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  • November Monthly Recap: Thankful for STEM

    November Monthly Recap: Thankful for STEM

    By Bela Koganti

    ~10 minutes

    November is about the three S’s: scarfing down Thanksgiving dinner, seeing family, and splurging on Black Friday. But we’d like to add a fourth: STEM! This November, we’ve advanced in everything from the environment to Jeff Bezos’ Blue Origin, so here’s what you need to know.

    November 3: Gone Glacier

    Antarctica’s Hektoria glacier recently became the quickest-retreating glacier in modern history, and a CU Boulder study published November 3 revealed how and why. From late 2022 to early 2023, over half of Hektoria disintegrated– that’s eight kilometers of ice, gone in just two months.

    Essentially, the flat bedrock (or ice-plain) under Hektoria set it afloat as it thinned, causing the glacier to shed parts into the sea. Such a shedding process is generally called “calving”, and it’s pretty rare. Here’s why it happened in Hektoria’s case:

    1. In the past, glaciers resting on ice-plains dissolved hundreds of meters each day, so Hektoria probably experienced the same process. 
    2. The ice-plain forced Hektoria to begin calving, and that exposure to the ocean created further cracks in the glacier. As the cracks met, they eventually calved the entire glacier.
    3. To confirm the process, scientists found a set of glacier-earthquakes that occurred in unison with the retreat.
    Between 2022 and 2023, broken fast ice allowed ocean water to reach the Hektoria glacier, shrinking it by half / Adrian Luckman / CNN Climate ©

    With this new discovery of how and why Hektoria retreated, scientists can now predict and expect other glacier retreats. However, prediction does not equal prevention. These models show that continued warming, driven largely by human greenhouse gas emissions, will only accelerate this process. In order to help out, let’s follow this guide from the University Corporation for Atmospheric Research (UCAR) to minimize our CO2 emissions; I mean, we might just save a glacier.

    November 8: Crispr for Cholesterol

    Cholesterol. We know it and sometimes fear it, but what is it? Cholesterol levels are determined by LDL cholesterol, a waxy compound that can clog arteries, and triglycerides, the most prominent type of fat in the body. Triglycerides can also harden arteries and artery walls. So, when we have high cholesterol, our arteries might be blocked and we have increased risk of heart attacks, heart diseases, and strokes.

    Around 25% of adults in the United States have increased levels of LDL and triglycerides. Ouch. But never fear, Crispr is here! Crispr, a Swiss biotechnology company that deals with gene-editing, recently tested a new infusion and presented its results on November 8. 

    Their one-time infusion of CTX310, a therapy delivered by liquid nanoparticles, attempted to turn off ANGPTL3, a gene in the liver. Because some people are born with a mutated ANGPTL3 gene that safely protects them from heart disease, the Crispr scientists tried to replicate that. The highest dose given reduced triglyceride and harmful LDL by about 50% in two weeks, and the results lasted through the end of the trial.

    With this initial success, Crispr plans to begin Phase II studies in 2026, and they hope to achieve an infusion that lasts a lifetime. Once safety of treatments is further explored and confirmed, CTX310 may even become a preventative measure. As senior author and chief academic officer of the Heart, Vascular, and Thoracic Institute at Cleveland Clinic Steven Nissen said,

    “This is a revolution in progress.” -Steven Nissen

    November 10: One of a Kind

    The universe cannot be replicated. We follow no simulation, no set mathematics, and no algorithm. Who knew? Well, physicists, apparently. At the University of British Columbia in Okanagan, physicists proved that the universe cannot be simulated.

    There’s a mathematical layer of quantum gravity dubbed the “Platonic realm” that creates even the concepts of space and time. However, these physicists proved that it cannot recreate reality purely with computation. Known as “Gödelian truths,” some things just cannot be understood with logic as they contradict themselves. Think about this for a minute: how would you prove the idea that “this true statement is not provable”? You can’t, and neither can a computer. Statements like this one exist all throughout our universe; when faced with them, computers’ logical algorithms fail.

    Thus, computers cannot know and compute everything about our universe, so they cannot replicate it. We are one of a kind.

    November 13: Bezos in Space

    On November 13, Jeff Bezos launched Blue Origin’s New Glenn rocket out of Florida. New Glenn deployed two of NASA’s Escapade Satellites to measure Mars’ atmosphere and magnetic field, and, for the first time, its reusable booster successfully made it onto a landing pad in the Atlantic Ocean. Blue Origin is now the second company in the world to do so, with Elon Musk in first. Watch the landing here. Okay, check back in 22 months—hm, that’s September of 2027—when the satellites arrive at Mars! 

