BioQuakes

AP Biology class blog for discussing current research in Biology

Author: megillies

The “Most Complicated” Cancer Treatment EVER

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On April 23, 2023

In Student Post

There are many approaches to treating cancer, ranging from invasive surgeries to extremely damaging radiation and chemotherapy.  The teeny-tiniest clinical trial ever began at UCLA in yet another attempt to find another way to eradicate cancer.  With only 16 participants, this trial combined two areas of research: gene editing and T-cell engineering.   The reason for the miniscule sample size is the intensely customized nature of the treatment.  Each patient’s tumor had completely unique mutations, so each patient needed equally unique T-cell engineering through gene editing.  

One reason cancer is so hard to treat is because they have adapted to be resistant to the body’s own immune response.  The patients that have cancers, especially ones in the later stages, have lost the battle against their cancer with their own immune system, so a new super-immune system must now be built.  This army of new T-cells (white blood cells, which identify and kill bad cells, seen below) will need “training” for its difficult battle ahead.  First, however, the researchers must determine how to train these cells so they will actually be successful.  They used algorithms to find identifiable mutations in the tumor, something that the T-cell can seek out to differentiate the cancerous cells from the normal cells.  Healthy Human T Cell

After testing to make sure that the T-cells can actually identify these mutations, T-cell receptors are designed specifically to their tumor.  Then, each patient’s blood is taken so that the DNA code for the new receptors can be inserted using CRISPR,  a genome editing technology at the cutting edge of genetic medical research.  The DNA code is transcribed to mRNA, which is then used in the ribosome to build polypeptides, in this case, the receptor proteins for the T-cells.  In order to ensure that these new T-cells (with the special receptors) are received, the patients had to take medication that suppressed the number of immune cells, so that the ones they are given can take hold.  

One month into treatment, 5 of the patients’ tumors stopped growing, and only 2 of the participants had associated side effects.  Although only 5 patients had the desired results, Dr. Ribas, one of the researchers, says that they “need to hit it stronger the next time” because they were limited to a small dosage of T-cells to start in order to establish safety.  Additionally, the technology will only get better and better as the research progresses and the T-cells can have more and more mutation targets to look for in a tumor.  

Attention all Concert Attendees: Hearing Loss Is Potentially Reversible

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On March 16, 2023

In Student Post

Organ of cortiThe most common cause of hearing loss is the damage and loss of cells that grow the hairs inside the inner ear.  These cells are aptly named cochlear hair cells.  Repetitive exposure to loud environments, such as construction zones, concerts, or military bases can damage these cells, which, until recently, were thought to be irreplaceable.  Normally, these cells enter the G0 phase after initial development ends when the organism is mature, which makes them similar to the brain cells we learned about in class.  When a cell is in the G0 phase, it is frozen in the cell cycle, so the cell does not proceed through mitosis.  This means that once the organism is done growing, there is no replacement of the damaged cells, as no cells are dividing.  

In the animal kingdom, however, these cells are known to regenerate.  Birds and fish have a mechanism which relies on a gene called ERBB2.  The artificial expression of this gene in mammals has also been proven to trigger cell growth in a trial led by Jingyuan Zhang, PhD.  They found that activating the ERBB2 gene triggered a cascading series of cellular responses which made the active cochlear hair cells multiply as well as trigger stem cells to become cochlear hair cells. 

The research found that the activation of the ERBB2 gene caused stem-cell like development through the expression of a few proteins.  The most important protein to this process, SPP1, signals the CD44 receptor, which exists on cochlear hair cells.  The theory is that because these receptors are triggered, they somehow promote mitosis in the cells.  The promotion of mitosis, the process of cell division in the cell cycle, would mean that these cells could be reproduced and the damaged cells could be replaced by new cells. 

When this process was tested in adult mice, this cascade happened as previously shown in growing mice, meaning that the possibility of the development of new cochlear hair cells is possible in mature mammals, it just needs to be stimulated correctly.  

The next step in the research is to determine whether or not these new cochlear hair cells are functioning mechanically. I don’t know about you, but I would maybe not stop wearing my earmuffs to use a jackhammer if I were you.  

