BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Cancer (Page 1 of 5)

CRISPR Reveals How mRNA Vaccines Work

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On April 8, 2025

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Dr. KIM V. Narry led an important study on mRNA vaccines, like COVID-19, and how cells take them up and respond, as described in the article “Cellular regulator of mRNA vaccine revealed… offering new therapeutic options” from the Institute for Basic Science. This research explains how these vaccines enter cells, carry out their functions, and eventually get degraded. These new insights could lead to the development of better mRNA vaccines and treatments for diseases like cancer and genetic disorders.

In the study, over 19,000 genes were analyzed using a CRISPR-based screen, which led to the discovery of three key factors that affect mRNA vaccine effectiveness. First, the cell surface molecule heparan sulfate (HSPG) was found to help mRNA enter the cell. Second, a protein called V-ATPase was shown to release mRNA inside the cell by creating an acidic environment. Third, the protein TRIM25 acts like a security guard, detecting and destroying foreign mRNA.

The scientists found that proton ions, tiny charged particles, act as signals that tell the cell to launch a defense. When mRNA enters the cytosol, these ions alert TRIM25 to take action. This is the first evidence showing that proton ions can function as immune signals.

Cas9 in complex with sgRNA and target DNA

This article relates to what we’ve learned in AP Biology about protein synthesis and how mRNA is used by ribosomes to make proteins. The study shows that foreign mRNA must avoid being destroyed for this process to happen. TRIM25, part of the innate immune system (which we also studied this year), works to break down foreign RNA, but mRNA vaccines use a modified base (m1Ψ) to protect it and allow translation. This ties into what we’ve just learned about gene mutations. The discovery of proton ions also connects to our unit on cell communication, as it shows how cells respond to threats through chemical signaling.

I found this article fascinating as it included content from almost every unit we have learned this year! Let me know your thoughts in the comments. Did you know a single chemical change in mRNA could make or break a vaccine’s success? Do you think understanding our cells better be the key to curing diseases like cancer?

Rewriting Cancer’s Script

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On April 7, 2025

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Imagine a film editor taking raw footage and cutting scenes to create entirely different movies while using all the same raw materials. This is remarkably similar to how cells process RNA, selectively splicing together different segments to produce various proteins from a single gene. This fine-tuned control is essential for normal cellular function, but when cancer hijacks this system, it rewrites the script for its own survival. A groundbreaking study from The Jackson Laboratory (JAX) and UConn Health, published in Nature Communications, reveals how cancer manipulates RNA splicing and introduces a potential therapy that could disrupt its deadly strategy.

In a recent study, scientists not only show how cancer hijacks this tightly regulated splicing and rearranging of RNA but also introduce a potential restorative strategy that could slow or even shrink aggressive and hard-to-treat tumors. In healthy cells, RNA splicing ensures that the right proteins are made at the right time as it removes all the introns and joins the exons back together. A key player in this process is poison exons, which are genetic elements that contain a premature termination codon targeting certain transcripts for decay, decreasing the amount of protein produced. This mechanism prevents excessive or harmful protein production. However, cancer cells have found a way to suppress these poison exons, particularly in the TRA2β gene. The study found that when poison exons are excluded from TRA2β RNA, the resulting protein accumulates, leading to uncontrolled tumor growth. Moreover, researchers observed that lower poison exon inclusion in TRA2β correlates with poor patient outcomes in aggressive cancers such as triple-negative breast cancer, brain tumors, and leukemia.

To counteract this, scientists experimented with antisense oligonucleotides (ASOs), synthetic RNA fragments designed Poison exonto force poison exon inclusion back into TRA2β RNA. By reactivating the gene’s kill switch, ASOs restored the cell’s ability to degrade excess TRA2β RNA and slow tumor progression. Interestingly, when researchers used CRISPR gene editing to remove the TRA2β protein entirely, tumor growth persisted. This suggests that targeting the RNA rather than the protein itself could be a more effective treatment strategy. Furthermore, preliminary results indicate that ASOs are highly specific and do not interfere with normal cell functions, making them promising candidates for future cancer therapies.

