a patient’s ability to fight cancer, could impair immediate and future fertility.
Its authors said studies in female patients were now needed to investigate the findings. In the meantime, fertility preservation through egg or embryo freezing should be considered for women using these immunotherapies.
“Initially these treatments were thought to be less damaging (than chemo and radiotherapy) in the context of off-target effects to the body in general,” Ms Alesi said. “However, it is now clear that inflammatory side effects in other organ systems are quite common with these drugs.
“Our study highlights that caution should be exercised by clinicians and their patients, for whom fertility may be a concern. Studies in women receiving these drugs must now be prioritised.”
Peter MacCallum Cancer Centre Specialist Medical Oncologist Professor in breast cancer and a senior author on the study Sherene Loi said further research into how these drugs impact the ovarian function and fertility of women receiving these drugs must be prioritised and should be included in future clinical trials involving women of reproductive age.
“Our study further highlights that fertility discussions are critical for all age appropriate women who are recommended to receive chemotherapy as well as immunotherapy,” Professor Loi said.
“Appropriate interventions that can preserve fertility and ovarian function can be implemented to facilitate pregnancies in the future, post completion of treatment. These interventions need to be implemented in a timely manner, so as not to delay anti-cancer treatment.
“Immunotherapy is now becoming a standard of care for many women with curable early stage breast cancer, due to impressive results in reducing breast cancer recurrences, but further research into the long-term effects of immunotherapy is needed.”
Apart from drugs that block ovaries from producing hormones during chemotherapy, and strategies to prevent premature menopause in younger women, Ms Alesi said egg and embryo freezing was the only fertility preservation measure available.
She said it was important to remember that embryo freezing was expensive, invasive and did not prevent ovarian damage. This meant that premature menopause could still be a risk for these women.
“Therefore, we are now prioritising investigation of targeted ovarian preservation strategies that aim to prevent the damage to the ovary from occurring in the first place, without interfering with the drugs’ ability to fight the cancer” she said.
Recent study shows that during the first year of the COVID-19 pandemic, the proportion of working-aged UAmerican adults without health insurance did not change despite increases in unemployment, and the prevalence of unhealthy behaviors decreased.
The findings, published by Wiley online in CANCER, studied individuals with and without a history of cancer. While cancer survivors often have high health care needs, they are more vulnerable to the effects of economic and health care disruptions, as happened during the first year of the COVID-19 pandemic.
File Photo of Johns Hopkins Covid-19 map
Xuesong Han of the American Cancer Society, and her colleagues used data from the nationwide, population-based Behavioral Risk Factor Surveillance System—an annual household telephone survey—to examine changes in multiple health-related measures in 2020 among cancer survivors.
Among adults aged 18–64 years, the uninsured rate did not change significantly in 2020 despite huge job cuts. The prevalence of unhealthy behaviors, including sleeplessness and smoking decreased in 2020, and health improved, regardless of cancer history, showed the analysis.
Declines in smoking were greater among cancer survivors than among adults without a cancer history, it noted. “Our findings suggest that the pandemic may have motivated people to adopt certain healthier behaviors, and national and regional policy responses to the pandemic regarding insurance coverage, unemployment benefits, and financial assistance may have contributed to the observed positive changes,” said Han.
Amid new diagnostic methods and treatment options, early detection is an emerging paradigm which seeks to decrease patient morbidity and mortality. And here comes saliva diagnostics with huge potential, possibly replacing the painful pricking on fingers or on wrists.
Saliva diagnostics is emerging as the latest and easiest way to detect disease at a phase where it is easily treatable. It is likely to provide new opportunities to use saliva liquid biopsy for early assessment of lung cancer because of the clinical performance of cancer detection, non-invasive collection process and the ease of collecting, transporting and storing saliva, said researchers.
At the 96th General Session of the International Association for Dental Research (IADR), held in conjunction with the IADR Pan European Regional (PER) Congress, David Wong, University of California, Los Angeles, USA presented his research “Saliva Diagnostics and Salivaomics” as part of the symposium “Will Saliva Translate to a Real Diagnostic Tool?” on Saturday, July 28, 2018 in London.
Research conducted on using saliva to measure stress hormones, enzyme levels, developmental disease biomarkers and even cancer mutations has revealed positive outcome, said researchers. “There are a variety of scenarios with which saliva can be used,” said Wong. “One of the most exciting emerging frontiers of saliva is liquid biopsy, which is a non-invasive means to assess the presence and characteristics of cancer in a patient with an indeterminate pulmonary nodule detected by low dose computerized tomography (LDCT).”
