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The Entire Spectrum of Colours and All the Forms, Manners and Expressions of Light are Made Invisible in This White: Or, Rather, Mix All the Colours and You Have This White: Or, Arrange All the Colours and Find an Infinite Rainbow: Or Take the Colours and Light Away and There Resides the Darkness But As Such That in Its Invisible Sphere There Still Remains Another Infinite Rainbow at Various States, That We Can Not See With Our Eyes: Take That All Away and You Have the Utter, Absolute and Primeval Duantum Darkness Within Which Our Matter Universe is Constructed and Does Function: Unless, We Remember This Every Nano-Second of Our Existence We Loose Our Sense and Joy of Eternal Wonder, Awe and Astonishment of This Magnificent Universe, Which is Outside, True, But Which is Nano-Seismically Constructed in the Human Physiology and Psychology: The Study of Medicine Will Always Remain and Fall Short Until It Sees and Learns That It is Dealing with the Universe, When It Goes About Learning and Healing This Human Physiology and Psychology: Alphansum Sovereign Necessarius: Munayem Mayenin

 

Cancers Engaged in Evolutionary Arms Race With the Immune System

 

 

|| Tuesday: January 21: 2020: The Institute of Cancer Research London News || ά. Aggressive, highly mutated cancers evolve to escape routes in response to immune attacks in an ‘evolutionary arms race’ between cancer and the immune system, according to a new Study. Gullet and stomach cancers with faults in their systems for repairing DNA build up huge numbers of genetic mutations, which make them resistant to treatments, such as, chemotherapy.

But their high number of mutations means they look ‘foreign’ to the immune system and leaves them vulnerable to immune attack, as well as, susceptible to new immunotherapies. Scientists at the Institute of Cancer Research, London, found that these ‘hyper-mutant’ tumours rapidly evolve with strategies to disguise their foreignness from the immune system and evade attack.

These findings underline the important role of Darwinian evolution in cancer and in how tumours respond to the immune system and, in the future, they could help optimise treatment with immunotherapy and other drugs, such as, chemotherapy. The Study is published in Nature Communications on Thursday and was funded by Cancer Research UK and the Schottlander Research Charitable Trust.

The research was part of a programme of work at the Institute of Cancer Research to understand how cancers adapt and evolve in response to changes in their environment, such as, by evading the immune system or becoming resistant to treatment. The ICR is the first organisation in the world to design a drug discovery programme, specifically, to meet the major challenge of cancer evolution and drug resistance, to be housed within its new £75 million Centre for Cancer Drug Discovery.

In the new Study, the researchers analysed in minute detail the genetic landscape of four tumours from the stomach and gullet which had a fault in one or more important DNA repair genes, making them ‘hyper-mutated’. The researchers analysed the genetic make-up of seven different areas from each patient’s tumour and in sites to which their cancer had spread.

The researchers found that the hyper-mutant stomach tumours had strikingly high levels of genetic variation, with an average of nearly 2,000 different gene impairments, much higher than the 436, found in skin cancer, the next most highly mutated cancer type analysed in the Study.

Different areas of the same tumour showed extreme variation in their mutations, much more than in other tumour types analysed in the new Study, which enabled the rapid Darwinian evolution. Importantly, the two stomach and gullet tumours with the highest level of infiltration from immune cells had each developed several mutations, that allowed them to evade immune attack.

These mutations occurred in genes, called, B2M, HLA and JAK1:2, which normally help immune cells to recognise and attack cancer cells. When the genes fail to function as normal, the immune system is unable to spot cancer cells despite their large numbers of mutations. The researchers believe that highly mutated cancers come under particularly strong selective pressure from the immune system and can draw on huge genetic variation to evolve more rapidly than other cancers, making them, particularly, hard to treat.

But hyper-mutated stomach and gullet tumours are highly sensitive to novel immunotherapies, showing that the immune system can effectively fight, even, the most rapidly evolving tumours. The new findings add to evidence that there is an evolutionary consequence to high mutation rates in sparking an arms race with the immune system and that this helps explain why these cancers are unusually sensitive to immunotherapy.