This study connects with what we’ve learned in AP Biology about gene expression regulation and alternative RNA splicing. In class, we discussed how alternative RNA splicing is part of how gene activity is controlled in eukaryotes. This gene regulation mechanism is part of RNA processing, which is right after transcription but before translation to make multiple types of proteins from the same RNA by ordering the exons differently. This research on the use of RNA splicing with poison exons to help mitigate tumor growth is a great example of how important a single stage of gene regulation can be. Beyond its scientific significance, this research is personally fascinating because it offers a glimpse into the future of cancer treatment. Traditional therapies like chemotherapy and radiation often come with severe side effects due to their inability to distinguish between healthy and cancerous cells. In contrast, ASOs offer a more targeted approach, potentially leading to treatments that are not only more effective but also less harmful. What do you think? Could ASOs revolutionize cancer treatment as we know it?

Poison Exons May be the Key to Reactivate Cancer’s Molecular ‘Kill Switch’

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On April 7, 2025

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In a study published in Science Daily, researchers from The Jackson Laboratory (JAX) and UConn Health have uncovered a crucial mechanism that cancer cells use to avoid the body’s natural defenses. They have identified a potential therapeutic approach that could slow, or even shrink, aggressive and hard-to-treat tumors. This discovery could be a critical for cancers such as triple-negative breast cancer and certain brain tumors, where current treatment options remain limited.

A crucial finding of the research examines genetic elements called poison exons. In healthy cells, poison exons regulate the levels of key proteins by triggering the destruction of RNA messages before they can be translated into harmful proteins. This process ensures that cellular processes remain tightly controlled.
In AP biology we learned that RNA splicing plays a critical role in gene regulation. It occurs in the nucleus of eukaryotic cells during RNA processing. It is a crucial process where introns are removed from mRNA transcripts, and coding regions exons are joined together to form mature mRNA, enabling protein synthesis.

However, in cancer cells, this critical safeguard is often suppressed. The research team, led by Olga Anczuków, an associate professor at JAX, discovered that cancer cells suppress poison exon activity in a key gene called TRA2β. As a result, TRA2β protein levels rise which causes tumor growth and proliferation. According to the National Library of Medicine, Tra2β protein is a splicing activator. “It binds to exons to regulate their alternative splicing inclusion.”

By analyzing data from various cancer types, the researchers uncovered a correlation between poison exon activity and patient outcomes. “We’ve shown for the first time that low levels of poison exon inclusion in the TRA2β gene are associated with poor outcomes in many different cancer types, especially in aggressive and difficult-to-treat cancers,” said Anczuków. This pattern was observed in cancers such as breast, brain, ovarian, skin, leukemia, and colorectal cancer.

Understanding how cancer suppresses poison exons was the first step. The research team then explored whether they could restore poison exon function and reactivate the natural “off” switch for the gene expression. They found Antisense oligonucleotides (ASOs) to be a possible solution. ASO’s are synthetic RNA fragments designed to increase poison exon inclusion. In an article from PubMed Central researchers Haoyu Xiong, Rakesh N Veedu, and Sarah D Diermeier, found that “oligonucleotide therapeutics are an emerging drug modality, which consists of modified or unmodified short nucleic acid molecules, and includes antisense oligonucleotides. The mechanism of action of oligonucleotide therapeutics mainly relies on Watson–Crick base pairing to targeted mRNAs, resulting in either gene silencing, a steric block, or altered splicing patterns, with the exception of aptamers, which recognize their targets by their three-dimensional structures”

When ASOs were introduced into cancer cells, they successfully tricked the cells into turning off their own growth signals by boosting poison exon inclusion. This, in turn, restored the body’s ability to degrade excess TRA2β RNA and slow tumor progression. “We found that ASOs can rapidly boost poison exon inclusion, essentially tricking the cancer cell into turning off its own growth signals,” explained Nathan Leclair, an MD/PhD graduate student at UConn Health and The Jackson Laboratory.