    New Glenn Launches NASA’s ESCAPADE, Lands Fully Reusable Booster / Blue Origin ©

    November 14: Crispr for Cancer

    And for the second time in one article, Crispr’s here! This time, however, it tackles chemotherapy resistance in lung cancer. A gene called NRF2 can cause resistance to chemotherapy in some cases of cancer, so Crispr scientists looked at disabling it in lung squamous cell carcinoma, an aggressive type of lung cancer that makes up around a quarter of all lung cancer cases.

    They infused R34G, a mutation in NRF2 that can regulate cellular stress reactions; when NRF2’s is overactive, it causes cancer cells to resist chemotherapy, so they used R34G to subdue NRF2’s behavior. Even when they only calmed NRF2 in less than half of tumor cells, it still reduced tumors and improved chemotherapy response.

    “The power of this CRISPR therapy lies in its precision. It’s like an arrow that hits only the bullseye,” Kelly Banas, lead author of the study, said. As Crispr will continue to perform and study trials, R34G might just be the future of cancer treatment.

    November 18: Gemini 3’s Release

    We’ve all seen the AI overviews embedded into Google’s search results. You’re just wondering how long to bake your snickerdoodles for, but the AI’s answer ranges from 8 minutes to 25. What? Then, you look and see twelve recipes referenced. Huh? There’s no way it’s that difficult, you wonder. Yeah, we’ve all been there. 

    However, Google just launched Gemini 3, and they proclaim it their “most intelligent model” yet. Maybe we’ll get a more precise answer on those snickerdoodles now! More confident than ever in Gemini 3, Google embedded it into its search engine on the first day of its release, which they had never done before. Normally, they gradually implant new versions over weeks, or even months. 

    Gemini 3 also brings new features to the table. Or, well, to the phone. “Gemini Agent” can book travel plans, organize your overwhelmed email, and do other multi-step jobs. Additionally, they updated the Gemini app to respond to prompts with answers so thorough they look like websites.

    Well, if you’re looking for a new AI model, Gemini 3 may very well be what you need. And if you’re looking for ridiculously incorrect and vague answers to make fun of, the jury’s still out on whether Gemini 3 is the platform for you or not.

    November 18: A Milky Way Model

    We already discussed computers’ inability to model our universe, but I never said anything about the Milky Way! Researchers from the RIKEN Center for Interdisciplinary Theoretical and Mathematical Sciences (iTHEMS) in Japan, The University of Tokyo, and the Universitat de Barcelona in Spain managed to accurately simulate 100 billion stars over the course of 10 thousand years. 

    Researchers Create First 100-billion-star Milky Way Simulation Using AI / NRAO / Orbital Today ©

    These researchers trained an AI model using high-resolution simulations, and it eventually managed to predict resulting gas expansions. Thus, it created a simulation of the galaxy’s overall dynamics as well as its smaller phenomena. Previous models of the universe would struggle to predict on a small-scale, but this new one can do exactly that. Also, it did so quickly! In just under 3 hours, it created a simulation of the galaxy over 1 million years.

    This new model could become popular for making other simulations that need small- and large-scale accuracy. Like lead researcher Keiya Hirashima said,

    “This achievement also shows that AI-accelerated simulations can move beyond pattern recognition to become a genuine tool for scientific discovery—helping us trace how the elements that formed life itself emerged within our galaxy.” -Keiya Hirashima

    November 18: Antimatter Aplenty

    Have you noticed that this is the third event from November 18? Sounds like a hat trick to me! Anyways, CERN’s Antimatter factory recently undertook a new project called the ALPHA experiment, and they published their findings on November 18. Essentially, they managed to create over 15,000 antihydrogen atoms in under 7 hours.

    Antihydrogen is the most basic form of atomic antimatter, and antimatter is a substance with the same mass and particles as another substance but opposite charges. For example, antihydrogen has the same mass and particles as hydrogen, but hydrogen’s protons have positive charges and its electrons have negative charges while antihydrogen’s protons have negative charges and its electrons have positive charges. When antimatter and matter meet, they destroy each other, creating an immense amount of energy. Antimatter is normally found in particle accelerators, cosmic rays, and medical imaging, but it’s fairly rare as creating it is a lengthy process.

