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Why was the human genome never completed?

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Why was the human genome never completed? So far, no human genome has been read completely. Scientists expect to pass this milestone for the first time this year.

Why was the human genome never completed?

Before the end of 2023, you should be able to read the complete human genome, which will be the story of a person; It will also provide insight into who he is and where he came from, and his future. The complete human genome is probably not very fun at first glance and it will be very, very long. But the online publication of the complete human genome without any flaws will be a very important moment.

At this point you may feel like you’ve heard this before: the human genome was published years ago. Was it not done perfectly?

In fact, the human genome had never been completely read. The first draft of the human genome was published in 2001, and then in 2003, a group of scientists from the Human Genome Project announced that they had completed the work. This sequence, which was prepared by combining DNA fragments from different people, became the reference sequence with which the DNA of other humans can be compared.

Compiling the human genome by combining the genomic information of several individuals was the best that scientists could do at the time, but it had significant flaws and errors. Later versions of the human genome improved, but many problems remained. Only in the last few years has technology advanced enough to read the entire human genome without gaps and with minimal errors.

But all human genome sequences published so far have been hybrid, using DNA from multiple individuals. This year, the entire genome of a person (a man named Leon Pushkin) is going to be published for the first time. This complete and single human genome will be a monumental technical achievement. It’s only been 70 years since Rosalind Franklin’s black-and-white image revealed the double helix structure of DNA and revolutionized scientists’ understanding of how genetic information is stored. Today, we have the ability to read the entire genetic book that gives rise to the unique characteristics of a human being.

But the project’s geneticists say this is just the beginning. They want to sequence the genomes of people from around the world to create a true picture of the genetic diversity of the human species. They want to find out what the previously unsequenced parts of the DNA do. They also want to introduce whole-genome sequencing into clinics to help doctors diagnose and treat diseases.

In short, the human genome will never be complete, and we will never finish reading it.

The first human genome

The Human Genome Major Project (HGP) was one of the largest scientific projects at a cost of about $3 billion. The goal of this project, which began in 1990, was to read the entire DNA that the average human carries in his cells. The first draft of the sequence was published a little over a decade later. In 2001, at the same time, another version of the human genome was published by Celera Genomics.

لئون پشکین

The human genome came with many promises. With the help of the human genome, we understand what genes do, especially genes that play a role in diseases. This enables personalized medicine where we receive treatments tailored to our genetic makeup.

The complete human genome also provides insights into our evolutionary origins: how exactly are we different from our closest living relatives, chimpanzees, and bonobos?

Some of these promises have happened and some have not yet been fulfilled. Our knowledge of the function of many genes and their roles in diseases ranging from breast cancer to schizophrenia has increased. However, most diseases are affected by hundreds of genes, so we are still a long way from genomic medicine.

Read More: Scientists have found a way to diagnose colon cancer more easily

A small number of inherited diseases are caused by a faulty gene, and the use of genetic screening to identify people at risk for rare diseases is largely limited to those at high risk.

Genetics has also changed our understanding of human evolution. For example, it has been shown that our ancestors interbred with other hominids such as Neanderthals.

Meanwhile, in the background of scientists’ efforts to provide a complete human genome, lies the unpleasant fact that the human genome has never been truly complete. While geneticists have been revising it since the first draft was published (last revised in February 2022), parts of the genome are still missing.

Repeated sequences

One of the problems is that parts of DNA are highly repetitive. In certain parts of the genome, the same sequences are repeated over and over, sometimes thousands of times.

Duplicated DNA often appears in similar parts of the genome. Our DNA is not stored as a long, continuous rope, but is divided into smaller pieces called chromosomes.

Chromosomes are X-shaped (except for the Y-shaped chromosome carried by males), and there are 23 pairs of them in human cells. Each of the chromosomes has duplicated DNA at the end of its four arms (telomeres) and at the central junction (centromeres), and both of these are important.

Telomeres act as protective caps and their damage is associated with aging. Meanwhile, centromeres are important for the process of cell division that underlies growth and reproduction. DNA rearrangements at centromeres play a role in the development of some cancers.

The Human Genome Project failed to sequence the duplicated DNA and did not attempt to do so. Their method could not solve this challenge. They didn’t read the entire genome at once, but instead divided it into small pieces a few hundred bases long, read them, and then put the sequences together using a computer. This method is not efficient for repeated segments, because the computer does not know in what order those segments are put together. “Eight percent of the copy that was officially completed in 2003 was missing,” says Adam Filippi, head of the genome informatics division at the National Human Genome Research Institute in Maryland.

