AP Biology class blog for discussing current research in Biology

Author: mitochondriadriana

Uncovering the Mysteries of Early-Onset Colorectal Cancer: A Growing Concern

In recent years, an alarming trend has emerged: more and more people under the age of 50 are being diagnosed with colorectal cancer. Once considered primarily a disease affecting older adults, colorectal cancer is now becoming increasingly prevalent among younger and middle-aged individuals. The shift in demographics has puzzled scientists and medical professionals alike, prompting a deep dive into understanding the underlying causes and warning signs of this concerning trend. Normally, colorectal cancer has been associated with older age groups (what is colon cancer?) However, recent studies have shown a significant increase in cases among individuals under 50. This shift in demographics has led to a growing concern within the medical community. As medical professionals try to figure out why this is happening, they notice that it cannot be attributed to a single cause. Researchers are exploring various factors, including obesity, diet, gut microbiome, and even birth cohort effects, to understand the complex interplay contributing to the disease. While the exact causes remain elusive, identifying early warning signs is crucial for timely diagnosis and treatment. Symptoms such as abdominal pain, rectal bleeding, diarrhea, and iron-deficiency anemia have been identified as potential red flags, emphasizing the importance of vigilance and proactive healthcare.

Blausen 0246 ColorectalCancerEnvironmental chemicals crashing our cellular party? It’s like a scene straight out of a sci-fi movie! Who knew our everyday exposures could have such far-reaching effects?

The topic of colon cancer rising in young adults is being explored by many people. The National Cancer Institute shared Doug Dallmann’s story, reflecting the reality faced by many young adults who experience symptoms but may dismiss them due to misconceptions about age-related risk. Dallmann noticed blood in his stool in his early thirties but didn’t think much of it until the bleeding became more frequent and intense. His story underscores the importance of paying attention to symptoms and seeking medical attention promptly, regardless of age.

The article delves into the growing body of research aiming to uncover the root causes of early-onset colorectal cancer. Factors such as obesity, diet, gut microbiome, and environmental exposures are being explored as potential contributors to the rise in cases among younger adults. As we strive to unravel the mysteries surrounding early-onset colorectal cancer, it’s crucial to raise awareness about the importance of vigilance and proactive healthcare. By sharing stories like Doug Dallmann’s we can empower individuals to take charge of their health and advocate for timely screening and intervention. It has become increasingly important to do this. 

As someone who enjoys a good Netflix binge, I never thought my TV habits could have anything to do with my colon health. Time to switch to more active hobbies, I guess!

ZG16 Expression in Normal and Tumor Tissues of the Colon

At the core of cellular proliferation lies the tightly regulated process of the cell cycle. This sequence that includes  phases such as G1, S, G2, and M, ensures precise DNA replication and distribution of genetic material. Cells progress through this cycle under the watchful eye of intricate signaling pathways and molecular checkpoints. In the context of colorectal cancer, disruptions to these fundamental cellular processes set off a chain reaction culminating in malignant transformation. Mutations in critical regulatory genes, including tumor suppressors like APC and oncogenes such as KRAS, upset the delicate balance of cell cycle control. This imbalance leads to uncontrolled proliferation and the formation of tumors. The article sheds light on the perplexing rise of early-onset colorectal cancer, providing a tangible context to explore these AP Biology concepts. As scientists try to find the root causes of this issue, they consider  the interplay between environmental exposures, genetic predisposition, and cellular dynamics. Moreover, the accumulation of mutations, fueled by disrupted DNA repair mechanisms and genomic instability, heightens the risk of malignant progression. Insights drawn from AP Biology concerning DNA repair pathways and genome maintenance offer invaluable perspectives in dissecting the molecular underpinnings of cancer.

As I delved into this topic, I couldn’t help but feel a sense of urgency. The increasing prevalence of colorectal cancer among younger adults serves as a stark reminder of the complex interplay between genetics, lifestyle, and environmental factors in shaping our health outcomes. It’s concerning to think that individuals in their prime years of life are being confronted with such a serious illness, often with delayed diagnosis due to misconceptions about age-related risk.

What are your thoughts on the potential factors contributing to the rise in early-onset colorectal cancer? Have you encountered cases or discussions about this issue in your own communities or healthcare settings? Share your insights and perspectives below! Let’s continue the conversation and raise awareness about this important health concern.

