Tag Archives: cancer

Yeast Matters

The cover photo is a cultivation plate with yeasts grown as a shape of heart on it.

Yeast on a cultivation plate

Yeasts appear in our life in many forms: the yogurt we drink, the bread we eat, the beer we love. We cannot live without these magnificent creatures, even though we cannot directly see them with our naked eyes.

But yeast matters even more than we think: currently, scientists are using special strains of yeast to develop drug targets that might be the key to discovering new treatments to fight human cancers. Why yeast?

The simplicity of yeast cells makes them a suitable tool for modern scientists to genetically engineer, study, and gain insights about human cells. More importantly, we bear disturbing similarities with yeasts. For example, the cell structure of yeast is almost identical to that of human’s cell but simpler.

Besides, yeasts also have two different genders: MATa and MATα (like male and female), just like us. But, because they do not have eyes, they have to find their “soul mates” with pheromones—a or α factor (chemicals released into the environment to send information).

During sexual reproduction, both MATa and MATα need to be physically in touch with each other for the exchange of genetic information. To locate the other type, yeasts can sense the pheromone produced by the opposite sex.

After knowing the existence of their partner, yeasts will extend toward the other type through a series of reactions including sensing, passing, and responding to the outside signals. Scientists can use those characteristics to artificially activate or deactivate the signaling pathways.

For example, in the experimental setting, we trick the yeasts. By using a single type of yeast cells (MATa), we can artificially add α factor to trigger the yeasts to grow towards imaginary partners (poor yeast!), which will activate the mating pathway. This procedure gives us greater control over the experiment to discover the function of similar pathways in humans.

Cells, including those of yeasts and humans, are like life factories. DNA is similar to a manager that controls the production: various types of proteins, which are made by different combinations of amino acids following instructions (mRNA). However, in both human and yeast’s cells, DNA usually stays in the nucleus and does not directly respond to outside changes. Therefore, little messengers on the cell membrane (receptors) need to find a way to inform the cell about certain changes, such as noticing the opposite sex.

Similarly, receptors often cannot leave the membrane as well, so they usually pass the information through a chain of signaling events using proteins, such as kinases (another type of messengers). For example, in the yeast mating pathway, the pheromone binds with receptors on the surface of the cell, a series of responses are triggered and will result in the changing of expression of the yeast gene.

In human cells, once the pathway for receiving information is messed up, cancer might grow.

Thus, finding out how signals are passed or received in yeast cells may tell us more about the origin of cancers and even provide a solution. There are multiple kinases linked to each other that change protein production in response to outside signals as shown in Figure 1. According to Wang and Dohlman, this signaling pathway in yeast is similar to those in human cells, which makes yeast a great tool for understanding our own cells.

Figure one explains the relationship between differenct components of yeast mating pathway to show the chain of command

Figure 1: Chain of command of yeast mating pathway

The cell must change constantly to fit the environment, which means the signaling pathway can also be regulated. For example, Dr. Dohlman explained that as you drink more and more coffee, you may find its effect diminishing, because the receptors are saturated with the stimulus (they are too busy to manage more messages), which is the result of desensitization.

Problem with pathway regulation is one of the reasons for messed up signaling that may cause cancers. Once we find out the function for each component of certain pathways in yeast, we may apply the results on human cells to find the targets in the problematic pathways.

Although it was mentioned above that DNA, the manager, does not usually respond inside the cell, histone methylation is an exception of pathway regulation. DNA is like a long, thin wire, so it needs to be organized and packed. Histone is a cube-like protein that allows DNA to twist around it in order to form chromosomes. The methylation of histone will add methyl groups, like little arms, to the histone, which will make the DNA wraps tighter or looser. Thus, the production of “the factory” will increase or decrease depending on where the methyl groups are added.

In human cells, SETD2 gene provides instructions for methyltransferases, which can perform such gene regulation. The mutation in SETD2 may lead to clear cell renal cell carcinoma (cRCC), a type of kidney cancer, according to Duns, or high-grade gliomas (HGGs), a type of brain tumor, based on Fontebasso’s result.

In yeast, SET2 gene codes for Set2 protein, the only methyltransferase that has such function. SET2 is like a close cousin of SETD2. Thus, studying how SET2 may regulate the mating pathway can shed light on the function of SETD2 in human cells that may provide a potential solution for drug targets.

Yeast has been studied as a standard model for years, which means we know all of its gene and numerous ways to manipulate different parts of its gene. It is a common practice for geneticists to remove or add certain genes into the yeast, just like LEGO pieces, to study the functions of genes.