    However, with the ALPHA team’s new method, they’ve managed to make antimatter 8 times faster than normal. Normally, the process involves creating and trapping antiprotons and positrons separately before cooling and merging them together to form antihydrogen, but ALPHA’s unique success came from the way they create their positrons. The general problem with creating antimatter is that trapped positrons refuse to stay still once trapped, and they don’t cool down enough. So, the ALPHA team approached the antihydrogen by adding laser-cooled beryllium ions to the positron trap. The beryllium makes the positrons lose energy through sympathetic cooling, which cools the positrons to around -266 °C and makes them more likely to merge with the antiprotons and form antihydrogen, creating more antimatter.

    Scientists thoroughly study any antimatter they can get, so, with this new abundance, they plan to study gravity’s effect on antimatter in the ALPHA-g experiment. Stay tuned because they may discover new properties and behavior of antimatter, which wouldn’t be possible without ALPHA’s new process.

    Okay, that’s all I have for November. Consider this my holiday gift to you. Enjoy December, and come back for Stemline’s next recap!

    References

    Cai, K. (2025, November 18). Google launches Gemini 3, embeds AI model into search immediately. Reuters. https://www.reuters.com/business/media-telecom/google-launches-gemini-3-embeds-ai-model-into-search-immediately-2025-11-18/
    ChristianaCare Gene Editing Institute. (2025, November 17). CRISPR breakthrough reverses chemotherapy resistance in lung cancer. Eurek Alert! https://www.eurekalert.org/news-releases/1106182
    CRISPR Therapeutics AG. (2025, November 8). CRISPR Therapeutics announces positive phase 1 clinical data for CTX310® demonstrating deep and durable ANGPTL3 editing, triglyceride and lipid lowering. CRISPR Therapeutics. https://crisprtx.com/about-us/press-releases-and-presentations/crispr-therapeutics-announces-positive-phase-1-clinical-data-for-ctx310-demonstrating-deep-and-durable-angptl3-editing-triglyceride-and-lipid-lowering 
    Harris, R. (2025, November 18). Breakthrough in antimatter production. CERN. https://home.cern/news/news/experiments/breakthrough-antimatter-production
    Lohnes, K. (2025, June 13). What is antimatter?. Encyclopedia Britannica. https://www.britannica.com/story/what-is-antimatter 
    Mullin, E. (2025, November 8). A gene-editing therapy cut cholesterol levels by half. Wired. https://www.wired.com/story/a-gene-editing-therapy-cut-cholesterol-levels-by-half/ 
    Riken. (2025, November 18). The simulated Milky Way: 100 billion stars using 7 million CPU cores. Riken. https://www.riken.jp/en/news_pubs/research_news/pr/2025/20251117_2/index.html 
    UCAR. (2020). How do we reduce greenhouse gases? UCAR: Center for Science Education. https://scied.ucar.edu/learning-zone/climate-solutions/reduce-greenhouse-gases 
    University of British Columbia Okanagan campus. (2025, November 10). Physicists prove the Universe isn’t a simulation after all. ScienceDaily. Retrieved December 13, 2025 from http://www.sciencedaily.com/releases/2025/11/251110021052.htm 
    University of Colorado at Boulder. (2025, November 3). Antarctic glacier retreated faster than any other in modern history. Eurek Alert. https://www.eurekalert.org/news-releases/1104274 
    Watch: Blue Origin rocket successfully lands booster for first time [Video]. (2025, November 13). BBC. https://www.bbc.com/news/videos/c5yd0zd6eddo 
  • Would you still love me if I were a worm?

    Would you still love me if I were a worm?

    By Michelle Cheng

    ~12 minutes

    How Scientists are Using Worms to Learn About Humans

    Worms and humans could not possibly be any more different. And yet, scientists have been studying C. elegans (caenorhabditis elegans) to learn more about the human body over 70 years. These unassuming worms have aided in groundbreaking findings in medicine for human diseases such as Alzheimer’s, AIDS, and stroke.

    What makes C. elegans so valuable is not its complexity, but rather its simplicity. Because so many of its biological pathways are conserved in humans, this worm provides a uniquewindow into the fundamental processes of life, including cell division, gene regulation, neural signaling, and aging. With a transparent body, rapid life cycle, and a genetic makeup that mirrors much of our own, C. elegans has become an essential organism in modern biomedical research. Understanding how scientists use these worms can help us appreciate not just what we’ve already learned, but also the vast potential that still lies ahead.