Huntington’s Unveiled: Delving into Delayed Onset and the Fun Side of Therapeutic Possibilities

Greetings, health explorers! Today, we embark on a riveting exploration into Huntington’s disease, where scientists, spearheaded by the brilliant geneticist Bob Handsaker, have unveiled a compelling clue about its delayed onset in this article

Picture this: Huntington’s disease stems from a mistakenly repeated segment in the HTT gene. Bucking the conventional belief that these repeats remain constant, the research illuminates their dynamic growth in specific brain cells over time. As these repeats breach a critical threshold, the very activity of numerous genes in the affected brain cells undergoes a dramatic transformation, ultimately leading to cell death. The tantalizing prospect arises – could preventing the expansion of these repeats be the key to halting the development of Huntington’s disease?

 But fear not! The study hints at a potential game-changer – curbing the expansion of these repeats might be the key to slamming the brakes on Huntington’s disease development.

HuntingtonLet’s summarize what the article’s main idea was. Scientists, led by geneticist Bob Handsaker, have uncovered a significant clue about the delayed onset of Huntington’s disease. The disease arises from a mistakenly repeated segment in the HTT gene. Contrary to the belief that these repeats remain constant, the research reveals their dynamic growth in specific brain cells over time. Once the repeats surpass a critical point, the activity of numerous genes in the affected brain cells changes drastically, leading to cell death. The study suggests that preventing the expansion of these repeats may offer a way to halt the development of Huntington’s disease.

But let’s not stop there – delve deeper into the intricacies.

Before we move on, let’s pause. Do you know what Huntington’s disease is? Before you move on, read this brief article on Huntington’s disease.  

Anyway, let’s continue! A study on the neurological manifestations of Huntington’s disease beckons us, offering insights into the broader impact on the brain. The article, GENETICS AND NEUROPATHOLOGY OF Huntington’s DISEASE, reveals a breakthrough in understanding Huntington’s disease, shedding light on why the fatal brain disorder takes a prolonged time to manifest and suggesting a potential strategy to halt its progression. The key finding is that in some brain cells, the repeats of a gene called HTT, responsible for Huntington’s disease, can grow to hundreds of copies over time. When the number of repeats surpasses a certain threshold, the activity of thousands of other genes in the brain cells changes drastically, leading to cell death.

ADAR Protein

This discovery is connected to this article   about CRISPR technology and its use in treating genetic disorders. The link lies in the common theme of genetic manipulation and its potential role in addressing hereditary diseases. In the case of Huntington’s disease, the research suggests that preventing the expansion of repeats in the HTT gene could stop the development of the disease. This aligns with the broader theme of genetic interventions discussed in the CRISPR article.

Moreover, the article highlights the role of MSH3, a protein involved in DNA repair, in inadvertently adding CAG sequences to the HTT gene. Lowering the levels of this protein may prevent the expansion of repeats. This mechanistic insight provides a potential target for therapeutic intervention, indicating a different approach from current strategies that focus on lowering levels of the huntingtin protein.

In AP Biology class, we covered cell signaling, where cells communicate through molecular signals to regulate various processes. Signaling pathways involve receptors, intracellular messengers, and cellular responses. The Huntington’s disease article reveals that the expansion of CAG repeats in the HTT gene leads to changes in the activity of thousands of genes in brain cells. This alteration in gene activity can be seen as a response to an abnormal signal, impacting cell function. Understanding how abnormal signals lead to cellular dysfunction is crucial to cell communication.

In conclusion, Handsaker’s research cracks the molecular intricacies of Huntington’s disease, providing a deeper understanding of its development and offering potential therapeutic routes. The connection to AP Biology principles underscores the relevance of this study in the broader context of cellular communication and genetic signaling. What are your views on this paradigm shift in Huntington’s research? How might targeting DNA instability revolutionize therapeutic strategies? Please share your thoughts, and let’s engage in a meaningful discussion on this fascinating topic.


Aftermath Mysteries of COVID-19

Greetings, health explorers! Today, we’re diving into the twists and turns of a new study that unveils what happens in the aftermath of COVID-19. To put this into context, let’s picture this: you have now gotten rid of COVID from your body after suffering for a few days, but the health challenges still linger. A fresh study with 140,000 US veterans reveals how risks, from diabetes to fatigue, can play the long game for at least 2 YEARS! Crazy right? 

The research revealed that patients initially hospitalized during their COVID-19 cases were more likely to experience these health problems. However, even those with milder initial infections were still at a higher risk for about one-third of the analyzed medical issues compared to those who didn’t test positive. The most common problems align with long COVID symptoms such as fatigue, memory problems, loss of smell, blood clots, metabolic issues, and gastrointestinal problems. The study found that for every 1,000 people infected with the coronavirus, a cumulative 150 years of healthy life is lost due to persistent symptoms, highlighting the significant impact of long COVID. 

