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The anti-tumor cells can be activated with common salt

 

In earlier days, cancer was supposed to be a death sentence. Presently, there have been many advancements in the treatment of cancer. Therefore, the rate of survival of cancer patients has increased, with many leading a good quality of life even after being diagnosed with cancer.

In recent years, adoptive T-cell therapy has particularly been developed as an effective cancer treatment tool. In this method, some of the body’s white blood cells, that is, the T cells, undergo such a modification that they gain the capability of recognizing and fighting tumor cells.

The efficacy of adoptive T-cell therapy depends on the metabolic activity of T cells. The T cells expression is generally suppressed in an immunosuppressive environment of tumor cells. Therefore, researchers had to identify factors that could overcome this suppression.

Historically, table salt was perceived as precious commodity. Its chemical name is sodium chloride. Today, common salt is a cheap commodity and used in kitchen recipes. A team of scientists led by Christina Zielinski have found that sodium ions, which are an integral component of common salt (sodium chloride), increased the efficiency of anti-tumor activity of T cells.

The researchers found that breast cancer tumors had a higher concentration of sodium as compared to healthy tissue. In particular, the T cells were acting strongly against tumors when the immediate environment had a high concentration of sodium.

The survival time increased in such cases. Furthermore, the researchers proved that the immune response of CD8+ T cells would be enhanced by sodium.

CD8+ T cells are immune cells that identify and kill tumor cells or cells that are infected with virus in the human body. In a previous study, researchers have reported that sodium can regulate other types of T cells, which are believed to be involved in autoimmune disease and allergies.

In this study, the researchers went on to know the effect sodium could specifically have on controlling the activity of CD8+ T cells in humans.

Various technologies were used by researchers to investigate how sodium regulated the genes and the metabolic process of CD8+ T cells. The human T cells were pre-treated with salt and then they were cultured with tumors.

A mouse model of the experiment involving T cells was also carried out. The researchers reported that in the presence of salt, the metabolic fitness of CD8+ T cells improved as the uptake of sugar and amino acids increased. Thus, energy production also increased in the cells.

Consequently, the immune cells were more capable of eliminating tumor cells, as seen in the experiments of cell cultures and mouse models. The researchers found that pancreatic tumors shrank in size in mice after they were injected with T cells that were pre-treated with salt.

 

 

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Damaged cartilage of joints could be regrown with new biomaterial

 

Scientists at the Northwestern University have successfully developed a novel biomaterial that could be used to regenerate high-quality cartilage of the knee joints. The study was conducted on a large-animal model. It has a rubbery appearance, and it is material of a complex network of molecules. These molecules together assembled create a natural environment of the human cartilage.

In this new study, researchers used this material to replace the damaged cartilage in the knee joints of animals. They got promising results within just six months. They observed evidences of the cartilage getting repaired. There was a growing new cartilage, which consisted of natural biopolymers, such as collagen II and proteoglycans. They facilitated mechanical resilience in joints, and the process took place without any pain.

However, researchers have to perform more work in this regard. They are of the view that the novel material has the potential to prevent complete knee replacement surgeries in the near future. The material could be effectively used to treat degenerative diseases, such as osteoarthritis. It can also be used to repair injuries of sportsmen. The study has been published in detail in the Proceedings of the National Academy of Sciences.

Samuel I. Stupp is the researcher who led this study at the Northwestern University. He said that cartilage is one of the most important components of the joints in human body. During the course of time, a cartilage can get damaged or may undergo a breakdown. This can severely impact the overall health and mobility of affected people.

In humans, adults do not have natural ability to heal the damage done to cartilage. With this new therapy, researchers could induce repair in the damaged tissue that does not regenerate naturally. The mode of treatment offered has the potential to solve a serious clinical problem.

In this study, the human cartilage was activated with the use of “dancing molecules.” They could boost the synthesis of proteins associated with the tissue matrix. In another related study, a hybrid biomaterial was used in place of “dancing molecules.” The new biomaterial has two components: the first component is a bioactive peptide that binds with TGFb-1 (transforming growth factor beta-1).

