HMN 2026: How Embryonic proteins are reactivated in lung tumors may drive faster growth

lung

Researchers have uncovered how proteins normally active only before birth can drive aggressive lung cancer, opening new avenues for future treatments. The study found that more aggressive lung cancers switch on a pair of embryonic proteins (proteins not usually found in healthy adult cells), resulting in poorer patient outcomes.

Lung cancer remains the leading cause of cancer death, driving urgency around research into novel ways to treat this cancer.

The experimental research conducted at Peter Mac showed that when these proteins were present in lung cancer cells, tumors grew more rapidly, confirming their role in cancer progression.

Laboratory Head, Associate Professor Melanie Eckersley-Maslin, said that the research demonstrates that some lung cancers are effectively hijacking an early developmental program to fuel their growth. The study is published in the journal Genes & Development.

“These embryonic proteins change how DNA is regulated inside cancer cells, making it easier for cancer-promoting genes to be switched on,” she said.

Inside cells, DNA is organized into a structure known as chromatin, which controls which genes are active or inactive. The researchers discovered that the embryonic proteins reshape the chromatin structure in lung cancer cells, opening up access to genes that promote tumor growth and survival.

“The molecular changes we see have not been described before in cancer cells,” said Dr. Janith Seneviratne, postdoctoral researcher in the Eckersley-Maslin laboratory and first author on the study.

“This is exciting as we’ve uncovered a new way cancer cells restructure their DNA to become more adaptable and difficult to treat,” he said.

Associate Professor Eckersley-Maslin commented that the research findings provided critical insight into the fundamental biology of lung cancer and how aggressive disease develops.

“By understanding the mechanisms that drive these dangerous cancers, we can start to think about new treatment strategies.”

Future treatments may include therapies that target embryonic proteins directly or reverse the chromatin changes they cause.

While further research is needed, the study lays important groundwork for the development of new approaches aimed at slowing or preventing the most aggressive forms of lung cancer.

Publication details

Janith A. Seneviratne et al, Embryonic stem cell factors DPPA2/4 amplify active H3K4me3–H2AK119ub chromatin domains in non-small cell lung cancer, Genes & Development (2026). DOI: 10.1101/gad.353102.125

Journal information:
Genes & Development


Clinical categories

OncologyPulmonary medicine


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