{"id":531,"date":"2026-03-05T05:16:25","date_gmt":"2026-03-05T05:16:25","guid":{"rendered":"https:\/\/sites.wp.odu.edu\/joneegrant\/?page_id=531"},"modified":"2026-04-18T00:02:52","modified_gmt":"2026-04-18T00:02:52","slug":"cell-biology","status":"publish","type":"page","link":"https:\/\/sites.wp.odu.edu\/joneegrant\/cell-biology\/","title":{"rendered":"Cell Biology"},"content":{"rendered":"\n
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CAR-T Cell<\/strong>
 
Jonee Grant<\/strong>
Cell Bio BIOL 293<\/strong>
February 27, 2026<\/strong>
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Medicine keeps advancing significantly and new breakthroughs continue to emerge. One of those breakthroughs comes in the form of cell therapies used to combat cancer and disease in a unique way. A unique cell being used is the CAR-T cell. A CAR is an enhancement added to a T-cell used in immunotherapy. The patients\u2019 own T-cells are modified by adding the Chimeric Antigen Receptor CAR. The addition of the CAR gives the T-cells the proper surface structure to bind to certain cancer cells and kill them (1). CAR-T cells are used in treatments for Tripple negative Breast Cancer and non-Hodgkin lymphomas as well as other hematological malignancies. As with any medical intervention there are some side effects of CAR cell treatments. Also, cell therapy is not always applicable as it depends on the patient\u2019s T-cell count to be adequate and a healthy immune system.
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CAR-T therapy is a multi-step process, with the therapy spanning over 1-2 months with once daily infusions. The patient\u2019s blood is drawn, and the white blood cells are put into a centrifuge to separate the T-cells from the blood. The CAR is added to the T-cell. The modified T-cell is then reintroduced into the patients\u2019 blood stream intravenously (1). The T-cells can now bind to the cancer cell. CAR T cells can be derived either autologously from T cells in a patient’s own blood or allogeneically from a donor. Once isolated, these T cells are genetically engineered to express a specific CAR, using a vector derived from an engineered lentivirus such as HIV. The CAR programs the T cells to target an antigen present on the tumor cell surface. For safety, CAR T cells are engineered to be specific to an antigen that is expressed on a tumor cell but not on healthy cells.
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Tripple Negative Breast Cancer or TNBC is an aggressive type of breast cancer where the. Triple-negative breast cancer (TNBC) is any breast cancer that either lacks or shows low levels of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2) overexpression and\/or gene amplification that comprises 15\u201320% of all breast cancer cases.  Limited treatment options for TNBC make cell therapies important. Immune checkpoint pathways regulate T-cell responses at distinct stages of the antitumor immune response, CTLA-4 primarily functions during the early \u201cpriming\u201d phase in secondary lymphoid organs, where it competes with CD28 for binding to B7 molecules (B7-1\/CD80 and B7-2\/CD86) on antigen-presenting cells, thereby limiting initial T-cell activation (2). These bonding sites are part of the immune checkpoint. The major histocompatibility complex (MHC) a genetic region that helps the immune system tell itself apart. By allowing peptides to be displayed on the cell surface the T-cell receptors can determine if a cell is abnormal. The tumor and the immune T-cell express the protein PD-L1 and PD-1, respectively. The T-cells PD-1 is an inhibitor that limits tissue damage and prevents autoimmunity. Some tumor cells have evolved to bond their PD-L1 to different sites on the T-cell causing T-cell exhaustion. The result is that the tumor cell is now able to get past the immune checkpoint. T-cell exhaustion causes a reduced ability to kill the tumor cell. Low cytokine production results in weak immune signaling and suppressed cytotoxic activity results in the tumor escaping the immune system (2). Some Patients with TNBC are at a higher risk of having the mutation BRCA1, this mutation maybe hereditary. Approximately 10\u201320% of TNBC patients harbor germline or somatic breast cancer susceptibility gene 1 and 2 (BRCA1\/2) mutations or exhibit homologous recombination deficiency (HRD), which contributes to genomic instability, TMB, and increased neoantigen load (3).
