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A potential method to detect cancer and the discovery of a new cell – Medical News of May 13, 2024

by C.J. Taylor | May 13, 2024 | Medicine, Personal

Before we start, a quick announcement; I have a podcast! If you’d like to listen to these stories and more, including The Vitals, where I tell you what you need to know about topics of your choice, tune into The Vitals Podcast on Spotify, or wherever you get your podcast! Sources to each story are below!

Counting atomic ratios in yeast and mouse cells to study cancer clues

Our first story comes from researchers Ashley Maloney and Sebastian Kopf and their joint research team made up of scientists at Colorado University and Princeton University, where tools often used in geology may be able to detect cancer on the atomic level.

To understand how this tool works, we need to know a little bit of chemistry; geochemist Maloney at Colorado University explains that hydrogen comes in two main isotopes, or flavors. Firstly, you have normal hydrogen, the hydrogen that bonds with Oxygen to make good ole H₂O, and the lighter one of the two. Secondly, there’s deuterium, which is heavier, and is outnumbered by normal hydrogen on Earth by a ratio of about 6,420 to 1.

While hydrogen has only 1 proton and 1 electron, deuterium adds a neutron. Geologists have used this difference to analyze anything from the origin and flow of bodies of water to the temperature of the Earth when a sheet of ice in the Arctic was formed.

Ok, so what’s the big deal? Well, in the research, Maloney and her colleagues grew cultures of yeast and cultures of mouse liver cells. The idea is that cancerous cells use a process called fermentation (like some yeast cells or cancerous mouse liver cells) while normal cells mainly use respiration (like other yeast cells and healthy mouse liver cells). The fatty acids that both processes produce, Maloney’s team suspects, could have different ratios of deuterium to hydrogen, which could help differentiate two different processes, and by extension, differentiate a cancer cell from a healthy cell.

As a brief refresher from biology class, normal cells in our bodies use cellular respiration to make energy, in which it takes in sugar (mainly glucose) and oxygen, and spits out carbon dioxide and water, along with some juicy ATP, which your cells use for energy. Glycolysis, the first stage, takes the glucose and essentially breaks it in half, creating pyruvates and NADH (stuff for the rest of cellular respiration), and two pieces of that sweet, sweet ATP. This process is anaerobic, which means it does not require oxygen, but that oxygen is used in later stages of cellular respiration. This is important.

Cancer cells (and fast replicating cells), on the other hand, do a LOT of glycolysis, and then a LOT of a process called lactic acid fermentation. This process is also anaerobic, so as you can guess, it is common when there isn’t much oxygen to go around, like in your muscles cells during an intense workout. Cancer cells, however, are known to ferment sugar even when there is oxygen; this is called overflow metabolism. Lactic acid fermentation results in a lot of (shocker) lactic acid, and when it builds up in your muscle cells as waste, it creates that burning sensation. Unfortunately, lactic acids also weaken the parts of your immune system responsible for attacking cancerous cells, which makes this ‘waste’ a lot more valuable to the cancer’s survival.

Microscopic picture of Saccharomyces cerevisiae cells, (Credit: CC image via Wikimedia Commons) — Microscopic picture of *Saccharomyces cerevisiae* cells (Credit: CC image via Wikimedia Commons)

In the study, the team of researchers found that respiring yeast cells had a higher ratio of deuterium to hydrogen atoms than fermenting yeast cells, even in the presence of oxygen (much like blood-supplied cancer cells). The researchers also tested this with healthy, respiring mouse hepatocytes (or liver cells) and fermenting cells within a hepatocellular carcinoma, or a liver tumor; this produced similar results.

Now while this is amazing, we don’t yet have a way to detect ratios of deuterium to hydrogen in actual live patients, but the potential is hopeful. Kopf points out that “If this isotopic signal is strong enough that you could detect it through something like a blood test, that could give you an important hint that something is off.” Detecting cancer early is invaluable to treating the disease, and thanks to Maloney, Kopf, and their team we may have a new, amazing tool in the near future to do just that.