The growth factor is an essential protein that promotes the growth and maintenance of the cartilage. The peptide modifies hyaluronic acid, which is a natural polysaccharide that is present in the cartilage. It also binds with the lubricating synovial fluid of joints.

Many people are well-versed with hyaluronic acid as it is a common ingredient of many skincare products. According to Stupp, it is also found naturally in most tissues of the human body, and this includes the brain and the joints. The researchers chose hyaluronic acid as it was very similar to the natural polymers of the cartilage.

The team of researchers were supervised by Stupp as they integrated the chemically modified particles of hyaluronic acid and the bioactive peptide. Thus, they strived to self-organize the nanoscale fibers into bundles, which resembled the natural structure of the cartilage. The main objective of the researchers was to create an enthralling scaffold for the cells in the human body. This would induce them to regenerate the cartilage tissue.

 

 

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ResearchGate and The Royal Society deepen their partnership of collaboration in the year 2024

 

The Royal Society and ResearchGate have joined hands to expand their partnership. They have decided to jointly cover all the journals of Royal Society, increasing the visibility and readership of 45000 articles at a global level.

Currently, the Journal Home product of Researchgate platform has increased the visibility of 10 journals of Royal Society publisher. These 10 journals are of open access and subscription model of publishing. In the year 2023, ResearchGate was provided content of journals published by Royal Society.

In the year 2024, both the parties have further strengthened their partnership as it was a successful collaboration. The readership and the reach of the content provided by the Royal Society has increased manifold due to ResearchGate platform.

It was found that in the year 2023, two open access journals of the Royal Society saw a 64% increase in their usage on the ResearchGate platform. The trend of increased usage continues for these two journals as their articles have been viewed more than 1.75 million times on ResearchGate in the past 12 months.

Using the platform of Researchgate, the Royal Society’s journals could get more engagement from researches who are in their early stage of careers. The publishers of Royal Society were targeting to increase their reach in this critical demographic group.

In the year 2024, ResearchGate has introduced a new product named Journal Home. There are dedicated profiles of all the journal titles of the Royal Society publisher. The important information and the content that is relevant is sourced from each journal and provided through the Journal Home platform of ResearchGate.

The branding of prominent journals is being done on all the associated pages dedicated to articles. Journal Home provides insights into unique network, paving the path to increase The Royal Society’s engagement with the journal community.

Each of the journals’ profiles contain the names of editors and authors. Thus, members of ResearchGate platform can understand how a journal is connected to a network of academic professionals.

Authors of the Royal Society publisher have benefitted additionally from the partnership of the publisher with ResearchGate. Their research work gets added automatically to their profiles on ResearchGate platform.

Thus, the visibility of the articles is boosted and the platform provides insights into who is currently reading the article and citing their research paper. Thus, the connectivity of the authors with the readers has increased significantly.

More 75,000 authors have benefitted as they have added their articles to their profiles on ResearchGate. The discovery and accessibility of these articles has increased sharply due to features of “Journals Home.”

 

 

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Immunotherapy efficacy increased with the discovery of a novel drug that bypassed inhibitory immune cells

The immune system was recruited to tackle tumor cells. The survival rates of millions of cancer patients improved after receiving immunotherapy. But, the treatment method also has a drawback: only one out of five patients had a favorable outcome to treatments of this kind. Researchers at the Washington University of Medicine in St. Louis wanted to understand and address the limitations of immunotherapy. They performed an extensive research study and found that in the fight against cancer, the immune system can act as its worst enemy.

In another study, researchers investigated a subset of immune cells, that is, type 1 regulatory T cells, or Tr1 cells in mice. They found that these cells performed their normal function of preventing an overreaction of the immune system. Meanwhile, they also inadvertently suppressed the cancer-fighting power of immunotherapy. According to senior researchers at the Department of Pathology and Immunology at Washington University School of Medicine, the Tr1 cells have a heretofore character that is considered to be an unrecognized obstacle to the efficacy of immunotherapy.