Saliva liquid biopsy delivers the best performance in the detection of circulating tumor DNA of lung cancer. This research was presented as part of the symposium. If validated biomarkers were combined with high-quality detection tools.
saliva would open up a new frontier in high-quality healthcare allowing physicians, dentists and patients to work and together for real-time health monitoring and high-impact personalized preventative medicine, said the study.
It’s more than a month since Bollywood actor Irrfan Khan, 51, who shot to fame with his role in Jurassic World, announced that he was suffering from a rare cancer and that he is going to the US for treatment.
Before leaving, he said:"I hope to be back with more stories to tell."
Diagnosed with neuroendocrine tumours, which may occur anywhere in the body, could non-cancerous or even malignant becoming fatal. The actor did not reveal at what stage of the condition his disease is. Instead, he chose to quote, Margaret Mitchell, saying, "Life is under no obligation to give us what we expect."
Film journalist Umair Sandhu has reportedly tweeted saying that his health is deteriorating. Citing family sources, Sandhu, wrote that Irrfan’s cancer was in its final stage and that the doctors were of opinion that he may not last for more than a month. But soon the tweet was retracted.
TimesNowNews has published the tweet that read, "BREAKING NEWS !! As per Family Sources of @irrfank ! His Cancer is at last Stage & Doctors are of the opinion that he may not last more than a month !!" — Umair Sandhu (@sandhumerry) April 8, 2018. However, it was reportedly removed later.
Irrfan Khan acted with ease in some memorable films of both Hollywood and Bollywood like "Paan Singh Tomar", "Talvar", "Maqbool", "7 Khoon Maaf", "Piku", "Hindi Medium" and "Blackmail" in Hindi.
In the West, he has starred in films like "The Namesake", "Life of Pi", "A Mighty Heart", "Slumdog Millionaire", "The Amazing Spider-Man" and "Inferno". His film ‘Hindi Medium’ has made more than Rs.100 in the Chinese market.
A new endoscopic system powered by artificial intelligence (AI) has today been shown to automatically identify colorectal adenomas during colonoscopy. The system, developed in Japan, has recently been tested in one of the first prospective trials of AI-assisted endoscopy in a clinical setting, with the results presented today at the 25th UEG Week in Barcelona, Spain.
AI-assisted endocytoscopy – how it works:
The new computer-aided diagnostic system uses an endocytoscopic* image – a 500-fold magnified view of a colorectal polyp – to analyse approximately 300 features of the polyp after applying narrow-band imaging (NBI) mode or staining with methylene blue. The system compares the features of each polyp against more than 30,000 endocytoscopic images that were used for machine learning, allowing it to predict the lesion pathology in less than a second. Preliminary studies demonstrated the feasibility of using such a system to classify colorectal polyps, however, until today, no prospective studies have been reported.
Prospective study in routine practice:
The prospective study, led by Dr Yuichi Mori from Showa University in Yokohama, Japan, involved 250 men and women in whom colorectal polyps had been detected using endocytoscopy1. The AI-assisted system was used to predict the pathology of each polyp and those predictions were compared with the pathological report obtained from the final resected specimens. Overall, 306 polyps were assessed real-time by using the AI-assisted system, providing a sensitivity of 94%, specificity of 79%, accuracy of 86%, and positive and negative predictive values of 79% and 93% respectively, in identifying neoplastic changes.
Speaking at the Opening Plenary at UEG Week, Dr Mori explained; “The most remarkable breakthrough with this system is that artificial intelligence enables real-time optical biopsy of colorectal polyps during colonoscopy, regardless of the endoscopists’ skill. This allows the complete resection of adenomatous polyps and prevents unnecessary polypectomy of non-neoplastic polyps.”
“We believe these results are acceptable for clinical application and our immediate goal is to obtain regulatory approval for the diagnostic system” added Dr Mori.
Moving forwards, the research team is now undertaking a multicentre study for this purpose and the team are also working on developing an automatic polyp detection system. “Precise on-site identification of adenomas during colonoscopy contributes to the complete resection of neoplastic lesions” said Dr Mori. “This is thought to decrease the risk of colorectal cancer and, ultimately, cancer-related death.”
A large long-term study found that breast cancer risk may be higher for women who live in areas with high levels of outdoor light at night.
The link between outdoor light at night and breast cancer was found only among women who were premenopausal and were current or past smokers, and was stronger among those who worked night shifts.
