Cobbers on the Brain – Page 3 – Student Commentary on the Neurological Sciences

Final Reflection: Integrating Neurochemistry, Liberal Learning, and Responsible Engagement

Posted on April 30, 2025 by Meg / 0 Comment

As I sit down to write my final blog post, I’m struck by how much this class has not only deepened my understanding of brain chemistry but also reinforced the core values of Concordia. The CORE curriculum—built on the idea of Becoming Responsibly Engaged in the World (BREW)—has shaped my academic journey in ways I couldn’t have anticipated when I first stepped onto campus. This neurochemistry course, in particular, has been a powerful synthesis of scientific rigor, real-world applications, and collaborative learning, all of which align with Concordia’s five goals for liberal learning.

Instilling a Love for Learning

One of the most profound lessons this course has taught me is that learning doesn’t stop at memorizing pathways or neurotransmitters—it’s about curiosity, questioning, and connecting ideas across disciplines. Neurochemistry is an inherently dynamic field, with new discoveries constantly reshaping our understanding of the brain. Whether we were discussing neurodegenerative diseases, synaptic plasticity, or the biochemical basis of psychiatric disorders, I found myself constantly wanting to dig deeper. Each week as I wrote my Wiki page, blog post, and prepped for the small-group discussion, I found myself immersed in the topic of the week, often falling down rabbit holes and reading far beyond the article for the week. I truly enjoyed learning more and more about each topic. That intellectual engagement is what liberal learning is all about: not just absorbing information but actively pursuing knowledge with enthusiasm.

Developing Foundational Skills and Transferable Intellectual Capacities

This course sharpened skills that extend far beyond neurochemistry. This course is centered around breaking down complex research papers, which required me to assess methodology, interpret data, and evaluate conclusions. Writing blog posts and presenting information on Wednesdays forced me to distill dense material into succinct explanations—a skill that will be crucial as I pursue my doctoral studies in the fall. Discussing the science with my peers in our Wiki page presentations and in our small group discussions helped develop my ability to communication and collaboration skills. These competencies are highly transferable. In my graduate studies and beyond, the ability to analyze, synthesize, and articulate complex ideas will be invaluable.

3 & 4. Understanding Disciplinary, Interdisciplinary, and Intercultural Perspectives & Cultivating an Examined Cultural, Ethical, and Spiritual Self-Understanding

Neurochemistry doesn’t exist in a vacuum—it intersects with psychology, ethics, medicine, and even philosophy. One of the most eye-opening moments this semester was discussing the ethics of autism treatment. We didn’t just talk about the physiology of the disorder, we discussed if teachers and faculty should be required to know if students have autism. Would it perpetuate prejudice or help make sure neurodivergent students don’t fall through the cracks of the education system? We also discussed if autism needs to be cured, or if further awareness and acceptance of the disorder is the best “cure” for the disorder.

In later weeks, we discussed cultural differences that impact perceptions of anxiety when discussing adverse memory formation, and differences in cultural diets when discussing metabolic disorders. These topics forced me to think about my own morals, ethics, and actions, fostering a deeper self-awareness. This kind of interdisciplinary dialogue—between ethics, culture, science, and beyond—is a hallmark of liberal arts learning. It taught me that solving real-world problems, like improving neurological treatments, requires more than just science; it demands an awareness of societal implications.

Encouraging Responsible Participation in the World

Perhaps the most significant takeaway from this course is that knowledge should inspire action. While I will not be entering a neuroscience-related field, I can still apply the knowledge from this course to responsibly participate in the world. Learning about various disorders allowed me to better understand how to prevent them, knowledge I can now share with my friends and family members. Most importantly, this course underscored the importance of empathy. Many disorders, from cancer to Alzheimer’s to obesity, are due to complex neurological pathophysiologies. While lifestyle choices may reduce risk, many of these disorders are multifaceted and largely out of human control. Learning about the pathogenesis of these diseases helped me to step into the shoes of those suffering and challenge any preconceived prejudices I carried to empathize at a deeper level.

A Liberal Arts Education: More Than Just a Degree

To me, learning at a liberal arts institution means breaking down barriers between disciplines. In this class, we didn’t just study neurotransmitters—we considered how they shape behavior and society. That holistic perspective is something I’ll carry forward, especially as I enter the interdisciplinary field of Industrial-Organizational Psychology.

How Neurochemistry Relates to My Future Goals: From the Classroom to Corporations

The skills and knowledge gained in neurochemistry directly support my future doctoral studies and career in Industrial-Organizational (I-O) Psychology by providing a strong scientific foundation for understanding human behavior in workplace settings. The course honed my ability to critically analyze complex systems—whether signaling pathways or organizational structures—and apply critical thinking to understand the interrelatedness of such systems. Additionally, the interdisciplinary perspective I developed, bridging neurochemistry with psychology, equips me to approach I-O challenges with unique insight. Transferable skills like oral and written scientific communication, ethical reasoning, and breaking down complex papers will be invaluable as I conduct organizational research and translate findings into practical workplace solutions. Ultimately, this course reinforced that behavior—whether in controlled lab settings or large corporate offices—is rooted in biology, neuroscience, and chemistry, an understanding that will help guide my future work.

Resume-Worthy Skill: Interdisciplinary Problem-Solving

If I had to highlight one competency I honed this semester, it would be integrating multiple perspectives to solve complex problems. At its core, neurochemistry is inherently interdisciplinary, but our discussions went beyond the fields of neuroscience and chemistry. For example, when examining neurodegeneration in Alzheimer’s disease, I considered the structure and formation of amyloid-beta plaques and tau tangles (biochemistry); possible genetic risk factors and predisposition to the disease (genetics); behavioral and cognitive consequences of Alzheimer’s (psychology); preventative strategies focusing on diet and lifestyle changes (public health); and dilemmas like early diagnosis without a cure or gene editing (ethics). This kind of multidimensional thinking is exactly what employers and graduate schools value.

Becoming Responsibly Engaged

This neurochemistry course has encapsulated my Concordia education—challenging me to think deeply, connect widely, and act thoughtfully. As I move forward, I’ll carry with me not just the MAPK pathway or the mechanics of action potentials, but also the critical, ethical, and interdisciplinary mindset that defines liberal learning.

To future students: Don’t just memorize the material—uncover how it matters in the real world. That’s what BREW is all about.

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What I’m Taking With Me

Posted on April 30, 2025 by smohame4 / 0 Comment

Looking Back

It’s wild how quickly time passes when you’re not paying attention. One moment, you’re trying to find your first college classroom, hoping you’re not in the wrong building. The next, you’re sitting down to write your final reflection, wondering how it all flew by. Somewhere in between, without even realizing it, you’ve grown through late-night writing sessions, hard conversations, unexpected connections, and quiet moments when something finally clicked.