Pockets Galore! Pockets of COVID-19 Antigens are Stuck in the Body and are Causing Long COVID

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On December 8, 2022

In Student Post

Do you know someone who has long COVID? It turns out that they may have pockets of SARS-CoV-2 hiding in their body! 

Researchers at University of Colorado’s Anschutz Medical Campus have found in a recent study that patients who suffer from long-term COVID symptoms (called PASC) have 100x more SARS-CoV-2 specific T cells than those who have recovered fully from the virus.  This discovery suggests that the virus itself lingers in the body, not that symptoms continue even after the virus has left.  

This evidence will allow doctors and researchers to shift the mentality surrounding treatment of PASC, as prevPaxlovidiously the only option was to treat exclusively the symptoms.  The shift has led them to antiviral medications (such as Paxlovid) and vaccines, both of which use adaptive immunity to their advantage.  The study found that the body’s natural adaptive immune response focused on systemic inflammation, pulmonary symptoms and reduced lung function because of the high levels of T-cells in the body.  The T-cells are very important in the primary stages of the infection because they help identify and destroy infected cells, however after controlling the infection, it creates longer symptoms, along with continued shortness of breath and lung damage.

About 20-30% of patients infected with COVID developed PASC.  Over the course of over 500 million COVID infections, healthcare systems are pressed to support 150 million patients with lasting symptoms, so a solution is a priority for physicians.  The upcoming solutions’ primary goal is to clear the virus from the body entirely so that T-cell levels decrease back to a normal level.  

In addition to identifying the higher levels of T-cells, the researchers found that the higher the level of SARS-CoV-2 specific T-cells there were in the body, the higher the inflammation levels there were in the body, showing that the T-cells play a role in creating lasting inflammation associated with PASC.  

The next step for the researchers is to continue to do research on the differences in lung cells between people with PASC and people who have not had COVID.  They claim that this research is vital because the “kitchen sink symptomatic treatments have not solved the problem” (Palmer).  

Shhhhhhh! Some Viruses Can Sneak into Cells and Cause Cancer

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On October 27, 2022

In Student Post

Viruses! We all hate the colds we get in the fall that come with a cough, a runny nose, and a sore throat.  These bugs have gone around since nursery school, so we were taught that viruses were transmitted through touching door knobs, getting coughed on, and touching someone who is sick.  While these are how viruses are spread from person to person, the infection that occurs on a cellular level is much more complex.  

For starters, only a handful of viruses are known to actually cause illness in humans, but the ones that do have adapted to do it very efficiently, and some are even known to cause cancer.  Viruses that cause cancer include human papillomavirus, Kaposi Sarcoma-associated Herpesvirus, and Epstein-Barr virus.  The way that these viruses get into the cells is very unique compared to the common cold virus, and a team at the University of Michigan Medical School decided to take a closer look at just how they invade to try and get a better grasp on how to prevent cancers caused by viruses in humans.

The virus they researched is called SV40 and it causes tumors in monkeys.  The way that SV40 infects monkey cells is by burrowing itself through the cell membrane and then into its nucleus in order to duplicate itself.  SV40 is used as a tool to understand how the cancer causing viruses work because of the biological similarities that monkeys and humans have.  An earlier team studied how SV40 travels through the cell.  It goes from the surface, through the endosome, the ER, and then enters the cytosol.  

The most recent study illuminates the rest of the virus’ passage through the cell. The way SV40 gets into the nucleus is through the nuclear pore complex.  This is how many viruses enter the nucleus, but the SV40 is too large to enter through this pore.   The virus must disassemble in order to gain access to the nucleus. This process partially disassembles the virus into a smaller package made of two proteins and genetic material (DNA).  As we have learned in class, the DNA is the macromolecule that codes for how to build the proteins that build the virus.  When the DNA for the virus is connected with the two proteins, it uses both the nuclear pore complex and another complex called LINC.  LINC connects the two membranes of the nucleus together.  Many other viruses grab onto the little fingers sticking out of the nuclear pore complex (seen below), while SV40 seeks out LINC in order to get into the nucleus.  

202012 Nuclear pore complex

The difference in entrances between more common viruses and SV40 could be what makes SV40 cancer-causing.  The next step is to research how SV40 exploits LINC in order to expand upon how other diseases could enter the nucleus, and hopefully find a way to trigger the immune system in order to expel or digest the viruses before it is too late.  

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