Tag Archives: cancer

Study Links High-Fat Diets To More Aggressive Breast Cancer Behavior

Posted on by
Reply

Researchers at Princeton University have found that high-fat diets may make certain breast cancers more invasive by altering tumor structure. The study, published March 3 in APL Bioengineering, examined triple-negative breast cancer using advanced 3D models. Scientists say the findings could help explain why diet influences cancer outcomes, though results remain limited to lab conditions.

In a controlled lab setting, researchers watched tumors change shape.

Not grow faster. Not shrink. Change form.

That shift, they say, may help explain why diet influences how some cancers behave.

A team at Princeton University has identified new links between high-fat diets and aggressive breast cancer, focusing on how fat alters the structure of tumors rather than simply accelerating their growth.

The study examined triple-negative breast cancer, a subtype that does not respond to many conventional therapies and is often associated with poorer outcomes.

High-fat nutrients linked to invasive tumor structure

Using 3D tumor models designed to mimic human biological conditions, researchers exposed cancer cells to different nutrient environments, including fats, cholesterol, insulin, and ketones.

The results showed a clear structural difference.

Tumors exposed to fatty acids and cholesterol developed hollow, branching extensions that spread outward from the tumor core. These structures are associated with invasive behavior, allowing cancer cells to penetrate surrounding tissue and potentially spread through the body.

Celeste Nelson, the study’s lead investigator, described these formations as characteristic of aggressive cancers.

“Aggressive cancers have these tendrils, and it’s the leading edges that end up invading into our normal tissues and making it into either a lymphatic or a blood vessel and escaping and metastasizing,” she said.

Notably, the tumors did not grow significantly faster under high-fat conditions. Instead, cells redistributed, moving from the center toward the edges, reshaping the tumor’s structure.

Gene activity points to possible mechanism

The team also identified increased activity of a gene known as MMP1, which is associated with the breakdown of collagen, a key structural component of tissue.

Higher MMP1 levels were strongly correlated with the structural changes observed in the tumors.

Researchers believe this may allow cancer cells to break down surrounding tissue more easily, creating pathways for invasion.

However, the study stops short of proving direct causation. Nelson said further research is needed to determine whether high-fat diets directly trigger this gene activity or if other factors are involved.

Future experiments may test whether blocking MMP1 changes how tumors respond to high-fat conditions.

Fluorescence images of sample tumors show invasions into surrounding tissue over several days. Branching invasions are most pronounced in the lower right frame. (Photo illustration from image provided by the researchers/Princeton University.)
Credit:Princeton University

Other diets showed limited impact in the model

The study also tested tumor responses under different nutrient conditions, including high insulin, glycerol, and ketones.

These conditions showed little difference from baseline tumors, which remained relatively compact and did not develop invasive structures.

One unexpected result involved a simulated ketogenic diet, which is typically high in fat and low in carbohydrates.

Researchers had expected it might slow tumor progression. Instead, the tumors did not show improved outcomes compared to baseline conditions within the model.

“We were expecting a ketogenic diet to be protective,” Nelson said. “Yet we didn’t see that here.”

She added that the model may not fully capture the complexity of how such diets interact with the human body, particularly immune responses and other systemic factors.

Study highlights limits of lab-based cancer models

The findings are based on 3D microfluidic tumor models, which aim to replicate aspects of real biological environments more accurately than traditional lab methods.

Unlike 2D cell cultures, which grow in simplified conditions, these models simulate both the physical and chemical environment of tumors. At the same time, they remain more controlled than animal studies, allowing researchers to isolate specific variables such as diet.

Even so, the researchers caution that the results are limited.

The tumors studied are simplified representations and do not include the full range of interactions present in the human body. That means the findings cannot be directly translated into dietary recommendations or clinical outcomes.

“Every tumor is an individual’s tumor,” Nelson said, noting the challenge of capturing the full diversity of cancer behavior in a single study.

New direction for diet and cancer research

The study adds to a growing body of evidence suggesting that diet influences cancer progression, though the mechanisms remain unclear.

By focusing on structural changes rather than growth rates, the Princeton team offers a different lens for understanding how nutrients interact with tumors.