This class didn’t feel like just another item on a checklist. It felt like a chance to pause and take a real look at how far I’ve come. And honestly? It caught me off guard in the best way. It made me reflect not just on what I’ve learned, but on who I’ve become while learning.

I remember hearing “Become Responsibly Engaged in the World” when I first got to Concordia. It sounded nice. A little abstract. Maybe something you’d put on a poster or hear during orientation. But somewhere along the way, especially in this class, it started to mean something. It showed up in the way I questioned things more deeply, listened more carefully, and cared more intentionally. It was less about memorizing definitions and more about thinking with purpose. About realizing that I don’t just want to exist in the world—I want to understand it, and help shape it for the better.

Finding Meaning Along the Way

There’s one night I keep going back to. I was exhausted—mentally, emotionally, just drained. I had a blog post due, and the article we were working with felt dense and hard. I couldn’t connect with it. I stared at a blank screen for a long time, until I gave up on trying to sound “smart” and just… wrote what felt true. I linked the science to something personal I’d seen in real life. And suddenly, it made sense. The writing flowed. Not because it was perfect, but because it was real.

That moment taught me something I didn’t expect: learning doesn’t always look like a neat, well-formatted essay. Sometimes, it shows up when you’re tired and just trying your best to make sense of something. And that’s okay. That counts, too.

This class challenged me to think in ways I hadn’t before. We tackled topics like brain inflammation, mental health, obesity, and the ethical side of research, not as separate ideas, but as threads woven into the same big picture. They weren’t just facts or headlines. They were human. And that’s what stuck with me. We weren’t solving puzzles for fun; we were exploring questions that affect people’s lives.

I remember one assignment that had me approaching a problem from multiple angles—neuroscience, psychology, and ethics. I realized quickly that no single discipline had all the answers. But when I let them overlap, the full picture became clearer. That shift in thinking across boundaries instead of staying inside one box has completely changed how I see the world. It’s how I read the news now. It’s how I listen to people. It’s how I try to understand the systems that shape our lives.

And then, there’s the writing. I’ve always enjoyed writing, but this class helped me write with more care. Not just about grammar or clarity, but about the person reading it. Could someone outside the field understand what I meant? Would they feel something when they read it? I slowed down. I rewrote sentences just to make them feel more human. I stepped out of my own head and tried to see things from someone else’s view.

That shift in how I communicate awareness of audience, tone, and empathy is something I’ll take with me long after this class. If I were to list one skill on my resume that truly grew this semester, it’d be this: translating complex ideas into something relatable and engaging. Whether I’m writing case notes, advocacy material, or educational content, I know this ability will serve me well.

Carrying It Forward

This semester wasn’t easy, and I won’t pretend otherwise. There were days I felt like I was just barely keeping up, when deadlines felt like dominoes and motivation was nowhere in sight. But I kept showing up. And sometimes, that’s the most important thing. I learned how to manage my time better (still a work in progress), how to give myself grace when I didn’t get it all right, and how to bounce back after slipping behind. That kind of growth doesn’t show up in a gradebook; it’s real. It’s lasting.

More than anything, Concordia and this course taught me that education is about more than checking off requirements. It’s about becoming someone who sees the world differently. Someone who’s curious. Someone who asks better questions. Someone who pays attention to the things that matter, even when they’re complicated or messy.

I’ve come to appreciate that learning in a liberal arts setting is about embracing complexity. It’s about seeing how everything connects, how culture, science, ethics, and emotion are all tangled together. It’s about developing not just your intellect, but your character. And that kind of learning changes you.

As I step into whatever comes next, whether it’s grad school, a career, or something I haven’t even imagined yet, I’m not just taking knowledge with me. I’m taking a mindset. A way of showing up. A belief that small moments of insight can lead to big change. And that learning isn’t over once the final paper is submitted.

If I ever forget that, I’ll come back to this reflection. To this pause. To the reminder that I am not the same person I was when I started. I’m someone who kept going. Someone who grew. And that’s something I’ll always be proud of.

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Cracking the Code of a Killer: How Glioblastoma Hijacks Cellular Communication

Posted on April 30, 2025 by adebleye / 0 Comment

In a quiet neuroscience lab lit by the blue glow of bioinformatics screens, a group of researchers stared at a common enemy—one that doesn’t knock, doesn’t wait, and doesn’t often lose. Glioblastoma. A tumor so aggressive and elusive that even with today’s best medicine, it often wins. But this time, the researchers weren’t trying to kill the tumor directly. They were trying to listen to it.

Because cancer, like everything in our body, talks.

Abstract by Alisha Debleye depicting the tumorous and dangerous growth in the human brain that can sometimes go untreated or undiagnosed.

It communicates using intricate molecular “languages” called signaling pathways—chemical networks that tell our cells when to grow, when to rest, and when to die. For healthy cells, this communication keeps everything running smoothly. But glioblastoma doesn’t play by the rules. Instead, it hijacks these pathways, manipulating messages to fuel chaos instead of harmony.

That’s what the article “Understanding and Exploiting Cell Signalling Convergence Nodes and Pathway Cross-Talk in Malignant Brain Cancer” is all about. It’s not just about what makes GBM grow. It’s about how GBM outsmarts nearly every treatment we throw at it—by rerouting, rewiring, and repurposing the very systems that keep our cells alive.

The Whispering Networks of GBM

Our bodies use three key signaling pathways to manage cell behavior: MAPK, PI3K, and cAMP. Think of them as information highways: MAPK fuels growth, PI3K ensures survival and movement, and cAMP acts as a cellular checks-and-balances system.

Figure 1 shows the MAPK pathway being activated by receptor tyrosine kinases, sending messages for tumor growth, survival, and movement. This pathway is often hyperactive in GBM, particularly when NF1—a negative regulator—is lost.

In glioblastoma, these systems are corrupted. The tumor amplifies MAPK and PI3K to accelerate growth and invasion, while it silences cAMP—the very pathway that normally tells damaged cells to self-destruct.

The PI3K pathway is slightly different. This is how it works.

Figure 2 illustrates the PI3K pathway, another powerhouse of tumor survival. It activates downstream molecules like Akt and mTOR, which promote cell proliferation and metabolic rewiring. Together, PI3K and MAPK form a dangerous duo.

It even discusses how the GPCR pathways, specifically cAMP pathway is effected.