Women who live in areas with higher levels of outdoor light at night may be at higher risk for breast cancer than those living in areas with lower levels, according to a large long-term study from Harvard T.H. Chan School of Public Health. The link was stronger among women who worked night shifts.
The study will be published online August 17, 2017 in Environmental Health Perspectives.
“In our modern industrialized society, artificial lighting is nearly ubiquitous. Our results suggest that this widespread exposure to outdoor lights during nighttime hours could represent a novel risk factor for breast cancer,” said lead author Peter James, assistant professor at Harvard Medical School’s Department of Population Medicine at Harvard Pilgrim Health Care Institute, who did the work while a research fellow in the Departments of Epidemiology and Environmental Health at Harvard Chan School.
Previous studies have suggested that exposure to light at night may lead to decreased levels of the hormone melatonin, which can disrupt circadian rhythms–our internal “clocks” that govern sleepiness and alertness–and, in turn, lead to increased breast cancer risk.
The new study, the most comprehensive to date to examine possible links between outdoor light at night and breast cancer, looked at data from nearly 110,000 women enrolled in the Nurses’ Health Study II from 1989-2013. The researchers linked data from satellite images of Earth taken at nighttime to residential addresses for each study participant, and also considered the influence of night shift work. The study also factored in detailed information on a variety of health and socioeconomic factors among participants.
Women exposed to the highest levels of outdoor light at night–those in the top fifth–had an estimated 14% increased risk of breast cancer during the study period, as compared with women in the bottom fifth of exposure, the researchers found. As levels of outdoor light at night increased, so did breast cancer rates.
The association between outdoor light at night and breast cancer was found only among women who were premenopausal and those who were current or past smokers. In addition, the link was stronger among women who worked night shifts, suggesting that exposure to light at night and night shift work contribute jointly to breast cancer risk, possibly through mechanisms involving circadian disruption. The authors acknowledged that further work is required to confirm the study findings and clarify potential mechanisms.
Stanford University scientists have described a new type of test that can detect genetic mutations in minute amounts of DNA released from cancer cells into the blood. The test, which is called single color digital PCR, requires only a fraction of a tube of blood and can detect as few as three mutation-bearing molecules in a single reaction. According to the report in The Journal of Molecular Diagnostics, this highly sensitive test has the potential to be personalized to recognize mutations unique to any individual cancer.
“For monitoring patient tumors, only a handful of blood tests are available which are limited to only several types of cancers. Nearly all cancer patients require monitoring by whole body imaging, which can be costly, complex, and time-consuming. In contrast, molecular tests like the one we have developed will enable patients to be monitored at every visit, and thus have the potential for quickly tracking cancer growth and spread. Moreover, the test’s rapid turnaround and relatively low cost, especially compared to next-generation DNA sequencing, provide a potential opportunity for universal monitoring of more patients than is currently done,” explained lead investigator Hanlee P. Ji, MD, Associate Professor in the Department of Medicine at Stanford University and Senior Associate Director of the Stanford Genome Technology Center.
The report describes the use of the test to analyze samples from six patients. Five patients were previously diagnosed with colorectal cancer and one with cholangiocarcinoma.
After generation of customized mutation detection assays, the researchers were able to identify tumor-derived circulating DNA from three out of six patients. In one patient, the assay was able to show the presence of three different mutations. The three patients, whose samples did not show elevated cancer DNA, were undergoing active treatment at the time of collection.
The single-color digital PCR test offers several advantages over other methods of circulating tumor DNA analysis, compared to next-generation targeted sequencing and fluorescent probe-based digital PCR assays. The main advantage is that the new technique does not rely on pre-amplification, which can introduce errors and biases.
“This test is simple enough to set up and analyze without extensive training, and therefore, it can be implemented by anyone, making it highly accessible to any laboratory. It has been truly motivating to work with a technology that will help transform the way that we monitor and treat individuals with cancer. I am excited to share our findings with the cancer research community,” noted lead author and researcher Christina Wood Bouwens, of the Stanford Genome Technology Center and the Division of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, California.
A tiny medical device containing gold specks could boost the effects of cancer medication and reduce its harm, research suggests.
Scientists have completed a study which showed that gold increased the effectiveness of drugs used to treat lung cancer cells.
Experts say that the findings could help researchers use the device to reduce side effects of current chemotherapies by precisely targeting diseased cells without damaging healthy tissue.
Gold is a safe chemical element and has the ability to accelerate – or catalyse – chemical reactions.
Researchers at the University of Edinburgh discovered properties of the precious metal that allow these catalytic abilities to be accessed in living things without any side effects.