Dr Marco Gerlinger, the Team Leader in Translational Oncogenomics at the Institute of Cancer Research, London, said, “Our new Study has shown that in highly mutated tumours, cancer and the immune system are engaged in an evolutionary arms race, in which they continually find new ways to outflank one another.

Watching hyper-mutated tumours and immune cells co-evolve in such detail has shown that the immune system can keep up with changes in cancer, where current cancer therapies can become resistant and that we could use immunotherapies to shift the balance of this arms race, extending patients’ lives. 

Next, we plan to study the evolutionary link between hyper-mutant tumours and the immune system as part of a new clinical trial looking at the possible benefit of immunotherapy in bowel cancer.’’

Professor Paul Workman, the Chief Executive of the Institute of Cancer Research, London, said, “Cancer evolution is the biggest challenge in cancer research and treatment today and deepening our understanding of how tumours evolve in response to treatment is absolutely key to finding ways of overcoming drug resistance.

This fascinating new Study shows how cancers can co-evolve with the immune system, with each responding to changes in the other. Without treatment, cancers will be destined to win this evolutionary arms race but, we can tip the balance in favour of the immune system through carefully designed use of immunotherapy.

I am keen to see our researchers harness their new insights into cancer evolution to help predict cancer’s response to immunotherapy and ultimately to enhance the way we use immunotherapies to maximise their impact.”

Professor Charles Swanton, Cancer Research UK’s Chief Clinician, said, “This Study emphasises the importance of understanding how cancers evolve and highlights likely selection pressures imposed by a patient’s immune system and the developing tumour.

The challenge in improving outcomes for people with cancer, is to fully understand cancer’s evolutionary rulebook. This will mean studying many more samples from patients with different cancers, as so far these researchers have analysed samples from four patients with a relatively uncommon form of cancer.

There’s still a long way to go but, we hope that as the rules of cancer evolution are uncovered, we can discover new ways to treat and care for patients with the disease.”

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New Way to Identify and Track the Progression of Huntington’s Disease

 

 

|| Monday: December 16: 2019: University of Southampton News || ά. Researchers at the universities of Southampton and Cambridge have developed a new technique to analyse biochemical changes unique to Huntington’s Disease. The breakthrough has the potential to lead to the improved diagnosis of the disease onset and, possibly, better ways to track the effects of new treatments.

Huntington’s Disease damages nerve cells in the brain and, typically, develops between the ages of 30 and 50. It leads to uncontrollable movement, loss of cognitive ability and changes in mood. Until now, it has been difficult to assess the progress of the disease, using biomarkers, molecules, found in blood, which indicate a condition. This is because the same markers can be associated with other diseases or aging.

In this new Study, researchers used two forms of spectroscopy, a way of examining molecules with light, to analyse blood samples from Huntington’s patients. From this the researchers were able to establish the patterns or ‘fingerprints’ of those biomarkers, which indicate the presence of the disease.

Determining these fingerprints allowed the research team to hone in on the specific biochemical signature of the disease. This could open the door to a better diagnosis of the onset and more effective tracking of the disease in the future. The development could, also, form the foundation for a tool to assess the effectiveness of therapies, aimed at slowing the condition. The research has been published in the journal Chemical Science. 

The Technology Lead of the Study, Professor Sumeet Mahajan of the Chemistry department at the University of Southampton says, “Currently, clinicians rely on physical signs and symptoms, such as, involuntary movements, to diagnose Huntington’s Disease. We have been able to identify those ‘fingerprint’ biomarker traits, which could, ultimately, help give a more accurate assessment of when their disease begins and how it is progressing. Just a tiny drop of blood serum is needed for rapid and easy detection.”

The researchers collected Raman spectral data by shining a low power laser on blood samples from patients, experiencing various stages of Huntington’s Disease. They, then, collected additional data by shining the same laser on blood samples, mixed with gold nano-particles. By combining results of these analyses, they were able to identify specific combinations of bio-chemical peaks, which occur in all patients with the disease and observe how they change in relation to the different stages of the condition.