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CAR-T cell therapy is considered by some as a living drug as it expands and multiplies through the body. It actively seeks out cells to be destroyed, and it can remain in the body long term (3). Low activity of MHC is what causes cancer cells to bypass the immune system. CAR-T cells can bind to cancer cells without the MHC. By using a single chain variable fragment as a sensor, it binds to the tumor and kills it. The CAR programs the T cells to target an antigen present on the tumor cell surface. For safety, CAR T cells are engineered to be specific to an antigen that is expressed on a tumor cell but not on healthy cells. The surface of CAR T cells can bear either of two types of co-receptors, CD4 and CD8, which have different and interacting cytotoxic effects. When CAR T cells come in contact with their targeted antigen on a cell’s surface, T cells bind to it and become activated, then proceed to proliferate and become cytotoxic, destroying the cancer cells through several mechanisms However, drawbacks include limited targeting of intracellular antigens and the risk of treatment failure (3). While CAR-T cell therapy is groundbreaking, there are limitations. CAR cells are not effective on intercellular antigens as they are not present on the cells\u2019 surface and CARs only bind to surface proteins. The quality of the patients\u2019 T cells plays a major factor in the effectiveness. There is also cost and patient accessibility to consider. To combat some of these hurdles, batch manufacturing is considered. This would require donation of blood containing healthy T-cells. Which could lead to lower cost and better accessibility. While autologous CAR-T cells remain the primary clinical application, advances in genome engineering and production methods are paving the way for more efficient and cost-effective allogeneic CAR-T cell therapies (3).
There are five generations of CAR cells since its development in 1987.Some studies show that CAR-T cell therapy aimed at CD19 has reconfigured treatment for B-cell malignancies. B-Cell malignancies are cancers that arise from B lymphocytes which are responsible for producing antibodies. This can cause cancers such as non-Hodgkin lymphomas. In a study of CAR-T cell effectiveness against CD19, magnetic activated cell sorting was used to isolate CAR-T products to determine how each subtype aides in killing the tumor. The results showed that CAR\u2011T cells can dampen therapeutic responses and may contribute to resistance.
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To conclude, CAR\u2011T cell therapy demonstrates noteworthy progress in modern cancer treatment, offering a targeted approach to how the immune system can be harnessed against disease. Adverse reactions to the treatment are possible, these reactions can affect any organ system, with common involvement of the skin, gastrointestinal tract, endocrine glands, lungs, and liver (2). There are serious side effects that result from CAR T-cells being introduced into the body, including cytokine release syndrome and neurotoxicity. Because it is a relatively new treatment, there are few data about the long-term effects of CAR T-cell therapy, meaning there are still concerns about long-term patient survival Even though cell therapy is not without limitations, ongoing research, improved manufacturing methods, and next\u2011generation CAR designs continue to address these challenges. There are over 400 ongoing clinical trials happening globally involving CAR T cells, with most of those trials target blood cancers. CAR T therapies account for more than half of all trials for hematological malignancies. CD19 continues to be the most popular antigen target, followed by BCMA.
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References

