AP Biology class blog for discussing current research in Biology

Tag: cancer research

Cancer-Causing Free Radicals Are the Key to Tardigrade Survival

Tardigrade (50594282802)

Many may recognize the resilience of tardigrades, the microscopic water bears that can seemingly endure any and all conditions—researchers have found that tardigrades possess this attribute because of their ability to harness free radicals, the infamous matter that causes cancer in humans.

Tardigrades have survived all five mass extinction events on Earth, and are thought to have been around since before the current eon. They can live through extreme temperature and radiation, and even the vacuum of space. But how are they capable of this immense resilience?

Traditionally, free radicals have been known to promote cancer, causing genetic mutations that allow cells to multiply uncontrollably. First, in mitosis, the mutated cell divides, then its offspring divides, and before long a mass forms. That mass, or tumor, grows uncontrollably, consuming vital nutrients and mechanically interfering with the body’s internal function. If left unchecked, the tumor will eventually overwhelm the body’s ability to survive. However, there’s a flip side to free radicals.

The tardigrade has managed to harness the destructive power of free radicals in its quest for survival. For years, scientists have been baffled by the tardigrade’s ability to undergo drastic transformation in times of extreme stress. The organism’s transformations are a part of cryptobiosis, which consists of (but is not limited to) anhydrobiosis and cryobiosis. In anhydrobiosis, the tardigrade decreases its water content by 99% and its metabolic rate by 99.99%, and remains in a “tun” state for five years or more, only to rehydrate and flourish once environmental conditions are back to normal. In addition, via cryobiosis and other cryptobiosis processes, the tardigrade can survive extreme heat (304° F) and cold (-458° F). And the trigger for all of these survival mechanisms: free radicals, the same extra-electron atoms and molecules that cause human cells to mutate and multiply to form tumors.

Recent research suggests that tardigrades initiate cryptobiosis and protect themselves by releasing intracellular reactive oxygen species (free radicals) that in turn reversibly oxidize cysteine, an amino acid that acts as a sort of regulatory sensor for responses to stressors. The obvious question is: why isn’t the tardigrade harmed by the free radicals? The answer might hold the key to better understanding how to prevent cellular mutation, and cancer, in humans. Additional investigation is needed in this area.

So, what do you think? Are there similar discoveries that may be able to help us combat cancer?

Researchers Discover Hacking Enzymes as New Cancer Treatment

We all know that mutations occurring in the synthesis of our cells lead to cancer, whether that be via ultraviolet light radiation, the inhalation of cigarette smoke over a long period of time, or otherwise. But how do these mutations actually occur, and if modern science knows that much, why can’t scientists step in before the mutation occurs in the cell and stop the creation of a cancerous one altogether? While the answer to this is evidently easier said than done, researchers such as Szymon Barcawz, Rahul Bhomick, Malgorzata Clausen, Marisa Dinis, Masato Kanemaki, Ying Liu, Katrine Lundgaard, and Wei Wu have found a way to limit the success of cancer-yielding cell mutations. 

In this study titled, ‘Mitotic DNA Synthesis in Response to Replication Stress Requires Sequential Action of DNA Polymerases Zeta and Delta in Human Cells,’ researchers studied the replication process of cells, also known as mitosis, in human body cells (all human cells except gametes, sex cells). In order to understand the study fully, a few biological concepts should be covered first; For starters, the activation of the oncogene in relation to developing cancer. ‘Oncogene’ is simply a term for a mutated cell which turns cancerous. The activation of such creates disorder to cells going through mitosis called DNA replication stress, the name of which essentially reveals its effect: when genetic material is being synthesized under these conditions, it is extremely difficult for the mitotic cell to correctly replicate, causing faulty, under-replicated DNA regions (UDRs) to be built. Since DNA replication is completed in the S phase of interphase, which technically is before the commencement of mitosis in a cell; enough genetic material needs to be available for the cell to split in order for it to be replicated. Therefore, if UDRs are going to occur in a cell, they are created during this time. 

However, our cells have developed clever adaptations to attempt to fight this type of cellular mistake. The strategy includes performing “‘unscheduled’ DNA synthesis in mitosis (termed MiDAS) that serves to rescue under-replicated” genetic material (Barcawz et al.). In studying this cellular defense mechanism, these researchers have discovered how exactly cells make up for a faulty S phase (the phase which copies DNA during mitosis) utilizing DNA gap-filling mechanisms (REV1 and Pol ζ) and DNA polymerases (group of enzymes) whose sole purpose is to replicate unfinished genomes (Pol δ). The study’s main goal, however, was to reveal which of these polymerases was the most crucial in the “rescuing” of under-developed genetic material, which were not, and which were not really necessary at all. 

The researchers were most interested in studying POLDI (a subunit of  Pol δ), REV 1, and REV 3 / REV 7 (both subunits of Pol ζ).  These are all different polymerases whose main job is to “[promote] the bypass of damaged DNA sites” (Barcawz et al.). Each one works to solve a different issue within DNA replication that could lead to a mutation. For example, a TLS polymerase called Pol ζ4 is better at “bypassing bulky regions” of genetic material than the others (Barcawz et al.); this can be defined as Pol ζ4’s ‘role.’  

