From Lab to Life: Cancer Drug Breakthrough

Cancerous tumors are phenomenally good at overcoming the body’s defenses.  Centuries, eons, of evolution have given them this ability.  Evolution has made we humans what we are – but also created a horde of diabolical enemies—and cancer is among the leading one.   Ten million people die of cancer yearly!  This is equal to the entire population of Israel.

Science Daily reports: “A new experimental drug called CS18 may help break through cancer drug resistance by disabling several of the defenses tumors use to survive treatment. It strengthened existing therapies, restored drug sensitivity in resistant lung cancer cells, and slowed tumor growth in animal models.”   **

** Fang-Tsyr Lin, Shwu-Jiuan Lin, Kang Liu, Yang Xiao, Lidija A. Wilhelms Garan, Helena Folly-Kossi, Weei-Chin Lin. Development of a structurally distinct TopBP1 inhibitor that enhances PARP blockade and reverses osimertinib resistance. Science Advances, 2026; 12 (32) DOI: 10.1126/sciadv.aeg1996

This research deserves a deeper description –  showing how human brainpower is confronting ‘cancer evolutionary deception’.

“Therapeutic resistance is a main obstacle to achieve effective and durable cancer treatments,” said corresponding author Dr. Weei-Chin Lin, professor of medicine – hematology and oncology and of molecular and cellular biology at Baylor. “While some therapies are effective at the beginning, many patients eventually relapse because cancer cells can activate compensatory and convergent biological pathways that allow them to overcome the toxic effects of therapy, promoting survival.”

“Rather than focusing on a single cancer pathway, the researchers set out to develop a drug that could interfere with a broader control center involved in several cancer-promoting processes at once. Their target was topoisomerase IIß-binding protein 1 (TopBP1), which the team describes as a ‘biological switchboard’ because it helps regulate multiple pathways associated with cancer growth and survival.   The researchers wanted to determine whether disrupting this central control point could produce longer-lasting treatment responses and help overcome resistance.”

“Of all the ‘biological switches’ on TopBP1, switch BRCT7/8 interacts with several key regulators of cancer growth, including MIZ1, a suppressor of cancer driver MYC; mutant p53, which can acquire cancer-promoting functions; and PLK1 and CIP2A, proteins that help cancer cells survive and divide,” said Lin, a member of Baylor’s Dan L Duncan Comprehensive Cancer Center. “All together, these diverse roles position TopBP1-BRCT7/8 as a promising target for intervention.”

In a sense, we are currently in a life-and-death matchup between cancer’s ‘smarts’, developed over centuries, many centuries – and the creative brainpower of scientists.  I believe we humans will eventually win, saving millions of lives, including our loved ones. But so far the process has seemed painfully slow.  Perhaps the Baylor research will be the start of a breakthrough, to improve our odds of success.