BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Cancer (Page 1 of 5)

Immune Evasion Unveiled: The Thrilling Genetic Drama of Tumor Suppressors and Their Sneaky Dance with Cancer Cells

Cancer, an unwelcome antagonist in our lives, often emerges as the thief of precious moments with our loved ones and friends. Ever wondered how it manages to disrupt the narrative of our lives, stealing the scenes we hold dear? Or perhaps, reflecting on those stolen moments, have you found yourself questioning the resilience of the human spirit in the face of such a formidable foe? Cancer perfectly reflects the quote that Alfred from  “The Dark Knight” said to Bruce  ‘Some men just want to watch the world burn”. In this case Cancer just wants to watch the world burn because it gains nothing.

Cancer stem cells text resized it

A study conducted recently at Howard Hughes Medical Institute by Stephen Elledge highlights the strange role played by altered tumor suppressor genes. Compared to the common belief that implies mutations in these genes only encourage unrestricted cell growth. The study revealed that in excess of 100 defective cancer suppressor genes in mice may impair the immune system’s ability to identify and eliminate cancerous cells.  Do you know how the immune system is able to detects and eliminate cancerous cells? If not this is how. The immune system is able to identify and eliminate the cancerous cells by using  T cells. These T cells constantly patrol the body to identify cells that display abnormal or mutated proteins on their surfaces. These proteins, known as antigens, can be indicative of cancerous changes. Dendritic cells then engulf and process abnormal proteins from cancer cells. They then present these antigens on their surfaces. They then present the cancer antigens to T cells.This activates specific T cells (cytotoxic T cells) that are capable of recognizing and targeting cells with the presented antigens. Activated cytotoxic T cells travel to the site of the cancer cells and release substances, such as perforin and granzymes, that induce apoptosis (programmed cell death) in the cancer cells. Successful elimination of cancer cells leads to the development of memory T cells. These memory cells “remember” the cancer antigens, providing a faster and more efficient response if the same cancer cells reappear. This challenges the conventional understanding that mutations in tumor suppressor genes primarily trigger unrestricted cell division. Instead, it suggests that such mutations can also impact the immune system’s ability to identify and eliminate cancerous cells through the T cell-mediated recognition process. This broader perspective underscores the complex interplay between genetic mutations, immune responses, and cancer development.

Tumor Growth

This has several key concepts that we covered in our AP Biology class, particularly related to cell regulation, cancer, and the immune system.

The immune system’s role in identifying and eliminating cancer cells is a significant aspect of the AP Biology curriculum. The discussion of T cells, dendritic cells, and the process of presenting cancer antigens aligns with the immune system’s functions and responses to abnormal cells. This aligns with what we learned in AP Bio regarding the immune system’s crucial role in defending the body against abnormal or potentially harmful cells, including cancerous cells because we got to see how the T Cells, Dendritic Cells, and Memory T Cells really work. We also got to see how the immune system also works directly with blood sugar levels. With various activities in class with the skittles as glucose and how the pancreases would either send a message to produce insulin or  glucagon depending on which the body needed to maintain a balanced blood sugar level.

 

Teaching Cancer to Fight Itself

Many of us know someone who has suffered from cancer and we have watched loved ones undergo the harsh treatments for it. With treatments such as chemotherapy, the side effects are hard to bear. So, what if your body could be taught to treat cancer on its own without having to experience the hair loss, fatigue, nausea, and anemia that external treatments can cause.

Cancer cells are very different from normal cells as they hide from the immune system which usually eliminates damaged or abnormal cells. Cancer cells also trick the immune system to help cancerous cells stay alive and grow. But, what if these cancer cells could be altered to teach the body’s immune system to fight the cancer that the cells come from?

7 Most Deadliest Cancers

In an experiment done by Stanford Medicine researchers used mouse leukemia cells to train T cells to recognize cancer in a way that could mimic the natural occurrence in the body, similar to vaccines. T cells recognize pathogens due to special antigen presenting cells (APCs) gathering pieces of the pathogen to show to the T cells what to attack. In cancer, the APCs would gather up the many antigens that characterize a cancer cell so T cells could be trained to recognize cancer antigens and wage a multi-pronged attack on the cancer.

Killer T cells surround a cancer cell

The researchers programmed mouse leukemia cells to be induced to transform themselves into APCs.  When they tested the cancer vaccine strategy on the mouse immune system, the mice were able to clear the cancer. The immune system was able to remember what the cells had taught them and when they reintroduced cancer to the mice 100 days they were able to have a strong immunological response to protect them. Additionally, they tried to see if the tactic used with leukemia would work with solid tumors so they used the same approach by using mice fibrosarcoma, breast cancer, and bone cancer. They found that the solid tumor transformation was not as efficient to that of leukemia, but it still had a positive result. With all three cancers, there was significantly improved survival rates.

They then went back to leukemia, but this time they studied acute leukemia in human cells. When the human leukemia cells APCs were exposed to human T cells from the same patient, they observed all of the signs that indicated the APCs were teaching the T cells how to attacked the leukemia.

This relates to what we have learned in AP Biology because we learned about cell division and how cancer differs from normal cell division. Cancer is a disease where some of the body’s cells divide and grow uncontrollably. This can start anywhere but also spread to other parts of the body very quickly. In its normal process, human cells grow and multiply through interphase and mitosis to form new cells as the body needs. Interphase is the phase in the cell cycle that prepares for cell division by growing cells and undergoing the process of DNA replication. The body has checkpoints that regulate the G1, S, and G2, phases of interphase. There are also checkpoints for mitosis, which is the division of cells that results in two daughter cells. When the cells become old or damaged, they die and new cells are regenerated. When this process breaks down and abnormal or damaged cells grow and multiply when they’re not supposed to, the body goes through a process called metastasis where cancerous tumors are formed. Cancer cells ignore the checkpoints and continue to divide and multiply.