It suppresses its fight against cancer. Therefore, in the mouse model, the researchers tried to circumvent this limitation. They could revitalize the cancer-fighting cells in the immune system. Thus, this finding is an important development in expanding the benefits of immunotherapy. More and more cancer patients can now avail the novel developments of immunotherapy. A detailed information of this study is available in the journal Nature.

Personalized form of immunotherapy is now available to cancer patients in the form of vaccines. Cancer vaccines are aimed at the mutant proteins, which are specific to a tumor in a patient. These vaccines encourage an attack on tumor cells by boosting the activity of killer T cells. At the same time, they allow the healthy cells to remain unaffected. In another study conducted by Schreiber’s group, it was found that helper T cells are also activated with vaccines that are more effective.

The helper T cells are another type of immune cells. They are used for recruiting and expanding the killer T cells. These cells are known to destroy tumor cells. These researchers tried to supercharge the cancer vaccine by adding an additional amount of helper T cell targets. They found that a different type of T cell was generated. This type of T cell suppressed the rejection of tumor cells.

In another study, a group of researchers laid down the following hypothesis: when the activation of helper T cells was increased, they could induce an enhanced elimination of sarcoma tumors in mice. They injected vaccines in groups of mice with tumors. These vaccines could activate the killer T cells in an equal manner and also trigger different extent of activation of helper T cells.

In their latest study, the researchers were surprised to know the activity of the vaccine. They had developed the vaccine to hyperactivate helper T cells. However, the effect of this vaccine was opposite and it suppressed the rejection of tumor cells. The researchers were of the view that the vaccine should have eliminate the sarcoma tumors in mice as it activated more and more T cells.

The vaccine contained helper T cell targets in higher doses, and this induced inhibitory activity in Tr1 cells. Thus, the elimination of tumor cells was blocked completely. In general, Tr1 cells control an immune system that is overactive. However, ours is the first study to show that they can dampen the fight against cancer. The brakes on the immune system are generally put by Tr1 cells. They prevent the immune system from attacking healthy cells of the human body. However, no previous study has investigated its role in cancer comprehensively.

Previously published data was investigated thoroughly by researchers. They found that more Tr1 cells were present in tumor patients who showed a poor response to immunotherapy treatment. The number of Tr1 cells was lesser in tumor patients who had shown a good response to immunotherapy treatment. When tumors grew bigger in size in mice, the number of Tr1 cells increased proportionately. This made the mice develop an insensitivity to immunotherapy.

Researchers wanted to bypass the inhibiting cells in mice, which were vaccinated. Therefore, they treated these mice with a drug that improved the cancer-fighting power of killer T cells. This drug was developed by Asher Biotherapeutics, which is start up in the field of biotechnology. The drug could carry out modifications in interleukin 2 (IL-2). Please note that IL-2 is a protein that boosts the activity of the immune system. The drug could specifically enhance the activity of killer T cells and reduce the toxicity associated with other treatments that do not modify IL-2.

The inhibition of Tr1 cells was overcome by the additional boost provided by the drug. Thus, the immunotherapy was found to be more effective. The lead researcher said that they are focusing on providing personalized immunotherapy and widening the efficacy of the treatment. The researchers said that in order to attain the most robust anti-tumor response, they had to understand how to trigger the immune system. For this purpose, they referred to related studies in recent decades. These studies investigated the basic immunology of the tumor. In our current study, the main aim of researchers was to improve the immunotherapy and to benefit more patients with cancer.

 

 

 

 

 

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Immunotherapy is now supported by epigenetically active drugs

 

Drugs that are active epigenetically would help a cell in reading the parts of a genome. These parts were either blocked earlier or inaccessible to the cells of the human body. Thus, new mRNA transcripts and proteins can be formed. This important finding has been presented by scientists of the German Cancer Research Center and the University Hospital of Tubingen.