One of the study’s most interesting findings was that completely removing TRA2β proteins using CRISPR gene editing did not stop tumor growth. This suggests that targeting the RNA instead of the protein may be a more effective strategy.

The schematic diagram of CRISPR-Cas9
While further studies are needed to refine ASO based therapies and explore their delivery to tumors, early results are promising. Preliminary data indicate that ASOs are highly specific, targeting cancerous cells without interfering with normal cellular function. This precision could make ASOs a highly effective and less toxic alternative to current treatments.

The discovery of how poison exons regulate cancer cell growth and how ASOs can be used to restore this natural defense opens the door to a new era of targeted cancer treatments. With continued research and clinical development, this approach may soon transform how we combat some of the deadliest forms of cancer. What do you think about this approach? Could RNA-targeted treatments change the future of medicine?

Electrical activity spurs growth of small-cell lung cancer

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On March 10, 2025

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Earlier this month, a team of scientists and researchers from across the United States, Taiwan, and the United Kingdom collaborated on a research study about the relationship between electrical activity and cancer. They explored how the neuroendocrine cells in small-cell lung cancer (SCLC) exhibit electrical excitability. In other words, cells that receive signals from the nervous system and respond by releasing hormones into the bloodstream, have demonstrated the ability to produce an electrical signal in response to a stimulus. The researchers ultimately found that electrical excitability plays a role in the growth of SCLC.

Neuroendocrine cells are similar to neurons in that both cell types are marked by calcium activity. The scientists tested whether the neuroendocrine cells in small-cell lung cancer would exhibit electrical excitability through the combined use of patch-clamp recording (a technique enabling researchers to measure current and voltages across a membrane through ion channels) and calcium imaging. They ultimately found that the non-neuroendocrine cells didn’t display electrical excitability, indicating that this signaling ability is only present in the neuroendocrine cells. Additionally, the researchers suggested that their finding of a significant increase in nerve fibers growing into early SCLC tumors indicates that the fibers form connections with cancer cells and interact with the cancer cells, similar to how nerves interact. Subsequently, the scientists proposed that electrical activity among neuroendocrine cells causes further development of SCLC.

Neuroendocrine cell hyperplasia

This study has given scientists potential avenues to finding new treatments for aggressive cancers like SCLC. The authors’ research, and studies similar to it, are crucial for developing a greater understanding of how cancer grows, and subsequently how to stop cancer from spreading.

Our most recent AP Bio unit on mitosis and genetics covered the topic of cancer as well. We learned that the cancer develops when a mutation in a cell bypasses checkpoints in the mitosis cycle, then begins to divide and grow. Additionally, we studied how mutations disrupt oncogenes, regulatory genes, and tumor suppressor gene, which ultimately results in cancer. SCLC, like other aggressive cancers, is typically caused by mutations in tumor-suppressor genes. While lung cancer and other aggressive cancers are notoriously difficult to treat, this study on electrical activity in cancer cells could hopefully lead to new treatment methods, as well as a deeper understanding of how cancer grows in the human body.

What do you think about the potential of studying electrical activity in cancer cells? Do you think it’s possible for scientists to develop new solutions based on the discovery of electrical activity in SCLC cells? I hope and believe that this research contributes to novel treatment methods for certain cancers.

The Unexpected Side effect of CAR-T Therapy

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On March 7, 2025

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There are many well-known side effects to cancer treatments, such as hair loss, nausea, pain, or fatigue. In rare cases, however, patients can experience a new side effect: a different cancer. The article “Rare side effects of cancer immunotherapy” by Anne Grimm of the Universität Leipzig discusses how new research shows that immunotherapy cancer treatments can trigger lymphoma to develop from modified T cells.

 As we learned in AP Bio and by the Cleveland Clinic, immunotherapy is a cancer treatment that utilizes your body’s immune system to detect and eliminate cancer cells. Your immune system recognizes and eliminates invaders, including malignant, cancerous cells. Similar to what we learned in class, the cells injected into the cancer patient undergo mitosis to rapidly divide for the patient to have as many cancer-killing cells in their body. Unlike these healthy cells, cancer cells are caused by uncontrolled mitosis, where cells divide uncontrollably due to mutations. While healthy cells go through checkpoints to ensure proper division, cancer cells bypass the checkpoints, allowing mutated cells to continue to divide.