Large enrichments in fatty acid 2H/1H ratios distinguish respiration from aerobic fermentation in yeast Saccharomyces cerevisiae | PNAS <– (Original Study Paper)

Geologists, biologists unearth the atomic fingerprints of cancer | ScienceDaily

Geologists, biologists unearth the atomic fingerprints of cancer | CU Boulder Today | University of Colorado Boulder

Discovering a new “Leader Cell” by studying the process of liver regeneration

Our second story comes from Dr. Neil Henderson and his team at University of Edinburgh in Scotland, where the discovery of a new repair-cell in your liver could mean more regenerative therapies on the way.

The liver has the remarkable ability to regenerate itself. Second to only the intestines, the liver is the most regenerative organ in the body. So regenerative, in fact, that, depending on many factors, the liver can be up to 70% damaged, and within months, fully grow back (even if it may not be at full capacity). Despite this, if damage is too extensive and exceeds the abilities to regenerate (like in Acute Liver Failure, or ALF), a patient’s only option may be to have a liver transplant. However, this may change.

Healthy hepatocyte culture (Credit: CC image via Wikimedia Commons)

Dr. Henderson and his team at the Centre for Inflammation Research wanted to study how the liver regenerates naturally to potentially innovate a new curative therapy as an alternative to liver transplant. Firstly, they took human liver samples from healthy patients, patients with chronic liver disease stemming from a range of causes, and patients with ALF stemming from either Hepatitis X (not to be confused with Hepatitis A, B, C, D, or E) or APAP toxicity (overdosing on acetaminophen, more commonly known as Tylenol). They then observed the growth of hepatocytes (liver cells) in the damaged area; ALF-afflicted liver samples had more active hepatocytes than the others, prompting the researchers to focus on these samples.

Upon observation, there was a problem; while the liver did heal some of its damage by replicating cells (what’s called “cell proliferation”), it did not fully heal. To take a closer look, they sequenced genes of the liver cells, creating a pan-lineage atlas of liver cells during human regeneration. Basically, they kept track of the activity of many types of liver cells while the regeneration process took place. This is when they found a unique gene protein, ANXA2+, belonging to the new cell.

They then found this same gene expressed in a similar cell in mice and studied its functions. This cell, dubbed the “leader cell,” seemed to come out to rapidly close the wound before cell replication could repair the damage. This suggests that these leader cells prioritized preventing infection from an open wound in the liver before regrowing the liver.
This discovery paves the road for new innovative therapies as an alternative to liver transplants, utilizing these novel leader cells to regenerate a liver beyond the superpowers our body already possesses. Thanks to Dr. Henderson and his team, hope is on the horizon.

Multimodal decoding of human liver regeneration | Nature <– (Original Study Paper)

Liver study pinpoints cell that helps healing process | The University of Edinburgh

Scientists discover new type of cell in the liver | Live Science

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Let us not become weary in doing good, for at the proper time we will reap a harvest if we do not give up.
Galatians 6:9 NIV

From Antibiotics to Phages: A Healing Evolution

by C.J. Taylor | Dec 25, 2023 | Medicine

On a fateful morning at the end of September 1928, Dr. Alexander Fleming, a bacteriologist from St. Mary’s Hospital, returned to his lab in London, having taken a summer vacation in Scotland. He found his lab bench messy, but it would prove one of the greatest mistakes in history. In multiple Petri dishes grew colonies of Staphylococcus aureus (a bacteria responsible for, surprise, staph infections). Still, Dr. Fleming noticed that a mold not intended to grow in the dish had dominated the controlled environment. This mold produced chemical weapons against the bacteria, which hindered the bacteria’s growth.

It took fourteen years for Dr. Fleming to harness the antibiotic he had discovered, to refine it, and to successfully treat the first patient, a ninety-year-old woman suffering from a streptococcal infection. From then on, humanity wielded Penicillin, and other antibiotics like it, as a potent drug against diseases that would otherwise mean death: the likes of Tuberculosis, Syphilis, Tetanus, Cholera, and E. coli.