    What is C. elegans?

    C. elegans is a free-living nematode that has become one of the most important model organisms in research. It measures approximately one millimeter in length and naturally lives in temperate soil environments, where it feeds on bacteria like e. coli. It is non-parasitic and exists in two sexes: hermaphrodites, which are capable of self-reproduction, and males, which occur at a less than 0.1% chance under normal conditions. The hermaphroditic reproductive mode allows for the maintenance of isogenic populations, which is advantageous for genetic studies.

    Anatomy of an adult C. elegans hermaphrodite / EnVivo Biosystems ©

    The adult C. elegans hermaphrodite has exactly 959 somatic cells while the adult male C. elegans has exactly 1,031 somatic cells. The worm’s relatively simple anatomy includes muscles, a nervous system, a digestive system, a reproductive system, and an excretory system. The organism develops through four larval stages before reaching adulthood, with a complete lifecycle taking just two to three weeks under laboratory conditions.

    The life cycle of C. elegans / National Institute of Health ©

    Genetically, C. elegans has a compact genome consisting of about 100 million base pairs across six chromosomes. It was the first multicellular organism to have its entire genome sequenced in 1998 in a project led by John Sulston and Bob Waterstons. Its genome is highly amenable to manipulation using a variety of modern techniques.

    Why do scientists study C. elegans specifically?

    First introduced into studies by Sydney Brenner in the 1960s to study neurological development and the nervous system, the nematode proved itself in the lab with its unique combination of genetic, anatomical, and practical features that make it exceptionally suitable for biomedical research. 

    Remarkably, around 60-70% of human disease-associated genes have counterparts in the C. elegans genome, making it an incredibly valuable model for studying human biology. Many genes responsible for critical cellular functions are evolutionarily conserved between worms and humans. Therefore, scientists can manipulate the function of these genes in C. elegans to study their roles in disease without the complexity or ethical challenges of working with human subjects or higher animals like mice or primates. 

    Analogous counterparts of the human nervous systems in C. elegans / Taylor and Francis Online ©

    Adult hermaphrodites’ cells, which remain the same in every single  worm, each of which has been identified and mapped, allowing for detailed tracking of development, differentiation, and cellular processes. Its transparent body enables real-time visualization of internal structures, including neurons, muscles, reproductive organs, and digestive tissues. The worm, which has a simple nervous system of only 302 cells, is one of the only organisms where every neural connection is known. Additionally, C. elegans has a short life cycle of two to three weeks and is easy to culture in large numbers, making it especially convenient for developmental and aging studies.

    How do scientists modify C. elegans in experiments?

    Scientists modify and study C. elegans using four primary methods: RNA interference (RNAi), CRISPR-Cas9 genome editing, transgenic techniques, and drug screening.

    Different modes of administration of dsRNAs for RNA interference / Biomed Central ©

    One of the most widely used techniques for modifying gene expression in C. elegans is RNA interference (RNAi). This method allows scientists to silence specific genes to observe the effects of their absence. In C. elegans RNAi can be easily administered by feeding worms with genetically engineered E. coli bacteria that produce double-stranded RNA (dsRNA) matching the gene of interest. Once ingested, the dsRNA activates the worm’s endogenous RNAi pathway, leading to the degradation of the corresponding messaging RNA and a reduction or elimination of the target protein. This method is highly efficient, non-invasive, and relatively easy to perform, making it ideal for large-scale genetic screens. Researchers can identify genes involved in key processes such as embryonic development, aging, metabolism, and neurodegeneration.

    The CRISPR-Cas9 system has revolutionized genetic research in C. elegans by enabling precise, targeted alterations to the genome. Scientists introduce a complex composed of the Cas9 enzyme and a guide RNA (gRNA) into the worm, which directs the Cas9 to a specific DNA sequence. Once there, Cas9 introduces a double-strand break in the DNA. The cell’s natural repair mechanisms then fix the break, and researchers can insert, delete, or replace specific DNA sequences. In C. elegans, CRISPR can create mutants mimicking  human disease alleles or study regulatory elements of genes. This method provides a level of control that surpasses RNAi, as it allows for permanent and heritable genetic modifications. Scientists often inject the CRISPR-Cas9 components directly into the gonads of adult hermaphrodites, ensuring that the genetic changes are passed onto the offspring.