The research also points to potential targets for future therapies, particularly genes involved in tissue breakdown and tumor invasion.

For now, the findings remain an early step.

They show how fat may change the way tumors behave under controlled conditions, opening new questions about how those processes unfold inside the human body.

Also Read:

New MetaRing Sensor Spots Breast Cancer Drug Response in 10 Minutes

Posted on by
Reply

Researchers at the Chinese Academy of Sciences have developed a biosensor that can quickly detect how breast cancer responds to paclitaxel. The system, called MetaRing, analyzes tiny biological samples and delivers results in about 10 minutes. The study, published recently, points to faster, more personalized chemotherapy decisions.

 

New strategy prevents pancreatic cancer removing microscopic lesions early

Posted on by
Reply

A recent preclinical trial using mice reveals that the precancerous cells of the pancreas can be disposed before they can develop into a tumor. Application of an experimental therapy to attack microscopic precancerous lesions in the pancreas was shown to increase survival in mouse models of a pancreatic ductal adenocarcinoma (PDAC) by nearly 2 times even when the same therapy was administered when the cancer was already present.

The study was carried out under the leadership of physician-scientists of the Perelman school of medicine in the University of Pennsylvania and Abramson cancer center of Penn medicine, which is released to date in Science.

It is also the first instance that scientists have demonstrated that a medical intervention could prevent growth of pre-cancerous lesions in the pancreas before it becomes pancreatic cancer and this is a good indication to the growing area of cancer interception.

I believe that the next age of cancer treatment will be interception, and I am confident that such an endeavor will be developed by cancer treatment experts like Robert Vonderheide, the director of the Abramson Cancer Center. Pancreatic cancer has had a stubborn poor prognosis, scarce treatment options as well as no tested screening and prevention measures. And should we be able to get a means of intercepting it–of detecting and counteracting abnormalities in their first beginnings of malignancy, it would be an issue game changer.

Cancer interception is different to cancer prevention.

Contrary to prevention approaches, like HPV vaccination or ceasing a smoking habit, which seek to ensure that the cancer never develops at all, cancer interception focuses on the first stages of a cell becoming malignant. Colonoscopy can be taken to illustrate an instance of a mechanical interception where the precancerous polyps are removed before they turn into colorectal cancer. Since the harder the malignancy is to treat, the larger it is, the idea of curing the malignant growths before they become cancer is quite a logical one in theory, yet challenging to be proven.

“The paper is a preclinical evidence-of-concept demonstrating that medical cancer interception is better than treatment of a diagnosis,” said the lead author, Minh Than, a clinical and research fellow in the field of Hematology-Oncology. “This research demonstrates the strength of using a proactive approach to cancer, as opposed to a reactive one. This will be interesting to test in our patients in the second stage of this work.”

RAS inhibition is an efficient way of intercepting cancer in mice.

In this research, the researchers employed two experimental inhibitors that are directed to the cancer causing gene, KRAS. KRAS mutations that cause more than 90 percent of pancreatic cancers are the most frequent cancer-causing gene mutation found in all cancers and has been traditionally thought to be undruggable.

The first KRAS inhibitor was approved in 2021 to treat non-small cell lung cancer and since that time, there have been additional KRAS inhibitors entering clinical trials treating various types of cancer, such as pancreatic cancer.

The majority of PDAC tumors are seen to be as a result of microscopic lesions referred to as PanINs (pancreatic intraepithelial neoplasias), which are too small to be detected through scans, and nearly all the PanINs have KRAS mutations. PanINs are typical in adult pancreases, but the few who become cancer only rarely; researchers are yet to understand the reason behind this unusual malignant conversion. Though this study did not aim at learning the biology or at better detection of PanINs, the research team hypothesized that removing these early lesions with the help of KRAS inhibitors, regardless of their awareness of which have malignant potential, would be an effective approach to preventing their ever transition into PDAC.

The group evaluated the two compounds identified by Revolution Medicines whose scientists participated in the analysis.

