By Elizabeth Shamgin
In third grade, I believed that Sherlock Holmes was a real person. I keenly wore my dad’s black trenchcoat and held a magnifying glass in my hands as I tiptoed around the shadowy halls of my house, investigating mysteries of who ate the last cupcake and where my sock went. I found joy in unraveling the unknown, just like Sherlock in the books I grew up reading.
My parents always supported my inquisitive mind, enrolling me in an honors math school as a kindergartener to develop my critical thinking skills. I spent every Sunday solving math problems, confidently scribbling the solution I had erected in my “brain attic”, as Sherlock would say, on the classroom whiteboard. The “Aha!” moments brought unrivaled satisfaction, as if I connected the red strings between photographs thumbtacked to a wall.
I was one of the best detectives I knew, yet one mystery I couldn’t seem to wrap my head around was my family’s extensive history of cancer. My mother had ductal-cell carcinoma; my grandfather, glioblastoma multiforme; my great-grandfather, bronchogenic carcinoma. The pattern stretched across generations as a fatal motif. Witnessing my family go through treatments, surgeries, and death felt like watching the same tragic story play out on repeat. I sat around in hospitals, dangling my legs from chairs in waiting rooms, no longer feeling like that almighty know-it-all I tried to be; I was a clueless child who couldn’t change the ending. Still, some part of me refused to stop searching for the clues that hide beneath the diagnosis. Here, I chose to face the most mind-boggling case of my sleuthing career. The game is afoot.
I found myself drawn to research on cancer genetics and pursued my expedition for knowledge in the Lander Lab at UC Irvine. Our assigned experiment seemed simple enough: inject Doxorubicin, an antitumor antibiotic, alongside Turmeric and Ashwagandha extracts into chick embryos to model tumor angiogenesis inhibition, to analyze interactions between natural and artificial drugs. Even with my optimism, science, like mystery investigations, rarely obeys expectation. All thirteen of my group’s embryos died within hours after drug administration, despite having meticulously checked our solution’s molarity calculations. Our hypothesis vanished like footprints in the snow.
For a moment, I felt that same helplessness as I did in those waiting rooms, watching monitors blink and doctors speak in hushed tones while I waited to hear about my mother’s procedures. Now, the helplessness carried a sense of guilt. Sacrificing over a dozen embryos for failed data, I felt like Moriarty, leaving casualties behind in the name of deduction.
Yet even in the face of obstruction, Sherlock never succumbs to despair. Discovery does not end with failure; it sparks adaptation. When angiogenesis was no longer detectable, my labmates and I spent hours tracing patterns in our mass spectrometry images. Finally, I noticed a significant contrast in drug absorption by the ectodermal and endodermal tissues of the embryo. Elementary!
The uneven uptake of drugs in the tiny embryo modeled a phenomenon seen in real tumors: tumor heterogeneity, where cancer cells differ in metabolic rate and therefore responsiveness to treatment. That cellular variation presents a key challenge in treating cancer; even if most tumor cells respond to a drug, the resistant minority can survive and fuel relapse. In learning that treatment could behave differently across a single tumor, we glimpsed how complex the fight against cancer truly is, and how each small insight propels the fight forward.
For over a decade, I believed that discovery meant always solving the case. Instead, it looks like standing in a lab coat with trembling hands, quietly tearing up over sacrificed embryos. It carries the fear born in hospital waiting rooms and channels it into micropipettes and data logs. It refuses to accept the “inevitable” and chases answers with a hope that one day, another family will sit in those waiting rooms and hear good news for once.