AP Biology class blog for discussing current research in Biology

Author: deukaryota

The Quest for the Cure: Could Modified CAR T-Cells Using CRISPR Technology Be the Key?

Cancer: difficult to talk about, but even harder to cure. Unfortunately, most, if not all of us have lost loved ones due to cancer, the disease which took the lives of over 600 thousand Americans in 2022. Lymphoma, one of the most common types of cancer, is cancer of the lymphatic system, which is part of the body’s immune system and includes the lymph nodes, bone marrow, thymus gland, and spleen. Although scientists have not yet discovered a cure for it, scientists across the globe have made significant amounts of discoveries which could help treat lymphoma.


One promising treatment option is CAR (chimeric antigen receptor) T- cell therapy, discovered in 2002 by scientists at Memorial Sloan Kettering Cancer Center. As we learned in AP Biology, T-cells are part of the body’s immune system, and some (helper T-cells) recognize antigens while others (T-Killer cells) kill infected or cancerous cells. Helper T-cells recognize fragments of the antigen on the surface of macrophages and signal for the immune system to destroy the infected cell, a task that is often carried out by T-killer cells. When scientists modify T-cells in a lab by inserting a gene for a chimeric antigen receptor (CAR), the T-cells can better identify and bind to cancerous antigen fragments and signal for the body to destroy the cancer cells. After modifying the T-cells, they are inserted back into the patient. 

However, one major problem with this treatment is that the T-cells often get “T-cell exhaustion,” which is when they are effective and efficient at first but quickly become worn-out and ineffective. To combat this problem, Dr. Michel Sadelain altered the T-cells’ genes through the use of CRISPR technology.

CRISPR (clustered regularly interspaced short palindromic repeats) technology is a cutting-edge method of genome editing which physically cuts and/or replaces nucleotides in DNA.  

CRISPR-Cas9 editing of the genome

As we learned in AP Biology, DNA, the genetic “code” in every living thing, is composed of two strands, in the shape of a double helix, which are made of a phosphate and deoxyribose sugar “backbone,” and bases which attach to each sugar. There are four bases: A (adenine), T (thymine), G (guanine), and C (cytosine). A base, sugar, and phosphate together form what is called a nucleotide, and these are what CRISPR replaces or deletes.

DNA codes for all characteristics of a living organism, so when it is altered, the genetic makeup and traits change. This is an essential fact when considering CRISPR technology, since it can alter the base sequence within DNA, causing potentially life-saving gene alterations. Dr. Sadelain used this technology to insert a gene in T-cells which makes them more resilient and less prone to T-cell exhaustion. Dr. Park of Memorial Sloan Kettering recently proved Dr. Sadelain’s discovery to be effective in a clinical trial which used Sadelain’s method to use CRISPR to insert CARs and a molecule called 1XX into T-cells which were then injected into patients with lymphoma.  The alterations Sadelain made were intended to create T- cells that work efficiently for longer periods of time and therefore will be more effective in destroying lymphoma cells. The results of the trial were very promising since it was very successful, safe, and used a relatively small amount of modified T-cells, meaning that the treatment could be accessible to more people if it is approved.  Do you think this treatment method will be a success?

As confirmed through this trial, the capabilities of CRISPR and CAR T-cell therapy are evolving to a mind-blowing extent and are providing safer and more effective treatments for cancer and other diseases every year. Although a universal cure for cancer has not yet been discovered, the discoveries of this study could alter the future of lymphoma treatment and save the lives of thousands.

Haven’t You Heard? Hearing Loss Could Be Reversible!


Hearing loss is a problem that affects almost a fifth of the world’s population, can cause feelings of isolation, and is closely correlated with dementia. Unfortunately, despite these drastic numbers and the fact that hearing loss can greatly worsen one’s quality of life, there is no way to reverse the effects of hearing loss.  Or is there?

Neuroscientists at the Del Monte Institute for Neuroscience at the University of Rochester Medical Center believe they may have come up with just the solution. The most common cause of hearing problems is the damage of cochlear hair cells in the ear, which detect sound waves and allow mammals to hear. Sound wave detection from inner cochlear hair cells make up about 95% of the auditory nerve’s signal to the brain, and outer cochlear hair cells amplify sound vibrations.  However, although mammals are unable to regenerate these cells, fish and birds can, allowing them to fix any hearing loss that they may encounter.Ear-anatomy-text-small-en

With this new study, the scientists discovered that the activating the ERBB2 growth gene, a gene that allows cochlear hair cell growth in birds and fish, triggers “a cascading series of cellular events by which cochlear support cells began to multiply and activate other neighboring stem cells to become new sensory hair cells.” 

Furthermore, the scientists tested cells with/without the ERBB2 growth gene in mice, and they found that cells with the ERBB2 gene stimulated stem cell-like growth by inducing the expression of many proteins. One such protein was SPP1, which signals through the CD44 receptor, a receptor found in cochlear hair cells.  This response signals mitosis, a process that we learned about in AP Biology, which is the process by which cells duplicate and, thus, grow. 

The cell cycle, or the cycle of processes of a cell’s life, consists of four main phases: gap 1 (cell growth), synthesis (DNA replication), gap 2 (cell growth & organelle duplication), and cell division.  In order for a cell to advance onto the next phase of the cycle, it must first pass checkpoints that affirm that the cell has completed the previous phases and is ready to move on.   However, for cells that do not grow regularly, such as neurons and cochlear hair cells, they enter a phase between gap 1 and synthesis, called gap 0. In this phase, cells exit the regular cell cycle and cease to duplicate unless they receive a signal to do otherwise.  This is why the SPP1 protein causes cell growth: because it gives the cochlear hair cells the signal to exit the gap 0 phase, continue on with the cell cycle, and duplicate, allowing the recovery of hearing.

