Leah Persaud, PhD
Lehman College, City University of New York; The Graduate Center, City University of New York, NY, USA
Leah is passionate about understanding the the molecular signaling pathways of new anti-cancer therapeutics. She is a City University of New York (CUNY) Science Scholar working in Dr. Moira Sauane's cancer research lab at Lehman College in The Bronx, NY. She is a PhD from the CUNY Graduate Center.
Leah completed undergraduate degrees in biology and forensic science from the University of New Haven in Connecticut. As an undergraduate, Leah performed research on highly specific DNA nucleases for gene therapy at Justus Liebig University in Giessen, Germany, which ignited her interest in molecular biology research and therapeutics.
As a mentor, she is able to share her passion for science research and encourage undergraduate and high school students to pursue careers in STEM fields.
Learn about Leah’s research
Title: Development of anti-cancer gene therapies through understanding of cytokine-induced programmed cell death
- Understand how cell lines are used to decipher molecular signaling pathways for the development of anti-cancer therapeutics
- Learn how IL-24 treatment kills cancer cells
The use of gene therapy is well studied due to its potential to treat cancer, the second leading cause of death worldwide. The goal of gene therapy is to introduce functional genetic material into human cells to be transcribed and translated in order to regulate, repair or suppress a molecular mechanism that contributes to a disease state. Compared to traditional cancer therapies such as surgery, chemotherapy or radiation therapy, gene therapy is a more personalized and targeted approach because it is based on understanding the genetic profile of a patient’s tumor. Genes being developed for cancer therapy code for a variety of proteins including tumor suppressors, specific antigens, transcription factors, cell cycle regulators, receptors and cytokines. The cytokine Interleukin-24 (IL-24), is of special interest for gene therapy because of its selective killing effect on numerous cancer cell types while having no effect on corresponding normal cells. Due to this property, IL-24 is being investigated in Phase II clinical trials as a gene therapeutic to treat cancer patients. To understand how IL-24 exerts its specific killing effect, our lab studies the signaling pathways that IL-24 activates to induce programmed cell death also known as apoptosis. We use various cancer cell lines to understand which proteins IL-24 modulates to produce its killing effect. Currently, we are exploring how IL-24 blocks protein synthesis in cancer cells to promote cell death. Our aim is to further develop IL-24 as an anti-cancer therapeutic for gene therapy and to reveal targets for combination therapies that will work synergistically with IL-24 to produce a cancer specific killing effect.
Watch the webinar
Presenter: Leah Persaud - PhD; Lehman College, City University of New York
0:00:01 – Slide 1
Moderator: Hello everyone, and welcome to today's live broadcast, Development of Anti-Cancer Gene Therapies Through Understanding of Cytokine-Induced Programmed Cell Death presented by Leah Persaud, a PhD candidate at Lehman College in City University of New York, the Graduate Center and City University of New York. I'm Susie Valdez and I will be your moderator for this educational web seminar presented by Labroots and sponsored by Thermo Fisher Scientific. To learn more about our sponsor Thermo Fisher Scientific, visit their website at thermofisher.com. (0:00:47)
Before we begin, I'd like to remind everyone that this event is interaction. We encourage you to participate by submitting as many questions as you want at any time during the presentation. Just click on that green Q&A button located at the lower left of your presentation window, type the questions into the box that appear on the screen and we'll answer as many questions as we have time for at the end of the presentation. (0:01:09) For questions not answered today we will follow up with our participants via e-mail. Also please notice that you will be viewing the presentation in the slide window. To enlarge that window just click on the icon located on the lower right of the screen. If you have any trouble seeing or hearing this presentation please click on the support button at the top right of the presentation window or use the Q&A button to let us know you're having a problem. (0:01:33)
Please join me now in welcoming Leah Persaud. Leah is passionate about understanding the molecular signaling pathways of new anti-cancer therapeutics. She is a City University of New York science scholar working in the lab with Dr. Moira Sauane's cancer research lab at Lehman College in the Bronx, New York. (0:01:55) She is a PhD candidate from CUNY Graduate Center. Leah has completed her undergraduate degrees in biology and forensic science from the University of New Haven in Connecticut. As an undergraduate she performed research on highly specific DNA nucleuses for gene therapy at Justice Liebig University in Giessen, Germany which ignited her interest in molecular biology research and therapeutics. (0:02:22) As a mentor, she's able to share her passion for science research and encourage undergraduate and high school students in pursuing their careers in stem fields. Join me now in introducing and welcoming Leah Persaud. Welcome, Leah.