The story, however, is not over.

Antibiotics hinder or kill bacteria by targeting their vital processes — the synthesis of the cell wall (their “hard” skin), the cell membrane (their “soft” skin), proteins (their building material), and nucleic acids (their DNA) — and plenty of bacteria share these processes. Antibiotics were praised as miracle drugs to humanity, and that reputation became a double-edged sword. On one hand, antibiotics saved millions of lives, but on the other hand, antibiotics became misused. The populous began overdosing on antibiotics or not finishing their antibiotics dosage. People took expired antibiotics for illnesses, animals were fed antibiotics for their meat, and humans took antibiotics for viral infections (antibiotics do nothing against viruses).

This HEAVY misuse of antibiotics constantly applied selective pressure on virulent bacteria and presented a perfect opportunity for new bacteria to evolve. Now take this concept, multiply it over dozens of patients (who may or may not wash their hands thoroughly) in a high-traffic area — say, a city hospital — and throw in the ability of bacteria to share these drug-resistant genes. It’s all but guaranteed that a multidrug-resistant strain will eventually arise from the sickening, germ-filled ashes. Basically, humanity forced bacteria to adapt, to become resistant to our drugs. Bacterial superbugs like Tuberculosis, Gonorrhea, and Methicillin-Resistant Staphylococcus Aureus (MRSA) are already raising concern in the medical community. If nothing is done, an ultimate superbug, if you will, that is infectious, deadly, and resistant to a wide variety of antibiotics could cause the next pandemic. An ultimate superbug is the nightmare scientists are trying to avoid.

The story is still not over.

A female scientist fighting pathogens with a rusted sword

In 1915, a British microbiologist named Frederick Twort discovered the bacteriophage, a virus fine-tuned to attack bacteria. Four years later, a French-Canadian microbiologist named Felix d’Herelle came up with the concept of phage therapy: a process in which a cocktail of these phages specific to a particular bacterium is injected into the host of a bacterial infection. These microscopic assassins are so precise, so specialized that human cells and good bacteria aren’t significantly affected; the phages only kill the virulent bacteria.

As simple as that may sound, the concept didn’t gain steam back in the 20th century in favor of antibiotics. Antibiotics were better understood and much easier to mass-produce. Antibiotic treatments, in many forms, were also much easier to sell to the public than injecting literal viruses into a patient. Nonetheless, phage therapy began to receive more attention as scientists looked for effective alternatives to antibiotics. And effective, I believe, phage therapy will prove to be.

Phages are the natural nemesis of bacteria and can be found wherever bacteria are: everywhere. If bacteria mutate and gain resistance against phages (as difficult as that is, considering the many genetically unique phages that may target a few strains), they may trade away resistance to our drugs; this means phages can be used in conjunction with antibiotics as treatment. While you only receive as many antibiotics as you are given, phages are programmed to multiply using bacteria; as they kill the targeted bacteria, the phages will become without a host and stop multiplying. They’re not harmful to humans, nor are they toxic to animals (think about your pets) or the environment.

Clinical trials have shown that there is some validity to the idea. The Center for Innovative Phage Applications and Therapeutics (IPATH) at UC San Diego School of Medicine published data from ten cases of phage therapy (through intravenous injection, or through the veins) to treat multidrug-resistant bacterial infections. Seven out of the ten cases had a successful outcome; there is hope, but many obstacles remain.

There is no way to mass-produce phages as of now. Definitive doses accounting for various factors are yet to be flushed out. Finding exact phages to target specific bacteria is tricky. The human immune system may react negatively to introducing, again, literal viruses to the body. Not all phages make for suitable treatments, and some bacterial strains may not have a phage associated with them at all.

The discovery of antibiotics still stands as one of the greatest advances in medical history; one of many monumental innovations in medicine like anesthesia, vaccination, insulin, and organ transplants. Phage therapy is the next weapon to be perfected and refined in this arms race against illness, ushering a new era of precision medicine and a healthier humanity.

NIAID

IPATH

Wikipedia