This research has introduced a new way that could eventually treat cancer in a more harmless way while also ensuring that the body can fight off recurrence. So do you think that this will be the new treatment for cancer?

 

To kill one, you must kill them all

Throughout your life, I bet you have heard hundreds of people mention the words cancer and chemotherapy, but have you ever wondered what this treatment does inside your body? Chemotherapy is a treatment method for cancer that involves the use of powerful drugs to kill cancer cells or stop them from growing and dividing. These drugs can be administered orally, intravenously, or through other routes and may cause various side effects due to their impact on rapidly dividing cells throughout the body. Doctors have not yet found a way to target only cancer cells. This means that chemo will attack all rapidly dividing cells including hair, the digestive system, and more. Finally, a recent study has found that chemo does not work the way that doctors have thought for many years.

Before I get into the discovery, I want to explain the process of mitosis and how cancer cells can divide so rapidly. In AP bio, we learned that mitosis is a fundamental process in cell division where a single cell divides into two identical daughter cells. It consists of several stages: prophase, Prometaphase, metaphase, anaphase, and telophase, followed by cytokinesis. During prophase, the chromosomes condense, the nuclear envelope breaks down, and spindle fibers form; in metaphase, the chromosomes align at the cell’s equator; in anaphase, sister chromatids separate and move towards opposite poles; finally, in telophase, new nuclei form around each set of chromosomes, completing the division process. In a normal cell, the rate of division is controlled by chemical signals from special proteins called cyclins. However, Cancer cells can divide without a signal; resulting in an extremely fast and dangerous pace of reproduction. For decades, researchers have believed that a class of drugs called microtubule poisons treat cancerous tumors by halting mitosis, or the division of cells. Now, a team of UW-Madison scientists has found that in patients, microtubule poisons don’t stop cancer cells from dividing. Instead, these drugs alter mitosis — sometimes enough to cause new cancer cells to die and the disease to regress. Beth Weaver, a professor in oncology and cell and regenerative biology found this discovery quite shocking. When hearing about this discovery she said “For decades, we all thought that the way paclitaxel works in patient tumors is by arresting them in mitosis. This is what I was taught as a graduate student. We all ‘knew’ this. In cells in a dish, labs all over the world have shown this. The problem was we were all using it at concentrations higher than those that get into the tumor.” With this discovery, scientists were inclined to see if other microtubule poisons work the same way. This led to an experiment conducted by Mark Burkard.

Binucleated cell overlay

In Burkard’s experiment, he used tumor samples from breast cancer patients who had received standard anti-microtubule chemotherapy. They measured how much of the drugs made it into the tumors and studied how the tumor cells responded. They found that while the cells continued to divide after being exposed to the drug, they did so abnormally. This abnormal division can lead to tumor cell death. In normal cell division, a cell’s chromosomes are split into two identical sets. Shockingly, weaver and her colleagues found that microtubule poisons cause abnormalities that lead cells to form three, four, or even five poles during mitosis while still only creating one copy of chromosomes. This then forces the chromosomes to be pulled in more than two directions causing the genome to scramble.”So, after mitosis you have daughter cells that are no longer genetically identical and have lost chromosomes,” Weaver says. “We calculated that if a cell loses at least 20% of its DNA content, it is very likely going to die.”. This experiment was crucial to the development of cancer treatment because it was able to take the scientists off the path of attempting to completely stop mitosis and instead has them attempting to screw it up. With this new finding, what else do you think scientists have missed in some of their treatments?

Cancer-Causing Free Radicals Are the Key to Tardigrade Survival

Tardigrade (50594282802)

Many may recognize the resilience of tardigrades, the microscopic water bears that can seemingly endure any and all conditions—researchers have found that tardigrades possess this attribute because of their ability to harness free radicals, the infamous matter that causes cancer in humans.

Tardigrades have survived all five mass extinction events on Earth, and are thought to have been around since before the current eon. They can live through extreme temperature and radiation, and even the vacuum of space. But how are they capable of this immense resilience?

Traditionally, free radicals have been known to promote cancer, causing genetic mutations that allow cells to multiply uncontrollably. First, in mitosis, the mutated cell divides, then its offspring divides, and before long a mass forms. That mass, or tumor, grows uncontrollably, consuming vital nutrients and mechanically interfering with the body’s internal function. If left unchecked, the tumor will eventually overwhelm the body’s ability to survive. However, there’s a flip side to free radicals.

The tardigrade has managed to harness the destructive power of free radicals in its quest for survival. For years, scientists have been baffled by the tardigrade’s ability to undergo drastic transformation in times of extreme stress. The organism’s transformations are a part of cryptobiosis, which consists of (but is not limited to) anhydrobiosis and cryobiosis. In anhydrobiosis, the tardigrade decreases its water content by 99% and its metabolic rate by 99.99%, and remains in a “tun” state for five years or more, only to rehydrate and flourish once environmental conditions are back to normal. In addition, via cryobiosis and other cryptobiosis processes, the tardigrade can survive extreme heat (304° F) and cold (-458° F). And the trigger for all of these survival mechanisms: free radicals, the same extra-electron atoms and molecules that cause human cells to mutate and multiply to form tumors.

Recent research suggests that tardigrades initiate cryptobiosis and protect themselves by releasing intracellular reactive oxygen species (free radicals) that in turn reversibly oxidize cysteine, an amino acid that acts as a sort of regulatory sensor for responses to stressors. The obvious question is: why isn’t the tardigrade harmed by the free radicals? The answer might hold the key to better understanding how to prevent cellular mutation, and cancer, in humans. Additional investigation is needed in this area.