The article describes a specific case where the genetically altered T cells in a 63-year-old patient developed T cell lymphoma following CAR-T treatment. According to the NIH (National Cancer Institute) CAR-T treatment is “A type of treatment in which a patient’s T cells (a type of immune system cell) are changed in the laboratory so they will attack cancer cells.” Researchers discovered that the tumor was caused by the CAR-T cell alteration and underlying alterations in the patient’s hematopoietic stem cells. They examined signaling networks and genomic alterations using next-generation sequencing. 

Mitosis cycle

While these side effects only occur in around 1% of patients who undergo CAR-T treatment, researchers are studying similar cases to examine the risks of immunotherapy. The article ends by describing new studies being conducted by research to ensure the well-being of the patient’s health after receiving immunotherapy, as it is becoming a more common treatment for cancer. To stress the urgency of the research, the author describes how, to begin a study, researchers must typically wait several weeks or months for approval and publication. Consequently, this study was accepted after no longer than a day due to its importance.

When first learning about immunotherapy in AP Bio, I thought it sounded almost to good to be true. However, after reading this article, I discovered that in some rare cases, immunotherapy can do more harm than good. This leaves me with some questions: Do you think researchers should spend time and money studying something so rare? Could early screening methods help predict and prevent these rare complications before treatment begins?

 

Nature’s Blueprint: Harnessing the Morpho Butterfly’s Light Manipulation to Create More Efficient Cancer Diagnosis

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On March 7, 2025

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Researchers at the University of California San Diego have developed an innovative method for cancer diagnosis inspired by the Morpho butterfly’s wing structures. The butterflies are known for shimmering blue wings, which are derived from microscopic structures that manipulate light rather than pigments. This is incredibly useful for cheaper, invasive-free cancer diagnosis.

Morpho Butterfly

One way that the degree of someone’s cancer is evaluated is through analyzing someone’s Fibrosis, which is the accumulation of fibrous tissue. In oncology, evaluating the extent of fibrosis in a biopsy sample can help determine whether a patient’s cancer is in an early or advanced stage. However, it is currently difficult to distinguish stages of fibrosis using current clinical methods, which includes physical exams, blood tests, bone marrow tests, genetic tests, and imaging tests. Existing techniques rely on staining tissues to highlight key structures in tumor biopsies, but interpretations can vary between doctors. While advanced imaging technologies offer greater detail, they require costly, specialized equipment that many clinics lack.

 

This is where the Morpho butterfly plays a crucial role. The researchers found that placing a biopsy sample on a Morpho butterfly wing and examining it under a standard microscope allows them to determine what phase tumor’s structure is currently at without requiring stains or expensive imaging equipment. This is critical because many clinics can’t afford the highest quality equipment. Also, the research team claims “It’s also more objective and quantitative than current methods,” which is amazing for patients. 

The researchers discovered that the microscopic and nanoscopic structures of the Morpho butterfly wing respond strongly to polarized light, which is a type of light that moves in a specific direction. Collagen fibers, a key structural component of fibrotic tissue, also interact with polarized light, but their signals are typically weak. By placing a biopsy sample on a Morpho butterfly wing, the researchers amplified these signals, making it easier to assess the density and arrangement of collagen fibers. To quantify these findings, the team developed a mathematical model based for analyzing polarized light. This model translates light intensity into a measurable indicator of collagen fiber density and organization, providing an objective metric to assess fibrosis in the tissue. 

This breakthrough is significant because early cancer detection is challenging in many parts of the world due to limited resources. This simpler and more accessible tool can help diagnose patients before the cancer reaches advanced stages. This current study focused on breast cancer, but they plan to expand their research to other tissue and parts of the body. 