For the purpose of studying the function of SET2, we can simply remove the SET2 in yeasts, grow them, and compare them with normal yeasts. In contrast with clinical trials or experiment on human cells, which usually take months or even years, it only takes less than a week for the yeast to show the influences of the missing gene.

Besides, with one single experiment, there are about 10,000,000,000 (ten billion) yeast cells involved, which are more than the combination of human’s population of the entire planet. This great number of samples provide an advantage for a more accurate result. We can now easily monitor the difference in mating pathway with the removal of SET2 to figure out how it influences the signaling pathway.

With the help of yeasts, scientists can solve human medical mysteries more efficiently. So please do not treat yeasts like magical little creatures that can only enrich your dinner; they are pioneers for human health research. Yes, yeast matters, and it matters more than you think.

By: H. Wang


Dohlman, H. G. (2002). Desensitization: Diminishing returnsNature418(6898), 591-591.

Duns, G., van den Berg, E., van Duivenbode, I., Osinga, J., Hollema, H., Hofstra, R. M., & Kok, K. (2010). Histone methyltransferase gene SETD2 is a novel tumor suppressor gene in clear cell renal cell carcinomaCancer research70(11), 4287-4291.

Fontebasso, A. M., Schwartzentruber, J., Khuong-Quang, D. A., Liu, X. Y., Sturm, D., Korshunov, A., … & Fleming, A. (2013). Mutations in SETD2 and genes affecting histone H3K36 methylation target hemispheric high-grade gliomasActa neuropathologica125(5), 659-669.

Wang, Y., & Dohlman, H. G. (2004). Pheromone signaling mechanisms in yeast: a prototypical sex machineScience306(5701), 1508-1509.

Image Credits:

Wang, H., “Yeast Matters”

Wang, Y., & Dohlman, H. G., “Pheromone signaling mechanisms in yeast: a prototypical sex machine


Medicine’s Very Own Mini Militia

nanobots and tumors

Nanobots surrounding cancerous tissues.

For the past 5,000 years, mankind has been arduously battling one of the most complicated diseases ever to exist: Cancer. Cancer has ravaged our world and overwhelmed centuries of medical science and technology. Just in 2018, it claimed the lives of an estimated 9.6 million humans and more people are being diagnosed with  this disease daily. The need for a cure has been imminent for a very long time now. Humans have dreamt and imagined different ways of gaining the upper hand in this archaic war.  From as early as the late 60’s, science fiction has portrayed nanoscale methods of curing human diseases, most especially cancer, in movies and books. At the time, one could only dream of such ever becoming a reality.  How often are the movies true and applicable to reality? It seemed like a dream and even now, many people are still dreaming of such advancements in technology.  Dream no more- a new scientific technology, known as nanomedical technology, may have the potential to end the war on cancer.

With the discovery of nanomedical technology, scientists have been able to create the world’s very first set of microscopic nanorobotic soldiers. These nanobots, as they call them, are carefully loaded with clot-forming proteins, such has thrombin, or chemotherapeutic drugs like methotrexate are able to track and kill cancer cells in different ways- the worlds very first microscopic spec ops mission. This incredible feat was achieved through nanomedical technology which started in the early 2000’s after being coined out of nanotechnology. Originally, it was not given much attention as it seemed impractical at the time but as years passed and our knowledge of technology continued to increase, it became more prominently known worldwide as a potential treatment of a wide range of diseases. The method of operation of this technology is characterized by swarms of nanoscale robots that swim through the blood to find the source of a diagnosed disease and then either administer drugs to that specific site or use in-built machinery like drills to destroy the source completely. For cancer treatment, they are designed to locate and destroy tumor cells or cancerous growths as the case may be.

Nanobots can be designed in different ways depending on the function they are intended to serve. The simpler nanobots, usually designed to cut off tumor’s blood supply, have simple structures analogous to any fuel tanker: a cylindrical containment containing cargo. The cylindrical containment is designed from an M13 rectangular bacteriophage DNA sheet using a technique called DNA origami which is characterized by folding DNA on an extremely small scale. Attached to the rectangular sheets are 4 thrombin enzymes designated at specific locations in the middle, tumor-targeting DNA at the vertices of the rectangular sheet and fastener strands that fasten the nanobot into a tubular shape in order to protect the thrombin cargo.