Both the compounds are meant to block the RAS when it is in the active or ON form and mediate cancer growth. RMC-9945 is a preclinical tool compound a selective inhibitor of KRAS G12D, the most frequent type of KRAS mutation in pancreatic cancer and it is one of a class of oral RAS(ON) G12D-selective inhibitors, such as the investigational drug candidate zoldonrasib (RMC-9805). RMC-7977 is a compound of clinical tool that targets several variants of RAS(ON) and is an example of oral RAS(ON) multi-selective inhibitors that contains an investigational drug candidate daraxonrasib (RMC-6236).

The research team considered the gold standard in the preclinical assessment of potential therapies of PDAC using an immunocompatible mouse model that was developed by Penn and that had a healthy and functional immune system. They firstly laid a baseline of PanIN to PDAC progression development in a control group. Then they treated an intervention group to either RMC-9945 or RMC-7977, following PanIN development, but prior to tumor development. It was also found that the reduction of the precancerous lesions occurred after 10 days of treatment and further reduced upon 28 days of treatment. In this milestone, Tumors took longer to form, and the survival of the mice was higher than in those mice that were not given the intervention. The team then discovered that extended administration of RMC-7977 to PanIN-bearing mice increased median overall survival time threefold in comparison with untreated control group with PanINs. Lastly, the intervention group that was treated earlier before the development of tumors had almost twice the lifespan compared to the group of mice that was treated after tumor development.

Further clinical trial to target high-risk patients.

The direct analogy in this paper places PanINs on the map as the possible targets of intercepting cancer and opens the field to investigate KRAS inhibitors in a new context, co-corresponding author Ben Stanger, MD, PhD, the Hanna Wise Professor in Cancer Research and director of the Penn Pancreatic Cancer Research Center. Nevertheless, due to the fact that PanINs are not visible on imaging tests and we are dealing with the case of treating people who are not cancer-diagnosed, we should seriously consider how to transfer this preclinical study to the appropriate population so that human trials can be conducted.

The team seeks to apply the research to a clinical trial where it targets high-risk patients who are already under monitoring over growths that exceed PanINs in size but still at a low risk of cancer but are usually removed once they attain a specific size. Should such a strategy proceed, the research group believes that it would be most relevant to people with a genetic susceptibility to pancreatic cancer, such as BRCA1, BRCA2, or PALB2 gene mutations, hereditary pancreatitis, precancerous cysts, or other high-risk factors. Eventually, the strategy could be considered for a broader range of individuals at intermediate risk.

How being squeezed contributes to risk of breast cancer cells

Posted on by
Reply

A recent study conducted by scientists working in Adelaide University and published in the journal Science Advances has shown the reason as to why certain cancers may grow and survive the body, whereas others do not. It happens that the hard mechanical stress to which the early cancer cells undergo as they are squeezed into a narrow area, causes some of the cancer cells to grow quicker, not to grow, as would otherwise be supposed.

This squeeze worked to the favor of the early breast cancer cells as scientists discovered.

The key point that was explained by the lead researcher, Professor Michael Samuel, of the Centre of Cancer Biology at Adelaide University and the Basil Hetzel Institute is that these breast cancer cells steal a particular sensor – one that our bodies rely on to sense touch – and use it to divide quickly and aid them in making their escape off the major tumour.

The process creates an indefinitely lasting mechanical memory in the breast cancer cells and it still contributes towards aggressive behaviour even after the pressure itself has been removed, Professor Samuel said.

The tumours which are solid are exposed to a lot of physical pressure when the disease is at its early stage of development, as the cancer cells grow in tissues that are limited in space, e.g. the milk ducts of the breast. Up to this day, the mechanism by which these cancer cells detect this pressure and whether or not it impacts the progression of the disease is unknown.

We have a tendency to believe that cancer is a genetic disease, but through this work we know that there is the same importance of physical forces within the tumours as the cause of cancer as there are genetic changes that cause cancer.

The researchers discovered that cancer cells respond to pressure via a molecule named PIEZO1, which is a hole in the cell that relates the interior of a cell to the exterior environment. Upon pressure stimulation, PIEZO1 enables the movement of calcium ions into the cell and subsequent signal transduction containing the Rho-ROCK pathway – a central regulator of cell movement, shape and growth.

The team demonstrated that mechanical pressure of a short duration that is obtained through compressing cancer tissue was sufficient to cause tumour growth to increase significantly. Mechanically compressed tumours in laboratory models of breast cancer became larger and the cancer cells in them fragmented faster than control groups.