Hello everyone. Thank you, Susie for that introduction and thank you everyone for signing in today. I'm Leah Persaud, a fourth year PhD student studying molecular cell and developmental bio at the City University of New York and the Graduate Center in New York City. (0:02:55) As Susie mentioned, I work with Dr. Moira Sauane at Lehman College, one of two senior colleges in the Bronx and this is where I perform the majority of my cancer biology research. Today I'm excited to talk to you all about how our lab is tackling cancer by developing anti-cancer therapeutics for gene therapy. So let's get started. (0:03:18)
0:03:20 – Slide 2
So as many of us know cancer is one of the leading causes of death worldwide right below heart disease. Over the years the rate of death due to heart disease has slowly declined but unfortunately we do not see any declines for the rate of deaths due to cancer. To control cancer, prevention and early screening is key. (0:03:42) According to the World Health Organization 30-50% of cancers could be prevented by reducing risk factors such as alcohol and tobacco consumption, unhealthy diet and getting vaccinated against cancer causing agents such as APV, also known as human papilloma virus or hepatitis B or C viruses to name a few examples. (0:04:05) Despite this, however, cancer can also be genetic and even arise spontaneously and it can go undetected if proper screening is not utilized. Once an individual forms a malignant tumor consisting of abnormally fast growing cells treatment is necessary to extend the life of a patient, to preserve quality of life and also to reduce suffering.
0:04:30 – Slide 3
So currently there are around five standard treatment options for individuals who have various stages of cancers. Generally when cancer is first detected surgery and radiation are used to physically remove or destroy cancer cells at a specific location in the body. When cancers have advanced they evade the body's immune system. (0:04:50) They become more aggressive and thus they can spread to other organs. Thus, more specialized treatments are needed to attack rapidly proliferating cancer cells. Some of these include hormone therapy, chemotherapy, targeting therapy such as gene therapy and personalized therapy.
0:05:12 – Slide 4
So gene therapy is very interesting because of its personalized approach. When developing any treatment plans for cancer patients it's very important to look at the patient's genetic history and the mutational status of the patient's tumor. Not all tumors are alike genetically and as a cancer advances even tumor cells can differentiate and become less sensitive to treatments that were once affected in said patients. (0:05:38) Because of this no one treatment fits all cancer patients. Depending on the composition of a patient's tumor, different therapies need to be given to different patients. Essentially the goal of gene therapy in cancer is to introduce functional genetic material into human cells to be transcribed and translated in order to regular, repair or suppress a molecular mechanism that contributes to cancer growth. (0:06:04) By understanding the composition of a patient's tumor, the goal is to only target cancer cells while leaving normal healthy cells alone. Thus, gene therapy goes hand in hand with personalized therapy.
0:06:18 – Slide 5
So of all gene therapy clinical trials worldwide over 64% of trials are for cancer diseases. Because of the ever changing nature of cancer, gene therapy is becoming a more popular approach. So essentially instead of having a one size fit all or most approach, the goal is to create tailor made therapies for patients who have tumors with different genetic profiles.
0:06:47 – Slide 6
And just recently the Food and Drug Administration announced the approval of ex vivo chimeric antigen receptor gene therapy also called CAR T therapy which will be the first gene therapy provided to the U.S. market to treat leukemia. The therapy was developed by a Swiss pharmaceutical company, Novartis, and basically it's a form of ex vivo gene therapy where a patient's T cells are removed and engineered to express receptors that will bind to patient cancer cells and then kill them once they are infused back into the patient. (0:07:20) The therapy was approved to treat pediatric and young adult patients with leukemia and this is really exciting news for the personalized treatment of cancer and we hope to see additional gene therapies approval in the coming years.
0:07:34 – Slide 7
So in addition to ex vivo treatment there are in vivo treatments where genes are directly put into a patient. Genes being developed for cancer therapy code for a variety of proteins including tumor suppressors, specific antigens, transcription factors, self-cycle regulators, receptors and cytokines. Our lab specifically studies a special cytokine called interleukin-24, as abbreviated IL-24. Interleukin-24 is of special interest in gene therapy because it has a selective killing effect on numerous cancer cell types while having no effect on corresponding healthy cells.