The article notes limitations. Some of these limitations include relying on electronic health records and potential skewing due to the predominantly male and older veteran population analyzed. It also did not include individuals who may have been infected but did not receive a positive test result in the early stages of the pandemic when testing was limited.

Wow, the impact of COVID-19 on long-term health is truly eye-opening! What are your thoughts on how we, as a society, can better address and manage the challenges posed by Long COVID? Share your insights below!

To set the stage, the World Health Organization (WHO) defines Long COVID, also known as Post-COVID Conditions, as the persistence or development of new symptoms three months post-initial SARS-CoV-2 infection, lasting at least two months with no other explanation. The Centers for Disease Control and Prevention (CDC) expand on this, noting that Long COVID encompasses a large variety of health issues affecting various body systems, even emerging after mild cases or in those who never tested positive for COVID.

Delving into the ideas, Dr. Akiko Iwasaki of the Yale School of Medicine and director of the Yale Center of Infection & Immunity, underscores that Long COVID is NOT A singular disease. Her research puts forward 4 hypotheses, suggesting that persistent virus remnants, autoimmunity triggered by B and T cells, reactivation of dormant viruses, and chronic changes post-inflammatory response may all contribute. SARS-CoV-2 without background

In AP Biology, we learned about the immune system and B and T cells. The immune system plays a crucial role in identifying and eliminating pathogens, but in some cases, remnants of the virus may persist. This situation involves the adaptive immune response, where B and T cells are responsible for recognizing and responding to specific pathogens. Autoimmunity is triggered by B and T cells. The immune system is designed to recognize and target foreign invaders. Sometimes, it can mistakenly attack the body’s own health cells, leading to autoimmune disorders. B and T cells are crucial to the adaptive immune response. 

How have your studies or interests in biology influenced your understanding of topics like the immune system and the function of B and T cells? Share your insights! Fimmu-11-579250-g003

Some statistics addressed in the Yale Medicine article, address the question of Long COVID’s trajectory, the Household Pulse Survey in the U.S. shows a potential decline, with reported symptoms dropping from 19% in June 2022 to 11% in January 2023. The true prevalence remains elusive, with estimates suggesting 65 million affected globally, potentially underreported due to the rise in at-home testing since 2022. 

Now, let’s connect this to the study involving 140,000 US veterans. The article  showcases the persistent health risks associated with COVID-19, unveiling that even individuals with milder initial infections face a higher risk of enduring medical issues. Some problems at the top of this list include: fatigue, memory problems, loss of smell, blood clots, metabolic issues, and gastrointestinal problems.  

For every 1,000 people infected, the cumulative loss of healthy life due to persistent symptoms amounts to a staggering 150 years. While the study acknowledges limitations, like reliance on electronic health records and potential population skew, it underscores the importance of protecting ourselves from COVID-19, given its potential long-term health consequences, even from seemingly mild infections. 

Long COVID demands continued attention, research, and comprehensive strategies for prevention and management. As we reflect on these findings, it is evident that understanding and addressing Long COVID is crucial.

What are your thoughts on this?

Shifting gears, another article from The Centers for Disease Control and Prevention (CDC)  delves into new guidance for healthcare providers treating patients with post-COVID conditions. The term “long COVID” is introduced, emphasizing that these conditions can affect individuals regardless of their initial symptoms. The CDC highlights a broad spectrum of symptoms, including heart palpitations, cognitive impairment, insomnia, and post-exertional malaise (PEM). While primary care providers can manage many cases, the CDC warns against relying solely on diagnostic results. People with post-COVID conditions are advised to continue preventive measures, and COVID-19 vaccines are highly recommended. The guidance is subject to updates as more information becomes available.

The FAIR Health study mentioned in the CDC article, indicates that over 23% of COVID-19 patients experience post-COVID conditions, with pain, breathing difficulties, hyperlipidemia, malaise, and fatigue being common. Half of hospitalized patients developed post-COVID conditions, and there’s a higher risk of mortality following severe treatment, more so for hospitalized individuals. The American Academy of Physical Medicine and Rehabilitation admires the CDC’s guidance for improving healthcare responses for long COVID.

As I did my research surrounding a health challenge that stretches far beyond the initial impact of the pandemic, the significance hits close to home. It’s not just data; it’s the lived experiences of individuals moving through the long-lasting effects of COVID-19. This isn’t just a call to action; it’s a call for our collective attention, research efforts, and a compassionate response. This health issue isn’t confined to statistics; it touches the lives of millions worldwide, making it a cause that resonates deeply within us all.