Figure 3 depicts the cAMP pathway—a tumor suppressor system that is unusually suppressed in GBM. Normally, this pathway promotes cell death and inhibits uncontrolled growth. But glioblastoma cells lower cAMP activity by reducing the enzyme adenylyl cyclase or increasing phosphodiesterases (PDEs) that degrade cAMP.

But these pathways don’t work in isolation.

Figure 4 shows how all three signaling networks converge on CREB, a central transcription factor. CREB integrates signals and activates genes responsible for growth, invasion, and immune evasion. It’s like the tumor’s master conductor—one that researchers now see as a promising therapeutic target.

But Why Should We Care About This At All?

Duh, Because its cancer! Also, GBM is the deadliest brain cancer. Its median survival rate is around 14 months, and fewer than 5% of patients survive five years with the disease¹. It doesn’t just grow—it infiltrates, migrates, and recurs. It touches memory, movement, and personality. It devastates not only the patient but everyone who loves them.

But the science we read this week gives us hope. The review showed that targeting convergence nodes—places like CREB where multiple pathways meet—might finally outmaneuver the tumor. Drugs like BKM120, a pan-PI3K inhibitor, and Vemurafenib, which targets RAF in the MAPK cascade, are being tested in clinical trials². Meanwhile, drugs like forskolin and PDE inhibitors, which restore cAMP signaling, show promise in triggering apoptosis, or programmed cell death³.

In fact, when researchers combined a cAMP activator with a MAPK inhibitor, some previously resistant GBM cells finally died⁴. This is a huge breakthrough. It suggests that combination therapy, hitting multiple pathways or convergence points at once, could finally disrupt the tumor’s carefully stolen communication.

What Can Society Do to Help The Cause?

Awareness is the first weapon. Glioblastoma symptoms often appear suddenly and worsen quickly. If you or someone you love experiences persistent headaches, personality changes, nausea, vision problems, or seizures, it’s important to seek medical attention quickly⁵. While there’s currently no routine screening for GBM, early diagnosis through MRI can sometimes buy precious time for surgery and treatment⁶.

Advocate for funding. Research into GBM receives a small fraction of overall cancer research funding⁷. By supporting organizations like National Brain Tumor Society or American Brain Tumor Association, the public can help fuel new discoveries—like the ones we studied this week.

And most importantly, don’t look away. Brain cancer may be rare, but its impact is massive. The more we learn about how it communicates, the better we can prepare, detect, and defeat it. We are on the cusp of a revolution in brain cancer treatment—not because we’ve found a cure, but because we’ve learned how to listen

Footnotes:

Stupp et al., 2005 – N Engl J Med ↩
Clinical Trial for BKM120 (NCT01349660) ↩
Sengupta et al., 2011 – Trends Pharmacol Sci ↩
Daniel et al., 2016 – Cell Death Dis ↩
Mayo Clinic – Glioblastoma Symptoms ↩
Johns Hopkins Medicine – GBM Diagnosis ↩
National Brain Tumor Society – Research Funding ↩

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Glio-not a blast-toma

Posted on April 30, 2025 by rhurley1 / 0 Comment

The article we have covered in a previous week, “Understanding and exploiting cell signaling convergence nodes and pathway cross-talk in malignant brain cancer” by Nok Him Funga, Corrina A. Grimaa, Samuel S. Widodoa, Andrew H. Kaye, Clarissa A. Whitehead, Stanley S. Stylli, and Theo Mantamadiotisa was an article about recently uncovered mysteries on cancer. Basically, we know already that cancer continues to evolve over time. However, due to this feature, we know that is why Glioblastoma is a very aggressive and invasive cancer.

The article informs us of what cancer specifically is in a intense detail. Though, the article specifically focuses mainly on the aspect of Glioblastoma. As a result of this article, we learnt much on this invasive condition.

Figure one, pictured above, from the article mentioned above is especially excellent at explaining this where it was needed (excellently timed, or in other words placed well). That piece is a diagram expressing the MAPK and the MI3K pathways to elaborate on the condition.^1 The myriad, but consistent colors complements the black words. Although, one slight problem could be that it could feel a large bunch overwhelming if you’re not too familiar with the applied terms and acronyms of figure one in the Neuroscience field. This was an excellent piece to me for it is maximized simplicity because, for clear reasons, that kind of thing strongly helps. The figure may also benefit people uninvolved in Neuroscience as well because figure one uses so much brief, yet descriptive, labeling, and I find that effective myself in general because it’s easy on the eyes to track or logicate.

Now, at this point, one, such as yourself, may wonder why people really should care about all the above information. Well, let’s answer with essential basics to answer ourselves by quickly asking ourselves something simpler first; what really is a cancer? Well, the answer is absolutely nothing short of deeply important, and very, very scary. According to the National Cancer Institute, a cancer is known as a scenario where a cells develops mutated in a harmful, bypasses various immune responses meant to kill this exact kind of thing, and then divides into clusters of mass.^2 Considering what we know about cancer long by now, it’s no shock to pretty much anyone that such a scenario can turn serious fast. Let us put this into perspective with similar topic.

In my class, I personally examined the various ways that something called a Xenograft benefits humanity. Surprisingly, I learned from Caroline Mitchellthat Xenografts are not some kind of scientific instrument like i originally suspected when I first heard it, but rather its actually the concept of using biological cells, tissues, and even organs beyond human origins.^3 Using pigs as an example, we can accept their hearts in our bodies to serve as our own, use their skin to temporarily treat burn victims, use their kidneys as our own when we lose to kidney failure and need new kidneys, and much more (including cancer treatments of course) all because we share a lot of biology with pigs. It is little short of incredible how essential Xenografts could very much be to resolve issues like the infamous organ donor hospitals dread worldwide. In the end, however, we must continue to strive toward scientific excellence to uncover the best possible solutions. As I conclude this blog post, I actually conclude my final blog on all, so I wish to shout out my teacher for being incredible to me.

References:
1) “Understanding and exploiting cell signaling convergence nodes and pathway cross-talk in malignant brain cancer” by Nok Him Funga, Corrina A. Grimaa, Samuel S. Widodoa, Andrew H. Kaye, Clarissa A. Whitehead, Stanley S. Stylli, and Theo Mantamadiotisa
2) https://www.cancer.gov/about-cancer/understanding/what-is-cancer
3) https://www.taconic.com/resources/what-is-xenograft (Caroline Michell)

Community/Disease/Health/Hot topics

Signaling Pathways in Glioblastoma: A Convergence of Pathways and a Convergence of Hope

Posted on April 30, 2025 by Meg / 0 Comment

Glioblastoma (GBM) is one of the most aggressive and treatment-resistant cancers, with a median survival of just 14 months despite advances in therapy[1]. The review article “Understanding and Exploiting Cell Signaling Convergence Nodes and Pathway Crosstalk in Malignant Brain Cancer” [2] dives into the complex molecular mechanisms driving GBM progression and treatment resistance, focusing on three key signaling pathways: PI3K, MAPK, and cAMP.