0:08:19 – Slide 8
So to give some background interleukin-24 is a secreted cytokine and it's a member of interleukin-10 cytokine family. It was first discovered in melanoma cells and initially named MDA-7 which is melanoma differentiation associated gene-7. Interleukin-24 is normally produced by immune cells and epithelial cells and under physiological levels it has various roles in other immunities, psoriasis and wound repair. For the past 15 years, however, interleukin has been studied as an anti-cancer molecule because it specifically target cancer cells and not normal cells.
0:09:01 – Slide 9
This is the really interesting thing about interleukin-24 because when it is overexpressed in cancer cells it kills a variety of cancer cells from melanoma to glioma, prostate, breast cancer and including breast cancer stem cells. Both overexpression in viral vectors and administration of recombinant interleukin-24 protein have been effective in inducing apoptosis in multiple cancer cell types including cancers in transgenic mice studies. (0:09:33) Interleukin-24 can also cause a bystander effect in which untreated cancer cells adjacent to treated cancer cells with interleukin-24 will undergo apoptosis as well. This is because it can induce its own expression of endogenous interleukin-24. So therefore it does regulate its own expression.
The most important thing about interleukin-24 is that it does not kill normal cells and this has been confirmed in many studies. (0:10:03)
So because of interleukin-24 cancer specific killing effect, it has been studied in Phase I clinical trials and it is currently in Phase II clinical trials to determine efficacy and evaluate safety.
0:10:21 – Slide 10
So as many of you know before a drug can be put on the market it has to be tested in a series of clinical trials and be approved by the FDA. Before any of this can happen, the drug must be understood on a cellular level. So currently interleukin-24 is being studied at Phase II clinical trials; however, these trials have been limited to patients with only melanoma. (0:10:45) To maximize the effect of interleukin-24 to different cancer cell types, the goal of our lab is to fully understand how interleukin-24 selectively kills cancer cells. We want to know its mechanism of action and what proteins it's interacting with to induce apoptosis, also called cell program death. Basically we want to know why molecular mechanisms are being changed due to interleukin-24's overexpression. The way we do this is by performing basic research using cell lines and protein analysis.
0:11:19 – Slide 11
So in our labs in order to do this type of preliminary pathway research we use cancer cell lines as our model. In general cancer cell lines replicate quickly. They are easy to take care of and they are inexpensive compared to working with live animals. Also there are a lot of data on cell lines because they are used in many labs across the world. So here we have a microscopic image of one of the most routinely used breast cancer cell lines called MCF-7. (0:11:50) This cell line originated from a 69-year-old Caucasian woman who had cancer of the human mammary gland in the breast. These cells could be cultured in an artificial environment and maintained for long periods of time, usually longer than primary cells which come from human or animal tissue, but they have a limited life span. These MCF-7 cells are called immortalized cell lines. So cell lines are essential for us to study the mechanism of action of anti-cancer therapies including interleukin-24. (0:12:24)
We can then plate cells in a variety of dishes for a variety of assays such as those that measure cell apoptosis, cell proliferation, mitochondrial function or reactive oxygen species production, also called ROSP.
In our lab we treat our cancer cells with an adenovirus that contains the interleukin-24 gene. This same virus has been used in clinical trials and is non-replicative. (0:12:50) We can treat cells with the virus protein inhibitors and determine if those proteins are essential for interleukin-24's killing activity. We can also use cell lines that have proteins that are mutated to determine if they are need for interleukin-24 mediated apoptosis.
We can also do really cool immunofluorescent experiments to determine if interleukin-24 expression translocates essential proteins to different parts of the cell which will give us an indication of their function and response to interleukin-24 expression.
0:13:28 – Slide 12
So despite all of these advantages that cell lines offer us, they do have several limitations. Our cancer therapy research needs to be progressed with translational studies first to pre-clinical animal studies and then clinical trials.
This of course takes time but it is necessary to learn how therapies work in a living in vivo system. As many of my fellow research also—they may also know contamination is also a major issue. Contamination of cell lines, whether it be the introduction of microbes such as these cells which you can see here or cross-contamination with other cell lines, it severely delay our experiments. (0:14:07) In addition if cell lines, especially cancer cell lines are grown for too long, they can start to accumulate genetic mutations and exhibit abnormal morphologies or altered functions. This can affect the reliability of our results. Despite these disadvantages we find cell lines extremely useful for our type of research which is the understanding of interleukin-24's mechanism of action on a molecular level. It is important to test your hypothesis in vitro first and then progress to animal studies to save time and also effort and also money. Thus overall before any drug can be made for market it must be discovered and tested in cell lines.