    Image of the pharynx of C. elegans expressing GFP / Leica Microsystems ©

    Transgenic techniques in C. elegans insert foreign DNA into the worm’s genome to monitor gene expression, trace cell lineages, or study protein localization. One common approach is to fuse a gene of interest to a reporter gene such as green fluorescent protein (GFP). When this gene is expressed, the fluorescent tag can be visualized in living worms using fluorescence microscopy. This allows researchers to observe where and when specific genes are active, how proteins move within the cells, and how cells interact during development or disease progression. Transgenes are typically introduced via microinjection into the syncytial gonads of adult worms, leading to the formation of extrachromosomal arrays inherited by the next generation. Stable lines can also be created through CRISPR or chemical integration methods. These visual tools are particularly powerful due to the worm’s transparent body, which makes it possible to track fluorescent signals in real time throughout the entire organism.

    C. elegans is an excellent system for drug screening and environmental toxicology due to its small size, short lifespan, and genetic tractability. Researchers can test the effects of thousands of compounds quickly and cost-effectively. In these experiments, worms are exposed to chemical agents in liquid or on agar plates, and their survival, movement, reproduction, or specific cellular markers are measured to assess the biological impact. Using genetically modified strains that mimic human disease pathways, scientists can screen for drugs that alleviate symptoms or restore normal function. These tests provide an efficient first step in drug development, singling out promising candidates before moving onto mammalian models.

    The cell lineage and the programmed cell death in C. elegans / Nobel Prize in Physiology or Medicine 2002

    One of the most groundbreaking discoveries made using C. elegans was the genetic basis of programmed cell death, or apoptosis, a critical process in both development and disease. The research was led by Dr. H. Robert Horvitz at the Massachusetts Institute of Technology. Horvitz and his colleagues began studying cell death in C. elegans in the 1980s by tracing the fate of every cell in the worm’s body during development. They discovered that exactly 131 cells always die in the developing hermaphrodite and that this process was genetically controlled. Through genetic screening, Horvitz identified three core genes that regulated apoptosis: ced-3, ced-4, and ced-9. By inducing mutations in these genes, the researchers could either prevent or accelerate cell death in the worm. This revealed that cell death is not a passive consequence of damage, but rather an active, genetically programmed event. The mammalian counterparts of these genes, like caspases and BCL-2, were later discovered to play central roles in cancer, autoimmune diseases, and neurodegeneration, making this research foundational to modern medicine. Horvitz was awarded the 2002 Nobel Prize in Physiology or Medicine for his work along with Sydney Brenner and John Sulston.

    In addition, C. elegans has contributed to our understanding of neurodegenerative diseases such as Alzheimer’s. One major study was led by Dr. Christopher Link at the University of Colorado in the late 1990s. Link developed a transgenic C. elegans strain that expressed the human β-amyloid (Aβ) peptide in muscle cells. This is the same peptide that forms toxic plaques in the brains of Alzheimer’s patients. In the study, the researchers observed that worms expressing Aβ developed progressive paralysis as they aged, mimicking aspects of human Alzheimer’s pathology. They then used this model to screen for genetic mutations and chemical compounds that could suppress the toxic effects of Aβ. Their work identified several genes involved in protein folding and stress response that modified Aβ toxicity. This demonstrated that C. elegans could be used as a fast and cost-effective in vivo system for identifying genetic and pharmacological modifiers of Alzheimer’s disease. The worm model has since then been adapted by numerous labs worldwide to study tau protein aggregation and mitochondrial dysfunction, expanding our knowledge of neurodegenerative pathways.

    Micrographs showing visible signs of aging in C. elegans from a 2-day old adult (A) to a 7-day old adult (B) to a 13-day old adult (C) / Whitehead Institute ©

    Another major discovery made using C. elegans was the link between insulin signaling and lifespan regulation. Dr. Cynthia Kenyon at the University of California, San Francisco, led a series of experiments in the 1990s that transformed the field of aging research. Kenyon’s team discovered that a single mutation in the daf-2 gene, which encodes an insulin/IGF-1 receptor, could double the worm’s lifespan. They found that when daf-2 signaling was reduced, it activated another gene, daf-16, which promoted the expression of stress-resistance and longevity-related genes. To test this, Kenyon used genetic mutants and tracked their development and survival across generations. The C. elegans with the daf-2 mutation lived significantly longer than their wild-type counterparts and were more resistant to oxidative stress and heat. These findings provided the first clear evidence that aging could be actively regulated by specific genetic pathways rather than being a passive deterioration process. Later studies found that similar insulin/IGF-1 pathways exist in mammals, including humans, opening new therapeutic avenues for age-related diseases, diabetes, and metabolic disorders.