Therefore, our duplicated DNA remained almost completely unread for 20 years. Then in 2021, Filippi and his colleagues announced that they had all read it.

What is the genome?

The genome is often compared to a book written in the DNA alphabet instead of the English alphabet. The DNA alphabet consists of only four letters: A, C, G, and T. Each of these letters represents different molecules called “bases” that are strung along the length of the DNA molecule. Any particular sequence of these letters constitutes a gene. The responsibility of translating this information lies with the molecular machines inside our cells. Some genes provide the information needed to make different proteins that have different functions in the body, while other parts of DNA have regulatory functions. What the Human Genome Project team achieved was the exact order of bases along the length of DNA; Something like CGATTTCCGAAAA and so on for over three billion characters.

Reading the human genome from beginning to end

The Telomere to Telomere (T2T) Consortium was not a big, famous, multi-billion dollar project. “It was really a public effort that took place during birth,” says Karen Miga, a geneticist at the University of California, Santa Cruz. In the eyes of many genomic experts, we appeared out of nowhere.

” A key advance was the ability to accurately read long stretches of DNA, says Evan Eichler, a professor of genome sciences at the University of Washington in Seattle. Previously, technologies capable of reading long sequences had been developed, but until recently they were not accurate enough. Therefore, improving the accuracy of these technologies was a key development. Also, the ability to read sequences that spanned over 100,000 bases was an important advance.

تشخیص بیماری های ژنتیکی

T2T’s first major breakthrough came in July 2020 when the project’s researchers published the complete sequence of the X chromosome. At the time, the best available sequence of the X chromosome had 29 gaps, and the T2T team filled in all the gaps. The following year, they published the complete sequence of chromosome 8. In 2021, they also published a preprint titled “The Complete Sequence of a Human Genome,” in which they filled in 8 percent of the missing sequence.

Reading repetitions

But the human genome had not been read completely yet. Ishler says the team used a little trick that some called cheating.

Most cells in our body have two copies of each chromosome: one from the mother and one from the father. This makes it more difficult to put the sequences together on the computer because the two versions differ very little. To solve this problem, T2T used abnormal cells that have two copies of the father’s DNA that are nearly identical. The mentioned cells were the result of a hydatiform mole (molar or baby-eating pregnancy), which is a type of failed pregnancy.

Eggs and sperm have only one copy of each chromosome, so when a sperm fertilizes an egg, the resulting embryo has two copies. However, sometimes the egg loses its DNA and is then fertilized. Then the egg cell, which has lost its DNA, replicates the sperm’s DNA. Hydatidiform moles form dangerous lesions that look somewhat like cancer and must be removed. This is what T2T sequenced. According to some researchers, they had read only half of the genome, because the complete genome has two copies of any particular sequence. Although overall, their sequence was a clear improvement over previous sequences and added more than 200 million letters and two thousand genes to the human genome.

Having a complete genome means finally being able to understand what the repetitive segments of DNA do, Miga says. “Now that we have these maps, I’m very excited to see what sequences are in these regions,” he says. But what is their main function? And if there is a problem in these areas, how can it contribute to our understanding of human disease and human health?”

Repetitive DNA contains many sequences that can move around the genome and are called “mobile DNA”. “Many of these elements have played a role in our recent evolution,” says Rachel O’Neill, a molecular geneticist at the University of Connecticut in Storrs. “Many evolutionary mutations, including placentation, loss of the tail, and some brain functions, can be attributed to this type of driver DNA.”

Meanwhile, Eishler refers to duplications, where long stretches of DNA that can contain multiple genes are duplicated at once. These sequences can evolve at an extraordinary rate. Ishler says: “The result of this phenomenon is the emergence of new genes that are specific to humans. “These genes contribute disproportionately to the differences that make us human.”

While the human and chimpanzee genomes are 99% identical, duplications are one of the ways in which important differences can arise between us and chimpanzees. The originally published human genome was largely devoid of these duplicated sequences.

Neuroscientists have shown that some duplicated genes are important in brain function. But geneticists couldn’t study them precisely because they were in repeats that didn’t occur in older genomes.

The T2T sequence was finally published in a special issue of the journal Science in March 2022. But at that time the team was moving forward.

