AP Biology class blog for discussing current research in Biology

Author: katealyst

New Potential Cancer Treatment!

CRISPR, a cutting-edge genetic technology, shows potential in fighting cancer by modifying genes responsible for triggering tumor formation. It works by using enzymes to target and modify specific sections of DNA. Scientists are exploring different ways to use CRISPR in cancer treatment. One way in which scientists are exploring using this new technology is by turning off harmful genes such as MYC

The MYC oncogene can affect cellular activities such as the “cell cycle, apoptosis, DNA damage response, and hematopoiesis”. When this gene gets deregulated, it can lead to the emergence of a range of cancers. In AP Bio, when reviewing cancer biology, we learned that an oncogene is a gene that has potential to cause cancer when it is mutated. Mutations or alterations in these genes can lead to their abnormal activation or over expression, disrupting normal cellular processes and contributing to the development of cancer. Specifically we learned that an oncogene is like a gas pedal that is stuck down, causing cells to divide uncontrollably. Because MYC is an oncogene, it can cause a variety of cancers which is what makes this new technology so important and current. Having worked at a summer camp for children with cancer and their siblings, I have seen how much cancer can disrupt not only a child’s life, but an entire family’s life. Research on CRISPR gives me hope. 

Furthermore, scientists also aim to use CRISPER in boosting the body’s immune response against cancer cells, and fixing genetic mistakes that cause cancer. This technique uses the CRISPR-Cas system which guides RNA molecules to locate and eliminate cancer cells while sparing the healthy cells. The process involves designing guide RNA molecules to bind specifically to cancer cell DNA, loading them onto a CRISPR-associated protein (Cas) complex, and introducing this complex into the one’s body through different methods. Once inside the cancer cells, the CRISPR-Cas complex cuts cancer-causing genes, leading to cell death. The goal is to make this approach viable for clinical use. In this photo, you can see the A pairing with T and C pairing with G which is something else we have learned about in AP Bio. 


The schematic diagram of CRISPR-Cas9

A New Way To Treat Genetic Epilepsy?!

Researchers at the Francis Crick Institute have discovered a promising treatment for CDKL5 Deficiency Disorder (CDD). CDD is a form of epilepsy that affects children.  Some symptoms included seizures, impaired cognitive development, and repetitive body movements. CDD is a devastating condition that can make a family’s life very difficult. Furthermore, it is a complicated disorder to manage. CDD was first identified in 2004 and as of now, the only treatment is medications to manage the symptoms. That is why this possible new method to treat the disorder is so interesting to me. A possible cure would change many lives. This video tells the story of a family with a child diagnosed with CDD.

CDD is an X-linked disorder. X-linked disorders refer to genetic conditions that are associated with mutations in genes on X chromosomes. This means that if a male is carrying this mutation, they will be affected because a man typically only has one X chromosome. A woman, on the other hand, typically has two X chromosomes so if she has a normal gene on the other X chromosome then she would likely be unaffected by the mutation, but has the risk of passing it on to her child. The ratio of boys affected by CDD to girls affected by CDD is roughly 8 to 1 according to PubMed Central.

Figure 13 01 05

CDKL5 stands for cyclin-dependent kinase-like 5 which is a gene located on the X chromosome. CDKL5 is involved in the “formation, growth, and movement of nerve cells” (MedlinePlus). We know from AP Biology that a kinase is an enzyme that catalyzes the transfer of phosphates groups. This enzyme transfers a phosphate group to different proteins that alter specifically brain function. We know that kinases are involved in signaling pathways which makes them essential for coordinating cellular responses. Specifically in AP Bio, we looked at tyrosine kinase receptors. In this case, the kinase removes a phosphate from ATP to add it to tyrosine to created a fully activated phosphorylated dimer which will control cell growth and cell division. CDKL5 codes for an enzyme that plays a role in brain function and is responsible for the synthesis of proteins that help the brain develop.

Researches had the idea to boost another enzyme’s activity to make up for the lack of CDKL5. They looked at mice who lacked the CDKL5 enzyme. Scientists measured the level of a molecule that is targeted by the CDKL5 enzyme called EB2. In the mice that did not produce CDKL5, researches still found that EB2 was being phosphorylated so there had to be a different enzyme similar to CDKL5 that was phosphorylating EB2 by transferring phosphates. EB2 was still getting phosphorylated because CDKL2 (cyclin dependent kinase like 2) was identified instead. Researches now aim to increase the level of CDKL2 in people who lack CDKL5 to see if this can stop symptoms of CDD from occurring. Increasing levels of CDKL2 could “uncover better treatments that could truly make a difference in the lives of the children with this devastating condition” (Margaux Silvestre).

My hope is that this research will not only help children with CDD, but also inspire research on other kinases and help find alternative kinases to cure more diseases.