The Complexity of Glioblastoma: Resistant and Persistent

GBM is characterized by intertumoral heterogeneity, meaning that different regions of the tumor may exhibit distinct genetic and molecular profiles. This heterogeneity complicates treatment, as therapies targeting one pathway may fail due to compensatory activation of another. The Cancer Genome Atlas has classified GBM into four molecular subtypes:

Classical – Driven by EGFR amplification.
Mesenchymal – Associated with NF1 and PTEN mutations.
Proneural – Linked to PDGFRA amplification and IDH1 mutations.
Neural – Lacks clear driver mutations but expresses neuronal markers[2].

Each subtype responds differently to treatment, creating an increased need for personalized therapeutic strategies.

Key Signaling Pathways in GBM

The MAPK Pathway: Cell Proliferation and Survival

The mitogen-activated protein kinase (MAPK) pathway is a critical regulator of cell proliferation, survival, and metastasis. In GBM, this pathway is frequently hyperactivated due to:

EGFR amplification (seen in ~40% of cases).
Loss of NF1, a negative regulator that inactivates Ras by converting GTP to GDP.

Upon growth factor binding (e.g., EGF), receptor tyrosine kinases (RTKs) dimerize and phosphorylate downstream adaptor proteins, leading to Ras → Raf → MEK → ERK activation. ERK then translocates to the nucleus, promoting transcription of oncogenes like c-Myc and CREB.

MAPK-based therapeutic implications:

Vemurafenib, a BRAF inhibitor, has shown promise in GBM patients with BRAF V600Emutations[2].
However, resistance often arises due to pathway redundancy, where tumors activate alternate survival mechanisms.

The PI3K Pathway: Regulating Cell Growth

The phosphoinositide 3-kinase (PI3K) pathway is another major player in GBM, regulating cell growth, metabolism, and survival. Key alterations include:

PTEN loss, leading to unchecked PIP3 accumulation and AKT/mTOR activation.
PI3K mutations, driving oncogenic signaling.

PI3K signaling promotes invadopodium formation, enhancing tumor invasiveness by upregulating matrix metalloproteinases (MMPs).

PI3K-based therapeutic implications:

BKM120 is a PI3K inhibitor, which could be used as a potential therapy.
Combining PI3K inhibitors with MAPK inhibitors may prevent resistance by blocking compensatory signaling[2].

The cAMP Pathway: Tumor Suppression

Unlike MAPK and PI3K, the cAMP pathway is generally suppressed in GBM, correlating with higher tumor malignancy. cAMP, produced by adenylate cyclase, activates protein kinase A (PKA), which can:

Inhibit Raf, suppressing MAPK signaling.
Induce apoptosis via Bim upregulation.

Therapeutic implications:

PDE inhibitors (e.g., IBMX) increase cAMP levels, promoting apoptosis in some GBM cell lines.
Combining cAMP activators with MAPK inhibitors may overcome resistance in tumors with high ERK activity[2].

Pathway Convergence: CREB as a Critical Molecule

A major theme in the review is pathway convergence on transcription factors like CREB (cAMP response element-binding protein) [2]. CREB integrates signals from MAPK (via ERK phosphorylation of Ser133), PI3K (via RSK and MSK kinases), and cAMP (via PKA).

CREB regulates genes involved in cell survival, proliferation, and stemness, making it an attractive therapeutic target. Small-molecule CREB inhibitors are being explored in leukemia and lung cancer, suggesting potential applicability in GBM[2].

Overcoming Drug Resistance: The Need for Combinatorial Therapy

A major challenge in GBM treatment is adaptive resistance, where tumors rewire signaling networks to bypass targeted inhibition. Strategies to overcome this include:

Dual PI3K/MAPK inhibition – Prevents compensatory pathway activation.
Targeting downstream molecules – Blocks multiple oncogenic signals simultaneously by targeting factors like CREB.
Combining pathway inhibitors with immunotherapy – Enhances anti-tumor immune responses[2].

Toward Precision Medicine in GBM

Understanding signaling crosstalk can inform better therapies for GBM. Future research should focus on identifying biomarkers to predict drug response and developing inhibitors targeting signaling hubs like CREB. For now, this review emphasizes the importance of understanding the convergence of pathways in tackling one of the most formidable challenges in neuro-oncology.

This article provides a fascinating glimpse into the molecular battlefield of GBM and the innovative strategies being developed to fight it. It’s a powerful reminder that cancer is not just a genetic disease, but a signaling disease—and defeating it will require disrupting its communication networks at multiple levels.

Glioblastoma is one of the most aggressive and treatment-resistant cancers AND is driven by hyperactive PI3K and MAPK signaling pathways that promote tumor growth and invasion. BUT these pathways exhibit crosstalk and redundancy, leading to drug resistance. THEREFORE, targeting downstream convergence points like CREB or using combination therapies may overcome resistance and improve treatment outcomes.

References

[1] “About Glioblastoma,” National Brain Tumor Society. Accessed: Apr. 29, 2025. [Online]. Available: https://braintumor.org/events/glioblastoma-awareness-day/about-glioblastoma/

[2] N. H. Fung et al., “Understanding and exploiting cell signalling convergence nodes and pathway cross-talk in malignant brain cancer,” Cell. Signal., vol. 57, pp. 2–9, May 2019, doi: 10.1016/j.cellsig.2019.01.011.

Disease/Health/Uncategorized

Inside the Tumor: The Complex Biology of Glioblastoma

Posted on April 30, 2025 by jcopiske / 0 Comment

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INSIDE THE TUMOR: THE COMPLEX BIOLOGY OF GLIOBLASTOMA

Glioblastoma (GBM) is a highly aggressive brain cancer that stems from glial cells, these cells known for their supportive role in the brain. This cancer is notorious for its high mortality rate and poor prognosis, and it is often regarded as the deadliest type of cancer. GBM is one of the most challenging cancers to treat, largely due to its resistance to current therapies.

Cell signaling regulates cell behavior; therefore, cell behavior influences tumor development. GBM rewires neuronal networks and intervenes with three common signaling pathways: PI3K, MAPK, and cAMP. The hyper-activation of these pathways drives tumor malignancy. This raises the question: Why is GBM so aggressive compared to other types of cancer?

WHAT IS GLIOBLASTOMA?

