By Sola Ogundipe 

Researchers in New York reviewed records from 11,000 cancer patients to evaluate long non-coding RNAs (lncRNAs), a type of RNA molecule that helps regulate gene behaviour and distinguish healthy from non-healthy cells. 

In a breakthrough that could transform cancer treatment, researchers in New York have identified a mysterious molecule that may fuel the deadliest form of breast cancer in young women—and found a way to shut it down.

Scientists at Cold Spring Harbor Laboratory have zeroed in on LINC01235, a previously overlooked RNA molecule, as a potential driver of triple-negative breast cancer (TNBC)—a fast-growing, treatment-resistant cancer that disproportionately affects women under 40. 

After sifting through the genetic data of more than 11,000 cancer patients, they discovered that LINC01235 supercharges tumour cells, likely by activating a cancer-linked gene known as NFIB.

Using advanced CRISPR technology, researchers turned off LINC01235 in tumour samples and observed something remarkable: cancer cells slowed their growth and lost their ability to form aggressive tumours. Without the rogue molecule, the cancer’s grip on the body loosened—raising hopes for a new generation of targeted therapies.

The gene NFIB, once activated by LINC01235, appears to suppress the production of p21, a protein that normally keeps cell growth in check. Without p21, cancer cells spread like wildfire. By disrupting this dangerous duo, scientists believe they could stop TNBC in its tracks.

Triple-negative breast cancer accounts for up to 15 percent of breast cancer cases yet it’s responsible for a disproportionately high number of deaths. Often found in younger patients and particularly common among Black women, TNBC lacks the hormone receptors that most breast cancer treatments target. That makes discoveries like this one **all the more vital.

To test their theory, researchers created miniature tumour “organoids” using patient tissue samples. These models clearly showed elevated levels of LINC01235 in cancerous cells compared to healthy ones. Disabling the molecule not only reduced tumour size, but also weakened its ability to spread.

“This could be the tip of the iceberg,” said Dr. David Spector, senior researcher on the study. The team is now exploring how to translate these findings into targeted therapies that could give young patients a fighting chance—especially those for whom standard treatments have failed.

With breast cancer diagnoses rising and aggressive forms like TNBC becoming more prevalent, this study—published in Molecular Cancer Research—marks a bold step toward understanding and eventually defeating one of cancer’s most elusive threats.