Unlocking the Secrets of Immortality: Bowhead Whales Defy Time and Cancer

When we look into nature, we often find remarkable solutions to some of our most pressing problems. From the camouflage skills of chameleons to the adhesive prowess of geckos, nature constantly astounds us with its ingenuity. Today, we’re diving into the fascinating world of bowhead whales, those majestic giants of the Arctic Ocean, and the incredible superpower hidden within their cells. Their unique DNA repair mechanisms might just be the key to unlocking groundbreaking advancements in cancer treatments for humans. But before we explore this potentially groundbreaking research, I want to share a personal connection to this topic. Whales, in particular, hold a special place in my heart—they are my favorite animals. This article resonates with my love for the ocean and its untapped potential to solve some of our most challenging medical puzzles, all thanks to a stuffed animal whale that was my cherished bedtime buddy!

I’m sure many of you also have a personal connection to the natural world or a favorite animal that has inspired your curiosity. Feel free to share your own stories or connections in the comments!

“Bowhead whales may have a cancer-defying superpower: DNA repair” by Meghan Rosen discusses the extraordinary longevity of bowhead whales, which can live for more than 200 years. Scientists have found that these whales possess a remarkable ability to repair damaged DNA, which could be the key to their cancer resistance.

A bowhead whale breaches off the coast of western Sea of Okhotsk by Olga Shpak, Marine Mammal Council, IEE RAS

The enormous size and large number of cells in the bowhead whale raise the possibility of cell mutations occurring during cell division, which in theory could raise the risk of cancer. A phenomenon known as Peto’s paradox states that large-bodied animals like bowhead whales appear to have robust cancer-prevention mechanisms that have evolved throughout time.

Bowhead whales appear to have a different technique from other huge mammals like elephants, which have additional copies of the tumor-blocking gene TP53 to get rid of damaged cells. Their cells are extremely effective at repairing double-strand DNA breaks, a type of damage that could cause cancer, as opposed to eliminating it. The less accurate DNA repair in other animals is contrasted with the effective repair process in bowhead whales.

It’s intriguing how different species have developed unique strategies to combat cancer. Share your thoughts on the varied approaches in the animal kingdom!

The study conducted by biologist Denis Firsanov and colleagues reveals that bowhead whale cells outperform human, mouse, and cow cells in repairing DNA damage, displaying an exceptionally efficient and accurate DNA repair system. The whales can tolerate more genomic damage because they possess a precise, rapid DNA repair mechanism. Moreover, bowhead whale cells produce higher levels of a DNA repair protein called CIRBP compared to other species studied. When human cells were engineered to produce bulk CIRBP, they exhibited improved DNA repair capabilities. The researchers conclude that the strategy of repairing damaged cells without eliminating them may be essential for the long, cancer-free lifespan of bowhead whales. Yale University cancer biologist Jason Sheltzer, though not involved in the research, finds this preprint fascinating, as it offers a new model for understanding how larger animals avoid cancer, possibly through superior DNA repair capabilities.


It is very important to fully understand how animals, such as bowhead whales, defend themselves against cancer because it may one day be possible to develop cancer cures for mankind. The importance of finding nature’s cures for medical problems is highlighted by research on animals with low cancer rates, as these methods could revolutionize human healthcare.
In AP Bio Unit 1 this quarter, I have learned the fundamental importance of cells.  Like we talked about, cells have proteins. In the research, the study identified two specific proteins, CIRBP and RPA2, that play a role in the DNA repair mechanism of bowhead whale cells. These proteins contribute to the efficiency of the repair process.

How have your studies or interests in biology influenced your understanding of topics like DNA repair and cellular mechanisms? Share your insights!

While human cells have their own set of DNA repair proteins, the specific proteins and mechanisms in human cells may differ from those in bowhead whales, potentially leading to variations in repair efficiency. We also talked about the Endomembrane System, including the Golgi apparatus, which is responsible for the processing and transport of molecules within the cell. In the context of the article, efficient intracellular transport of repair proteins and DNA repair products within bowhead whale cells is essential for their cancer resistance. Additionally, lysosomes in the endomembrane system are responsible for cellular waste disposal. In the context of the article, understanding how bowhead whale cells efficiently repair damaged DNA is also linked to the concept of maintaining cellular integrity and reducing the need for cellular degradation and recycling.

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