    So what does the future hold?

    The future of C. elegans in scientific research is remarkably promising, with its applications continually expanding as technology and genetic tools advance. With the rise of CRISPR-Cas9, optogenetics, and high-throughout screening techniques, researchers can now manipulate C. elegans with unprecedented precision to study complex biological processes such as epigenetics, gut-brain interactions, and real-time neuronal activity.
    In the coming years, C. elegans is expected to play an even greater role in personalized medicine and systems biology. Its potential as a predictive model for human gene function could aid in understanding the consequences of mutations found in patient genomes, leading to more tailored treatments. The worm’s short life cycle, fully mapped genome, and conserved biological pathways make it an ideal model for rapidly identifying new therapeutic targets and testing drugs, especially for age-related and neurodegenerative diseases. Despite its simplicity, this tiny nematode continues to open doors to complex human biology, proving that even the smallest organisms can have the biggest impact on science and medicine.

    References

    Alvarez, Javier, et al. “Modeling Alzheimer’s Disease in Caenorhabditis Elegans.” Biomedicines, vol. 10, no. 2, 1 Feb. 2022, p. 288, http://www.mdpi.com/2227-9059/10/2/288/htm#B52-biomedicines-10-00288, https://doi.org/10.3390/biomedicines10020288.
    Apfeld, Javier, and Scott Alper. “What Can We Learn about Human Disease from the Nematode C. Elegans?” Methods in Molecular Biology (Clifton, N.J.), vol. 1706, 2018, pp. 53–75, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6391162/, https://doi.org/10.1007/978-1-4939-7471-9_4.
    “C Elegans: The Early Worm Gets the Sequence.” Yourgenome.org, 2024, http://www.yourgenome.org/theme/ic-elegans-i-the-early-worm-gets-the-sequence/.
    “C. Elegans 101: A White Paper – InVivo Biosystems.” InVivo Biosystems, 26 Jan. 2024, invivobiosystems.com/disease-modeling/c-elegans-101-a-white-paper/.
    Chiu, Hui, et al. “C. Elegans as a Genetic Model to Identify Novel Cellular and Molecular Mechanisms Underlying Nervous System Regeneration.” Cell Adhesion & Migration, vol. 5, no. 5, 2011, pp. 387–394, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3218605/, https://doi.org/10.4161/cam.5.5.17985.
    Edgley, Mark. “What Is Caenorhabditis Elegans and Why Work on It? – Caenorhabditis Genetics Center (CGC) – College of Biological Sciences.” Umn.edu, University of Minnesota, 2022, cgc.umn.edu/what-is-c-elegans.
    Félix, Marie-Anne. “RNA Interference in Nematodes and the Chance That Favored Sydney Brenner.” Journal of Biology, vol. 7, no. 9, 2008, p. 34, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2776389/, https://doi.org/10.1186/jbiol97.
    Link, C. D. “Expression of Human Beta-Amyloid Peptide in Transgenic Caenorhabditis Elegans.” Proceedings of the National Academy of Sciences, vol. 92, no. 20, 26 Sept. 1995, pp. 9368–9372, http://www.pnas.org/content/92/20/9368.short, https://doi.org/10.1073/pnas.92.20.9368.
    Riddle, Donald L, et al. “The Biological Model.” Nih.gov, Cold Spring Harbor Laboratory Press, 2014, http://www.ncbi.nlm.nih.gov/books/NBK20086/.
    “The Nobel Prize in Physiology or Medicine 2002.” NobelPrize.org, 2019, http://www.nobelprize.org/prizes/medicine/2002/press-release/.
    Venkatesan, Arun, and Krishma Adatia. “Anti-NMDA-Receptor Encephalitis: From Bench to Clinic.” ACS Chemical Neuroscience, vol. 8, no. 12, 7 Nov. 2017, pp. 2586–2595, https://doi.org/10.1021/acschemneuro.7b00319.
    Wheelan, Sarah J, et al. “Human and Nematode Orthologs — Lessons from the Analysis of 1800 Human Genes and the Proteome of Caenorhabditis Elegans.” Gene, vol. 238, no. 1, Sept. 1999, pp. 163–170, https://doi.org/10.1016/s0378-1119(99)00298-x.
    “Whitehead Institute of MIT.” Whitehead Institute of MIT, wi.mit.edu/unusual-labmates-how-c-elegans-wormed-its-way-science-stardom.
    Wolozin, Benjamin, et al. “Watching Worms Whither: Modeling Neurodegeneration in C. Elegans.” Progress in Molecular Biology and Translational Science, vol. 100, 2011, pp. 499–514, http://www.ncbi.nlm.nih.gov/pubmed/21377635, https://doi.org/10.1016/B978-0-12-384878-9.00015-7.
    “Wonderous Worms.” NIH News in Health, 3 July 2025, newsinhealth.nih.gov/2025/07/wonderous-worms. Accessed 1 Aug. 2025.
    Zhang, Siwen, et al. “Caenorhabditis Elegans as a Useful Model for Studying Aging Mutations.” Frontiers in Endocrinology, vol. 11, 5 Oct. 2020, https://doi.org/10.3389/fendo.2020.554994.
  • Gene Editing in Focus