Minute fragments, known as gold nanoparticles, were encased in a chemical device by the research team to control these highly-specific reactions in exact locations.
The device was shown to catalyse a directed chemical reaction when implanted in the brain of zebrafish, suggesting it can be used in living animals.
Gold nanoparticles also activated anti-cancer medicines that had been applied to lung cancer cells in a dish, increasing the drugs’ effectiveness.
Some 450 people die from cancer every day in the UK. A cancer diagnosis is made every two minutes. Medications are improving, but often damage healthy cells.
The study was carried out in collaboration with researchers at the University of Zaragoza’s Institute of Nanoscience of Aragon in Spain. It was part-funded by Cancer Research UK (CRUK), and the Engineering and Physical Sciences Research Council and is published in the journal Angewandte Chemie.
Dr Asier Unciti-Broceta from the University of Edinburgh’s CRUK Edinburgh Centre, said: “We have discovered new properties of gold that were previously unknown and our findings suggest that the metal could be used to release drugs inside tumours very safely.
“There is still work to do before we can use this on patients, but this study is a step forward. We hope that a similar device in humans could one day be implanted by surgeons to activate chemotherapy directly in tumours and reduce harmful effects to healthy organs.”
Dr Áine McCarthy, Cancer Research UK’s senior science information officer said: “By developing new, better ways of delivering cancer drugs, studies like this have the potential to improve cancer treatment and reduce side effects. In particular, it could help improve treatment for brain tumours and other hard-to-treat cancers. The next steps will be to see if this method is safe to use in people, what its long- and short-term side effects are, and if it’s a better way to treat some cancers.”
Rashtriya Swasthya Bima Yojana (RSBY), a centrally sponsored scheme, provides health insurance coverage to Below Poverty Line (BPL) families and including other 11 categories of Unorganized Workers (UOWs) who are enrolled under the scheme.
Senior Citizen Health Insurance Scheme (SCHIS) is also implemented w.e.f. 01.04.2016. Under this, health coverage is available for Rs.30,000/- per annum per senior citizen for treatment packages, over and above RSBY entitlement.
Each family enrolled in the scheme is entitled for hospitalization benefits in Government empanelled hospitals (including both private and public). RSBY and SCHIS cover oncology treatment within prescribed benefits ceiling.
Under comprehensive Primary Healthcare, operational guidelines for Prevention, Screening and Control of Common Non-Communicable Diseases: Hypertension, Diabetes and Common Cancers (Oral, Breast, Cervix) have been issued under National Health Mission which envisage preparation of Health Cards for individuals above 30 years of age. These Cards primarily will be health records of individuals listing health issues/diseases/disabilities and exposures to risk factors of common NCDs including cancer.
The Minister of State (Health and Family Welfare), Smt Anupriya Patel stated this in a written reply in the Rajya Sabha here today.
Periodontal disease was associated with increased risk of several types of cancer in postmenopausal women, even in women who had never smoked.
Journal in Which the Study was Published: Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research.
Author: Jean Wactawski-Wende, PhD, a professor in the Department of Epidemiology and Environmental Health and dean of the School of Public Health and Health Professions, State University of New York at Buffalo, was senior author. Ngozi Nwizu, BDS, MMSc, PhD, assistant professor of oral and maxillofacial pathology at The University of Texas School of Dentistry, was lead author.
Background: In recent years, research has shown that periodontal disease is a risk factor for certain cancers, including breast cancer, oral, and esophageal cancers. However, few studies have analyzed the overall risk for all types of cancers.
How the Study Was Conducted and Results: The researchers conducted a prospective cohort study of 65,869 women aged 54 to 86 who were enrolled in the Women’s Health Initiative Observational Study. The women self-reported periodontal disease on questionnaires administered between 1999 and 2003. The researchers monitored cancer outcomes through September 2013. Over an average follow-up time of 8.32 years, the researchers identified 7,149 cases of cancer.
The study showed that a history of periodontal disease was associated with a 14 percent higher risk of developing any cancer. The strongest association was for cancer of the esophagus, which was more than three times more likely in women with periodontal disease than women who did not report periodontal disease. Lung cancer, gallbladder cancer, melanoma, and breast cancer were also associated with significantly higher risk.
The researchers noted that certain cancers, such as breast cancer, lung cancer, and gallbladder cancer, were associated with higher risk in women who smoked and had periodontal disease. Others, such as melanoma, were associated with higher risk in the women who had never smoked but did report periodontal disease.