So, what do you think? Are there similar discoveries that may be able to help us combat cancer?

A New Approach to Wound Care

Researchers at Linköping University in Sweden have made an incredible contribution to the field of medicine, specifically in wound care and infection detection that does not interfere with the patient’s healing process.

In medicine, wounds are typically treated with a dressing, which is changed often to avoid infection. In order to detect infection, healthcare providers have to frequently open the wound’s covering, which can be painful and can potentially disrupt the healing process. Additionally, each time the wound is opened, the risk of infection is increased. The researchers were alarmed by this issue, and developed a wound dressing comprised of nanocellulose that has the ability to display early signs of infection without further tampering with the wound or lifting the dressing. Daniel Aili, a professor involved in the study, has confidently stated that “being able to see instantly whether a wound has become infected, without having to lift the dressing, opens up for a new type of wound care that can lead to more efficient care and improve life for patients with hard-to-heal wounds. It can also reduce unnecessary use of antibiotics.”

The new wound dressing is made of a tight mesh nanocellulose material, which prevents bacteria and other harmful microbes from entering the wound. However, the mesh-like material allows airflow in, which is critical in the wound healing process. However, if the wound does become infected, the nanocellulose dressing will display a shift in color, notifying healthcare providers that the wound needs care. pH also plays a major role in this creation. Wounds that are not infected maintain a pH value of about 5.5. If an infection occurs, the wound starts to become basic and can increase to a pH value of 8, or higher. The increase in pH occurs because the wound’s bacteria shift their pH to properly fit their optimal growth environment. As we learned in AP Biology class, bacteria and enzymes have an optimal pH level to grow and function. If this level is not maintained, they cannot function properly. So, the bacteria increase their pH in response to infection if the optimal level is compromised. This elevated pH level in the wound can be detected by the nanocellulose dressing before any physical signs of infection.

pH Value Scale

In order to make the nanocellulose display infection with an elevated pH value, the researchers used bromthymol blue, a dye that reacts to a change in pH value. The bromthymol blue shifts from yellow to blue if the pH value increases past 7. The material of the bromthymol was then able to be combined with the dressing material without ruining the nanocellulose. As a result, the researchers successfully developed a safe-to-use, noninvasive wound dressing that will display a blue color if an infection occurs.

Bromothymol blue colors at different pH levels

 

The “Most Complicated” Cancer Treatment EVER

There are many approaches to treating cancer, ranging from invasive surgeries to extremely damaging radiation and chemotherapy.  The teeny-tiniest clinical trial ever began at UCLA in yet another attempt to find another way to eradicate cancer.  With only 16 participants, this trial combined two areas of research: gene editing and T-cell engineering.   The reason for the miniscule sample size is the intensely customized nature of the treatment.  Each patient’s tumor had completely unique mutations, so each patient needed equally unique T-cell engineering through gene editing.  

One reason cancer is so hard to treat is because they have adapted to be resistant to the body’s own immune response.  The patients that have cancers, especially ones in the later stages, have lost the battle against their cancer with their own immune system, so a new super-immune system must now be built.  This army of new T-cells (white blood cells, which identify and kill bad cells, seen below) will need “training” for its difficult battle ahead.  First, however, the researchers must determine how to train these cells so they will actually be successful.  They used algorithms to find identifiable mutations in the tumor, something that the T-cell can seek out to differentiate the cancerous cells from the normal cells.  Healthy Human T Cell

After testing to make sure that the T-cells can actually identify these mutations, T-cell receptors are designed specifically to their tumor.  Then, each patient’s blood is taken so that the DNA code for the new receptors can be inserted using CRISPR,  a genome editing technology at the cutting edge of genetic medical research.  The DNA code is transcribed to mRNA, which is then used in the ribosome to build polypeptides, in this case, the receptor proteins for the T-cells.  In order to ensure that these new T-cells (with the special receptors) are received, the patients had to take medication that suppressed the number of immune cells, so that the ones they are given can take hold.  

One month into treatment, 5 of the patients’ tumors stopped growing, and only 2 of the participants had associated side effects.  Although only 5 patients had the desired results, Dr. Ribas, one of the researchers, says that they “need to hit it stronger the next time” because they were limited to a small dosage of T-cells to start in order to establish safety.  Additionally, the technology will only get better and better as the research progresses and the T-cells can have more and more mutation targets to look for in a tumor.  

New CRISPR Technique can Potentially be a Treatment for Leukemia

An article published on December 11, 2022 on newscientist, shares fascinating information on a 13 year old patient with leukemia, having no detectable cancer cells after being the first person to receive a new type of CRISPR treatment, to attack cancer.  

The 13-year-old leukemia patient, Alyssa, has had many treatments that have been unsuccessful in helping her condition. Leukemia is caused by immune cells in the bone marrow dividing and growing rapidly. This relates to what we learned about in Biology class in how cancer cells become cancerous by cells dividing uncontrollably. It is also related to how cancer is caused by changes to the DNA (mutations) that alter important genes and change the behavior of them. Leukemia is also caused by the mutations in DNA.