The researchers now plan to extend their studies to include patients, who have the Huntington’s gene but, have not yet developed features of the condition, in order to pinpoint when changes begin. The Clinical Lead of the Study, Professor Roger Barker of the University of Cambridge, says, “Longer-term, we want to see our research benefitting people, who have or may develop the disease by creating a portable device, which can be used in clinics for diagnosing and tracking disease.”

|| Readmore  || :::ω::: ||   reginehumanicsfoundation.com || 171219 ||

 

 

 

 

 

New Immune Pathway Involved in Resistance to Parasite Worms Found in Undercooked Pork

 

 

 

|| Monday: April 29: 2019: Lancaster University News || ά. Scientists from Lancaster University have discovered that immune responses, originally found to prevent fungal infections, are, also, important in eliminating Trichinella Spiralis, a round worm and the causative agent of Trichinosis. People acquire Trichinellosis by consuming raw or undercooked meat, infected with the Trichinella parasite, particularly, wild game meat or pork.

Consumption of contaminated meat contains ‘nurse cells’ of the parasite. Once in the stomach these ‘nurse cells’ hatch, releasing infective larvae, which, then, bury themselves within the lining of the small intestine. Previously, immune responses to expel the parasite have been shown to rely on white blood cells, called, T-helper two cells, specialised for eliminating gastro-intestinal parasites. However, scientists at Lancaster discovered that following this T-helper two response, a second T-helper 17 response, previously, shown to be specialised for eliminating fungal infections and certain bacterial infections occurred.

In collaboration with Professors Mark Travis and Richard Grencis from the University of Manchester, they were able to identify how these T-helper 17 cells arose and that they were key in maintaining the intestinal muscle contractions needed to flush out the worms.

The findings have been published in the journal PLOS Pathogens and show that mice, lacking the ability to activate a key signalling molecule, important in producing T-helper 17 cells have a reduced ability to expel the parasite. Interestingly, they saw a delayed transit time in the small intestine hinting at alterations in muscle contraction.

In isolating the small intestine they demonstrated that a key molecule, produced from T-helper 17 cells, termed IL-17, could increase intestinal contraction and restoring levels of this IL-17 in their mice rescued their ability to expel the parasite.

“We were quite surprised by what we found during this study. Normally, these immune responses are thought of as acting quite distinctly, depending on what type of infection you, may, have. It’s well established that the T-helper two response is beneficial during gastro-intestinal worm infections, so, traditionally, any other response would be thought of as hindering worm expulsion. So, it was quite surprising to see that this late acting T-helper 17 response was actually beneficial to the mouse’s ability to resolve an infection and get rid of the worm.’’ said Dr John Worthington from the Department of Biomedical and Life Science in the Faculty of Health and Medicine led the research.

“Our study provides novel insights into how the immune system interacts with muscle contraction during intestinal inflammation. Although, the occurrence of this infection is very rare in the developed world, we hope, it will help us to design new treatments for the many millions of people, who suffer from intestinal parasitic infections worldwide and, may, even, inform other intestinal diseases, involving altered muscle function.”::::ω.

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Antibody Therapy Training Phagocytes to Destroy Tumours Now Tested on Patients
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

|| February 25: 2019: University of Turku News || ά. Developed by researchers at the University of Turku, an immune-therapeutic antibody therapy re-educates macrophages to activate passivated cytotoxic T-cells to kill cancer. The antibody therapy prevented the growth of tumours in several mouse models. The development of the therapy has now progressed to patient testing in a phase I:II clinical trial. One reason behind many unsuccessful cancer treatments is the cancers’ ability to hijack the immune system to support its own growth.

This is assisted by the so-called tumour-associated macrophages, that can be educated by cancer cells to dampen anti-tumour immune responses. Macrophages are phagocytes, that form the first line of defence towards invading pathogens and they have a crucial role in maintaining tissue homeostasis. Macrophages have a large repertoire of functions in immune activation and resolving inflammation. In collaboration with Professor Sirpa Jalkanen, of Immunology, Dr Maija Hollmén’s research group investigated the possibility to utilise tumour-associated macrophages to increase the immunological detection and killing of cancer cells.