A crucial realization in this study was that the polymerases Pol ζ and Pol δ may actually be switching roles at some point within the rescuing process by switching their subunits, which we defined earlier as POLDI, and REV3 / REV 7. But, this still doesn’t answer the question of whether or not all the aforementioned polymerases are essential in the process of fixing mutations in the copying of genetic material during mitosis. 

The study at hand was successful at answering this question. It found that POLDI, REV1, and REV 3 are crucial to MiDAS, while REV7 is not at all. Additionally, it was discovered that POLDI and REV1 colocalize with another substance (FANCD2) in mitosis, which reveals how they both indeed play a role in the ‘rescue’ of under-replicated regions” (Barcawz et al.).

However, something unexpected about REV1 was also discovered. While it was found to be useful in mending UDRs in conjunction with POLDI and FANCD2, it actually does more harm than good: When REV1 was removed from the rescuing process in a situation where all the cell’s defense mechanisms failed at stopping the synthesis of a cancer cell, cancer cells were much less likely to survive in the human body. This suggests that it is very possible for a new and effective way to treat cancer to be the inhibition of the presence of REV1 polymerase. 

In the coming years, if the inhibition of REV1 is found to be possible and turns out to be a promising way of preventing cancer cells from surviving in the body, we could be looking at a groundbreaking advancement to modern medicine and the world of cancer treatment as we know it changing forever.

Cancer cells

Real image of cancer cell under a microscope.

A new evolution in cancer metastasis research


Perhaps the greatest fear of any cancer patient is metastasis.  According to Cancer.Net, metastasis is the process by which cancers spread throughout the body.  Furthermore, according to, “Metastatic cancer is notoriously difficult to treat, and it accounts for most cancer deaths.” However, a new study in Nature, as outlined in an article in The Scientist, unearths new truths about how cancer cells metastasize that could perhaps spark a new wave of research.  

As stated in The Scientist, “Previous studies have shown how, counterintuitively, cells pick up the pace as they move through thicker solutions.”  Recent studies have elaborated on this accepted facet of cancer reaction, and have discovered that Cancer cells have the ability to detect, and even memorize the viscosity of their environments.  Researchers noticed that cancer cells initially exposed to viscous environments retained their speedy movement even after they were moved to watery environments, at a level not represented in those constantly in watery solutions, thus indicating a sort of memory of environment in cancer cells.  This phenomenon of “cell memory” is similar to the memorization features seen in T-memory cells we discussed in class during the unit on the immune response.

Breast cancer cell (2)

Later, that same team of scientists released study that aimed to determine how cancer cells are able to move quickly through viscous substances.  According to an article in The Scientist, “cancer cells move by taking up water at the front of the cell and squirting it out the back, propelling themselves like octopuses through narrow spaces.”  Some researchers believe that new drug research could aim to target the ion channel that causes this transportation: TRPV4, but others are not so convinced.  According to Miguel Valverde of Pompeu Fabra University, “Animal knockouts for the TRPV4 channels develop normally,” indicating that the newly discovered transportation mechanism may not be as essential as researchers may believe.

Still, the discovery of a new transportation method for cancer cells explaining its peculiar preference for viscosity is an important breakthrough, that will undoubtedly guide future research in cancer metastasis. 

For Cancer Cells, it’s Halloween All Year Long– New Research Finds That They Masquerade as Normal Cells by Covering Themselves in “Sugary Costumes”

Dr. Rachel Willand-Charnley and her team of biochemist researchers at South Dakota State Univerity have achieved a “sweet victory” in cancer research. Their recent findings determine how cancer cells utilize sugar to deceive our immune systems. Their research suggests that cancerous cells mimic normal cells’ glycans due to genetic mutations, and because of this similarity, the immune system then confuses the cancer cell for a normal, healthy cell. This is because glycans on cell membranes of the cell are inspected by T-cells belonging to the immune system

Macs killing cancer cell

This is revolutionary to understanding the behavior and function of cancer cells which could help create more effective cancer treatments. Potential new treatment methods include stripping or altering the sugary layer of the cancer cell, allowing the immune system to recognize it as a threat and take care of it itself.

Milestones in cancer research are significant because as of right now, there is no cure for it. As we have learned in AP Biology, normal cells comply with signals that direct themselves into apoptosis, or programmed cell death. This process involves the expulsion of lysosomal enzymes into the cytosol which kills off the cell. This occurs when the cell is deemed inefficient or unable to function. If cancerous cells are detected by the immune system, those cells could avoid destruction by evading apoptosis signals and continue to progress within the human body which often leads to death. 

How could a cancer cell bypass something like this? Well, it seems that their newly adapted sugary coating could play a role in avoiding those signals. This is because T-cells from the immune system inspect glycans in the extracellular matrix for deviations. When deviations are present, an immune response is triggered, which could also trigger apoptosis of the deviated cell. So, the modified glycans on the cancer cell’s extracellular matrix help cancer evade a process like apoptosis.

Isn’t it astonishing that a single genetic modification could actually make cancers resistant to immunotherapy and chemotherapeutics? What do you think about this discovery?


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