    Gene Editing in Focus

    By Maggie Wright

    ~6 minutes

    Advancements in genetic engineering have brought revolutionary tools to the forefront of biotechnology, with CRISPR leading as one of the most precise and cost-effective methods of gene editing. CRISPR, which stands for Clustered Regularly Interspaced Short Palindromic Repeats, allows scientists to alter DNA sequences by targeting specific sections of the genome. Originally discovered as part of a bacterial immune system, CRISPR systems have now been adapted to serve as programmable gene-editing platforms. This paper explores how CRISPR works, its current uses, its future potential, and the ethical considerations surrounding its application in both human and non-human systems.

    How CRISPR System Works

    The CRISPR-Cas system operates by combining a specially designed RNA molecule with a CRISPR-associated protein, such as Cas9 or Cas12a. The RNA guides the protein to a specific sequence in the genome, where the protein then cuts the DNA. Once the strand is cut, natural repair mechanisms within the cell are activated. Researchers can either allow the cell to disable the gene or insert a new gene into the gap. As described by researchers at Stanford University,

    “The system is remarkably versatile, allowing scientists to silence genes, replace defective segments, or even insert entirely new sequences.” (CRISPR Gene Editing and Beyond)

    This mechanism has been compared to a pair of molecular scissors that can cut with precision. For example, the Cas9 protein is programmed with a guide RNA to recognize a DNA sequence of about 20 nucleotides. Once it finds the target, it makes a double-stranded cut. The repair process that follows enables gene knockouts, insertions, or corrections. This technology has dramatically reduced the time and cost associated with gene editing, making previously complex tasks achievable in weeks rather than months. According to a 2020 review,

    “CRISPR/Cas9 offers researchers a user-friendly, relatively inexpensive, and highly efficient method for editing the genome.” (Computational Tools and Resources Supporting CRISPR-Cas Experiments)

    A simple guide to CRISPR / Javier Zarracina / Vox ©

    CRISPR’s Application in Medicine

    CRISPR’s influence extends across many fields, but its role in medicine has attracted the most attention. Scientists are using CRISPR to treat genetic diseases such as sickle cell anemia by editing patients’ own stem cells outside the body and then reinserting them. In 2023, researchers published results showing that a single treatment could permanently alleviate symptoms for some patients with these genetic diseases (Zhang 4.) Another area of exploration includes its potential for treating cancers by modifying immune cells to better recognize and destroy cancerous tissue. According to Molecular Cancer,

    “Gene editing technologies have successfully demonstrated the correction of mutations in hematopoietic stem cells, offering hope for long-term cures.” (Zhang 3)

    Current gene-editing uses / Royal Society ©

    CRISPR in Agriculture

    Beyond human health, CRISPR has transformed agricultural practices. Scientists are using it to develop crops that resist pests, drought, or disease without the need for traditional genetic modification methods that insert foreign DNA. One of the longer processes of traditional modifications in DNA could include conjugation. This is moving genetic material through bacterial cells in a direct contact. Conjugation is just one example of many of the traditional genetic modification methods.

    CRISPR has been used to produce tomatoes with longer shelf lives and rice varieties that can survive in low-water environments. According to the World Economic Forum,

    “CRISPR can help build food security by making crops more resilient and nutritious.” (CRISPR Gene Editing for a Better World)

    Such developments are increasingly critical in addressing global food demands and climate challenges.