Professor Jalkanen has studied the function of Clever-1 for a long time. Previously, her group has observed that Clever-1 controls leukocyte trafficking between tissues. Published in the journal Clinical Cancer Research, the Study found that blocking Clever-1 function on macrophages activated the immune system and was highly effective in inhibiting cancer progression.

By inhibiting Clever-1 functions, tumour-associated macrophages, that, normally, impair adaptive immune cell activation, such as, cancer cell killing by cytotoxic T-cells, were managed to be re-educated so that they had increased ability to present antigen and secrete pro-inflammatory cytokines, leading to increased activation of killer T-cells.

‘’These results are highly promising and present a completely new way to activate anti-cancer immunity.’’ says Doctoral Candidate Miro Viitala, who is the main Author of the Paper.

‘’Macrophages are an ideal drug development target as they express several molecules, that can be activated or impaired to transfer the macrophages into cells, that destroy cancer. In itself, this would increase beneficial inflammation in the tumour micro-environment, which would improve the efficiency of immune checkpoint inhibitors in those patients, whose response is weak due to lack of tumour-specific T-cell activation.’’

The antibody therapy, targeting Clever-1 worked in the studied tumour mouse models as efficiently as the PD-1 antibody therapy, that is in clinical use. The PD-1 antibody maintains the functionality of the killer T-cells. It is notable that the Clever-1 antibody therapy, targeting macrophages, also, increased the activity of the killer T-cells efficiently.

In certain mouse models of cancer, a combination of anti-Clever-1 and anti-PD-1 therapies prevented tumour growth and formation of metastases more effectively than either treatment alone.

‘’Every cancer is different. Therefore, it is important to explore the types of cancer where Clever-1 antibody therapy most effectively works on and to find biomarkers, that can be used to identify beforehand the patients, that will benefit the most from this kind of therapy.’’ Viitala says.

The Paper: Immunotherapeutic Blockade of Macrophage Clever-1 Reactivates the CD8+ T Cell Response Against Immunosuppressive Tumors: Miro Viitala, Reetta Virtakoivu, Sina Tadayon, Jenna Rannikko, Sirpa Jalkanen, Maija Hollmén: Published in the journal Clinical Cancer Research:  February 12: 2019

More information: Maija Hollmén:::ω.

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New Clinical Trial for Osteo-Arthritis Drug Gets Funding

 

 

 

|| February 22: 2019: University of Liverpool News || ά. An innovative treatment for Osteo-arthritis, being trialled at the University of Liverpool, has been awarded a grant from Innovate UK, the leading government innovation agency. Osteoarthritis is the most common type of Arthritis in the UK, affecting more than eight million people and is the leading cause of joint pain and stiffness in older people. The University’s Clinical Trials Unit, in partnership with AKL Research and Development Ltd and the NHS, is leading a clinical trial to test a potential new drug treatment for Osteo-arthritis.

As part of their research and development programme, AKLRD identifies promising phytochemicals, found in natural products, which can be synthesised. Trials have identified two molecules, which act synergistically and have been brought together to create the ‘APPA’, a patented drug, which is an investigational medicine and not yet approved for use. In a variety of pre-clinical animal testing trials, APPA clearly demonstrated significant pain relief from Osteo-athritis, improved functionality and the slowing of cartilage destruction. These results led to the clinical trial being launched.

Innovate UK is part of UK Research and Innovation with a remit to drive the science and technology innovations, that will grow the UK economy. It has recognised APPA’s potential as a powerful treatment despite it only being at the Phase One trial stage, awarding AKLRD £675,000. This will contribute to the development of APPA in its Phase Two trial, which is expected to commence later this year, based on anticipated favourable results in the Phase One trial.

The trial, which is a partnership between the University of Liverpool, the pharmaceutical Industry and the NHS, is being led by Rheumatologist Professor Robert Moots from the University’s Institute of Ageing and Chronic Disease and is occurring in the Phase I unit at the Royal Liverpool University Hospital.