Normal and cancer cells structure

The most common treatments for leukemia are known as killing all bone marrow cells with chemotherapy and then replacing it with a transplant. If this treatment is unsuccessful, an approach known as CAR-T therapy is used. This involves adding a gene to a type of immune cell known as a T cell that causes it to destroy cancerous cells. This also relates back to how in biology class we learned about the functions of T- cells being vital because they protect us from infection. The modified cells are called CAR-T cells. Alyssa’s leukemia was caused by T cells so if they used this technique to modify CAR-T cells to attack other T cells, it would lead to these cells killing each other. Wasseem Quasim at the University College London Great Ormond Street Institute of Child Health, has discovered many drawbacks with this treatment. Due to the many problems conventional gene editing can cause, Qasim and his team used a modified form of the CRISPR gene-editing protein, and Alyssa is the first person ever to be treated with. Alyssa received a dose of immune cells from a donor that had been altered to attack the cancer, and tests revealed 28 days later she had no signs of cancer cells. CRISPR is technology that can be used to edit genes. It finds specific DNA inside a cell and then changes that piece of DNA. It has also been discovered that CRISPR can be an effective tool for cancer  treatment. This new approach to CRISPR treatments could be hugely beneficial  to cancer patients and Many other treatments involving CRISPR base editing are being developed.  

 

 

 

 



 Cancer Detection Using CRISPR Gene Editing

Currently, many are accustomed to invasive cancer diagnostic methods such as endoscopies, colonoscopies, and mammograms. Driven by the desire to discover new methods, a group of researchers from the American Cancer Society developed an alternative method, which is a significant contribution to cancer detection.

Utilizing CRISPR gene editing as their approach, the group of ACS researchers developed an easy-to-use mechanism for detecting small amounts of cancer in plasma. CRISPR gene editing is a method that scientists and researchers have been using to modify an organism’s DNA. CRISPR gene editing is often done for numerous reasons, such as adding or removing genetic material, creating immune defense systems, and repairing DNA. Their detection method also allows healthcare professionals in diagnostics to decipher between malignant and benign cancer-related molecules that they may discover.

CRISPR Gene-Editing

The first step that the researchers made to develop this approach was to design a CRISPR system that creates a manufactured exosome out of two reporter molecule fragments, which they cut. An exosome is a small vesicle that carries material such as lipids, proteins, and nucleic acids after branching out from a host cell. Exosomes are typically involved in detecting cancerous cells because they provide a glimpse into the host cell they branched out from. Therefore, cancerous cells are shown in their exosomes through biomarkers, like micro RNAs (miRNA). In AP Biology class, microRNAs are described as materials that bind to complementary mRNAs to prevent the translation from occurring. MiRNAs are a recent discovery, identified in 1993. It is now concluded that most gene expression is influenced by them, so the researchers made efficient use of miRNA in their experiment. The two fragments of the reporter molecule came together and interacted with the CRISPR’s materials.

Micro RNA Sequence

The researchers concluded that if the targeted miRNA sequence was evident in the combination, the CRISPR system they made would become activated and cut apart the reporter molecule. The researchers specifically targeted miRNA-21, which is often involved in cancer development. The researchers were able to detect miRNA within a combination of similar sequences and later tested their method on a group of healthy exosomes and cancerous exosomes. Their CRISPR system successfully differentiated between the healthy and cancerous exosomes, which makes this system effective for cancer detection. The researchers are confident that their CRISPR gene editing approach to cancer detection will make diagnosis easier on patients and a more efficient process overall.

 

The Chemotherapy-Free Way Of Curing Cancer

Introduction 

Chemotherapy has been one of the only ways to cure cancer for a long time, but this is not the case anymore. According to a report in the journal Nature, CAR-T cell therapy has shown long-lasting success in treating blood cancer, with two patients remaining cancer-free over a decade later. This can be a new efficient way to cure cancer and it will also allow for less severe side effects like our fast-growing cells to still function properly. 

Life of a Cancer Cell

How it works 

The treatment uses genetically engineered immune cells to target and kill cancerous cells. CAR-T cells are a type of immune cell that is engineered in a laboratory to recognize and attack cancerous cells. The process of creating CAR-T cells involves extracting T-cells, from blood. These T-cells are then genetically modified in the laboratory to produce antigen receptors. These are engineered to recognize and bind to cancer cells. After CAR-T cells binds it triggers death to the cancer cell, ultimately getting rid of the cancer.

 

Connection to AP Biology

CAR-T cell therapy reflects what we learned in AP Biology. Unlike chemotherapy which kills fast-growing cells. CAR-T cell therapy selectively targets cancerous cells which eliminates possible symptoms. This is also similar to the topic of the immune system in AP Bio. For example, we learned that Cytotoxic T cells are part of the adaptive group of the immune system. When the Cytotoxic T cell sees an infected cell it binds to it and causes apoptosis (self destruction of cell )to occur.

How a killer T cell destroys a cell infected with viruses

Potential Drawbacks

Though the treatment seems ideal, there are still drawbacks. The treatment does not work for everyone and can have dangerous side effects. Researchers are working on expanding the therapy’s effectiveness by understanding how and why it works. CAR-T cell therapy is still new but has potential in the near future for curing cancer. 

Side effects listed:

  • High fever and chills.
  • Trouble breathing.
  • Severe nausea, vomiting, and/or diarrhea.
  • Feeling dizzy or lightheaded.
  • Headaches.
  • Fast heartbeat.
  • Feeling very tired.
  • Muscle and/or joint pain.

 

 

Detecting Cancer Early in Dogs

Scientists have discovered different factors that may be able to predict a dog’s cancer diagnosis. Previous studies done on this have mostly focused on European breeds, but the doctors in this study wanted to focus on breeds that are most commonly found in the United States. Dr Andi Flory, a veterinary oncologist, led this research by collecting data from 3,452 dogs. They found that the median age at which the dogs were diagnosed was 8.8 years. 

We have learned in AP Bio about what causes cells to become cancerous in humans, and sadly, it’s similar in dogs. If cells become damaged, this can affect their ability to know when to stop reproducing, causing them to reproduce uncontrollably. Other factors, such as mutations in onco genes, can cause similar uncontrollable cell reproduction. Cells that become cancerous are different from normal cells in that they will divide even if they haven’t received a signal to do so or if the area they belong in is filled with cells already.