The remaining large gap was the Y chromosome, which is only present in males. Sperm usually carry only one sex chromosome (either an X chromosome or a Y chromosome). Because the hydatidiform mole DNA used by T2T came from sperm that contained an X chromosome, the Y chromosome was not sequenced. The team needed a male donor to finish their work, so they used Pushkin.

DNA donor

Pushkin is a systems biologist at Harvard Medical School in Boston, Massachusetts. Much of his research focuses on understanding the mechanisms of aging and how to slow them down. He believes that the human life span has no limit and can be increased. Genomics is a big part of his work. Pushkin has donated his DNA to a number of major sequencing projects.

Pushkin’s first donation was to the Personal Genome project, which was launched in 2015. The goal of the project was to attract volunteers who were willing to share their DNA publicly to enable faster and more efficient research, as well as to overcome fears about the potential misuse of genomic data.

A decade later, Pushkin’s DNA was again used by the GIAB project. The goal of the project was to sequence the genomes of cell lines that could be grown indefinitely in the laboratory and make it easier to study the effects of mutations. Pushkin’s genome was favorable because he had also enrolled his parents in the project and provided them with information on his mother, father, and son.

تعیین توالی ژنوم

Pushkin does not regret his choices, although he points to an unpleasant consequence. “I can’t go to labs that work with my cells, because if my immortal cells somehow get into my body, my immune system won’t recognize them, and there’s a chance that the immune system will go into overdrive, and it’s a dangerous situation,” he says. come.” He is delighted to have his DNA sequenced again by T2T, this time in full.

In December 2022, T2T published another preprint paper describing the complete sequence of Pushkin’s Y chromosome. Since this chromosome has many repetitions and complications, more than half of the chromosome was not present in the past genomes. The new sequence added more than 30 million characters including dozens of genes.

The team is now working on Pushkin’s complete genome, including both copies of each chromosome. “We’ve finished sequencing and reconstructing it,” says Filippi. The resulting genome is complete and without defects and takes duplications into account. All that remains is the review. Filippi says there are a handful of errors we can check. He says their final genome should be published this year.

Pan Genome

Will the human genome be completed this year? The answer is no because there is no single human genome. Each person’s DNA is different and these differences are important. We won’t really understand the genome unless we have a record of how it differs between different populations.

The initial HGP project attempted to address this problem by drawing its sample from a few individuals, all from New York. The sequence that was released was a combination of all of them. Indeed, they tried to provide an average genome, but an American city cannot represent the full spectrum of human genetic diversity. This is why many members of the T2T Consortium are also enrolled in another project: the Human Pangenome Reference Consortium. The goal of this project is to sequence the genomes of hundreds of people from all over the world.

The project’s genomes will not be complete, as they will lose some degree of completeness in exchange for using automated methods that allow them to include more people in the study. In July 2022 the team published a preprint describing the 47 sequenced genomes that they had combined to create a draft “pangenome.”

They are now collaborating with researchers from around the world. “We don’t want this to be done exclusively in one place,” says Ishler. I think it is better to have genomes, especially from populations whose genetic diversity we have not identified well, and to do this in their own communities and by their own people.”

Pangenome’s effort has already paid off. Filippi is a co-author of a study published in January that identified a mechanism for a genetic abnormality. About 1 in 1,000 babies have a Robertsonian translocation, in which two chromosomes fuse together. If the genetic material is not destroyed, the health of the person is not affected, but in some cases, it can lead to conditions such as Down syndrome.

There appears to be a conserved sequence of DNA (that is, a sequence that is the same across species) that is found on multiple chromosomes. This can confuse the cellular mechanisms of DNA replication and cause chromosomes to fuse together. The critical sequence is located in a region that is both repetitive and highly variable between individuals, so it cannot be studied without multiple complete genomes.

Such findings explain why many project researchers want whole genome sequencing to be done in hospitals as well. “My ultimate goal is to be able to replicate T2T genomes in the clinic for any disease,” says Filippi. The methodology we have developed is in this direction. The cost of genome sequencing has fallen dramatically over the decades, so much so that the cost of the T2T project was much less than the cost of the original HGP.

Clearly, there is still much to learn from our genome. As new techniques reveal more secrets of the genome and make it possible to sequence more genomes, there is no end in sight. “As long as humans exist, the Human Genome Project will continue,” says O’Neill.

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Why do people listen to sad songs?

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Why do people listen to sad songs?
Perhaps the main reason for listening to sad music is not to enjoy the feeling of sadness, and people listen to this type of music because of the sense of connection. So why do people listen to sad songs?