Professor Moots, said, “Millions of osteo-arthritis patients are suffering every day with severe pain because the current prescription drugs available are, often, not effective or can not be used long-term. “APPA has the potential to be an effective treatment for OA, that could not only tackle the pain it causes but, do so with excellent tolerability and, also, we hope, stop the disease from causing further joint damage. It’s incredibly exciting that Innovate UK has clearly recognised the potential of this new drug, which could transform the lives of OA patients.”

Mr David Miles, the Chief Executive Officer of AKLRD, said, “For APPA to be recognised as a disruptive innovation is incredibly exciting. The award from Innovate UK will allow us to secure the future development of what we believe could be an important medicine for OA patients, who currently have limited treatment options. We believe APPA not only tackles pain but will, also, put the brakes on the inflammatory cascade, that we know is responsible for the devastating consequences of OA.”

Mr Chris Sawyer, Innovation Lead, at Innovate UK, said, “This is an exciting area of research in a disease with high incidence and major debilitation in many sufferers. Supporting AKLRD to pursue the development of this important medicine is aligned perfectly with Innovate UK’s objective to support UK business growth in the health and life sciences sector.

AKLRD underwent a highly competitive process to be awarded the grant, with five independent expert assessors evaluating its submission. The assessors praised the ‘strong’ and ‘exciting proposal with large potential’ and described AKLRD’s work as an ‘exciting area of research in a disease with high incidence and major debilitation in many sufferers.”

Innovate UK is part of UK Research and Innovation with a remit to drive the science and technology innovations that will grow the UK economy. Since 2007 Innovate UK has committed more than £01.8 billion to innovation, helping 8,000 organisations with projects, estimated to add more than £16 billion to the UK economy and nearly 70,000 jobs. Innovate UK competitions provide grants between £25,000 and £10 million.

The forthcoming Phase II trial will be recruiting nationally in collaboration with Aintree University Hospital NHS Foundation Trust.:::ω.

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New Rapid Test for Sepsis Could Save Thousands of Lives

 

 

 

|| February 21: 2019: University of Strathclyde News || ά. Researchers at the University of Strathclyde have developed an innovative, low cost test for earlier diagnosis of Sepsis, which could save thousands of lives. The simple system for sensitive real-time measurement of the life threatening condition is much quicker than existing hospital tests, which can take up to 72 hours to process. Using a micro-electrode, a bio-sensor, this device is used to detect, if, one of the protein biomarkers of Sepsis, interleukin-6, is present in the bloodstream.

IL-6 is a molecule, secreted by the immune system and the levels of it in the blood increase in many of those, who have the condition. The results of the research project show that increased levels of the molecule can be detected by the test as quickly as two and a half minutes. The small size of the devices, micro-electrodes on a needle shaped substrates, makes them ideal for initial testing and, also, continuous monitoring for Sepsis, which is notoriously difficult to diagnose. Dr Damion Corrigan, from the department of Biomedical Engineering at Strathclyde, said, “The research shows that the tools we’ve developed could underpin a rapid test for Sepsis.

We’ve developed a needle shaped sensor with different electrodes and have shown we can detect one sepsis biomarker in almost real time, at the clinically relevant levels. When levels go up, as they do in Sepsis, we can detect that, too. Sepsis is quite complex and difficult to diagnose but IL-6 is one of the best markers.

Our research so far shows you can measure a single Sepsis marker but, there are, actually, eight sensors on the needle, each about the same diameter as a human hair and the idea is that in the future we can get multiple markers on the one microchip for a more comprehensive test.”

The device takes a pin prick of blood, which is, then, put on the chip for the result to be read. Its needle shape means it can, also, be implanted and used on patients in intensive care. The UK Sepsis Trust estimates that around 52,000 people in the UK die every year and six million globally from the condition, yet, with early diagnosis and the correct treatment, most people make a full recovery.

Sepsis develops, when the chemicals the immune system releases into the bloodstream to fight an infection instead cause inflammation throughout the entire body. Without quick treatment, it can lead to multiple organ failure and death. A delay of just one hour for giving the corre