Canis lupus familiaris.002 - MonferoMale dogs were generally diagnosed at a younger age than females. Furthermore, fixed dogs had earlier detection as well, compared to dogs that had not been fixed. Purebred dogs had cancer detected at a younger age compared to mixed-breed dogs. There are many things that could cause cancer in dogs. It’s possible that a cell was damaged or altered, or that an outside factored changed their DNA, which therefore could affect their genes that influence the behavior of cells. 

The scientists have concluded that, based on the findings, pet owners start cancer screenings for the dogs at age seven. 

PetDx, the pet diagnostics company that conducted the study, has created a blood-based canine cancer test. This liquid supposedly detects cancer in dogs by looking for “genomic alterations” in blood. However, doctors question the validity of this test. In general, there are few tools that are successful in early cancer detection in jobs-even ultrasounds and x-rays, and including these liquid biopsies previously mentioned. That being said, the test’s ability to identify true cases is 54.7% accurate. Additionally, they can identify metastasized cancers (cancers that have spread) at a rate of 87.5 %, but only at 19.6% for small cancers. However, these tests do not officially detect cancer. Veterinary oncologist Cheryl London acknowledges that this study is especially useful for recognizing patterns in dogs’ diagnosis, and for encouraging pet owners of certain types of dogs to get screened sooner for early detection. The earlier the diagnosis, the earlier the treatments can begin. As we learned in class, treatments can be either chemotherapy, which is killing the rapidly dividing cancer cells, or the treatment can be a physical removal of the cancerous tumor. 

Hot dogs, Fries, and Chicken Nuggets Aren’t Good For Me?

Although foods such as soft drinks, chips, and breakfast cereals have been normalized as good meals, these foods are ultra-processed, and new research shows just how dangerous these foods can be. A recent study from the Imperial School of Public Health in London provides new and convincing evidence that ultra-processed foods lead to cancer, especially ovarian and breast cancer.

Now, you may be wondering how one develops cancer. One develops cancer when cells divide uncontrollably. These uncontrollable divisions begin due to a mutation in genes, sections of DNA. Proto-Oncogenes are genes involved in normal cell growth; these genes cause cells to divide. A mutation in a single allele of a proto-oncogene causes a protein to be produced that will exponentially increase the rate of cell division. Tumor suppressor genes are involved in the stopping of cell growth. When both alleles in a tumor suppressor gene are mutated, it leads to an inability to stop cell division.

Cancer

So, how does ultra-processed food cause mutations in your genes? It is believed that these foods can eventually lead to the mutation of alleles in proto-oncogenes and/or tumor suppressor genes. All ultra-processed foods share the commonality of being created by substances extracted from foods: Fats, starches, added sugars, and hydrogenated fats. A diet consisting of these types of food can lead someone to develop type II diabetes. People with type II diabetes are twice as likely to develop liver or pancreatic cancer. These people also have a much higher risk of developing bladder, colon, or breast cancer. When someone has a lot of excess fat around vital organs, it makes it very easy for cancer cells to get the nutrition they need to keep uncontrollably dividing. The fat from glucose is what the cancer cells need to continue to divide; cancer cells are known to metabolize glucose at 200x the normal rate. When one has Type II diabetes, they have increased blood sugar. If the cancer cells have access to blood flow, the increased blood sugar gives the cancer cells even more nutrients to keep dividing. Even though one can not say for sure, it seems increasingly apparent that avoiding ultra-processed foods is best for your health. So, the next time you want a snack, maybe an apple and a glass of water are your best bet.

 

Can Cancer in Dogs be Predicted?

Cancer in dogs is not an uncommon thing. While unfortunate, about 1 in 4 dogs unexpectedly develop cancer throughout their lifetime. Scientists have recently raised the question of the possibility of predicting when a dog might develop cancer. Veterinary Oncologist and researcher Andi Flory and her team at PetDX (pet-diagnostics firm) began research to find out if certain traits and factors are associated with a dog’s development of cancer.

As an AP Biology Class, we have gained a significant amount of background information on cancer as a result of our studies throughout this unit. Cancer in dogs is very similar to cancer in humans. As we know from class, when a cell becomes cancerous, it divides uncontrollably, and its DNA becomes damaged as a result of some form of mutation (as a result of radiation, high fat, etc.). Unlike a healthy cell, a cancer cell does not stop dividing when it is crowded, and through metastasis, cancer cells travel through the blood system and create tumors. Cancer treatment for both dogs and humans can also be very similar, one major example (similarity) being chemotherapy, a process in which chemicals attempt to kill the fast-spreading cancer cells in a living organism.

Differences in glycolysis pathways between normal cells and cancer cells

After using data and samples from three previous studies, one at University of California- Davis combined with Colorado State University, the second at Ohio State University, and the last at the University of Wisconsin- Madison, Flory and her team concluded their results. They concluded that the median age for cancer development and discovery in dogs was approximately 8.8 years old, with the males being slightly younger than females during cancer diagnosis. They found that neutered and spayed dogs, on average, were diagnosed later than those who have not been “fixed.” With regards to breeds, the study found that West Highland White Terriers and American Staffordshire Terries formed cancer the latest out of all breeds, and Mastiffs and Saint Bernards formed cancer the earliest compared to other breeds. These results may be useful to anyone looking to get or adopt a new dog.