The immune system would be able to identify cancer cells, thanks to the activity of “therapy-induced epitopes.” Immunotherapies are now being provided to treat patients with different types of cancer. But, all the cancer patients do not benefit from immunotherapy. The treatment fails in some cases because the immune system of the patient is not able to identify cancer cells.

Antigens are protein structures, which are transported by cancer cells onto their surface. At this stage, the T cells of the immune system recognize and differentiate them from healthy cells in the human body. In such cases, immunotherapy is effective and successful.

The antigens can be proteins associated with cancer, and they are also known as tumor-associated antigens. Antigens could also be proteins that have been modified by mutations. They are known as completely new gene products. These products are formed in tumor cells when completely new areas of the genes are being read.

Researchers of this study decided to make the immune system quite visible to cancer cells. The cells were equipped with completely new antigens. This was possible due to the help offered by cancer drugs, which were epigenetically active. Many cancer patients are prescribed such types of drugs. The epigenetic markers of the DNA or the proteins associated with the DNA are subjected to these drugs.

Thanks to the epigenetic markers, researchers could determine whether certain parts of the ist genome in mRNA could be translated by cancer cells. Decitabine or the HDAC inhibitors are a class of demethylating drugs, which have epigenetic effect. They help in reading those parts of the genome, which were either blocked or were inaccessible earlier. Thus, new mRNA transcripts can be created in the cells.

In this study, a lung cancer cell line was treated with decitabine and HDAC inhibitor in a culture dish. This induced the formation of several new transcripts, which were detected by RNA analysis. The origin of most of the new transcripts could be traced to endogenous retroviruses. The sequences of these transcripts accounted for upto 8% of the human genome, so they were considered as relics of retroviral infections.

In general, epigenetic mechanisms block their transcription. In cancer cells, the effect of the neoepitopes is much stronger than that in healthy cells. These neoepitopes are induced by Decibtabine and HDAC inhibitors. Cancer cells have high proliferation rate. The researchers now had to determine whether the therapy-induced transcripts could be used for coding segments of immunogenic proteins, that is, peptides.

Mass spectrometry was used for analysis in this study. The researchers were able to identify 45 neoepitopes, which were present on the surface of cancer cells post-treatment. The results obtained were reproducible with a large number of different cancer cell lines. In the culture dish, the cytotoxic T cells could be activated by therapy-induced neoepitopes.

 

 

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A new 5-year agreement was signed by Wiley and Germany’s DEAL Consortium

 

Wiley, a leading academic publisher of STEM journals, recently announced its decision to enter into a five-year agreement with DEAL Consortium in Germany. This consortium represents a collaboration of more than 1000 academic institutions of Germany.

The drift in scholarly communications has favored open access publishing, and the evolution of the hybrid model of publishing. The needs of the scholarly community will be better addressed by this partnership.

Thanks to this five-year deal, Wiley will now offer open access articles freely to authors of leading institutions in Germany. Thus, the readability and access to content would increase from Wiley’s portfolio of journals. Let us understand how this agreement benefits the research ecosystem of Germany.

The deal will facilitate a better understanding of all the scholarly institutions associated with OA publishing in Germany. The investment needs of journals would be recognized as they deliver high quality content with greater impact to researchers.

The deal also enables the development of a better infrastructure in terms of workflows. Thus, both the parties have agreed to support readers, authors, and librarians involved in the OA movement. Finally, all the institutions of the consortium will benefit from training sessions and workshops held by the well-established team of Wiley.

The deal between DEAL Consortium and Wiley is going to support a new wave of Open Access movement in Germany. This would be immensely beneficial to gain path-breaking results in the research community of Germany.

Kudos to the five-year agreement that dwells on supporting both the publishers and researchers associated with OA movement. The collaborative approach of Wiley has been much appreciated by DEAL Consortium of Germany. The cooperation model is sustainable.