Why do people listen to sad songs?

There is a paradox in sad music: we don’t enjoy sadness in real life, but we enjoy art that makes us feel that way. Countless researchers since Aristotle tried to solve this contradiction. Perhaps through music, we experience a kind of catharsis of negative emotions. Catharsis here means refinement and cultivation of the soul. Maybe there is an evolutionary advantage in this feeling of sadness, or maybe we want to value our suffering. Maybe our body produces hormones in response to anxiety disorder, music that leads to a sense of comfort.

According to the New York Times, Dr. Nob, an experimental philosopher and psychologist at Yale University, in a new study published in the Aesthetic Education Journal, raised the question, “What is the purpose of sad music?” He tried to solve the contradiction of this kind of music. Over the years, he came to the conclusion that people often have two perceptions of the same thing. For example, they can consider people as artists if they have a set of characteristics such as an innate talent for working with a brush; But if they don’t have abstract values ​​such as creativity, curiosity or interest and just recreate old masterpieces for profit, we can say they are not artists. According to Dr. Nob and his former student Tara Venkatsan, a cognitive scientist, perhaps sad music also has a dual nature.

A girl listening to sad music

The aforementioned research shows that our emotional response to music is multidimensional; You don’t necessarily feel happy when you listen to a beautiful song, and you don’t necessarily feel sad when you listen to a sad song. According to a 2016 study, the emotional response of 363 listeners to sad songs was divided into three categories: sadness and strong negative emotions such as anger, panic, and despair, nostalgia, quiet sadness and self-compassion, and finally sweet sadness is pleasant pain. It comes from consolation and understanding. Many respondents reported a combination of all three. The researchers called this research “Fifty Blue Spectrums”.

Given the layers of emotion and the ambiguity of language, it’s no wonder that sad music creates a paradox; But it is not clear why it induces a sense of pleasure or meaning. Some psychologists have investigated how certain aspects of music, such as position, pitch, rhythm, and resonance, are related to listeners’ emotions. According to research, certain forms of songs have an almost universal function: for example, among different countries and cultures, lullabies have similar acoustic characteristics that make children and adults feel safe. Thomas Irola, a musicologist at the University of Durham in England and researcher of the “Fifty Spectrum” study, says:

Throughout life, we learn to make connections between our feelings and what we hear. We recognize emotional expression in speech, and often these cues are used in a similar way in music.

Other researchers, such as Patrick Joslin, a music psychologist from Uppsala University in Sweden, believe that such findings reveal the value of sad music. Sad music, he writes in an essay, asks why “the second movement of Beethoven’s Eroica symphony evokes a sense of sadness?” It leads to the question, “Why does a slow step lead to a feeling of sadness?”

According to the findings of Joslin and his colleagues, there are cognitive mechanisms through which feelings of sadness are induced in listeners. These mechanisms include unconscious reactions in the brain stem, synchronization of the rhythm with the internal rhythm such as the heartbeat, conditional reactions to certain sounds, the arousal of memories, emotional contagion, and reflexive measurement of music. Perhaps because sadness is such a strong emotion, it can evoke an empathetic and positive response. In fact, understanding other people’s grief provokes a social response.

Why do people listen to sad songs?

The purpose of listening to sad music is not necessarily to convey sadness; Rather, it is creating a sense of connection.

Dr. Nob, along with Dr. Venkatsan and George Newman, a psychologist at the Rotman School of Management, designed a two-stage experiment to test the hypothesis. In the first part of the experiment, they gave one of four song descriptions to more than 400 participants. In the description of the first song, it was written: “transmitting complex and deep emotions, but technically full of errors.” The second track was described as: “music without technical errors that do not convey complex and deep emotions.” The third song was described as “highly emotional and technically flawless” and the fourth song was described as “technically flawed and non-emotional”.

Sad girl playing guitar

Subjects were asked to indicate on a seven-point scale whether their song conveyed the intent of the music or not. Their goal was to show how important it is for music to express emotion and generally happiness, sadness, hate, or any other emotion on an intuitive level. Overall, subjects reported that deeply emotional but technically flawed songs best reflected the nature of music. In other words, the emotional expression had a more prominent value than the technical aspect.

