Eighth Annual Three Minute Thesis Competition

[Speaker: Mindula Kaumadi Wijayahena] The bad news is, nothing lasts forever. The good news is, nothing lasts forever. Has anyone in this audience heard about PFAS? They are human-made chemicals, which are strongly bound together. Because of their unique water and oil proof properties, they have been used in lots of applications. Basically, they are found everywhere. Have you ever noticed pizza boxes and disposable paper cups, even food package, keep their shape even with hot stuff in them? How nonstick pants work fine without oil, or how raincoats keep us dry? All these contain PFAS. So PFAS can enter our body when we eat, when we drink, even when we breathe. So, why do we care? Of course, they can harm our health. So, they can cause cancer, increase your cholesterol level, and reduce the vaccine responses, even for COVID vaccines. PFAS, also found in breast milk. Imagine mothers passing PFAS into their babies. So, part of my research investigates to what extent we are contaminated with PFAS. I do this with blood testing, and 95% of all the blood samples I tested contained PFAS. In other words, everyone here in this room might have PFAS in your body. This is very alarming. So the problem with PFAS is they don't break down in the environment or in our body. That's why we call them forever chemicals. But don't worry, I have the solution. We found a bacteria who can destroy these toxic PFAS. In other words, imagine a bustling kitchen. But instead of Gordon Ramsay, I'm the head chef with the new challenge on the menu, PFAS. But wait, I'm not alone. I have a team of little chefs, our bacteria buddies, who's ready to roll up their sleeves and chop up these toxic PFAS nearly 100% into smaller pieces. They only need few days. So, that means you cannot call them forever chemicals anymore. So my goal is to turn these toxic PFAS into smaller compounds, like water. So, my discovery holds the key to wiping out these PFAS from the world. So remember, nothing lasts forever. Thank you.

(audience applauding)

[Speaker: Alber Aqil] Today, I'll tell you a story, a story of a woman, a story that begins in Southeast Alaska. Now, when we zoom in on this region, we see that it is home to two types of indigenous nations. Ones that live away from the coast, the interior nations, and ones that live right at the coast, the coastal nations, including the Tlingit. Now, inside the Tlingit territory is a cave, and within that cave was found a bone, about this big, presumed to be from a bear. But preliminary analysis revealed that we were in fact looking at a human bone, a bone from a woman who lived 3,000 years ago. We stopped our research. We went to the tribal elders of the Tlingit and asked them if it is okay for us to study what is potentially their ancestor. They said yes, but she will no longer be just a subject. She would have a name and her name would be Tatook yik yees shaawat, the young woman in the cave. With this, we got back to work. We extracted DNA from the bone and compared it against the DNA of modern day indigenous people from the same region. The genetic results are shown on the graph. Here, every point is an individual. Blue points are coastal individuals. Red are interior individuals. The closer together two points are on this graph, the more closely related those two individuals are genetically. Here we see that Tatook yik yees shaawat, the black star, is more closely related to the blue coastal individuals including the Tlingit, than the red interior individuals. Well, the close relationship between the Tlingit and Tatook is consistent with Tatook being an ancestor to the Tlingit people. And this is interesting, because this tells us that the Tlingit people are living today in almost exactly the same place where their ancestors lived 3000 years ago. This is a remarkable case of genetic continuity over a strip of land no wider than a few hundred miles. This sort of continuity is rare in other parts of the world, which makes the story of Tatook and the Tlingit people extraordinary. Now, the story that I have told you today highlights how much we can learn about the astounding history of an entire population based on nothing more but a few faint echoes from the past. Thank you.

(audience applauding)

[Speaker: Sabrina Orsi] As the most feared illness in America, no one ever wants to hear those three scary words, you have cancer. But with 2 million new cancer cases in 2023 just in the United States, I'm sure everyone in this room knows someone who has heard those words. Personally, I have lost many family members to cancer, but losing my grandma, Holly, hit me the hardest. Witnessing firsthand how her long battle with cancer affected her and our family, I was left wondering why the currently available therapies weren't good enough and why we couldn't do any better for patients like her. Even though this was almost 10 years ago, cancer is still a major public health issue that has severe social, financial, and psychological consequences, and that's why researchers like me are working hard to make discoveries that improve our ability to treat patients. Now, in order to find these new and improved therapies, it's important to understand how a regular cell becomes cancerous in the first place. So let's pretend our cells are like cars. There are lots of different roads you can drive on to reach the same destination, which in this case is a cancer cell. In the cancer I study, the cells are known to take the road for increased metabolism, which makes it a great therapeutic target or road to put that stop sign on. So what is metabolism exactly? Just like how cars need gas to drive, our cells are fueled by nutrients broken down from what we eat and turned into energy by metabolism. Naturally, cancer cells are rapidly growing, and dividing, and spreading, so they need a lot more of this energy than regular cells do. And this is the weakness that I'm targeting in my thesis, because what you eat directly feeds into these energy producing processes, in my thesis, I'm using dietary restrictions like fasting to deprive cancer cells of that necessary fuel to slow them down. Now, of course, we can't cure cancer just by cutting some calories, but when combined with traditional anti-cancer drugs, we are able to take treatment one step further, so that instead of just slowing that car down, now we're stopping it. Unfortunately, not all tumors are alike, and much like how some cars use regular gas and others use diesel, different tumors have different energy needs. And this is why my ongoing work involves figuring out exactly how cancer cell metabolism is changed by these different diets, so that we can piece together which specific diet and drug combinations are most effective for different subtypes of cancer. For everyone out there like me who has or had a loved one with cancer, you know how important it is to find treatments like this one that are safe, affordable, and effective. By providing the scientific evidence for why and how dietary restrictions work with traditional therapy, my research is improving the future of cancer care one snack at a time, thank you.

(audience applauding)