 

 

 

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A partnership between ResearchGate and Taylor & Francis eases access to scholarly publications

A partnership has been announced between ResearchGate and Taylor & Francis, making it a new development in the field of STEM publishing. ResearchGate is a leading professional network of researchers, enabling collaboration and sharing of research publications.

Taylor & Francis is a renowned publisher of journals and books in the academic world. With this partnership, Taylor & Francis would provide access to 200 high quality journals to researchers registered at ResearchGate.

ResearchGate has specifically designed a new service entitled “Journal Home” to cater to the growing demands of journals. All the 200 journals would get enhanced visibility on ResearchGate platform. A profile will be created for each journal on ResearchGate, which would be accessible to researchers throughout the platform. Every journal title will also have an article page, benefitting sharing, collaboration, and networking.

This development is interesting as it plans to make more than 100,000 recorded versions of open access articles freely readable on ResearchGate platform. All the articles written henceforth will be included in the 70 completely OA journals and be available for viewership on ResearchGate.

Taylor & Francis is an important name in the field of academic publisher. It has published cutting-edge research from various disciplines, such as sciences, social sciences, and humanities. Since Researchgate platform has more than 25 million researchers, this partnership would benefit the publisher immensely. It would increase the readership of viewers and engage the interest of new audiences.

The founders of ResearchGate have expressed their gratitude to the publishers: Taylor & Francis. They will be embarking on a new journey as they make so many articles freely accessible. Most scientific content is hidden till today under the restrictions of a paywall, thanks to subscription journals. ResearchGate supports the OA model of publishing in academia, paving a new way for researchers in developing countries.

 

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A promising drug delivery system for brain cancer

A preclinical study was conducted to treat the most common form of brain cancer in humans, that is, glioblastoma. This experimental study was conducted by researchers at the University of Texas at Dallas and the UT Southwestern Medical Center. They have developed a novel technique that delivers medication through the barrier between the bloodstream and the brain. The research study was performed on mice and published in Nature Communications magazine.

In the USA, the most aggressive form of brain cancer is glioblastoma. Every year, about 12000 patients are diagnosed with glioblastoma in the US. The average survival rate of these patients is just 15 to 18 months, post-diagnosis. Presently, the conventional modes of treatment, such as chemotherapy, radiation, and surgery, are not really effective in most cases. Most chemotherapeutic agents cannot pass through the blood-brain barrier, making them ineffective in destroying glioblastoma tumors.

The primary function of the blood-brain barrier is to restrict and prevent substances from the bloodstream from entering the parenchyma in the brain. The blood-brain barrier shows high selectivity as a filter and acts a protective barrier in the human brain. The blood-brain barrier is the biggest hindrance in the treatment of any disease related to the brain. Although it is just 1 micron in thickness, it obstructs about 98% molecules from entering the brain.

Our current research study was conducted on experimental mice, which were engineered genetically to contain mutations of human glioblastoma. The researchers used gold nanoparticles to co-deliver medication and to target the blood vessels. The nanoparticles were administered through an injection in the bloodstream. When they reached the mouse skull, they were activated with non-invasive laser pulses.

Owing to laser treatment, thermomechanical waves were formed in the brain of mouse model. The blood-brain barrier became permeable within a short span of time, thereby enabling the medication to enter the target area. In this experiment, researchers used a chemotherapeutic drug named paclitaxel. This drug is usually used to treat ovarian, lung, and breast cancers. On its own, the drug molecule fails as it cannot surpass the blood-brain barrier in patients with brain cancer.

As the novel drug delivery method could permeate through the barrier, the technique was successful. The size of the brain tumour shrank in size; the overall survival rate of experimental mice was more than 50%. These preclinical procedures need to be guided by further research studies on humans. This is a novel mode of treating diseases like brain cancer, offering hope to patients with high mortality.

 

 

 

 

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Researchers identify the switch that activates programmed death of cancer cells.

The UC Davis Comprehensive Cancer Center has conducted an in-depth research study. The focus was to activate programmed death of cancer cells. A crucial epitope has been identified on the CD95 receptor, and it triggers the death of cells. An epitope is a section of protein that activates the larger protein. As cell death can now be programmed, cancer treatment methods have become effective.