This connects to AP Biology because in many organisms, color arises from pigments, molecules that absorb certain wavelengths of light and reflect others. For example, chlorophyll in plants absorbs red and blue light while reflecting green, which is why leaves appear green. However, the Morpho butterfly does not rely on pigments for its brilliant blue color; instead, it uses its structure, where microscopic structures manipulate light to produce color. These structures interact with light to show their color. In addition, collagen fibers, long, fibrous proteins that make up part of the extracellular matrix. Collagen is a structural protein composed of amino acids, forming a triple helix structure that gives the fibers strength and flexibility. The collagen also interacts with polarized light, but their signals are typically weak. By placing a biopsy sample on a Morpho butterfly wing, the wing’s nanostructures amplified these weak signals, making it easier to analyze the tissue without using chemical stains. To me, the most compelling part of this research is that it is simply utilizing a phenomenon of a species. What other species could we try to utilize in research like this? What are your thoughts on this new discovery and its potential implications?

Lighting the Way: A Smart Bomb Against Breast Cancer

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On March 7, 2025

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Imagine a treatment so precise that it destroys cancer cells while sparing healthy ones, all activated by the simple power of light. Thanks to recent research from the University of California, Riverside, and Michigan State University, thisBreast cancer cell could soon be a reality for patients with aggressive breast cancer. Scientists have developed light-sensitive chemicals, called cyanine-carborane salts, that show remarkable potential in treating metastatic tumors with fewer side effects than traditional therapies.

Photodynamic therapy (PDT) has long been used to treat cancers such as skin and bladder. It is a two-stage treatment that combines light energy with a photosensitizer medicine. This process involves activating the photosensitizer from light causing it to become toxic to the targeted tissue which kills cancerous and precancerous cells. While this procedure mainly leaves healthy cells unharmed and only breaks down cancer cells from the inside, traditional PDT has significant limitations: prolonged light sensitivity post-treatment, poor tissue penetration, and off-target toxicity. These flaws can limit the effectiveness of the treatment, ultimately leading to the recurrence of the cancer if the tumor is not completely destroyed. 

The development of cyanine-carborane salts offers a promising solution to these challenges. Unlike their predecessors, these salts clear from the body more quickly, remain concentrated in cancerous tissue and can be activated by near-infrared light that penetrates deeper into the body. This means fewer side effects and a broader range of treatable tumors. The ability of these new chemicals to exploit a natural weakness in cancer cells makes them especially effective. Tumors overexpress certain proteins called OATPs, which help transport the cyanine-carborane salts directly into cancerous cells. This precision targeting eliminates the need for costly additional chemicals often required for PDT. Also, once inside the cancerous cells, the salts are activated by near-infrared light, leading to highly localized cancer cell destruction while sparing healthy tissue. The light used with the cyanine-carborane salts is also able to penetrate deeper into tissues, unlike the traditional wavelengths of light used in PDT. 

This breakthrough in PDT technology could redefine how we approach cancer treatment. Not only does it offer a safer and more effective method for eradicating aggressive breast cancer, but researchers believe these salts could be modified to work with other energy sources beyond light, potentially increasing their reach even further. I think that research into more effective and safer treatments for cancer is incredibly important. Having lost a family member to cancer, I understand the deep sense of helplessness that comes with watching a loved one endure grueling treatments, only to become too sick for further procedures. Innovations like this give hope for a future where treatments are not only more effective but also far less punishing for the patient. Do you think this technology can be adapted for other diseases beyond cancer? How do you see advances in targeted therapy shaping the future of medicine? The topic of cancer itself is explained through the cell cycle in AP Biology. Cancer occurs when cells acquire genetic mutations often in the proto-oncogenes and tumor suppressor genes that alter their normal behavior, leading to uncontrolled growth and division. Within the cell cycle, many checkpoints regulate the stop-and-go signals of the cycle, however, a mutation in the genes of the cyclin or other gene causes the cell cycle to continue even if the cell fails the checkpoint and should not keep dividing. Understanding how cancer cells differ from normal cells at the molecular level allows scientists to develop such targeted treatments, demonstrating the real-world application of molecular biology in medicine.