West Highland White Terrier PippaAmericanStafforshireTerrierMastiff - English MastiffGrupp 2 SANKT BERNHARDSHUND, Dein Hards Monday Muffin (24180113462)

As a result of this study, specifically the fact that, on average, the younger ages of cancer diagnosis in dogs was around 7 years old, veterinarians recommend that dog owners begin cancers screening right around the 7 years-old-mark. While there isn’t enough technology yet to detect cancers at very early stages, scientists and veterinarians still say that it is better to begin cancer checkups early rather than later. As a dog owner, I agree with the fact that cancer screenings in dogs should start earlier rather than later. Even though it might be an added expense, if cancer happens to be detected earlier, the dog will begin treatment sooner, and the chance for recovery increases.

A new evolution in cancer metastasis research

 

Perhaps the greatest fear of any cancer patient is metastasis.  According to Cancer.Net, metastasis is the process by which cancers spread throughout the body.  Furthermore, according to Cancer.gov, “Metastatic cancer is notoriously difficult to treat, and it accounts for most cancer deaths.” However, a new study in Nature, as outlined in an article in The Scientist, unearths new truths about how cancer cells metastasize that could perhaps spark a new wave of research.  

As stated in The Scientist, “Previous studies have shown how, counterintuitively, cells pick up the pace as they move through thicker solutions.”  Recent studies have elaborated on this accepted facet of cancer reaction, and have discovered that Cancer cells have the ability to detect, and even memorize the viscosity of their environments.  Researchers noticed that cancer cells initially exposed to viscous environments retained their speedy movement even after they were moved to watery environments, at a level not represented in those constantly in watery solutions, thus indicating a sort of memory of environment in cancer cells.  This phenomenon of “cell memory” is similar to the memorization features seen in T-memory cells we discussed in class during the unit on the immune response.

Breast cancer cell (2)

Later, that same team of scientists released study that aimed to determine how cancer cells are able to move quickly through viscous substances.  According to an article in The Scientist, “cancer cells move by taking up water at the front of the cell and squirting it out the back, propelling themselves like octopuses through narrow spaces.”  Some researchers believe that new drug research could aim to target the ion channel that causes this transportation: TRPV4, but others are not so convinced.  According to Miguel Valverde of Pompeu Fabra University, “Animal knockouts for the TRPV4 channels develop normally,” indicating that the newly discovered transportation mechanism may not be as essential as researchers may believe.

Still, the discovery of a new transportation method for cancer cells explaining its peculiar preference for viscosity is an important breakthrough, that will undoubtedly guide future research in cancer metastasis. 

Improvements for Kidney Cancer Treatments

Cancer is a disease where some of the body’s cells grow uncontrollably and spread to other parts of the body. Approximately 39.5% of men and women will be diagnosed with cancer in their lifetime and an estimate of cancer survivors in 2030 will be around 22.2 million – this study was done in 2020. In 2021 statistics showed that roughly one in every two people will get cancer in their lifetimes the biggest reason being that people are living longer lives, with the main range of people getting cancer being those over 70 years old. Recently the HSE – which is the Health and Safety Executive (HSE) is Britain’s national regulator for workplace health and safety. It prevents work-related death, injury, and ill health – has “discovered genes that are specific to the most aggressive subtype of clear cell renal carcinoma”. Clear cell renal carcinoma or ccRCC is a type of kidney cancer. The kidneys cleanse the blood of toxins and change the waste into urine, the two kidneys together filter 200 liters of fluid every 24 hours – balancing the body’s fluids. ccRCC is a rare type of cancer where when one looks at the cells under the microscope the cells look clear. For adults, ccRCC is the most common type of kidney cancer and it is more common in adults than in children. ccRCC makes up between 2-6% of childhood and young adult kidney cancer cases. Patients who are diagnosed with ccRCC tend to have a worse prognosis than patients diagnosed with different subtypes of RCC “with 5-year disease-specific survival rates of 50-69%, compared with 67-87% for papillary RCC and 78-87% for chRCC“. This recent genetic discovery by Grigory Puzanov, a research fellow at the HSE Faculty of Computer Science International Laboratory of Bioinformatics, could change the clinical treatment course of ccRCC patients.

Histopathology of renal clear cell carcinoma

Puzanov analyzed data from 456 patients with the disease identifying cancer subtypes that have favorable or unfavorable prognoses. His study reveals the ccRCC subtypes that are more dangerous than others and what specific human genes appear responsible for the progression of the disease. The discovery of this is significant for the early detection of tumors and for designing a personal treatment for the patient – this is especially important because most patients are diagnosed after ccRCC has already advanced to later stages. The way that Puzanov analyzed the data from the 456 tumor samples was using the k-means method – where the algorithm randomly chooses a centroid for each cluster – to create subgroups with similar characteristics. Through this Puznov was able to select 2,000 genes with high “variable expression patterns in ccRCC“. Gene expression “is the appearance in a phenotype of a characteristic or effect attributed to a particular gene” which allows the gene to be read and copied producing RNA (which is then used to synthesize proteins). He ran this algorithm on each tumor 100 times based on the 2,000 subgroups he had found previously. There were multiple testing stages run during this research study, in the first stage, each subgroup’s characteristics were tested on how their genetic factors could influence the course of ccRCC. Then Puzanov identified the crucial genes in particular for high to low survival subgroups and created a system of interaction for “proteins whose synthesis is encoded by these genes”. From this, he determined which genes created the highest number of “network connections”. Some of the key genes they found were noticed to affect the anti-tumor therapies they were running on patients with ccRCC  –  like CP, FGA, and FGG genes – this can help doctors in the future choose better working treatments for patients with malignancies. In our biology class, we have gone over mRNA and what it does, and how it is vital for protein production. It carries information from the DNA in the cell’s nucleus to the cytoplasm. Since mRNA carries information scientists can use mRNA vaccines to treat diseases, it also allows researchers to create mRNA cancer vaccines that activate the immune system to attack cancer cells. The known research on mRNA and the new information found from Puzanov’s research is bringing cancer treatment further.