0:14:55 – Slide 13
So back to our protein of interest, interleukin-24. Thus far this is what we know about interleukin-24. Interleukin-24 inhibits metastasis and also angiogenesis and it induces apoptosis in many cancer cell types. It is able to inhibit metastasis by up regulating and down regulating factors involved in cell adhesion and migration. (0:15:19) It also inhibits angiogenesis by down regulating angiogenic factors such as VEGF, FGF and TGF. These are various growth factors. Most importantly interleukin-24 activates apoptosis or program cell death by endoplasmic reticulum stress, also called ER stress.
Interleukin-24's effect on ER stress in cancer cells has been well studied and is believe that this is one of the main mechanisms in which interleukin-24 induces cell death.
0:15:56 – Slide 14
So in general cancer cells are in a constant state of ER stress. The ER is extremely important for cancer cells to thrive because this is the primary site for protein symphysis which is essential for the rapid proliferation of cancer cells. And because cancer cells rely heavily on protein symphysis there is an accumulation of misfolded mutant proteins which causes a constant state of ER stress. (0:16:23) With the higher ratio of survival and proliferation signals to death signals the cancer cells can adapt to this condition and survive. In terms of interleukin-24 action we and others have showed that interleukin-24 is potentiating ER stress to such an extent that cancer cells cannot recover. Thus signals are amplified and the cells thus undergo apoptosis. (0:16:51) More specifically interleukin-24 induces a buildup of cytosolic calcium, ceramides and reactive oxygen species which can lead to an apoptotic response. Our lab has also discovered that interleukin-24 interacts with a ligand mediated receptor called the Signal 1 receptor in the ER. This interaction antagonizes the signal 1 receptor and it is necessary for interleukin-24 to induce its apoptotic effect. (0:17:25) Oftentimes in cancer cells Signal 1 expression is up regulated. In our experiments when Signal 1 receptor is overexpressed by adenovirus vector interleukin-24's killing activity is actually decreased.
0:17:42 – Slide 15
So to further understand how interleukin-24 induces apoptosis through ER stress, we have to understand what happened in response to ER stress. So in general the cell will activate three different pathways to restore cellular homeostasis by increasing folding capacity protein degradation or by decreasing translation or protein symphysis. So these pathways include IRE1, PERK pathway and the ATF6 pathway. (0:18:14) So as I just mentioned extreme and prolonged stress conditions of the ER can contribute to the induction of apoptosis. So we believe that interleukin-24 is doing this through the inhibition of protein symphysis by activating the PERK pathway which is responsible for translation attenuation so for the decrease of protein symphysis. We and others have shown that interleukin-24 does activate PERK to induce apoptosis. So one of our main objectives, one of our main projects was to determine if interleukin-24 specifically blocks protein symphysis when it is over expressed in cancer cells.
0:18:58 – Slide 16
So the reason why this would be promising is because therapeutics that attack translations are essential to killing cancer cells because they can disable the machinery necessary for cancer cells to grow and proliferate. Pursuing translation inhibition can also be a more targeted and effective approach that can be used against a variety of cancer cell types that exploit different mutated pathways based of their genetic profile. (0:19:31) So these therapies could be used against tumors that are heterogenic in which the subsets of cells in the same tumor can have varied morphological , genetic or metabolic or metastatic characteristics. And since interleukin-24 exhibits a broad anti-cancer effect in many tumor cell types, it's killing affect could be attributed to the inhibition of translation as a downstream pathway of ER stress.
0:20:00 – Slide 17
So more specifically we wanted to look at translation initiation which is the first step of protein synthesis. To initiate translation the Ternary Complex must be created. This complex contains being a thymine tRNA, GPP and eukaryotic initiation factors to begin translation at the start code on. So a key eukaryotic initiation factor is called eIF2a. The phosphorylation of EIF2a on CRN51 specifically can block translation initiation which is the rate limiting step in protein symphysis. (0:20:40) We know from previous experiments that interleukin-24 activates ER stress and phosphorylates eIF2a lung and prostate cancer cells. So also in addition interleukin-24 is able to increase the expression of downstream markers of the Ternary Complex. So our goal here was to definitively determine if the anti-proliferative affect of interleukin-24 is mediated by phosphorylation of eIF2a and Ternary Complex depletion in different cancer cell types. So thus we want to determine if interleukin-24 is an inhibitor of translation initiation through this main mechanism.