 

CRISPR: Rewriting the Script in Cancer Treatment

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On January 20, 2025

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Cancer continues to impact millions of people each year around the world; however, new breakthroughs in cancer treatment using CRISPR technology are set to transform how we can combat this complex disease. By leveraging CRISPR’s gene-editing capabilities, researchers are unlocking new possibilities to enhance immune responses, optimize therapies, and develop more precise and effective treatments.

A groundbreaking study from Harvard Medical School, led by LaFleur et al. and Milling et al., explored how CRISPR can reprogram T cells to more effectively fight cancer. Cancer cells typically evade the immune system by downregulating antigen presentation or suppressing the immune system. The researchers addressed these challenges by targeting specific genes in T cells to enhance target recognition(improved the T cells’ ability to recognize tumor antigens), increase the length of the immune response, and strengthen activation(amplifying the response on the detection of cancer). These genetically modified T cells show significant improvements in combating cancer in laboratory and preclinical models than the typical T cell. This showcases their potential to develop more effective immunotherapies, especially for cancers resistant to traditional treatments.

CAR T-Cell immunotherapy diagram by (OHC CAR-T team)

Another innovative study by Lei et al. explored CRISPR’s role in enhancing CAR(Chimeric Antigen Receptor) T-cell therapy, a promising approach that modifies a patient’s T cells to target cancer cells. While CAR T-cell therapy has shown success, it faces challenges like limited efficacy against solid tumors, safety concerns, and high costs. CRISPR offers potential solutions by improving efficacy(Enhances T-cell function and persistence through precise gene edits), enhancing safety(disables genes responsible for adverse effects like cytokine release syndrome), and reducing costs(streamlining the manufacturing process to make the therapy more accessible)

This study emphasizes how CRISPR can address existing barriers, making CAR T-cell therapy safer, more effective, and available to more patients.

The potential of CRISPR extends beyond these studies. CRISPR has opened up a new frontier in cancer research by directly editing the genes within cancer cells, disrupting oncogenes, and reshaping immune responses. For example, recent findings revealed that CRISPR can target oncogenes in leukemia cells, reducing their ability to proliferate and making them more vulnerable to existing treatments (Carlo et al.).

These advancements directly connect to what we’ve studied in AP Biology. The role of CRISPR in gene editing demonstrates the power of manipulating transcription and translation, concepts which are directly related to nucleic acids. Additionally, the focus on T-cell activation and immune responses ties into our understanding of cell communication and the immune system’s intricate pathways.

I chose to write about this topic because it represents a deeply personal and hopeful turning point in cancer treatment. My mom battled breast cancer, and seeing her fight the disease made me acutely aware of the challenges cancer patients and their families face.

What do you think about CRISPR’s role in transforming cancer treatment? Could we one day eliminate certain types of cancer altogether? Share your thoughts and let’s discuss!

Covid-19: Could it’s immune cells fight cancer?

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On December 16, 2024

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Were you one of many who faced an extreme case of COVID-19? You may have lost your sense of smell, but now you may have tumor shrinking immune cells!

A recent study suggests that the immune cells produced during a severe case of COVID-19 may be more helpful than you think. In her article Julia Goldenberg explains how COVID-19 immune cells may shrink cancer tumors.

The study was done by a group of researchers. They realized that certain monocytes lose CCR2, ultimately becoming nonclassical monocytes with anticancer properties.

SARS-CoV-2 without background

Monocytes are a type  of white blood cell built to destroy pathogens. With an infection or injury, white blood cells work together and collude to heal the injured or infected area.

In our AP Biology class, we learned how the immune fighting cells are created. These monocytes will ingulf the virus and produce interleukin to activate T-Helper cells. The T-Helper Cells then trigger a humoral response so B cells can split and create B plasma cells which secrete antibodies, and B-memory cells too prevent reinfection. These cells are the immune fighting cells that fight against the tumors.