In a healthy brain, glial cells regulate their gene expression very precisely to support neurons and maintain homeostasis. However, in glioblastoma, these cells undergo malignant transformation, which is frequently accompanied by the over-expression of certain genes and proteins, such as EGFR (Epidermal Growth Factor Receptor). EGFR is involved in cell signaling pathways that control cell division and survival. When mutations occur, an excess of EGFR appears on cancer cells, causing them to divide more rapidly.

Figure 1. early stage of glioblastoma versus tumor cells in the advanced stage.

The over-expression of EGFR drives the over-activation of signaling pathways such as PI3K/AKT and MAPK as shown in Figure 1. The tumor environment also has an increasing number of peripheral cells that accumulate within the tumor tissue, further promoting tumor progression. This progression can impair the blood-brain barrier (BBB), as shown in Figure 2. which is the semi-permeable membrane that regulates movement between the blood and the brain. Such impairment can manifest as inflammation.[1]

Glioblastoma - an overview | ScienceDirect Topics — Figure 2. GBM presence in the BBB

FOUR SUBTYPES OF GLIOBLASTOMA

Classical GBM:

Amplified EGFR signaling but minimal TP53 mutations.
Responds well to aggressive treatment.

Mesenchymal GBM:

Frequent NF1 and PTEN mutations, along with altered MAPK and PI3K pathways.
Aggressive therapy improves survival.
longer average survival time

Pro-neural GBM:

Common in younger patients, with mutations like IDH1 and TP53 and amplified PDGFRA.
Longer survival but poor response to aggressive treatments.

Neural GBM:

Characterized by neuronal gene expression, with no obvious mutations.
Offers the worst survival prognosis.
symptoms only slightly improve with treatment

The Multifaceted Metabolism of Glioblastoma | SpringerLink — Figure 3. subtypes of Glioblastoma

HOW GLIOBLASTOMA DISRUPTS NEURONAL SIGNALING

Glioblastoma invades the brain, rewiring neuronal networks and disrupting signaling:

PI3K and MAPK Pathways

These pathways use cellular signaling to regulate cell proliferation and survival. In GBM, PI3K and MAPK are cross-regulated, which poses a challenge for research because it becomes difficult to target a singular pathway.

cAMP

cAMP is distinct from the PI3K and MAPK pathways because it generally exerts tumor-suppressive effects rather than driving cell proliferation. cAMP, which stands for cyclic Adenosine Monophosphate, is produced by adenylyl cyclase in response to various extracellular signals. Elevated levels of cAMP activate protein kinase A (PKA), which then phosphorylates downstream targets that promote cell cycle arrest, differentiation, and apoptosis. In contrast, the PI3K and MAPK pathways typically generate proliferative signals that support tumor growth.

WHAT IS CROSSTALK

Crosstalk is a term that indicates the interaction between different signaling pathways. In GBM, a tumor will disrupt the communication between the pathways. dysregulated pathways—such as PI3K/AKT, MAPK, and cAMP—don’t operate in isolation. Instead, they interfere with and amplify each other’s signals, leading to a network of communication that is difficult to shut down with targeted therapies. [2]

TREATMENT CHALLENGES

Despite decades of intense research, GBM remains one of the most challenging cancers to treat. Drug resistence is driven by mulitple factors in GBM, making it difficult to achieve lasting therapeutic responses. As targeting GBM is a major focus of research, two main strategies have been pursued:

EGFR

Researchers have investigated EGFR inhibitors to counter the over-expression of EGFR, which promotes rapid cell division and survival. However, clinical results with EGFR inhibitors have often shown limited benefits, partly because the drugs are unable to fully inhibit downstream signaling and overcome intrinsic resistance mechanisms.

PI3K/AKT/mTOR

Regulatory PI3k/Akt/ mTOR as shown in Figure 4. This pathway supports cell proliferation, survival, and metabolic reprogramming such as promoting glucose dependency. Glioblastoma cells leverage PI3K/AKT signaling to enhance glucose metabolism, which facilitates rapid growth while protecting them from apoptosis. A hyper-activation of PI3K, often combined with the loss of PTEN function, drives this process. The frequent occurrence of PI3K hyper-activation, PTEN loss, and AKT mutations underscores the central role of this pathway as a key driver of oncogenesis and treatment resistance in GBM.[3]

WHY YOU SHOULD CARE!

Understanding the complex signaling pathways involved in GBM is crucial because it explains the underlying reasons for its aggressiveness and resistance to therapy. With GBM being one of the deadliest cancers and given its ability to rewire neuronal networks and activate multiple survival pathways simultaneously, finding effective treatments remains one of the greatest challenges in oncology. Overcoming these challenges could lead to significant advancements in therapeutic strategies and ultimately improve the survival rate and quality of life for patients with this devastating disease.

REFRENCES

[3] Barzegar Behrooz, A., Talaie, Z., Jusheghani, F., Łos, M. J., Klonisch, T., & Ghavami, S. (2022). Wnt and PI3K/Akt/mTOR Survival Pathways as Therapeutic Targets in Glioblastoma. International journal of molecular sciences, 23(3), 1353. https://doi.org/10.3390/ijms23031353

[2] Fung NH;Grima CA;Widodo SS;Kaye AH;Whitehead CA;Stylli SS;Mantamadiotis T; (n.d.). Understanding and exploiting cell signalling convergence nodes and pathway cross-talk in malignant brain cancer. Cellular signalling. https://pubmed.ncbi.nlm.nih.gov/30710631/

[1] Wu, L., Chai, R., Lin, Z., Wu, R., Yao, D., Jiang, T., & Wang, Q. (2023). Evolution-driven crosstalk between glioblastoma and the tumor microenvironment. Cancer biology & medicine, 20(5), 319–324. https://doi.org/10.20892/j.issn.2095-3941.2022.0771

Disease/Health/Uncategorized

Untangling the Deadliest Brain Tumor: Why We Must Care About Glioblastoma Research

Posted on April 29, 2025 by ttiongso / 0 Comment

Glioblastoma (GBM) is the deadliest form of brain cancer, and despite decades of effort, survival rates have barely improved. While we’ve learned a lot about cancer pathways, glioblastoma remains particularly elusive because of its complex, tangled web of signaling networks. New research has revealed how major pathways like PI3K, MAPK, and cAMP interact and offer potential new targets for therapy. Therefore, understanding these pathways could be the key to finally outsmarting this brutal disease.

Why Glioblastoma Matters

GBM isn’t just another cancer—it’s an aggressive, invasive, and heterogeneous beast. After initial surgery, chemotherapy (typically temozolomide), and radiation, tumors almost always return within months. Median survival is just 14 months, with a 5-year survival rate of less than 5%[1].