In the second part of the experiment, which included 450 new subjects, the researchers gave each participant 72 descriptions of emotional songs that convey feelings such as “humiliation,” “narcissism,” “inspiration,” and “lust.” For comparison, they gave participants phrases that convey conversational interaction in expressing people’s feelings. For example, one of the phrases was: “An acquaintance is talking to you about the past week and his feeling of passion”. In general, the emotions that the subjects receive are strongly rooted in the “purpose of the music” and are similar to the emotions that make people feel close to each other in conversation: emotions such as love, joy, loneliness, sadness, ecstasy, and relaxation.

Mario Etti Picker, a philosopher at Lowell University of Chicago, finds the results of this study interesting. After reviewing the data, he came up with a relatively simple idea: “Perhaps the reason we listen to music is not just an emotional response, but we do it to understand the connection with others; Because, according to the reports of many subjects, sad music is not necessarily enjoyable despite its artistic dimensions. In other words, according to the paradox of sad music, our love of music is not the result of direct praise of sadness; Rather, it is the result of valuing communication with others.”

Dr. Irola also concluded in his research that empathic people are likely to be moved by unfamiliar sad music. They tend to engage in this kind of imaginary grief. These people also show significant hormonal changes in response to sad music. But sad music, like an onion, has many layers, and this explanation can give rise to other questions. For example, who should we communicate with? Artist or with our own past? Or even with an imaginary person?

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Inventing a new drug to treat influenza

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Inventing a new drug to treat influenza!

A new drug developed to treat severe influenza works in a unique way, unlike what a drug would expect, to treat lung disease and infection.

Inventing a new drug to treat influenza!

A new drug to treat severe flu successfully keeps patients at the right level of lung inflammation to protect against lung damage while still allowing the immune system to fight infection. This drug has been effective in mice even a few days after infection.

According to New Atlas, if you’ve ever had the flu, you’ve most likely contracted the influenza A virus (IAV). Compared to influenza B virus, infection with type A often causes more severe symptoms. But, while many of us have experienced the fever and chills, headache and muscle aches, fatigue, sore throat, and cough of the common flu, severe infection with the animal IAV strain is different and potentially life-threatening.

Severe infection of this type of influenza causes a special type of cell death called necroptosis in infected cells. While this is a natural process designed to limit viral spread by actively eliminating infected cells and mobilizing the immune system to respond, necroptosis can activate a hyperinflammatory response and cause collateral lung damage that is potentially fatal. Is. Other than managing its symptoms, there are few treatment options for treating severe influenza.

In a new study, researchers from Tufts University School of Medicine, St. Jude Children’s Research Hospital, the University of Houston, and Fox Chase Cancer Center collaborated to test a drug called UH15-38 that could prevent this flu-related lung damage in mice. It prevents and allows the immune system to fight the virus.

“Our drug significantly increased survival and reduced symptoms of influenza virus infection,” said Paul Thomas, co-author of the study. The new drug reduced dangerous inflammation and even seemed to improve the adaptive response to the virus.

Achieving the Goldilocks effect, or the effect of the right amount of the drug on inflammation, required researchers to use clever chemistry along with a thorough understanding of the underlying mechanisms of necroptosis.

Receptor-interacting protein kinase 3 (RIPK3) is an essential part of the necroptosis cell death pathway, but it also controls another cell death pathway called apoptosis. Both types of cell death trigger opposing immune responses. Apoptotic death usually results in muted immunological responses, while necroptosis releases molecules that cause inflammation. UH15-38 was designed to prevent the stimulation of the necroptosis pathway by RIPK3, while still allowing cell death and removing infected cells in a less inflammatory manner.

Alexei Degterev, an associate professor of developmental, molecular, and chemical biology at Tufts University School of Medicine and one of the authors of the paper, says: “If you eliminate necroptosis, you will still limit virus replication without severe damage to the lungs.” Necroptosis does not appear to be necessary to limit viral activity, so if we can block it, we can protect the host by reducing inflammation in the lungs.

Read more: Testing a vaccine that reduces liver tumors

The researchers tested the drug UH15-38 in mouse models and found that high doses of the drug provided protection against the usually fatal IAV influenza. At low doses, the UH15-38 drug protected mice against similar amounts of influenza that humans experience. Notably, the mice were protected even if they received the drug several days after being infected with the disease.

“This drug can do something we haven’t seen before,” says Thomas. We can start five days after the initial infection and still see benefits. Completely removing the RIPK3 protein is not a great choice because then the immune system cannot clear the virus. When we removed only the necroptosis, the animals did better because they still had apoptosis and could still get rid of the infectious cells, but their condition was not as severely inflammatory.