The tumor-targeting DNA is then able to track tumor cells by binding to specific proteins located only on tumor cells. When this happens, the tubular nanobot is unfolded and the thrombin cargo is released into the blood vessel and the body responds naturally to the thrombin’s presence in the blood by forming a blood clot in the blood vessel, blocking the supply of blood to the tumor and causes the tumor to die due to oxygen shortage.

A group of scientists from Arizona State University and the National Center for Nanoscience and Technology of Chinese Academy of Sciences actually manufactured a large number of these nanobots and studied their effects on the progression of cancerous tumors in mice models to see if they actually perform as intended. Incredibly, the median survival time of the mice was increased and the mice showed signs of tumor regression.

Another group of scientists from medical science universities in Iran, used nanoparticles (another name for simple nanobots) loaded with chemotherapeutic drugs, doxorubicin and methotrexate, on rats with chemically induced cancer to assess their efficacy as opposed to orally delivering these drugs. The nanoparticles proved to be more efficient as they caused a significant drop in the rate of cancer cell proliferation as well as the degree of malignancy of the tumors. Below is an infographic explaining the structure and design of these nanobots.

Cylindrical nanobots

Image of the structure of simple nanobots and their function in treating tumors

The more structurally complex nanorobots however, have designs hypothesized to contain nanoscale biosensors, radiation cameras, drills and chemotherapeutic drug storages embedded into a machine roughly half the size of a cell. Given the difficulties of creating something so tiny, the hypothesized nanobots would be printed using 3D printers and loaded with drugs using specially designed machines.

Prior to being injected into the patient, the patient would be given a dose of radiotracers, a harmless radioactive substance that accumulate at regions of cancerous growth. Once deployed, the battalion of nanobots use their gamma ray cameras to detect positrons emitted by the radioligands in the radiotracers and calculate the shortest possible path towards those regions using its microprocessors. After determining which route to take, the nanobots use motors designed to flow with the blood and biosensors to dodge blood constituents and obstacles until it reaches its destination. Once at the target, the nanobot is remotely instructed to inject chemotherapeutic drugs to the cancerous cells, or drill through them entirely in a completely painless procedure. Amazingly, after these soldiers accomplish their mission, they are instructed to go through the body’s excretory system and come out in your feces.

Currently, seeing as modern technology does not have the capabilities of creating a nanoscale robot packed with so much equipment, large prototypes of this hypothesized design are being experimented. One scientist, R.Maheswari, has manufactured a prototype for the nanobot. The prototype is able to use the navigation system of a nanobot to successfully maneuver obstacles courses designed to mimic the bloodstream. Right now, the only problem he faces is to scale the robot down to nanoscale.

Even though this breakthrough sounds promising, this technology has a long way to go before it becomes widely used as a medical treatment but on thing is for sure, as the level of modern technology continues to rise, we are destined to get a cure for cancer soon and this incredible breakthrough is an indicator of how close this inevitability is from now.



Li, S., Jiang, Q., Liu, S. et al. A DNA nanorobot functions as a cancer therapeutic in response to a molecular trigger in vivoNat Biotechnol 36258–264 (2018). https://search.proquest.com/docview/2011288340?pq-origsite=summon

Moradzadeh Khiavi, M., Rostami, A., Hamishekar, H., Mesgari Abassi, M., Aghbali, A., Salehi,           R., … Sina, M. (2015). Therapeutic Efficacy of Orally Delivered Doxorubicin Nanoparticles in Rat Tongue Cancer Induced by 4-Nitroquinoline 1-Oxide. Advanced pharmaceutical bulletin5(2), 209–216. doi:10.15171/apb.2015.029https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4517077/?tool=pmcentrez&report=abstract

R., Maheswari, et al. “Cancer Detecting Nanobot Using Positron Emission Tomography.” Procedia Computer Science, vol. 133, 2018, pp. 315-322.,https://www.sciencedirect.com/science/article/pii/S1877050918309840?via%3Dihub


Photo credits: 

Image 1: The Nanorobotics Laboratory, Polytechnique Montreal. https://www.polymtl.ca/salle-de-presse/en/newsreleases/legions-nanorobots-target-cancerous-tumours-precision

Image 2: The Biodesign Institute, Arizona State University . https://asunow.asu.edu/20180212-discoveries-cancer-fighting-nanorobots-seek-and-destroy-tumors



Telomeres: Fountain of Youth or Grim Reaper?

Kailyn Valido

The majority of people dread the inevitability of aging, a genetically programmed process. It is evident that many wish that they could somehow rewind time to relive their 20’s and 30’s—a range of years where most people do not have wrinkles, graying hair, and frequent thoughts about the enigmatic nature of “The Great Unknown.”