In molecular biology, CD95 receptors are known as Fas and death receptors. These receptors are proteins present in cell membrane. They evoke self-destruction of cells by releasing a signal. This happens when CD95 receptors are activated. By modulating the activity of Fas, researchers extended its benefits to CAR T-cell therapy. This was effective in destroying solid tumours of ovarian cancer.

Managing cancer with better therapies

The conventional method of treating cancer includes chemotherapy, radiotherapy, and surgery. In cases where cancer is diagnosed at an initial stage, these methods are effective. However, cancer cases may relapse, especially when they are therapy-resistant. Recently, CAR T-cell immunotherapy and an immune checkpoint receptor molecule have shown to activate antibodies, and thus they are promising candidates that destroy the cycle of cancerous growth.

These immunotherapeutic agents are effective against only few types of cancer cells, such as ovarian cancer, breast cancer, lung cancer, and pancreatic cancer. In CAR T-cell therapy, researchers engineer the specific type of immune cells, that is, T cells. They graft these cells on a specific antibody that targets specific tumours. The grafted T cells are quite effective in battling leukaemia and other types of blood cancer.

The engineered T cells have not been effective in combating solid tumours; the microenvironment of these tumours drives off T cells and other immune cells. Thus, they cannot provide a therapeutic effect to solid tumours. Although the immune receptor activates antibodies, the T cells cannot infiltrate without additional spaces.

The activity of death receptors

Now, let us understand the activity of death receptors. Through targeted therapy, we can trigger them into programming cell death of tumours. Thus, chemotherapeutic drugs should be such that they induce the activity of death receptors. Many pharmaceutical companies have been slightly successful in targeting the death receptor-5. But the clinical trials of Fas agonists have failed.

Developing the right target

The activity of immune cells is effectively regulated by Fas. However, researchers have proposed that cancer cells can be targeted selectively if they identify the correct epitope. After identifying the targeted epitope, researchers of this study have designed a new type of antibodies. These antibodies show selectivity while binding and activating Fas. With this strategy, specific tumor cells can be destroyed.

 

 

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A promising approach for treating pancreatic cancer

 

A new study has reported about a promising approach for treating pancreatic cancer. The study was conducted on mice by researchers of the Queen Mary University of London. They identified the cells that caused metastasis of pancreatic cancer, and they also explained how the weakness of these targeted cells could be explored to mitigate pancreatic cancer with existing drugs.

These researchers have reported that certain types of cells known as amoeboid cells were present in most patients with pancreatic cancer. The activity of these fast-moving cells was aggressive and invasive, thereby weakening the immune system of patients.

These amoeboid cells are also reportedly to have been found in patients with other types of cancer, such as liver cancer, breast cancer, and skin cancer. The survival rate of such patients is poor. However, this is the first study to report these cells in pancreatic cancer patients.

Researchers also found high levels of expression of a molecule named CD73 in patients with pancreatic cancer. This molecule is believed to be produced by amoeboid cells and it drives the metastasis of cancer, thereby weakening the immune system. The activity of this CD73 molecule had to be blocked. Thus, tumour tissues would not have spread to the liver.

The amoeboid cells were reportedly detected in late as well as early-stage patients with pancreatic cancer. This implies that the activity of CD73 molecule should be blocked at an early stage of the disease and the aggressive nature of amoeboid cells can be curtailed. Thus, the damage caused to the body can be reduced, thereby indicating a new hope for patients with pancreatic cancer.

Currently, the rate of survival and patient outcomes of pancreatic cancer are poor. Presently, every year more than 10000 people are diagnosed with pancreatic cancer in the UK. The conventional mode of treatment enables just 7% of patients to survive for five years after detection. Presently, chemotherapy, radiotherapy, and surgery are not working well for most patients.  This novel mode of treatment has given promising results in mice and human clinical trials need to be conducted soon.