What the Science Shows Us

The article, Understanding and Exploiting Cell Signalling Convergence Nodes and Pathway Cross-Talk in Malignant Brain Cancer, explores three crucial pathways:

PI3K pathway: Promotes cell survival, proliferation, and invasion. Mutations in genes like PTEN often hyperactivate this pathway in GBM.
MAPK pathway: Drives cell division and survival. EGFR mutations, common in GBM, turbocharge this cascade.
Figure 1 [1]
cAMP pathway: Normally suppresses tumor growth, but GBM often has abnormally low cAMP activity.

Each of these pathways individually promotes tumor growth.. PI3K and MAPK can activate each other, bypassing single-drug therapies. Meanwhile, cAMP can suppress parts of MAPK and PI3K, offering a potential therapeutic counterbalance.

How This Could Change Treatment

Glioblastoma (GBM) is hard to treat because it can quickly find new ways to grow when one path is blocked. It’s like cutting off one road, only to have the tumor take a different route. That’s why treating just one pathway at a time often doesn’t work for long. But new research suggests smarter ways to attack the tumor:

Combining Treatments

Instead of blocking just one pathway, scientists are now trying to block two or more at the same time, like PI3K and MAPK. These pathways often work together, so stopping both may prevent the tumor from finding a new route to grow [2].

Targeting Key Hubs

Some proteins, like CREB, sit at the center of many important growth signals. By targeting CREB, we could shut down several tumor pathways at once. This might make it harder for the tumor to adapt and could also target the cells that help tumors grow back [1,3].

Restoring Natural “Off” Signals

Healthy brain cells use cAMP signaling to control growth and trigger cell death. GBM cells often shut this down. Some drugs can boost cAMP, pushing the cancer cells back toward normal behavior or even killing them. But if MAPK is too active, the tumor resists this effect, so blocking MAPK at the same time could make these drugs work better [4].

So Why Should the Public Care?

Glioblastoma is deadly because it quickly adapts to treatments by switching between different growth pathways. These new strategies focus on combining therapies, targeting key control points like CREB, and restoring natural tumor-blocking signals like cAMP.
By attacking multiple weak spots at once, we could finally slow tumor growth, prevent resistance, and improve survival. Instead of reacting to the tumor’s changes, we could stay one step ahead.

[1] Fung NH, Grima CA, Widodo SS, Kaye AH, Whitehead CA, Stylli SS, Mantamadiotis T. Understanding and exploiting cell signalling convergence nodes and pathway cross-talk in malignant brain cancer. Cell Signal. 2019 May;57:2-9. doi: 10.1016/j.cellsig.2019.01.011. Epub 2019 Jan 30. PMID: 30710631.

[2]Julien, L. A., Carriere, A., Moreau, J., & Roux, P. P. (2010). mTORC1-activated S6K1 phosphorylates Rictor on threonine 1135 and regulates mTORC2 signaling. Molecular and cellular biology, 30(4), 908–921. https://doi.org/10.1128/MCB.00601-09

[3] Mantamadiotis T, Papalexis N, Dworkin S. CREB signalling in neural stem/progenitor cells: recent developments and the implications for brain tumour biology. Bioessays. 2012 Apr;34(4):293-300. doi: 10.1002/bies.201100133. Epub 2012 Feb 13. PMID: 22331586.

[4] Daniel PM, Filiz G, Mantamadiotis T. Sensitivity of GBM cells to cAMP agonist-mediated apoptosis correlates with CD44 expression and agonist resistance with MAPK signaling. Cell Death Dis. 2016 Dec 1;7(12):e2494. doi: 10.1038/cddis.2016.393. PMID: 27906173; PMCID: PMC5261024.

Community

Final Reflection: Connecting the Dots

Posted on April 26, 2025 by gsparks1 / 0 Comment

As I wrap up my time at Concordia, I find myself reflecting on just how much this experience brought together the skills and knowledge I’ve developed over time. Majoring in Chemistry with an ACS certification and minoring in Biology and Mathematics, I have spent the last few years diving deep into the world of science, but this class pushed me to connect all of that in new ways. It challenged me to think differently, apply information creatively, and communicate complex ideas in ways that make sense beyond a lab setting.

This course reminded me why the liberal arts education model matters. It gave me the tools to see beyond just facts and equations and to ask deeper questions about how science fits into the broader world and how I can use that knowledge responsibly and meaningfully moving forward.

Expanding My Knowledge: Learning in New Ways

Throughout the semester, I gained a deeper understanding of key signaling pathways in the brain, such as MAPK, PI3K, and cAMP. These pathways are vital not just for understanding basic brain function but also for grasping how diseases like glioblastoma, anxiety, and obesity develop. I had learned about chemical signaling before, but this class pushed me to think about it on a systems level and to consider how disruptions ripple outward and cause real-world disease.

One of the most valuable things I took away from this class was improving my ability to read and process scientific articles. Academic research papers can be intimidating, even for students deep into their majors. However, this course pushed me to work through dense information, pull out key ideas, and translate them into my own words. Especially through writing weekly blogs aimed at a general audience.

Another important area of growth for me was learning to form hypotheses based on given data and to interpret new information critically. The signal interpretation tasks were some of my favorite assignments because they required me to predict outcomes based on pathways we had studied by not just memorizing but truly applying what I knew. This kind of thinking will be crucial as I move forward toward my future goals in graduate school and research.

Building Skills for the Future

The skills I developed this semester directly relate to the career I hope to pursue. After graduation, I plan to attend graduate school for chemistry, focusing on research. In that world, critical thinking, problem-solving, and the ability to communicate scientific ideas clearly are absolutely essential.

Through this class, I have become better at not just analyzing scientific data, but also connecting concepts across fields such as chemistry, biology, neuroscience, and even broader societal issues. Being able to see those connections will help me think more creatively and innovatively as a researcher.

If I were to highlight one major skill I’ve strengthened this semester on my resume, it would be critical thinking and problem-solving. Whether through analyzing a faulty signaling pathway, understanding a complicated article, or explaining a disease mechanism in simple language, this course constantly pushed me to solve problems from multiple angles and with multiple tools.

Liberal Arts Learning: Why It Matters

Studying at a liberal arts college like Concordia has been a huge part of shaping the way I think. Instead of focusing only on one narrow specialty, I have been exposed to a variety of disciplines ranging from science and math to history, philosophy, and the arts.

That exposure helped me understand that real-world problems are complex and interconnected. Diseases like glioblastoma or conditions like anxiety are not just chemical issues; they involve psychology, sociology, ethics, healthcare policy, and more. Liberal arts learning has taught me how to bridge those gaps, to ask better questions, and to think critically about the world around me.