Goldenberg goes on to explain how the inflammatory conditions during COVID-19 allow this change to occur. When blood tests of patients were taken, they found that the monocytes that were produced from COVID-19 contained a specific receptor. This even occurred with mice! The researchers studied a variety of mice with different types of stage four cancers. When the monocytes were induced, the tumors shrank for all four types of cancer. This is because the monocytes activated natural killer cells.

The researchers are hoping that this can work in humans. However, this wouldn’t work with the current COVID-19 vaccines that are on the market since they their RNA sequence is differs from severe COVID-19. But with more work, hopefully an advanced vaccine can be developed.

Throughout the years we have focused on how negative COVID-19 has been. As it is dangerous and has caused extreme long lasting symptoms for many people, one can only wonder, are there any more benefits to this nasty virus?

New Technology Can Detect Cancer Using Blood Samples

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On April 17, 2024

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With over 150,000 diagnoses per year, cancer is the leading cause of illness and death in Australia. Cancers in organs such as the liver and kidneys often require surgery for a diagnosis, however, researchers have recently created a device to diagnose cancer that does not require invasive biopsy surgeries.

A biopsy can take many different forms. Some examples include a needle biopsy, the most general type, which is when a small needle is inserted into the skin to collect cells or fluid. An image-guided biopsy can include an x-ray, MRI, or ultrasound. A surgical biopsy is a surgery that includes making an incision in the skin in order to remove suspicious tissue. The complexity of the surgery varies depending on the the part of the body. Biopsies can be difficult for many reasons such as the price, the amount of risk, its consuming of time, and the possibility of bad side effects; however before this new method was finalized, they were necessary for a definite diagnosis and effective treatment.

Scientists have created a device called the Static Droplet Microfluidic device, which identifies the metabolic signature of cancer cells to identify ones that have broken away from a tumor and entered the bloodstream. Professor Warkiani states that the device has 38,400 chambers, which are capable of classifying the tumor cells, making it easier to distinguish a single cancer cell among billions of normal blood cells. This device is also crucial in discovering metastasis, which is when cancer cells travel through the blood and grow in different parts of the body. Metastasis leads to 90% of cancer-related deaths.

Diagram showing cancer cells spreading into the blood stream CRUK 448.svg
By <a href=”//commons.wikimedia.org/wiki/User:Cancer_Research_UK_uploader” title=”User:Cancer Research UK uploader”>Cancer Research UK uploader</a> – <span class=”int-own-work” lang=”en”>Own work</span>, CC BY-SA 4.0, Link

As learned in AP Biology, cancer cells are created when a cell loses its ability to regulate cell division. This inability could be caused by mutations that affect the activity of the cell cycle regulators. For example, a mutation could cause a lack of activity of cell cycle inhibitors, which allows the cell to continue to divide without limits. There could also be too much activity of positive cell cycle regulators, which can lead to cancer because it causes the cell to divide too much.

Differently from normal cells, cancer cells can continue to divide whether they have growth factors or not. Some have growth factors that are always “on,” some have the ability to make their own growth factors, and some can use neighboring cells to make growth factors for them. They also have “replicative immortality,” which is their ability to replicate many more times than the average cell. The enzyme telomerase is created, which reverses the shortening of chromosomes that normal cells experience during cell division. This characteristic is why cells have a limited life span. Cancer cells are difficult to stop because they do not undergo apoptosis (programmed cell death) like normal cells.

The Static Droplet Microfluidic Device will allow doctors to diagnose and treat cancers in a safe and cost-effective way. I have family members who have undergone painful surgeries in order to officially diagnose cancer, and technology using blood would have greatly improved their process of diagnosis. I invite any and all comments to share experiences or other information!

 

 

 

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

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On February 27, 2024

In Student Post

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

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On February 27, 2024

In Student Post

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

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On February 27, 2024

In Student Post

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

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On February 27, 2024

In Student Post

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

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On May 7, 2023

In Student Post

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

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On April 23, 2023

In Student Post

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

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On April 23, 2023

In Student Post

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

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On April 23, 2023

In Student Post

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

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On March 15, 2023

In Student Post

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

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On March 15, 2023

In Student Post

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. 

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