Activation of ERBB kinases

Growth of the cochlear hair cells would allow mammals, including, eventually, humans, to regain their hearing after suffering from hearing loss.  Scientists plan to continue researching and experimenting with this newfound information and hope to one day use this knowledge to reverse hearing loss at any stage of a person’s life.  Just think about someone you know who has hearing loss: a grandparent? An uncle? A friend? Or maybe even you? This new research about the ERBB2 gene could heal the way they listen to music, watch TV, have a conversation, and live their everyday life.


Is Brain Fog Becoming Clear?

Has anyone ever tried to talk to you the second after you woke up?  It’s almost impossible to comprehend what they’re saying within those first ten seconds that you’re awake, right? Now imagine if those ten seconds lasted weeks, months, or even years, and you’ll be imagining the life of someone with post-COVID-19 brain fog.

“Brain fog,” is a feeling of confusion, inability to concentrate, fatigue, and overall “cloudy” mindedness that is a common residual symptom of the SARS-CoV-2 virus, affecting about forty percent of people who experience “long COVID” symptoms.  Although unable to be detected through any sort of medical examination or test, post-COVID brain fog can have an overwhelming presence, causing people to be unable to work and frequently lasting for over a year.  However, because brain fog only became an extremely common complaint of patients since the COVID-19 pandemic started, scientists know very little about the symptom.

SARS-CoV-2 without background

In an attempt to discover more, scientists at Karolinska Institute, led by Carl Sellgren, researched how the SARS-CoV-2 virus affects the brain by infecting organoid brain cells with SARS-CoV-2.  The experiment revealed that the virus caused neuron synapses to be destroyed at an unnaturally high rate.  As we learned in AP Biology, neurons are signaling cells that exist throughout the body but make up most of the brain.  Neurons are not actually connected- a small gap, called a synapse, between the end of one neuron (or the presynaptic membrane) and the start of the next (called the postsynaptic membrane) separates the two cells.  Neurons signal each other by sending small particles called neurotransmitters across the synapse and into the next cell.  Another common brain cell is microglia, which are immune system cells that dispose of dead cells and repair synapses.  Microglia also destroy synapses, or connections between neurons, when they are no longer needed.  

Complete neuron cell diagram en

Sellgren’s study revealed that SARS-CoV-2 causes microglia in the brain to amplify the rate at which they destroy synapses, preventing many neurons from being able to make connections with other neurons.  Assuming that a full human brain would respond the same way as brain organoids, this discovery explains why long-COVID patients with brain fog experience difficulty thinking.  Amplified microglia activity is also associated with aging, which further supports the results of Sellgren’s experiment because people oftentimes become more forgetful with age.

With this new discovery to open the gates to more knowledge, scientists can begin to understand post-COVID brain fog more deeply and potentially hope for treatment for this symptom that affects the lives of thousands of people.

TMEM251: A Gene Come True?

Have you ever finished a painfully long math problem, only to realize you made a mistake in the very first step?  Although you probably panicked because your final answer was embarrassingly far away from the correct one, fixing your one small mistake may have actually revealed that the mess was not truly all that complicated.  Identifying the root of a seemingly drastic problem quite frequently uncovers the underlying simplicity of the matter, but who would have thought that this basic concept could save generations of victims of a viciously lethal disease?


Mucolipidosis type II is an extremely rare inherited disease that causes physical, mental, and visual deformities and usually claims its victims before they turn seven years old (oftentimes much sooner).  What causes Mucolipidosis type II?  Simply put, it is when lysosomes do not receive the enzymes necessary to digest materials, making them not only ineffective, but also dangerous.  When lysosomes are unable to perform the necessary recycling functions that you have learned about in AP Biology, materials are instead stored in the cell, causing Mucolipidosis type II and its seemingly infinite list of tragic symptoms such as scoliosis, neurological disabilities, ectrodactyly, enlargement of the heart, and more.   

Blausen 0785 Scoliosis 01

In fully functional cells, mannose-6-phosphate biosynthetic pathway, or M6P, signals the transport of hydrolytic enzymes into the lysosomes.  Inversely, when M6P is either not functional or not present, the hydrolytic enzymes do not make it to the lysosomes, causing Mucolipidosis type II.  Now that we know what happens when M6P is dysfunctional, let’s take one more step back.  What causes M6P to stop working in the first place?  Well, it turns out that a team of scientists at the University of Michigan had the same question. Lysosomes Digestion

Using CRISPR technology, the team tested individual genes’ effects on cellular functions, and they found the answer to our previous question: TMEM251.  This gene is responsible for creating an enzyme called GNPT, which signals M6P to transport the enzymes to the lysosomes, and when this one singular gene fails to work, it causes the lifelong adversities of Mucolipidosis type II.  Also, TMEM251 is located in the Golgi apparatus, and you (hopefully) already learned in AP Biology that lysosomes are created from this organelle.  Therefore, this fact further supports the validity of the new finding.

CRISPR-Cas9 Editing of the Genome (26453307604)

The disease currently has a 100% fatality rate because scientists have not yet discovered a cure.  Or have they?  Now that scientists have identified the root of the problem, non-functional TMEM251 genes, they are experimenting with enzyme replacement therapy- the supplementing of missing lysosomal enzymes into the cell through endocytosis– to rehabilitate the cells to their proper, functional forms.  It may be too early to place bets, but this groundbreaking discovery could turn out to be the hope that scientists around the globe have been searching for.

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