 

 

 

 

 

 

Shhhhhhh! Some Viruses Can Sneak into Cells and Cause Cancer

Viruses! We all hate the colds we get in the fall that come with a cough, a runny nose, and a sore throat.  These bugs have gone around since nursery school, so we were taught that viruses were transmitted through touching door knobs, getting coughed on, and touching someone who is sick.  While these are how viruses are spread from person to person, the infection that occurs on a cellular level is much more complex.  

For starters, only a handful of viruses are known to actually cause illness in humans, but the ones that do have adapted to do it very efficiently, and some are even known to cause cancer.  Viruses that cause cancer include human papillomavirus, Kaposi Sarcoma-associated Herpesvirus, and Epstein-Barr virus.  The way that these viruses get into the cells is very unique compared to the common cold virus, and a team at the University of Michigan Medical School decided to take a closer look at just how they invade to try and get a better grasp on how to prevent cancers caused by viruses in humans.

The virus they researched is called SV40 and it causes tumors in monkeys.  The way that SV40 infects monkey cells is by burrowing itself through the cell membrane and then into its nucleus in order to duplicate itself.  SV40 is used as a tool to understand how the cancer causing viruses work because of the biological similarities that monkeys and humans have.  An earlier team studied how SV40 travels through the cell.  It goes from the surface, through the endosome, the ER, and then enters the cytosol.  

The most recent study illuminates the rest of the virus’ passage through the cell. The way SV40 gets into the nucleus is through the nuclear pore complex.  This is how many viruses enter the nucleus, but the SV40 is too large to enter through this pore.   The virus must disassemble in order to gain access to the nucleus. This process partially disassembles the virus into a smaller package made of two proteins and genetic material (DNA).  As we have learned in class, the DNA is the macromolecule that codes for how to build the proteins that build the virus.  When the DNA for the virus is connected with the two proteins, it uses both the nuclear pore complex and another complex called LINC.  LINC connects the two membranes of the nucleus together.  Many other viruses grab onto the little fingers sticking out of the nuclear pore complex (seen below), while SV40 seeks out LINC in order to get into the nucleus.  

202012 Nuclear pore complex

The difference in entrances between more common viruses and SV40 could be what makes SV40 cancer-causing.  The next step is to research how SV40 exploits LINC in order to expand upon how other diseases could enter the nucleus, and hopefully find a way to trigger the immune system in order to expel or digest the viruses before it is too late.  

Is a Vaccine for Cancer Getting Closer?

Vaccines for cancer have long been seen as a possible, but incredibly far-fetched idea. However, the possibility of being vaccinated for cancer, like a polio or flu shot, is getting closer. Scientists and medical doctors are becoming increasingly optimistic about the possibility for a successful vaccine to certain forms of cancer.

Testing vaccine in laboratory. Holding syringe with protective medical gloves closeup. (51714051263)

One type of these vaccines is a dsRNA vaccine, which is designed to replicate the protein that is able to take over a cell by tricking the receptor proteins on the plasma membrane into accepting it. The immune system then learns how to respond to this event and can do so in the future with actual malignant proteins. This works similarly to the COVID-19 mRNA vaccine.

Pancreatic cancer is a promising target – for those in remission, the chance of fatal recurrence is 70-80%, yet relatively easy to detect early with careful testing. The safety study, conducted by the Johns Hopkins Hospital Cancer Center, had no recurrence out of 12 patients. Although very early in the trial process, these are promising initial results that bode well for the future of the trial.

Although not every study is quite as promising. In a more comprehensive, though also not peer-reviewed, study of vaccination against colon cancer, there was no significant difference between the cancer rates of the control group and the experimental group. However, there is promise in the concept, and the field must be explored further before judgment can be cast. At the same time as these other therapies are being developed, inoculation such as the HPV vaccine is preventing cancer by protecting against cancer-causing illnesses. Cancer prevention is a recent, but flourishing field, and one that must be developed further.

Will Microscopic Worms Replace Dogs in Sniffing Out Cancer?

It is very rare that doctors are able to find cancer at its early stages, however, on the rare occasion that they do there is a much higher chance that the patients survive. You may be asking yourself: Why isn’t there a way to find this cancer earlier inorder to save more lives? A recent study shows that microscopic worms are able to sniff out cancer as early as stage 1. While dogs are also able to smell cancer from human breath, urine, and blood, keeping cancer sniffing dogs in a lab is not practical. These tiny worms create a more practical solution to this problem. 

Specifically, lung cancer is found by doing a biopsy or different kinds of imaging tests. However, these kinds of tests are not able to detect lung cancer until it is in its later stages and more severe. As we learned in AP Biology, cancer is caused by cells that uncontrollably divide. In normally dividing cells there are checkpoints the cell must pass in order to divide. These checkpoints are at the G1, S, and G2 phases. If the cell needs to divide there will be an influx of cyclin concentration and MPF activity. Cyclins are proteins that control the progression of the cell through its checkpoints by activating cyclin-dependent kinases. MPF, or maturation promoting factors, promotes the cell’s entrance into the M phase from the G2 phase. In cancer cells there is a genetic mutation, sometimes it is hereditary, however it can also be caused by caused by tobacco smoking, radiation, etc. This genetic mutation causes these proteins to not work properly. Because of the malfunction of these proteins, cells do not know when to stop dividing and continue to divide. 

A team of scientists from Myongji University in Korea found a type of worm called C. elegans that is attracted to the floral scent of lung cancer cells. 

