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Scientists Discover Way to Send Information into Black Holes Without Using Energy

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Why Some Cancers Are Worse Than Others?

In a quiet laboratory at Virginia Tech, graduate student Megan Sweet performs a task that sounds almost surgical in its precision—and strangely meditative in its repetition.

She slices tumors.

Inside a chilled metal box, Sweet carefully positions a tiny tumor grown in a lab mouse. With steady hands and intense focus, she slowly brings the tissue closer to a razor-sharp blade. Then comes the rhythmic sound: chunk, chunk, chunk.

“This is the hardest and most time-consuming part,” Sweet explains. “But it’s also kind of meditative.”

What she produces are not ordinary cuts. The tumor slices are so thin they become almost translucent. Each one is carefully transferred onto a glass slide, later stained, and examined under a high-powered microscope.

Slice. Stain. Stare. Compare.

This cycle repeats daily in labs at Virginia Tech, forming the backbone of research that is helping scientists understand one of medicine’s biggest mysteries: why some cancers are aggressive and deadly, while others grow slowly or remain contained.

The findings from this research have been published in leading scientific journals including the Proceedings of the National Academy of Sciences and Cancer Research.

Why slicing tumors matters

At first glance, slicing tumors may seem simple. But each thin slice contains a detailed map of cancer’s internal world—its structure, its behavior, and its hidden weaknesses.

After staining, different cellular structures inside the tumor become visible. Under the microscope, researchers can see how cancer cells are arranged, how they grow, and how they interact with surrounding tissue.

These tiny slices help answer big questions:

  • How does cancer spread?

  • Why do some tumors grow faster than others?

  • What makes certain cancers resistant to treatment?

For Megan Sweet and her colleagues, every slide brings them a step closer to understanding these patterns.

The science of “replicating errors”

To understand cancer, researchers first need to understand how normal cells behave.

Most healthy human cells are diploid. That means they contain two copies of each chromosome—one from each parent. This balanced system is essential for normal growth and repair.

But sometimes, mistakes happen when cells divide. A cell may accidentally gain or lose chromosomes. When this error repeats itself, it can lead to serious consequences.

It’s like a printing press making a mistake and then copying that mistake over and over again. Eventually, the error spreads and grows.

This is one of the pathways that can lead to cancer.

Working with cell biologist Daniela Cimini, Sweet and graduate student Mat Bloomfield have spent years studying these abnormal cells, especially those with incorrect chromosome numbers.

When cells double: the tetraploid problem

In their experiments, researchers created a special type of abnormal cell called a tetraploid cell.

Normally, a diploid cell divides into two new diploid cells. But in this experiment, scientists forced cells to duplicate their chromosomes but skip division. The result: a cell with four full sets of chromosomes.

These are called tetraploid cells.

At first, this might sound like just a lab curiosity. But in real life, tetraploid cells can appear during tumor development in humans. And when they do, it is often linked with more aggressive cancer and worse outcomes.

Scientists suspected these cells might play a bigger role in cancer progression than previously thought.

A surprising discovery inside tumors

To test this idea, Sweet and Bloomfield compared two types of tumors in mice:

  • Tumors formed from normal diploid cancer cells

  • Tumors formed from tetraploid cancer cells

What they discovered surprised them.

Even though tetraploid cells became fewer over time inside the tumors, the tumors themselves grew much faster and became much larger.

Why?

The answer was not what scientists expected.

Instead of simply multiplying, tetraploid cells were influencing their environment. They were recruiting stromal cells—non-cancerous cells that normally provide structural support to tissues.

But in this case, those support cells were being turned into helpers for the tumor.

As Megan Sweet explained, “The presence of even a small fraction of these tetraploid cells can promote the recruitment of extra non-cancerous cells that support further tumor progression.”

In other words, a small number of abnormal cells can “reprogram” the surrounding tissue to help cancer grow.

Not all tetraploid cells behave the same

The second major discovery came as a surprise during another set of experiments.

When Bloomfield created tetraploid cells from human cancer samples and grew them into separate clones, he expected all the cells to be the same size—roughly twice as large as normal cells due to extra chromosomes.

But they were not.

Some clones were 25% to 30% smaller than expected.

Even more surprising: these smaller cells were far more aggressive.

“The smaller clones are more tumorigenic,” said Mat Bloomfield. “They grow faster, are more invasive, and more tolerant of common anti-cancer and stress-inducing drugs.”

This was unexpected because scientists usually assume larger cells with more genetic material would be more dominant. Instead, the smaller tetraploid cells were proving more dangerous.

Testing in animals and humans

To confirm their findings, the team tested these cells in mice. Tumors containing smaller tetraploid cells grew faster and became more aggressive than those with larger ones.

What made this even more important was that the pattern held true across different cancer types, including breast and colorectal cancer.

This suggested the phenomenon was not limited to a single disease.

But the researchers went further.

Using data from the The Cancer Genome Atlas, which contains thousands of patient samples, they found a similar trend in humans.

Patients with cancers linked to smaller tetraploid cells tended to have worse outcomes and lower survival rates.

Why cell size may predict cancer behavior

These findings led to a powerful conclusion: size matters in cancer cells more than previously thought.

As Daniela Cimini explained, scientists already knew tetraploidy could make cancer more aggressive. But now, they understand that cell size can help predict how dangerous those tumors might become.

This opens new possibilities for cancer research:

  • Better prediction of tumor aggressiveness

  • Improved understanding of cancer evolution

  • Potential new biomarkers for diagnosis

In the future, doctors might not only look at genetic mutations—but also at physical traits like cell size.

What comes next

The research is still ongoing. Scientists now want to understand why smaller tetraploid cells behave more aggressively. Is it due to gene regulation? Metabolism? Stress resistance?

There are still many unanswered questions.

But each answer begins the same way in the lab:
Slice. Stain. Stare. Compare.

And for Megan Sweet, that routine continues—quiet, careful, and deeply focused.

Because sometimes, the smallest slices of tissue can reveal the biggest truths about cancer.

References: (1) M.L. Sweet, M. Bloomfield, N. Keen, N. Bano, X. Pan, N.C. Baudoin, B. Udayasuryan, R.N. Ahmad, E. Riddervold, E. Klaiber, S.S. Verbridge, E.M. Schmelz, J. Chen, & D. Cimini, Oxidative stress and serum deprivation influence the evolution of newly formed tetraploid cells during tumorigenesis, Proc. Natl. Acad. Sci. U.S.A. 123 (22) e2522077123, https://doi.org/10.1073/pnas.2522077123 (2026). (2) Mathew Bloomfield, Sydney M. Huth, Daniella S. McCausland, Ron Saad, Nazia Bano, Tran N. Chau, Megan L. Sweet, Nicolaas C. Baudoin, Andrew McCaffrey, Kai Fluet, Eva M. Schmelz, Uri Ben-David, Daniela Cimini; Cell and Nuclear Size Is Associated with Chromosomal Instability and Tumorigenicity in Cancer Cells That Undergo Whole Genome Doubling. Cancer Res 1 May 2026; 86 (9): 2126–2142. https://doi.org/10.1158/0008-5472.CAN-24-3718

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