What if one can extend this period of youthfulness and vivacity? What if one can delay this seemingly undesirable process of aging?

This is where the notion of telomeres comes into play.

Telomeres are essentially repeated sequences of DNA at the end of eukaryotic chromosomes. These sequences are in the form of repeated TTAGGG bases on one strand of DNA and AATCCC bases on the complementary DNA strand. Analogous to the plastic tips on shoelaces, telomeres ultimately provide the chromosome with protection—up to a certain point.

Synthesized by the enzyme telomerase, telomeres get shorter every time a cell undergoes division. Because there is not enough telomerase for somatic—or body—cells, the gene for telomerase is inactive and telomeres consequently shorten. The shorter the telomere length, the lesser amount of times a cell can divide. Once the telomeres become too short, the cell can no longer divide, and so it ages and inevitably dies.

For this reason, telomere shortening has been linked to the aging process. Through his research, geneticist Richard Cawthon at the University of Utah discovered that shorter telomeres correlate with shorter lives. Working with a group of people older than 60 years old, he and his colleagues found that those who had significantly shorter telomeres were three times more likely to die from heart disease and eight times more likely to die from infectious disease.

The main issue with this finding, however, relates to the correlation versus causation argument, in which it is commonly believed that correlation does not equal causation. Scientists are currently unsure of whether telomere shortening is merely a sign of aging, such as wrinkles, or an actual contributing factor.

If telomere shortening is proven to be a definite cause of aging, this information would be an immense breakthrough in the medical field. Scientists may be able to extend human lifespan greatly by somehow devising a mechanism to restore or preserve telomere length, allowing cells to divide more and not become senescent.

In a small-scale scientific study at the University of California at San Francisco, scientists wanted to research if telomere length can be affected by certain lifestyle changes. In this study, which began in 2008, 35 men who had early-stage prostate cancer were closely monitored. Ten men altered their lifestyle habits by having a plant-based diet, moderate exercise six days a week, and stress reduction exercises. Additionally, they attended a weekly support group. The 25 other men who had early prostate cancer were not asked to make any major lifestyle alterations.

After five years of surveillance, the 10 men with the lifestyle changes had an increase in telomere length by about 10 percent. In contrast, those 25 men who did not change any lifestyle habits had significantly shorter telomeres, about 3 percent shorter when the study was concluded.

This pilot study has major implications. Because of the small size of the study, however, the legitimacy of this research finding needs to be confirmed by more large-scale studies to assess the sample size and find repeatability in results. The scientists at UCSF hope to inspire larger research studies for confirmation.

The lead scientist in this study, Dean Ornish, MD, powerfully states, “Our genes, and our telomeres, are not necessarily our fate…[The] findings indicate that telomeres may lengthen to the degree that people change how they live.”

If scientists can preserve telomere length, one might be wondering then, will humans be able to attain that much desired Fountain of Youth and ultimately become immortal like many science fiction movies portray? Very unlikely.

Although the concept of telomere lengthening and preservation can potentially postpone aging, unnaturally active telomerase and incessant division of cells may be problematic. Cancer cells, for instance, escape their death by having a consistently active telomerase, preventing telomeres from shortening. This, in turn, allows these cells to grow an abnormal amount of times and form tumors. Scientists are aware that replicative aging of cells occurs to combat against these malignancies.

This complex part of telomerase and its product, telomeres, is what is still confounding experts today. If telomerase can be systematically lengthened to extend one’s lifespan, would that increase that person’s risk of cancer? Questions similar to these and their respective multifaceted issues are currently being explored. Perhaps one cannot delay the aging process without certain repercussions, such as a higher chance of having cancer.

Scientists, however, are still hopeful. Many are attempting to utilize the notion of telomeres as a target for cancer treatment. If they can find a way to shorten cancer cell telomeres and allow these cells to age and die, it can be revolutionary.

Some researchers have already started testing this in the lab with prostate cancer cells, but results had unfortunate consequences, such as significant impairment of both fertility and production of immune cells. Knowledge is still being gathered about how differentiation in normal cells and cancer cells can be related to telomeres and the enzyme telomerase.

Despite scientists’ extraordinary efforts in fighting against the aging process by manipulating and observing telomeres, the only seemingly possible result is to delay aging rather than terminating the process altogether. In addition to the preservation of life, research on telomeres could be a key to unlocking the cure to cancer— a colossal discovery that would prevent a lot of emotional, physical, and mental suffering in the world.