Caenorhabditis elegans hermaphrodite adult-en

During their experiment, scientists placed the worms in a center chamber. On each side of the chamber was a petri dish, one with lung cancer cells and one with normal cells. The scientist found that these worms were more likely to move towards the lung cancer cells than the regular cells. Now, researchers hope to increase the accuracy of the worm’s attraction to the lung cancer cells and use these worms to detect lung cancer during its early stages. Worms that have already been exposed to the lung cancer cells will be used to detect cancer in patients urine, saliva, and even their breath. These researchers will continue to work with doctors to test their theory and see if these microscopic worms will replace dogs in sniffing out cancer.

 

Can Cancer Cell’s Medication Immunity Be Stripped?

Cancer is one of the hardest diseased to fight. If a tumor begins to grow inside of a patient, they may be given drugs to fight off the corrupt cells. The problem with this is that the cancer cells could become immune to these drugs. Through the use of CRISPR. In Novel Crispr imaging technology reveals genes controlling tumor immunity, a new way of fighting cancer is revealed. Instead of targeting the whole tumor, Perturb-map marks cancer cells and the cells around cancer cells. Once this is completed, it is able to identify genes controlling cancer’s ability to become immune to certain drugs.

Mitosis appearances in breast cancer

To fight cancer cells, scientists use thousands of CRISPRs at the same time. This identifies every gene in a sequence and allows them to be studied. Through Perturb-map, scientists can now dive deeper and find where the cell immunity to drugs originates. A certain pathway in the cell is controlled by the cytokine interferon gamma or IFNg, and a second is by the tumor growth factor-beta receptor or TGFbR. When the cell had a gene with TGFbR2 or SOCS1, the latter of which regulates IFNg, tumor cells grew. When the cell lacked one of these, it shrunk. Moreover, it was discovered that tumors with SOCS1 were susceptible to attacks by T cells, but TGFbR cells had immunity against them. This stayed true even when both types of cells lived in the same environment. With findings like these emerging more and more, the future of cancer treatment is looking brighter than ever.

Chromosome DNA Gene unannotated

CRISPR Causes Cancer, Sort Of

          Scientific researchers are always looking for ways to improve modern science and help create new treatments. Currently, CRISPR, “a powerful tool for editing genomes,” holds the ability to help advance medicine, specifically gene editing, so long as the kinks in this specific method are worked out. One of these problems is the DNA damage caused by CRISPR “activates the protein p53,” which tries to protect the damaged DNA. This raises not one, but two concerns as present p53 can diminish the effectiveness of this technique, however when there is no p53 at all cells grow rapidly and become cancerous. As we learned in AP Biology class, typical cells communicate through chemical signals sent by cyclins that ensure the cell is dividing the right amount. Cancer cells, however, contain genetic mutations that prevent them from being able to receive these signals and stop growing when they should. “Researchers at Karolinska Institute” have discovered that “cells with inactivating mutations of the p53 gene” have a higher survival rate when contingent on CRISPR. To further their research, they discovered genes with mutations similar to those of the p53, and also “transient inhibition” of the gene could help prevent “the enrichment of cells” that are similar. Although seeming antithetical, these researchers proved that inhibiting p53 actually makes CRISPR work better and prevent enrichment of mutated p53 and other similar genes. 

CRISPR logoDNA animation

           These results give crucial information, helping advance CRISPR and make it more usable in current medicine. Additionally, the researchers have uncovered the possibility that the damage CRISPR causes to DNA might be key in creating a better RNA sequence (the RNA sequence tells us the “total cellular content of RNAs”) guide, showing where DNA should be changed. In future tests, these researchers want to try and get a better idea of when the enhancement of mutated p53 cells from CRISPR becomes a problem.    

CRISPR Causes Cancer? Or Does It?

CRISPR illustration gif animation 1

The ground-breaking scientific break through of gene editing is finally here with the technique called CRISPR. CRISPR, or gene cutting, is the method of cutting a strand of DNA and letting the DNA repairer function repair the cut by itself. But it is at this instant where scientists introduce some changes to the genes, which the DNA will reproduce; DNA naturally grows back the mutated Genes. This CRISPR sounds great in the world of science, where certain genes can be modified onto a person. Though there are different opinions on gene-modifying, CRISPR has yet to be fully perfected. One of these hurdles is P53; a tumor suppressing protein. P53 is known as the “guardian of the genome” as this protein determines “whether the DNA will be repaired or the damaged cell will self-destruct” (MEDICINEPLUS). While this is good news, it is observed that “a dataset of >800 human cancer cell lines identified additional factors influencing the enrichment of p53-mutated cells.”(aacrjournals). So a lot of cancer cells have had a mutated P53 protein. So why does this happen? Why is the guardian of the genome being mutated?

 

P53 mutations are “missense mutations,” meaning they mutate in relation to a gene being edited, which creates different amino acids. By creating a whole new set of amino acids, the cell completely changes and in this case, mutates the P53. By mutating the P53 protein, P53 can no longer stop the cell division cycle, immensely increasing the chance of cancer cells. Although I make CRISPR sound like a dangerous operation to do(*I am not a scientist*), Researchers at Karolinska Institutet say to” have found new links between CRISPR, p53 and other cancer genes that could prevent the accumulation of mutated cells without compromising the gene scissors’ effectiveness.”

Another new research point mentions that although a lot of P53 mutations occur when subject to CRISPR, “cells with mutations are there from the start.” This is still a huge unknown to scientists, as CRISPR does cause P53 to mutate, there are already mutated P53 cells beforehand. Though this does prove that P53 is affected by other factors instead of only affected by CRISPR. Scientists still have much to uncover about gene-editing and in the future, they could possibly change somebody’s genes for a good cause.

 

 

 

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