    Research is also underway to apply CRISPR in animal breeding and disease control. In mosquitoes, scientists are testing ways to spread genes that reduce malaria transmission. In livestock, researchers are working to produce animals that are more resistant to disease. These experiments, while promising, require cautious monitoring to ensure ecosystem stability and safety.

    Future Potential

    Looking ahead, new techniques are refining CRISPR’s capabilities. Base editing allows researchers to change a single letter of DNA without cutting the strand entirely, reducing the off-targeting effect such as prime editing, a newer method that uses an engineered protein to insert new genetic material without causing double-stranded breaks. These tools provide even more control. According to the Stanford report,

    “Prime editing may become the preferred approach for correcting single-point mutations, which are responsible for many inherited diseases.” (CRISPR Gene Editing and Beyond)

    Possible Concerns

    Despite its potential, CRISPR also raises important ethical concerns. One of the most debated topics is germline editing, or the modification of genes in human embryos or reproductive cells. Changes made at this level can be passed down to future generations, leading to unknown consequences. In 2018, the birth of twin girls in China following germline editing sparked international outrage and led to widespread calls for stricter regulation. The scientific community responded swiftly, with many organizations calling for a global prohibition on clinical germline editing. As CRISPR & Ethics – Innovative Genomics Institute (IGI) states,

    “Without clear guidelines, genome editing can rapidly veer into ethically gray areas, particularly in germline applications.”

    Another concern is the potential for unintended consequences, known as off-target effects. These are accidental changes to parts of the genome that were not intended to be edited, which could lead to harmful mutations or unforeseen health problems. I will expand on this later in the article. Researchers are actively developing tools to better predict and detect such errors, but long-term safety remains a topic of study. The possibility of using CRISPR for non-therapeutic purposes, such as enhancing physical or cognitive traits.

    Cost and accessibility are also significant factors. Although the CRISPR tools themselves are affordable for research institutions, the cost of CRISPR-based therapies remains high. According to Integrated DNA Technologies,

    “Therapies based on CRISPR currently cost hundreds of thousands of dollars per patient, limiting their availability.” (CRISPR-Cas9: Pros and Cons)

    Bridging this gap requires investments in infrastructure, policy development, and global partnerships to ensure that developing countries are not left behind.

    In conclusion, CRISPR is reshaping the landscape of genetics and biotechnology. It has already brought major advances to medicine, agriculture, and environmental science. While the technology is still evolving, its precision offers a glimpse into the future of human health. CRISPR the potential to unlock solutions to some of humanity’s most pressing challenges.

    References

    “5 Novel Uses of CRISPR Gene Editing.” Genetic Engineering & Biotechnology News, http://www.genengnews.com/topics/genome-editing/5-novel-uses-of-crispr-gene-editing. Accessed 31 July 2025.
    “CRISPR Gene Editing and Beyond.” Stanford News, Stanford University, 2024, news.stanford.edu/stories/2024/06/stanford-explainer-crispr-gene-editing-and-beyond. Accessed 31 July 2025.
    “CRISPR-Cas9 Gene Editing.” Broad Institute of MIT and Harvard, http://www.broadinstitute.org/news/crispr-cas9-gene-editing-explained. Accessed 31 July 2025.
    “CRISPR Gene Editing for a Better World.” World Economic Forum, 2024, www.weforum.org/stories/2024/04/crispr-gene-editing-better-world. Accessed 31 July 2025.
    “CRISPR-Cas9: What Are the 10 Pros and 7 Cons?” IDT DNA, Integrated DNA Technologies, www.idtdna.com/pages/community/blog/post/crispr-cas9-what-are-the-10-pros-and-7-cons. Accessed 31 July 2025.
    “Current Gene Editing Uses.” National Human Genome Research Institute, http://www.genome.gov/about-genomics/fact-sheets/Genome-Editing. Accessed 31 July 2025.
    Lino, Cathryn A., et al. “Delivering CRISPR: A Review of Methods and Applications.” Drug Delivery and Translational Research, vol. 8, no. 1, 2020, pp. 1–14. PubMed Central, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7427626/. Accessed 31 July 2025.
    Zhang, Yujing, et al. “Gene Editing in Cancer: Opportunities and Challenges.” Molecular Cancer, vol. 22, no. 48, 2023, https://molecular-cancer.biomedcentral.com/articles/10.1186/s12943-023-01925-5. Accessed 31 July 2025.