In many ways, this class embodied the spirit of Concordia’s liberal learning goals. It reinforced a love for learning by encouraging curiosity about brain function and disease. It built on my foundational skills of analysis and communication. It gave me new interdisciplinary insights by combining neuroscience, psychology, chemistry, and even public health ideas. It asked me to think about the cultural and ethical implications of diseases and treatments. And most importantly, it prepared me to engage responsibly with the world as a future scientist.

Solving Problems Across Disciplines

One specific example of using several disciplinary perspectives came when we discussed treatments for diseases like obesity. Understanding obesity is not just a question of biology, it also involves chemistry (how molecules interact in the body), neuroscience (how the brain regulates hunger and reward), psychology (how behaviors and emotions influence eating), and sociology (how social environments shape habits).

By looking at the issue from all those angles, we could better understand why obesity is so difficult to treat and why a one-size-fits-all solution won’t work. This kind of interdisciplinary thinking will be critical in any future research I do, especially if I want my work to have real-world impact.

Looking Ahead

As I move forward toward graduate school and a future career in chemistry, I know the skills and experiences I gained in this course will stay with me. Being able to critically analyze information, synthesize ideas across disciplines, communicate clearly, and solve problems creatively are skills that matter in every field but especially in science, where the challenges we face are rarely simple.

This class helped remind me that the ultimate goal of education isn’t just to learn facts. It’s to become someone who can take knowledge and use it to make a difference. Whether through research, communication, or collaboration, I hope to keep building on what I’ve learned here at Concordia and to always keep growing as a learner, a thinker, and a responsible global citizen.

I also want to take a moment to express my gratitude for the dedicated professors here at Concordia. Throughout my time as a student, and especially in this course, I have been consistently supported and challenged by faculty who truly care about their students’ success. Their passion for teaching and commitment to helping us grow not just academically, but also personally, has made a lasting impact on me. I am incredibly thankful for their guidance, encouragement, and the countless ways they have helped me become a more thoughtful learner and a more prepared future scientist.

Disease/Health

Cracking the Code of Brain Cancer: How Glioblastoma Outsmarts Us and How We’re Fighting Back

Posted on April 26, 2025 by gsparks1 / 0 Comment

abstract created by Gabe Sparks.

Cancer is one of the most recognized and feared diseases in our society. It has been the focus of decades of research, with countless efforts dedicated to finding a cure. Thanks to these advances, we now have a range of treatments that can successfully target many types of cancer. However, there is still much we don’t understand, and some forms of cancer continue to cause trouble for even our best therapies. While breast cancer and skin cancer are commonly known, one of the most aggressive and deadly forms often goes overlooked: glioblastoma (GBM). This malignant brain tumor is notorious for its poor survival rates, with most patients living only months after diagnosis. Despite aggressive treatment with surgery, radiation, and the chemotherapy drug temozolomide, glioblastoma remains devastatingly difficult to control.¹

But new research is beginning to crack the code of how GBM survives and thrives. Potentially offering hope for smarter, more effective ways to fight back.

Understanding the Science

To understand the development of glioblastoma (GBM), it’s essential to look closely at three major signaling pathways: MAPK, cAMP, and PI3K. These pathways are critical for regulating key cellular functions, including metabolism, proliferation, survival, invasion, and stemness.¹ Under normal conditions, they work together in a carefully balanced system to maintain healthy cell growth and tissue stability. However, when these signaling networks become disrupted or unbalanced, they can trigger uncontrolled cell growth which sets the stage for the development of GBM.

The MAPK pathway begins with the activation of a receptor tyrosine kinase (RTK) on the cell surface. Once the receptor binds its specific ligand, it triggers a cascade of intracellular events: adaptor proteins like GRB2 and SOS activate Ras, which in turn activates RAF. RAF then phosphorylates MEK, which subsequently activates MAPK. Activated MAPK moves into the nucleus, where it phosphorylates transcription factors such as CREB, leading to the recruitment of additional regulatory proteins and RNA polymerase to initiate the expression of genes that promote growth and survival.¹Under normal conditions, this pathway is regulated by negative feedback mechanisms, including the tumor suppressor NF1.¹ However, in GBM, NF1 is often deleted or inactivated, allowing the pathway to remain unchecked.

The PI3K pathway also starts with the activation of an RTK. Activation of PI3K leads to the conversion of PIP2 to PIP3, which then recruits and activates PDK1. PDK1 then activates AKT which is a key regulator that can translocate into the nucleus and promote gene expression that drives survival, growth, and metabolic activity.¹ This pathway is normally kept in balance by PTEN (phosphatase and tensin homolog), a tumor suppressor that dephosphorylates PIP3 back to PIP2.¹ In GBM, PTEN is frequently mutated, deleted, or silenced, resulting in hyperactivation of PI3K signaling.

The cAMP pathway operates through a different mechanism. It begins with the binding of a ligand to a G-protein-coupled receptor (GPCR), leading to activation of adenylyl cyclase. This enzyme catalyzes the conversion of ATP to cAMP, which activates protein kinase A (PKA). PKA serves as an important modulator by inhibiting signaling at the RAF step of the MAPK pathway, thus helping to regulate cell growth. In GBM, cAMP levels are often reduced, weakening this inhibitory control and further contributing to the imbalance among pathways.

In glioblastoma, the MAPK and PI3K pathways are often hyperactivated, driving rapid and uncontrolled tumor cell proliferation, while the regulatory influence of the cAMP pathway is diminished.¹ This imbalance between growth-promoting and growth-suppressing signals creates an environment where cancer cells can thrive. Figure 1 is a pictural representation of the three pathways and how they interact with one another. Here is a link to an article that goes into great detail on how these pathways play a role in GBM.

Figure 1. Pictorial representation of the multiple pathways involved in GBM.

Fortunately, recent advances in research are uncovering new strategies to target these disrupted signaling networks and bring new hope in the fight against GBM.

Emerging Treatments

Despite the major challenges presented by glioblastoma’s complexity and resistance to treatment, several promising new therapies are under active investigation. One major area of focus is immunotherapy, which aims to help the body’s own immune system recognize and attack tumor cells. Immune checkpoint inhibitors that target proteins like PD-1, PD-L1,and CTLA-4 are being tested, often in combination, to boost immune activation against GBM.² Another exciting strategy is CAR T-cell therapy, where a patient’s T cells are genetically engineered to recognize specific tumor markers such as EGFRvIII and IL13Rα2.² While these approaches show great promise, challenges like tumor relapse and immune evasion remain, highlighting the need for further investigation.