Author Comment: Wactawski-Wende said the biological mechanisms that connect periodontal disease and cancer are not yet fully understood. She said one possible explanation is that oral pathogens could potentially be carried in saliva and dental plaque, or through diseased periodontal tissues into the blood circulation to reach other body sites and contribute to carcinogenesis; this may possibly explain the strong association in esophageal cancer.
“The esophagus is in close proximity to the oral cavity, and so periodontal pathogens may more easily gain access to and infect the esophageal mucosa and promote cancer risk at that site,” Wactawski-Wende said.
“Our study findings serve to provide further evidence that periodontal disease is linked to cancer, and support the need for further investigation into how periodontal disease contributes to increased cancer risk,” said Nwizu.
The authors said the study’s large size adds to the strength of the findings.
“This study is the first national study focused on women, particularly older women,” Wactawski-Wende said. “Our study was sufficiently large and detailed enough to examine not just overall risk of cancer among older women with periodontal disease, but also to provide useful information on a number of cancer-specific sites.”
Limitations: The authors said that because the study used self-reported data, the prevalence of periodontal disease may have been under-reported. They said further research that uses more precise assessments of periodontal disease could be useful in confirming the link between periodontal disease and cancer, they added.
Postmenopausal women who have a history of gum disease also have a higher risk of cancer, according to a new study of more than 65,000 women.
The study, led by researchers at the University at Buffalo, is the first national study of its kind involving U.S. women, and the first to focus specifically on older women. It’s also the first study to find an association between periodontal disease and gallbladder cancer risk in women or men. The findings were published today (Aug. 1) in the journal Cancer Epidemiology, Biomarkers & Prevention.
“This study is the first national study focused on women, particularly older women,” said Jean Wactawski-Wende, the study’s senior author.
“Our study was sufficiently large and detailed enough to examine not just overall risk of cancer among older women with periodontal disease, but also to provide useful information on a number of cancer-specific sites,” added Wactawski-Wende, dean of UB’s School of Public Health and Health Professions and a professor of epidemiology and environmental health.
The study included 65,869 postmenopausal women enrolled in the Women’s Health Initiative, an ongoing national prospective study designed to investigate factors affecting disease and death risk in older American women. The average age of the participants was 68, and most were non-Hispanic white women.
As part of a follow-up health questionnaire, participants were asked “Has a dentist or dental hygienist ever told you that you had periodontal or gum disease?”
Women who reported a history of gum disease had a 14 percent increased risk of overall cancer. Of the 7,149 cancers that occurred in the study participants, the majority — or 2,416 — were breast cancer.
“There is increasing evidence that periodontal disease may be linked to an increased cancer risk and this association warrants further investigation,” said the paper’s first author, Ngozi Nwizu, who worked on the research while completing her residency in oral and maxillofacial pathology in UB’s School of Dental Medicine and her doctorate in pathology (cancer epidemiology) at UB’s Roswell Park Cancer Institute Graduate Division. Nwizu is now an assistant professor of oral and maxillofacial pathology at the University of Texas Health Science Center at Houston.
The risk associated with periodontal disease was highest for esophageal cancer, the researchers reported. “The esophagus is in close proximity to the oral cavity, and so periodontal pathogens may more easily gain access to and infect the esophageal mucosa and promote cancer risk at that site,” Wactawski-Wende said.
Gallbladder cancer risk also was high in women who reported a history of gum disease. “Chronic inflammation has also been implicated in gallbladder cancer, but there has been no data on the association between periodontal disease and gallbladder risk. Ours is the first study to report on such an association,” Nwizu said.
The esophageal and gallbladder cancer findings are significant, Nwizu said. “Esophageal cancer ranks among the most deadly cancers and its etiology is not well known, but chronic inflammation has been implicated,” she said.
“Certain periodontal bacteria have been shown to promote inflammation even in tiny amounts, and these bacteria have been isolated from many organ systems and some cancers including esophageal cancers. It is important to establish if periodontal disease is an important risk of esophageal cancer, so that appropriate preventive measures can be promoted.”
Periodontal disease also was associated with total cancer risk among former and current smokers.
The findings for this particular age group are significant because they offer a window into disease in a population of Americans that continues to increase as people live longer lives.
“The elderly are more disproportionately affected by periodontal disease than other age groups, and for most types of cancers, the process of carcinogenesis usually occurs over many years,” said Nwizu. “So the adverse effects of periodontal disease are more likely to be seen among postmenopausal women, simply because of their older age.”