UH15-38 improved survival by preventing collateral necroptosis damage to type 1 alveolar epithelial cells, a special type of cell in the lungs that facilitates gas exchange. Damage to these cells can make it difficult for oxygen to enter the blood and carbon dioxide from it, and cause symptoms such as shortness of breath, wheezing, and chest tightness. The drug also reduced the number of immune cells associated with inflammation, such as neutrophils, in the mice.

Often, the worst part of the flu happens after the virus is under control when inflammation destroys lung cells, Thomas says. UH15-38 can reduce influenza-induced inflammation while leaving viral clearance and other functions of tissue and immune responses intact. This makes the drug a promising option to move towards clinical use.

The next step is clinical and human trials safely. Researchers are testing whether UH15-38 is effective in treating other respiratory diseases.

While the worst of COVID-19 may be upon us, another pandemic is expected, and we need something that protects the host regardless of how it is infected, Degtref says. This study demonstrates the possibility of achieving such a goal and renews interest in how cell death occurs against infections.

This study was published in the journal Nature.

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Testing a vaccine that reduces liver tumors

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Testing a vaccine that reduces liver tumors

Testing a vaccine that reduces liver tumors. A combination of a vaccine and an immunotherapy drug has reduced advanced liver cancer in trials.

Testing a vaccine that reduces liver tumors

A third of patients with advanced liver cancer who received a personalized vaccine in a small trial saw their liver tumors shrink.

According to IA, Geneos Therapeutics has announced the publication of positive safety data, immunogenicity, and effectiveness of its solution in Nature Medicine magazine.

According to this study, hepatocellular carcinoma is the most common type of primary liver cancer and is also one of the leading causes of cancer-related deaths worldwide. The disease is responsible for more than 12,000 deaths each year in the United States alone.

Hepatocellular carcinoma or hepatocellular carcinoma (HCC) is the most common type of primary liver cancer in adults and is currently the most common cause of death in people with cirrhosis. This disease is the third leading cause of cancer deaths worldwide.

Hepatocellular carcinoma occurs in conditions of chronic inflammation of the liver and is most associated with chronic viral hepatitis infection (hepatitis B or C) or exposure to toxins such as alcohol, aflatoxin, or pyrrolizidine alkaloids.

Although advances have been made in the treatment of advanced liver cancer, the five-year survival rate remains below 10%.

current study

The first and last patients were enrolled in the study on June 16, 2020, and June 14, 2023, respectively, and all 36 patients in this study received their personalized vaccine.

In this study, researchers used samples from patients’ tumors to make vaccines based on the new mutations found in each patient’s tumor.

Liver cancer contains fewer mutations that reduce the effectiveness of immunotherapies. The results show that vaccines based on mutations present only in the patient’s tumor can boost the immune system. This is done in a way that improves the ability to detect and attack cancers.

The vaccine essentially trains the immune system to recognize antigens that are being ignored, says Dr. Mark Yarkwan, who led the study.

Read more: The relationship between high blood insulin levels and pancreatic cancer

Patients were given vaccines along with widely used immunotherapy. With this combination, they experienced a 30% tumor reduction. Three of them had a complete response, meaning no detectable signs of tumor remained after a median follow-up of 21.5 months.

“This certainly shows that the vaccine has indeed increased clinical efficacy,” Yarkvan added.

Side effects and adverse reactions

There were no serious side effects for the patients, and the only complication was pain at the injection site.

Genius’ innovative treatment involves a DNA vaccine that delivers the genetic code of mutated proteins to cells via a tiny electrical impulse. Each vaccine can target up to 40 mutated genes.

Despite the small size of the study, its results are important for the advancement of the field, says Niranjan Sardsai, president of Genius. “Our mechanism validates every step from vaccination to tumor reduction that is necessary to explain the immunological basis of the observed clinical responses,” he said in a statement.

Yarkvan also said that larger trials were being planned, but declined to provide details.

According to this study, more than 800,000 people worldwide are diagnosed with this type of cancer every year. It is also the leading cause of cancer deaths worldwide and accounts for more than 700,000 deaths annually.

It is predicted that the number of new cases of liver cancer will increase by about 55% each year between 2020 and 2040. It is also predicted that 1.3 million people will die from liver cancer in 2040.

Preliminary findings of the study were presented at the American Association for Cancer Research in San Diego.

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