1. Explore CAR T. Explore Cell Therapy. https:\/\/www.explorecelltherapy.com.

2. Alharbi, Shaimaa, Farah Faozi Qasem, Mahsa Taleb Talebi, Nourhan E. Omran, Rifat Hamoudi, and Rania Harati. \u201cImmunotherapy Approaches for the Treatment of Triple\u2011Negative Breast Cancer.\u201d Cancers 18, no.3 (2026): 464.

3.Buono, Giuseppe, Monica Capozzi, Roberta Caputo, Vincenzo Di Lauro, Daniela Cianniello, Michela Piezzo, Stefania Cocco, Claudia Martinelli, Annarita Verrazzo, Margherita Tafuro, Claudia Calderaio, Alessandra Calabrese, Francesco Nuzzo, Martina Pagliuca, and Michelino De Laurentiis. 2025. \u201cCAR\u2011T Cell Therapy for Breast Cancer: Current Status and Future Perspective.\u201d CancerTreatmentReviews133.

4. Sun, Y., J. Liu, D. Zhan, J. Wei, L. XianShi, R. Zhang, C. Duan, D. Zhang, X. Tang, T. Lin, L. Li, and X. Lai. \u201cDepletion of Tregs from CD4\u207a CAR\u2011T Cells Enhances the Tumoricidal Effect of CD8\u207a CAR\u2011T Cells in Anti\u2011CD19 CAR\u2011T Therapy.\u201d FEBS Journal 292, no. 8<\/p>\n<\/div><\/div>\n\n\n\n\n\n\n\n

Jonee Grant<\/p>\n\n\n\n

Cell Biology<\/p>\n\n\n\n

03\/26\/2026<\/p>\n\n\n\n

The Role of Foxo3 in Developmental Cell Fitness Surveillance<\/p>\n\n\n\n

In 2024 the Osaka University published a scientific study \u201cThe longevity factor Foxo3 mediates ‘unfit’ cell elimination to ensure healthy body construction.\u201d on a cellular quality control system called cell competition. The article states that life begins at conception, and as mitosis occurs errors that arise in the form of \u201cunfit\u201d cells are corrected with cell competition. Researchers\u2019 used zebrafish for their experiment to observe this \u201ccleaning up\u201d quality control process. The article also states that through the study they have uncovered how developing organisms identify and remove the \u201cunfit\u201d cells.<\/p>\n\n\n\n

During early development organisms depend on the preciseness of cell multiplication, mitosis, for growth and development. This is how tissues ,organs and body structures are formed. however, unlike DNA replication in meiosis which is a largely error free or quick error correcting process, cell division is complex process where each cell is self-replicating thus it has the potential to have more errors. These errors will  lead to defective cells that are compromised in their functions. Defective cells could upset the physiology or have fatal effects on organism. Cell competition is a necessary corrective process to ensure survival.<\/p>\n\n\n\n

The scientists focused on the spinal cord tissue and muscle of the zebrafish, examining how these tissues are formed during the fish\u2019s development. For the experiment, the cells\u2019 ability to initiate apoptosis was inhibited. Apoptosis is a built-in self-destruct that prevents damaged cells from self-replicating and causing harm, thus maintain a healthy environment for the other cells. This is a system that is   crucial for shaping tissue and preventing disease. Researches observed that  the blocking of apoptosis caused disruptions to the normal pattern in the spinal cord and muscle. Confirming that a programed cell death is essential. The observation also raised the question of what determines the defective cells and identified them as unfit removed?<\/p>\n\n\n\n

To answer this question the researchers utilized a protein known as Sonic hedgehog (Shh).  It is a signaling molecule that<\/strong> provides positional information to cells it tells them where to go and what to become in a developing embryo. It also creates a gradient with some areas having higher Shh levels and some having low Shh levels. Cells with abnormal Shh level for their position in the gradient showed elevated markers for apoptosis. The abnormal cells accumulated when apoptosis was blocked thus distorted the gradient. Confirming that cells with improper Shh signaling are normally eliminated to maintain correct developmental patterning.<\/p>\n\n\n\n

Now that they had an answer to the first part of their question the next step was to identify how cells sense the differences in Shh activity in the other cells around them. N-cadherin , a membrane adhesion protein was identified by the research team as a key component in the signaling that enables adjacent cells to compare their signaling sites with one another allowing them to detect when a neighbor is behaving abnormally. When an unfit cell is identified the elimination process is a specific pathway involving Smad proteins<\/strong>, Foxo3<\/strong>, reactive oxygen species (ROS)<\/strong>, and Bcl2<\/strong>.<\/p>\n\n\n\n