Nanocarrier-mediated therapy is another cutting-edge field. Researchers are developing nanoparticles designed to cross the blood-brain barrier and deliver drugs directly to tumor cells.² By targeting cancer cells more precisely, these nanocarriers hope to improve treatment effectiveness while minimizing side effects. Magnetic nanoparticles, in particular, are entering clinical trials and may offer a new solution for delivering therapies deep within the brain.²

While many of these new therapies are still in early stages of development, they are already showing encouraging results. Together, they represent an exciting shift in how we approach one of the most challenging cancers. Here is a link to an article that explores many of the new treatments being developed.

Conclusions

GBM is a devastating form of cancer that too often goes overlooked. While more common cancers like breast and skin cancer receive widespread attention, it’s crucial that we shine a light on all forms of cancer especially those as aggressive and lethal as GBM. Increasing public awareness can drive not only a deeper understanding of this disease but also greater support for the research needed to develop new, life-saving treatments. By broadening the conversation around cancer, we can help accelerate progress and offer hope to those affected by glioblastoma and other under-recognized cancers.

References

(1) Fung, N. H.; Grima, C. A.; Widodo, S. S.; Kaye, A. H.; Whitehead, C. A.; Stylli, S. S.; Mantamadiotis, T. Understanding and Exploiting Cell Signalling Convergence Nodes and Pathway Cross-Talk in Malignant Brain Cancer. Cellular Signalling. Elsevier Inc. May 1, 2019, pp 2–9. https://doi.org/10.1016/j.cellsig.2019.01.011.

(2) Angom, R. S.; Nakka, N. M. R.; Bhattacharya, S. Advances in Glioblastoma Therapy: An Update on Current Approaches. Brain Sciences. Multidisciplinary Digital Publishing Institute (MDPI) November 1, 2023. https://doi.org/10.3390/brainsci13111536.

Uncategorized

Final Reflection: My Capstone Experience

Posted on April 26, 2025 by jdeitz1 / 0 Comment

Every ending is also a beginning — and as I close this chapter at Concordia, I find myself reflecting on how this journey has shaped who I am and how I see the world. As I reflect on my experience in this course and my broader education at Concordia, I realize how much the CORE curriculum and the philosophy of liberal learning — to Become Responsibly Engaged in the World (BREW) — have truly shaped my academic and personal growth. This class served as a culmination of the many skills, competencies, and perspectives I have gained during my time at Concordia, allowing me to not only apply what I have learned across disciplines but also to better understand my role in the larger global community.

Throughout the semester, the knowledge I gained from participating in this class was both academic and personal. Academically, I strengthened foundational skills such as critical thinking, comprehension and processing of research articles in a variety of fields, communication, and collaboration. Each of our weekly assignments not only made me better understand the topics discussed in each of the articles, but also it challenged me to think beyond surface-level understanding, encouraging me to connect theoretical knowledge to real-world applications. Personally, the group discussion aspect of this course pushed me to reflect more deeply on my values, my approach to problem-solving, and my ability to engage with diverse perspectives. Learning, for me this semester, was an active process of integration — weaving together threads from different courses, disciplines, and experiences into a cohesive understanding of complex issues.

The skills and competencies I gained this semester are directly aligned with my future goals. As I look toward a career in the field of chemistry that requires not only technical knowledge but also the ability to think critically, adapt, and lead ethically, I am grateful for the emphasis Concordia has placed on transferable skills. Whether it is analyzing data, finding and researching scientific topics of interest, creating stories and communicating them in a way that fit my audience, navigating intercultural communication, or leading a team with empathy and responsibility, the liberal learning goals have prepared me to meet these challenges. In particular, developing interdisciplinary perspectives has been invaluable. Problems in the real world are rarely isolated within one field, and my education has trained me to draw from multiple disciplines to find creative and effective solutions.

Learning at a liberal arts institution like Concordia has meant more than simply mastering content; it has meant developing a mindset of lifelong curiosity and responsibility. It has taught me to ask not just “How?” but also “Why?” and “For whom?” Concordia’s commitment to cultivating an examined self — culturally, ethically, physically, and spiritually — has encouraged me to be mindful of the broader impact of my actions. It has challenged me to think about my place in society and to recognize my responsibility to contribute positively to my community and beyond. In a world that is increasingly complex and interconnected, I believe this kind of education is more important than ever.

If I were to highlight a few skills I really strengthened this semester, I would definitely focus on communication, research and information literacy, and time management. Over the past few months, I had so many opportunities to practice different forms of communicating clearly — whether it was writing scientific based papers or blog posts, giving presentations, or simply explaining my thoughts and ideas in class discussions. I learned that good communication isn’t just about sharing information; it’s about telling a good story and making sure your message connects with your audience, and that’s something I know I’ll carry into my future work. I want to specifically highlight the opportunities that I have had to communicate in a public speaking manner. Public speaking or just clearly communicating my thoughts out loud to any size of audience has always been a struggle for me. I have gone through a lot of speech therapy throughout my life, especially in my childhood, and so public speaking is scary and difficult for me as I usually revert back to bad habits that make it hard to understand what I am trying to say. I have had plenty of practice with this over the years, but I think in this class as well as through senior chemistry seminar has been extremely influential in helping me feel more confident in my abilities and has given me hope that I can give solid scientific talks in the near future.

This semester also pushed me to become much more confident in my research skills. Finding reliable sources, evaluating information critically, and weaving different perspectives into a clear argument has become almost second nature. I realized how important it is not just to find information, but to understand and use it responsibly — a skill that’s incredibly valuable in any career path.

And finally, managing all the moving pieces of this semester really tested — and improved — my organizational skills. Being my fifth and final year here at Concordia came with some exciting opportunities to show off what I have done and learned such as senior chemistry seminar. This added to the process of balancing academic deadlines, looking for my next career step, and other outside commitments which forced me to plan ahead, stay focused, and adjust when things didn’t go exactly as planned. I struggled a lot with staying healthy this and last semester which really took me out of the flow that I have gotten used to being in during college. The previous semester showed it in terms of my academic performance and my struggles with bouncing back from being behind. However, I think I was able to learn from that experience, and even though I was dealing with similar issues this semester, I handled the situation much better and got back into the swing of things much more efficiently. I can honestly say I’m ending this semester more confident in my ability to stay organized and handle competing priorities, which will definitely help me moving forward.

Overall, this course — and my education at Concordia more broadly — has instilled in me a deep love for learning, an ability to think across disciplines, and a commitment to being a responsible, engaged participant in the world. I now see liberal learning not just as an academic ideal but as a lifelong practice — one that calls me to continue growing, questioning, and contributing, wherever my future may take me.