Some tumors eliminate healthy neighboring cells to grow, study reveals

by Institute for Research in Biomedicine (IRB Barcelona)

edited by Gaby Clark, reviewed by Alexander Pol

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Chromosomal instability is a common feature in many solid tumors and is associated with greater aggressiveness. For years, its main contribution to cancer was thought to be driving the evolution of tumor genomes, causing cells to gain chromosomes with growth-promoting genes or lose chromosomes with tumor-suppressor genes.

A study led by Dr. Marco Milán's laboratory at IRB Barcelona shows that chromosomal instability promotes tumor growth through a completely new mechanism. The work, published in EMBO Reports, reveals that tumor cells with an incorrect number of chromosomes can become senescent and release signals that alter the behavior of neighboring tissues.

The study, conducted in Drosophila melanogaster, shows that these senescent cells not only promote tumor growth and invasiveness but also induce the death of nearby healthy cells. This, in turn, fuels the tumor's growth.

"What we are seeing is that the tumor doesn't just grow due to its own internal alterations. It also interacts with the surrounding healthy tissue, preventing its cells from proliferating and ultimately killing them. And that process is necessary for the tumor to grow further," explains Dr. Marco Milán, an ICREA researcher and head of the Development and Growth Control laboratory at IRB Barcelona.

Cells that stop dividing but remain active

When a cell has an incorrect number of chromosomes—a condition known as aneuploidy—its internal functioning becomes unbalanced. When cells can no longer properly manage the accumulated damage, they trigger alarm signals. Often, they enter senescence, a state in which they stop dividing, increase in size and release molecules that influence surrounding cells.

In principle, senescence is a protective mechanism. In specific situations, such as an injury, senescent cells help attract the immune system to repair tissue. The problem arises when these cells are not cleared and persist in the body chronically. When that happens, their sustained activity can generate inflammation and promote pathological processes such as aging or cancer.

In this work, the team studied senescent cells caused by aneuploidy—that is, cells with an abnormal number of chromosomes. Although these cells present highly diverse alterations, the researchers observed that they share a common response. This shared program includes halting cell division, activating stress response mechanisms and an increased capacity to secrete signals into their environment.

The research was carried out in Drosophila melanogaster, a model that allows scientists to observe in a living organism how cells with chromosomal instability interact with surrounding tissues. Many of the behaviors described here, such as aneuploidy, senescence and the secretion of inflammatory signals, have also been observed in mammalian cells.

A tumor that modifies its environment

Milán's laboratory has spent more than a decade studying how chromosomal instability contributes to tumor development. Previous work by the group had identified signals secreted by senescent cells that promote tumor growth, invasion and systemic effects on the body.

In this new study, the team describes a fourth function of these cells: their ability to damage neighboring healthy tissue. The researchers identified several molecules secreted by senescent cells that act on nearby normal cells. Some of these molecules, such as Dilp8 (relaxin in humans) and ImpL2 (IGFBP7 in humans), reduce the proliferation of neighboring cells. Others, such as the cytokines Upd1 and Upd3 (IL-6 in humans) and Eiger (a molecule equivalent to TNF in mammals), help induce the death of these nearby healthy cells.

"We know that the tumor needs these neighboring cells to die in order to grow more. What we don't yet know for sure is why. One possibility is that the death of these cells releases nutrients, such as amino acids or other metabolites, which the tumor can then exploit," explains Kaustuv Ghosh, co-first author of the study alongside Aishwarya Kunchur.

Moving forward, the team wants to study the heterogeneity of these aneuploid senescent cells with greater resolution.

To do this, "we plan to use single-cell analysis to see if the gain or loss of specific chromosomes is associated with specific behaviors within the tumor," Dr. Milán says.

Publication details

Kaustuv Ghosh et al, A tumour-host feed-forward loop contributes to the growth of chromosomal instability-induced tumours, EMBO Reports (2026). DOI: 10.1038/s44319-026-00811-7

Journal information: EMBO Reports

Key medical concepts

Chromosomal InstabilityAneuploidyCellular Senescence

Clinical categories

Oncology Provided by Institute for Research in Biomedicine (IRB Barcelona) Who's behind this story?

Gaby Clark

MA in English, copy editor since 2021 with experience in higher education and health content. Dedicated to trustworthy science news. Full profile →

Alexander Pol

PhD nano-engineering from Delft University. Published researcher and journal reviewer. Brings scientific insight to content standards. Full profile →

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