Foxo3 a protein linked to longevity showed expression reliably marks unfit cells in both zebrafish and mice, demonstrating that its function in cell competition is evolutionarily conserved. This positions Foxo3 as a valuable biomarker for detecting defective cells across a wide range of biological settings. The ability to precisely identify naturally arising unfit cells will deepen our understanding of developmental processes and may uncover previously unrecognized sources of cellular abnormalities.<\/p>\n\n\n\n

Refrences <\/p>\n\n\n\n

Osaka University. “The longevity factor Foxo3 mediates ‘unfit’ cell elimination to ensure healthy body construction.” ScienceDaily. ScienceDaily, 18 December 2024. <www.sciencedaily.com\/releases\/2024\/12\/241217131237.htm><\/p>\n\n\n\n\n\n\n\n

Jonee Grant<\/p>\n\n\n\n

Cell Biology<\/p>\n\n\n\n

April 17, 2026<\/p>\n\n\n\n

End\u2011of\u2011Term Reflection<\/strong><\/p>\n\n\n\n

I\u2019ve learned many things from this course, but what I am most proud of is how the material has interacted naturally with my other three courses genetics, pre\u2011calculus, and art history helping me creating meaningful connections in those subjects.<\/p>\n\n\n\n

This course helped me realize just how delicate and precise the cell\u2019s systems of checks and balances are, and how processes as \u201csimple\u201d as ion transport, cell\u2011signaling pathways, and apoptosis support nearly every major biological function. These systems became much clearer when paired with reading scientific articles demonstrating how catastrophic the consequences can be when these pathways fall out of balance. This connected directly to my genetics course, where I learned about base\u2011substitution mutations and how even a single altered amino acid can change a protein\u2019s structure such as the missense mutation that causes sickle\u2011cell anemia. The connections didn\u2019t stop there. In pre\u2011calculus, I could see how ion movement changes membrane potential in predictable, graphable patterns, showing how biological processes can be modeled mathematically.<\/p>\n\n\n\n

 Understanding the physiology behind movement added depth to how artists depict the human body; glycine, a major inhibitory neurotransmitter helps regulate motor control and prevent excessive muscle activation and an invisible process behind every life like sculpture such as Michelangelo\u2019s Bacchus<\/em>.<\/em> <\/strong>Even artists like Van Gogh, whose neurological and psychiatric struggles may have involved disrupted neurotransmitter signaling, illustrate how deeply biology and art can intertwine.<\/p>\n\n\n\n

When these connections diffuse across disciplines the material truly sinks in as a result, strengthening my understanding of both the human body and the world around me.<\/p>\n","protected":false},"excerpt":{"rendered":"

CAR-T Cell Jonee GrantCell Bio BIOL 293 February 27, 2026  Medicine keeps advancing significantly and new breakthroughs continue to emerge. One of those breakthroughs comes in the form of cell therapies used to combat cancer and disease in a unique way. A unique cell being used is the CAR-T cell. A CAR is an enhancement added … Continue reading Cell Biology<\/span><\/a><\/p>\n","protected":false},"author":23831,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"_links":{"self":[{"href":"https:\/\/sites.wp.odu.edu\/joneegrant\/wp-json\/wp\/v2\/pages\/531"}],"collection":[{"href":"https:\/\/sites.wp.odu.edu\/joneegrant\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/sites.wp.odu.edu\/joneegrant\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/sites.wp.odu.edu\/joneegrant\/wp-json\/wp\/v2\/users\/23831"}],"replies":[{"embeddable":true,"href":"https:\/\/sites.wp.odu.edu\/joneegrant\/wp-json\/wp\/v2\/comments?post=531"}],"version-history":[{"count":5,"href":"https:\/\/sites.wp.odu.edu\/joneegrant\/wp-json\/wp\/v2\/pages\/531\/revisions"}],"predecessor-version":[{"id":661,"href":"https:\/\/sites.wp.odu.edu\/joneegrant\/wp-json\/wp\/v2\/pages\/531\/revisions\/661"}],"wp:attachment":[{"href":"https:\/\/sites.wp.odu.edu\/joneegrant\/wp-json\/wp\/v2\/media?parent=531"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}