New COVID-19 Vaccine

Did you know that different variants of COVID-19 can have SUB variants as well? Because the Omicron variant is now the world’s most prevalent strain, it has been able to mutate into different sub variants. The XBB sub variants stood out because they contain a high number of genetic mutations compared to other variants. These mutations or changes help the virus avoid the body’s immune response even if one has been vaccinated for COVID-19 already. Specifically the XBB. 1.5 sub variant (also known as Kraken) has a mutation that helps the virus bind to cells making it more contagious. Scientists believe that XBB. 1.5 binds “more tightly to cells in the human body that the predecessors” (Andrea Garcia). This was the dominant strain in June 2023. 

COVID-19 vaccines (2021) A

The updated COVID-19 vaccine is now being recommended by the CDC and has been approved by the FDA as of this September. It is a monovalent or single component version that specifically targets this sub variant of Omicron (XBB. 1.5). This vaccine is meant to broaden vaccine-induced immunity and provide protection from other XBB sub variants as well. This is similar to how the flu shot works in that the formula changes every year depending on which strain is spreading the most at the time. The vaccine will not prevent every version of COVID-19, however, unless there is a great change in the genetics of the virus, it should provide at least partial protection from other strains as well. The treatments for COVID-19 such as antivirals will still work against this new XBB. 1.5 sub variant. 

In AP Biology, we learned about the immune system and how memory T cells and B cells are made to fight the same virus in the future. A virus enters the body through a macrophage or dendritic cell. Viral antigens are then presented on the surface of the dendritic cells or macrophages and infected cells. The viral antigen then binds to the Helper T cell and causes cytokines to be released to stimulate B cells and cytotoxic T cells. This creates a memory helper T cell. B cells divide to create plasma cells and memory B cells. The plasma cells secrete antibodies for this virus. 

This process is why it is important to receive this vaccine even if one has already been infected by COVID before or if one has received the vaccine before because of the new variants such as XBB. 1.5 that are emerging. The previous COVID-19 vaccine does not necessarily protect against the XBB subvariants and having COVID-19 previously and getting those antibodies through the process described above does not mean you have the antibodies for the new strains.

I still got COVID after having the vaccine because it was a different strain of the virus than the one being targeted in the vaccine. This is very common but hopefully this vaccine means that there will be one less sub variant to worry about! 

Stimulating the Vagus Nerve Can Control Traumatic Bleeding

60,000 Americans die each year from uncontrolled bleeding and bleeding is responsible for 35% of pre-hospital deaths. New research in mice shows that through electrical stimulation of the vagus nerve, it is possible to prohibit bleeding. But, how does bleeding stop? Bleeding stops in a process called hemostasis.Figure 16.4.4 : Blood ClotAn important part of this process is the activation of platelets to form a platelet plug to prevent further blood flow. Platelets activate when a blood vessel is injured and the vessel wall constricts to reduce blood flow. Platelets are involved in the The Neural Tourniquet that becomes activated using vagus nerve stimulation. The Neural Tourniquet shows the vagus nerve and its connection to the spleen via the celiac ganglion. Stimulation of the vagus nerve harnesses the acetylcholine secreting Choline Acetyltransferase (CHaT+) T-cells to stimulate calcium uptake and alpha granule secretion via alpha 7 nicotinic acetylcholine receptors found on platelets and therefore activates platelets and accelerate clotting. This made researches believe that the splenic CHaT+ T-cells secrete acetylcholine to regulate the function of platelets. How can this be proven?

One way in which this was proven was by using immunohistochemistry to explore the interactions between the CHaT+ T-cells and platelets. Immunohistochemistry is a technique in which antibodies are used to label cell structures so we can take close up photos of cells. The zoomed out photo below is a photo of the spleen. The purple is the white pulp where lymphocytes are located and the green is the red pulp where platelets and all other circulating blood cells can be found. The zoomed in photo below shows the interactions between CHaT+ T-cells (pink with purple halo) and platelets (green) directly touching proving that the stimulation of the vagus nerve activates platelets.

The next step for this research is beginning a clinical trial to see if these interactions can exist in humans as well. Procedures will be repeated in humans. To optimize the assays for the clinical trial, flow cytometry (a technique that will allow one to study single cells using fluidics, optics, and electronics) will be used to determine which anticoagulants work best to keep the platelets from activating without an agonist.

In AP Bio, we learned about that the Rough ER is directly connected to the cell nucleus. The Rough ER is similar to the celiac ganglion in which the celiac ganglion is directly connected to the vagus nerve and allows it to connect to the spleen. The Rough ER allows the cell to function by producing proteins and the celiac ganglion allows the vagus nerve to connect to the spleen via the parasympathetics nervous system showing that their connection to other parts of the cell or body is what makes them essential.

(I took these photos at the Feinstein Institute this summer!)

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