0:21:26 – Slide 18
So one of the first things we did was to measure eIF2a phosphorylation in a variety of cancer cell types such as melanoma, breast cancer, cervical cancer and squamous cell carcinoma. The way we would do this is first we would grow our cancer cells and then we would treat our cells with the interleukin-24 gene in adenovirus. The cells would uptake the adenovirus within two hours and then we could perform assays on the cells within 24 to 72 hours depending on the type of assay we wanted to do. (0:22:03) So some of these downstream assays include Western Blot. So Western Blot is for protein analysis to determine if specific proteins are affected by interleukin-24 expression. We can also do cell viability assays or cell proliferation assays that measure whether the cells are living after interleukin-24 treatment. We can also do annexin V apoptosis assays that measure how many cells are undergoing apoptosis using flow cytometry. And we can also do qRT-PCR to determine what genes are getting expressed in a response to interleukin-24 treatment.
0:22:45 – Slides 19
So here I’m going to show you some data. Here we use watch and wait analysis to show that in all of these cell lines interleukin-24 phosphorylates eIF2a at Serine 15 and below we have our sub-proliferation and apoptotic assays. So all of the cell proliferation assays indicated that interleukin-24 was indeed killing these cancer cells. The same results were seen with the Annexin V apoptosis assay. So interleukin-24 was indeed inducing apoptosis in these cancer cells. So next we wanted to directly determine whether eIF2a was necessary for interleukin-24's killing effect.
0:23:30 – Slide 20
So here we use Western Blot analysis to show that interleukin-24—well, before we show the interleukin-24 does indeed phosphorylate eIF2a. Next we wanted to employ eIF2a mutant cells. So here basically we were able to get cancer cells from our collaborator at Harvard and these cancer cells contained a mutant form of eIF2a. So these cancer cells were genetically engineered so that the eIF2a, this phosphorylation site would be mutated. (0:24:25) So instead of the serine at specific immuno acid 51 the serine was mutated to an alanine. So in effect what would occur is that interleukin-24 or any other kinases would not be able to self-correlate the specific eIF2a. So basically what we hypothesized was that if this specific eIF2a could not be phosphorylated, then we would not have a decrease in global protein symphysis. So if interleukin-24 is unable to pause phosphorylation of the mutant eIF2a then translation initiation would still occur and we would get protein symphysis and the cells will continue living.
0:25:12 – Slide 21
So here I have some data. We treated both mutant cells lines and wild-type cell lines with increasing concentrations of interleukin-24. So as expected the wild-type cells show chilling effect in response to interleukin-24. So as we increase the concentration the cells died. We can also see that in our apoptosis assay, the cells were increased in their apoptotic effect in response to increasing concentrations of interleukin-24. When we looked at the mutant cells that did not have the phosphorylateable form of eIF2a there was no significant change in apoptosis or cell viability. (0:26:01) So we also performed a Western Blot to show that with increasing concentrations of interleukin-24 we see increasing levels of eIF2a phosphorylation in the wild-type and no phosphorylation with the mutant cells confirming that our mutant worked and the inhibition of interleukin-24's killing effect was due to the fact that eIF2a could not be phosphorylated.
0:26:27 – Slide 22
So overall we show that interleukin-24 phosphorylates eIF2a to induce apoptosis in cancer cells. And it does this by defeating the Ternary Complex which cannot initiate translation and create new proteins for the cancer cells. Currently we are working on another arm of translation initiation in which interleukin-24 may also decrease the eIF4 complex here which is required for mRNA binding at the five prime untranslated region for protein symphysis. Many oncogenic proteins that promote tumor growth contain long five prime untranslated regions. (0:27:07) So if the eIF4F complex is not available maybe due to interleukin-24, these mRNA's cannot be translated to protein which will decrease cancer cell survival signals leading to cell death. So here we are. If both of these arms affected by interleukin-24 overexpression, that will inhibit translation and thus allow the cells to undergo apoptosis and cause cancer cell death.