In addition to promoting growth, compression was also identified to drive cancer cells into a more aggressive, invasive, state in a process known as epithelial-mesenchymal transition. When either of the PIEZO1 or the Rho-ROCK pathway had, however, been inhibited with the help of suitable drugs, compression did not propel cancer aggressiveness, making their role in this process definite.

Co-lead author Dr Sarah Boyle mentioned that one of the most significant findings was that the cancer aggressiveness effects of compression remained even after removal of the force itself.

According to Dr Boyle, even relatively short durations of pressure can lead to a mechanical memory by altering the way the DNA is packed into the cell, by chemically modifying the histone proteins.

These changes, which are called epigenetic changes, are modifications of the interpretation of the DNA code by the cell, which enables the process of switching on some genes that promote tumour growth and aggressiveness.

This type of epigenetic mechanical memory offers a molecular basis to the long term effects of short term mechanical forces on the cell level of the behaviour of tumours.

Notably, the research established that PIEZO1 is over-expressed in human breast cancers compared to normal breast tissue, and that the level of PIEZO1 differs among the patients. The high PIEZO1 levels have been linked to low patient survival implying that the identical pressure-detecting system found in test animals would probably be applicable in human cancer.

The results indicate a little-known role of mechanical pressure in the development of cancer aggressiveness and represent the PIEZO1 -Rho-ROCK pathway as a possible new therapeutic objective that can be used as an early intervention.

According to the researchers, future therapies can restrict tumour growth and invasiveness by interfering with the sensory and response of cancer cells to mechanical pressure. The results can also be applied in diagnosing the patients who are susceptible to aggressive breast cancers due to excessively high concentrations of PIEZO1.

That work has opened up a whole new field of so-called mechanotherapy – the use of treatments that disrupt the mechanical signals that tumours are dependent on to develop and spread out, as cancers grow to be mechanically responsive diseases, said Professor Samuel.

Use of Boron in Proteins to Create New Treatments to Cure Cancer: Study

Posted on by
Reply

A large number of the most important proteins of modern medicine and science are insoluble. These comprise a host of signalling proteins and protein hormones, and all of the receptors embedded in the cell membranes, which are directed at approximately 60 percent of the active ingredients presently utilized in medicines. When the concentration of these proteins crosses some given level, they will form clumps and become useless.

This aggregation renders synthesis of these molecules in lab impossible. Since specialised production with specialised synthesing robots always needs more than a single fragment to be conjugated into a full protein, a single poorly soluble fragment of protein is usually sufficient to inhibit production. The reason is that the current techniques employed by chemists to assemble protein fragments merely perform successfully when the fragments exist in solution and in very high concentrations.

A team of researchers, headed by Jeffrey Bode, professor at the Laboratory of Organic Chemistry at ETH Zurich has now discovered how to couple even the poorly soluble portions of proteins into functional proteins. In order to do this, they utilized special properties of a chemical compound comprising an element named boron.

The slow carbon chemistry has a concentration constraint.

The only major difference between the ETH technique and the traditional strategies is in the rate of the coupling reaction. Unlike in biochemistry, which occurs extremely fast in cells of living organisms, through enzymes, reactions such as these typically need to be carried out at unnatural concentrations within the laboratory. The reason behind this is that the slower the reaction is taking place, the greater the concentration of the reacting substances should be so that the reaction processes take place as intended.

The novel coupling technique invented by the team of Bode is approximately 1000 times faster and thus was also applicable in 1000 times lower concentrations.

Boron opens up new opportunities bio-chemistry

The ETH chemists hastened the reaction by including Boron atoms to the carbon-based molecules. These are not found in natural molecules.

In several of its properties, the metalloid boron behaves in a somewhat different way. On bonding with metals, it forms very tough and heat-resistant metal alloys. Alternatively, it is capable of bonding with the nonmetals carbon, oxygen or nitrogen in the lab to form molecules that tend to have bizarre reaction characteristics. In 2010, Akira Suzuki, a Japanese researcher and Richard Heck, an American researcher, won the Nobel Prize in Chemistry due to the development of boron-based coupling reactions to enable laboratory synthesis of natural substances.

