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Meet Ashka Shah, the 17-year-old New York student who studied how a cancer-driving protein enters the cell nucleus and found a way to block its harmful signalling while preserving its normal function


Meet Ashka Shah, the 17-year-old New York student who studied how a cancer-driving protein enters the cell nucleus and found a way to block its harmful signalling while preserving its normal function
Ashka Shah (Jericho Senior High School, Jericho, NY)

A 17-year-old student from New York has developed a targeted method to stop cancer cells from growing, earning national recognition for tackling one of the biggest challenges in cancer research. Ashka Shah, a senior at Jericho High School on Long Island, developed a method that blocks the harmful activity of a key cancer-driving protein without stopping its important functions in healthy cells. Her research earned her a place as a finalist in the 2026 Regeneron Science Talent Search, one of the oldest and most prestigious science and maths competitions for American high school students. The project focuses on the Wnt signalling pathway, an important biological system that controls normal cell growth, stem cell maintenance and tissue repair. When mutations occur, a key protein in this pathway, beta-catenin, can build up in large amounts and move into the cell nucleus. There, it activates genes that help aggressive tumours grow, especially in liver and colorectal cancers.

Separating cancer growth from healthy function

Scientists have struggled to target beta-catenin because the protein has two very different roles in the body. Outside the nucleus, beta-catenin helps form important structures that hold healthy cells together. Completely blocking the protein can therefore cause serious toxicity and damage healthy tissues. Shah focused instead on how mutant beta-catenin gets into the nucleus and causes harm. According to her project profile published by the Society for Science, Shah found that a helper protein called Gid8 helps mutant beta-catenin enter the nucleus, where it switches on genes linked to cancer growth. Using fruit fly models, cultured human liver cancer cells and molecular binding experiments, Shah identified a small section of the beta-catenin protein that could interfere with this process. By introducing the targeted peptide, she was able to block the Gid8-assisted transport system. This stopped the mutant beta-catenin from reaching the nucleus and driving uncontrolled cell growth, while allowing the protein to continue performing its important structural role in healthy tissue. Her project, formally titled “Selective Dual Inhibition of beta-Catenin in Wnt-Driven Cancers via Gid8-Assisted Translocation and a Precision Peptide-Based Gene Therapy,” presents a possible new approach to precision cancer treatment.

National recognition for her research

Shah was selected as one of 40 national finalists from 2,612 applicants across the United States. It was the largest group of applicants to the competition since 1967. The Society for Science selects finalists based on the originality of their research, scientific quality and leadership. According to official competition records, each of the 40 finalists receives at least 25,000 dollars, while the top awards can reach 250,000 dollars. The final judging takes place in Washington, D.C. Shah’s work in molecular biology is only one part of her wider academic and community involvement. She is president of Jericho High School’s Medical Minds Club, captain of the school’s varsity fencing team and involved in local community service projects.

A possible path towards precision cancer treatment

Finding treatments that can block cancer-related activity without damaging healthy cells remains a major goal in cancer research. Many current treatments affect both cancerous and healthy cells, which can lead to serious side effects. Shah’s research takes a more targeted approach by focusing on the Gid8 mechanism that helps move beta-catenin into the nucleus. By blocking this specific interaction, her work suggests that the cancer-driving activity of beta-catenin could potentially be stopped while leaving its normal functions in healthy cells untouched. The research presented to the Society for Science points towards the possibility of using peptide-based gene therapies to target this transport process. Such an approach could eventually provide a more precise option than treatments that affect healthy organs along with cancer cells.



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