0:27:41 – Slide 23
So in terms of our continuing and future studies we are looking at how interleukin-24 expression affects the different pieces of the eIF4F complex. We want to find out also how does interleukin-24 affect mRNA stabilization for protein symphysis so this is one of the continuing projects that we are currently working on. We want to also verify if interleukin-24 does down regulate oncogenic mRNAs. (0:28:12) We are also looking at additional mediators of interleukin-24 induced apoptosis. We recently found that protein kinase A also called PKA is a major cell regulator that plays a role in regulating interleukin-24's mediated extrinsic apoptosis which works through death receptors rather than internal signals that tell cells to die. We are exploring the role of PKA in various different pathways that interleukin-24 normally activates to kill cancer cells. So we're trying to find out of PKA is a major regulator in interleukin-24 mediated cell death. (0:28:52) We also want to know how interleukin-24 mediates its own expression. So what transcription factors are involved in expressing the interleukin-24 gene and what proteins are involved in stabilizing interleukin-24's mRNA. Also signal 1 receptor is involved. So as I mentioned earlier interleukin-24 will bind to Signal 1 receptors to potentiate ER stress in the cancer cell to cause apoptosis, so we are interested to know if Signal 1 has any additional roles in respect to interleukin-24 expression of mRNA.
0:29:34 – Slide 24
So overall in basic research through our studies of the signaling pathways and respective proteins what we hope to achieve is to find new targets for anti-cancer therapeutic. If we understand the proteins that interleukin-24 targets to kill cancer cells, we could possibly create drugs from those binding domains to treat cancer patients with. Also by understanding these pathways we can develop combination therapies and personalized therapies with interleukin-24 that will kill cancer cells in a more effective and synergistic manner. (0:30:08) So there have already actually been studies showing that in combination with interleukin-24 well-known therapies such as Herceptin and Cisplatin, they actually work better with interleukin-24 treatment. We also want to expand the positive results seen with melanoma patients in clinical trials to patients with other cancer cell types. (0:30:32) And as we have shown interleukin-24 targets the protein translation which is an essential process to all cancer cells. So this would be a key in developing interleukin-24 as a potent anti-cancer therapeutic against multiple cancer cell types, not only melanoma.
0:30:53 – Slide 25
So overall to conclude I would like to thank of course Dr. Moira Sauane. She's an amazing mentor. I've been working with her for the past two years and she always has really great ideas and inspires me every day to be a great scientist. I definitely wanted to thank my current and former lab members, Xuelin, also known as Sean, Anna, Hilal, Marifer, Carlos and Jordan. Special thanks to our collaborators, Dr. Aktas from Harvard Medical School and Dr. Redenti and Fellow PhD Student Jason who are our lab neighbors at Lehman College and of course none of this research could have been done without funding from NIH and the National Cancer Institute. So thank you everyone for signing in today to listen to my presentation. I'm happy to answer any questions and I welcome you to connect with me on Twitter or LinkedIn if you would like to learn more about what we do at Lehman College. Thank you.
End Presentation: 31:58
Get to know Leah
What motivates you to succeed in your field?
My family has always been a motivating force behind my career because of their sacrifices. My parents emigrated from Guyana to New York City to pursue the “American dream”. Through their own examples of achieving a level of education that they could not attain in Guyana and developing careers in fields which they are now successful, my parents inspired me to do the same from a very young age. I am also motivated because I am a woman. As many of us know, there are not enough women and women of color in STEM fields particularly, as leaders. Since representation matters, I see myself as role model for female students who want to pursue science as a career. This is what keeps me motivated during the ups and downs of doing a PhD.
Describe yourself in three words
Optimistic. Open-minded. Proactive.
Is outreach/STEM important to you? Why?
STEM outreach is one of the most important things that we scientists need to take part in. Young talent in the STEM fields is equally distributed across the globe but the opportunities for disadvantaged youth in STEM are not. Investment in STEM education needs to be a priority for us because as a society we need more thinkers, innovators, and problem-solvers to tackle challenges that we face in various fields such as medicine, the environment, and energy.
What is your favorite phrase?
The future is female.
Why did you become a scientist?
Curiosity. It is instinctive for us to ask questions and want to learn more about the world we live in. I think this is why many people pursue science and specifically, research as a career. Learning how things work, especially how biology works has always been a driving force behind me becoming a scientist. It can be mind-boggling as well. The fact that just a few atomic elements can create self-sustaining biological life will always amaze me.
Who inspires you to be better?
Everyone who has invested time, love, and energy in me- my husband, my family, close friends, past teachers, my mentor. Also, my future children.
How do you relax after a hard day of work?
A good workout, good food, and good TV.
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