According to Bode, “We reach an ultimate limit of reaction rate with purely carbon based systems. It is further expansion into previously untapped boron based reagents that places us in a space where even the most recalcitrant reactions that bring large biological molecules together can occur in a very brief time.”

cancer cells/photo:en.wikipedia.org

Protective acids: a rocky road

As shown by Bode and colleagues in 2012, this was the first study to demonstrate that it was possible to add an element of a hitherto unexplored chemical group to proteins fragments and do so with great speed and stability. Nevertheless, this compound was not stable with strong acids hence could not be utilized in automated synthesis.

To endure the tough environment that was applied to the sensitive boron compound in normal laboratory robots, the compound would require protection in the form of a chemical packaging, but this was easier said than done. The researchers experimented with a number of strategies in four years to little effect.

The discovery was made by mistake and eventually, the discovery occurred when a doctoral student tried an experimental method that the team had indeed thought was ineffective. The resulting protective compound binds to the boron group on three sides, therefore, being unable to be terminated in the acids in protein production.

According to Bode, such fundamental research, in which there is no assurance of success, is feasible only due to the unrestricted funds provided by the Swiss National Science Foundation and ETH.

Inorganic amino acids and cancer treatment

The ETH method implies that new peptide and protein drugs or drugs of medical interest to cure cancer that are prone to clumping, can now be produced via the usual laboratory protocols.

Moreover, special amino acids that are not natural can also be incorporated in the location of choice on the poorly soluble proteins. As an example, the chemists can functionalized these building blocks in a protein in a specific way in case they wish to attach it to an active substance on a particular location. Some of the applications of antibody-drug conjugates prepared through this method include cancer treatment procedures that do not damage normal tissues.

The way in which the method will be applied to clinical practice is not yet clear. In 2020 Bode co-founded the ETH spin-out Bright Peak Therapeutics, which applications the technologies invented in his lab to build immunotherapies to fight cancer. A therapeutic agent has already entered clinical trials and the new method based on boron may assist in increasing the size of the product pipeline of the spin-off.

What’s your poison? Alcohol linked to higher risk of pancreatic cancer

Posted on by
Reply

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.

2022 Nobel Prize in Chemistry: Former Berkeley Lab scientist Carolyn Bertozzi wins

Posted on by
Reply

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.

 

World Food Programme gets 2020 Nobel Prize for Peace

Immune targets for chemotherapy-resistant breast cancers identified

Posted on by
Reply

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.”

Not just chemotherapy, now phototherapy is here for cancer treatment [Details]

Posted on by
Reply

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.

Non-invasive ‘FAST device’ measures the changing size of tumors below the skin

Posted on by
Reply

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.

  1. It provides continuous monitoring, as the sensor is physically connected to the mouse/human patients and remains in place over the entire experimental period.
  2. 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.
  3. 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.
  4. FAST packs are also reusable, cost just $60 or so to assemble and can be attached to the mouse/human patients in minutes.
  5. 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.”

Obesity drug may decrease type 2 diabetes risk: Study reveals

Posted on by
Reply

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/curbing sitting time likely to lower breast cancer risk:Mendelian randomisation study reveals

Posted on by
Reply

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.”

JOURNAL

DNA screen: World-first preventative saliva test for cancer and heart disease risk

Posted on by
Reply

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 Victoria facility.

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

 

Some cancer immunotherapy treatments may damage fertility, women’s hormonal health

Posted on by
Reply

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.

 

Early COVID-19 pandemic induced cancer survivors to reduce smoking: Study

Posted on by
Reply

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.

Saliva diagnostics? Saliva to replace blood test as a real diagnostic tool?

Posted on by
Reply

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.

‘Blackmail’ is hit but ‘Irrfan Khan critical’, says Tweet, retracted now

Posted on by
Reply

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.


​

Artificial intelligence: Is this the future of early cancer detection?

Posted on by
Reply

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.”

Outdoor light at night linked with increased breast cancer risk in women

Posted on by
Reply
  • 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.

New blood test may transform the way cancer is monitored and treated

Posted on by
Reply

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.