• Home
  • Technology
  • Gaming
  • Entertainment
  • World & Business
  • Science
  • Sports
  • AI
HomeTechnologyGamingEntertainmentWorld & BusinessScienceSportsAI
Science
Report

Colon cancer cells reportedly shifted toward normal-like states in lab tests

A post describing KAIST research says a computational model identified three genes to suppress in colon cancer cells.

Brian RoemmeleBR
1 Source, 5h ago, first seen 5h ago

TLDR

A post describing KAIST research says suppressing MYB, HDAC2 and FOXA2 gave colon cancer cells normal-like traits and reduced their proliferation in three cell lines. It says tumors formed from reprogrammed cells were smaller than controls in mice. The research is preclinical; no human trials are described.

Combined views

122.4K

1 Source, first seen 5h ago

2.4K likes67 comments2.3K saves537 reposts

Combined views

122.4K

1 Source, first seen 5h ago

2.4K likes67 comments2.3K saves537 reposts

Sentiment

Positive——Negative

Summary

Not enough discussion yet.

No sentiment analysis available yet.

Featured Source

Sentiment

Positive——Negative

Summary

Not enough discussion yet.

No sentiment analysis available yet.

1 Source

Brian Roemmele@BrianRoemmeleTHIS IS BIG! The Cancer Cells That Changed Their Minds A KAIST team just reversed cancer without killing a single cell — and the method may matter more than the result. For a century, oncology has had exactly one strategy: find the cancer and destroy it. Chemotherapy poisons it. Radiation burns it. Surgery cuts it out. Immunotherapy teaches the body to hunt it. Every weapon differs in precision, but not in philosophy. The tumor is an enemy. You win by killing. Now a team at South Korea's KAIST has proposed a heresy: *what if the tumor doesn't need to die?* In a study led by Professor Kwang-Hyun Cho of the Department of Bio and Brain Engineering, published in Advanced Science ("Control of Cellular Differentiation Trajectories for Cancer Reversion," DOI 10.1002/advs.202402132), researchers took colon cancer cells and — without poisoning, irradiating, or cutting them — turned them back into normal cells. Not dead. Not damaged. Just normal again. The tumors, grown in mice, shrank dramatically. The surrounding tissue was left intact, because there was never an attack to survive. This is early research — cell lines and animal models, no human trials, real obstacles still unsolved. But the conceptual break is the story. For the first time, cancer treatment has a second verb. Not just destroy. Also: convert. The digital twin of a cell The KAIST team's insight begins with a redefinition of what cancer is. The conventional view treats cancer as a pile of broken machinery: mutations accumulate, checkpoints fail, cells proliferate. Cho's group looked at the same evidence and saw something different — a trajectory. During oncogenesis, they observed, normal cells don't just break. They regress, sliding backward along the differentiation path they followed when they matured. A colon cell becomes, in effect, a confused stem cell: immature, proliferative, lost. If cancer is a wrong turn on a developmental road, then the treatment question changes. You don't blow up the road. You build a map and find the turn. That map is what the team calls a digital twin — a complete computational model of the gene network governing a cell's differentiation. Using data from 4,252 intestinal cells, they reconstructed a network of 522 interacting components, capturing how genes regulate one another as a cell matures or degrades. Then they did the audacious thing: they asked the simulation which levers, flipped together, would push a cancer cell back down the road toward normalcy. The answer came through a system they built called BENEIN (Boolean Network Inference and Control), which models gene interactions as logical relationships and systematically tests which interventions redirect the network's state. The simulation pointed to three master regulators — the genes MYB, HDAC2, and FOXA2 — acting together as the switch that holds the cancerous state in place. Turn all three off simultaneously, the model predicted, and the cell would stop proliferating and differentiate into something resembling a normal intestinal cell. They tested it, and it worked. In three colon cancer cell lines, suppressing MYB, HDAC2, and FOXA2 together strongly induced differentiation into normal-like cells. The cancer cells began expressing markers of healthy intestinal tissue. Proliferation collapsed — not because the cells died, but because they grew up. In animal models, tumors formed from the reprogrammed cells were dramatically smaller than controls, and under the microscope they looked far more like normal tissue. The signature achievement, and the one that would matter most to any patient reading this: there was no collateral damage. Nothing was poisoned, burned, or irradiated. The healthy tissue never came under fire, because there was no fire. 1 of 25h
    • Home
    • Technology
    • Gaming
    • Entertainment
    • World & Business
    • Science
    • Sports
    • AI

    1 Source

    Brian Roemmele@BrianRoemmeleTHIS IS BIG! The Cancer Cells That Changed Their Minds A KAIST team just reversed cancer without killing a single cell — and the method may matter more than the result. For a century, oncology has had exactly one strategy: find the cancer and destroy it. Chemotherapy poisons it. Radiation burns it. Surgery cuts it out. Immunotherapy teaches the body to hunt it. Every weapon differs in precision, but not in philosophy. The tumor is an enemy. You win by killing. Now a team at South Korea's KAIST has proposed a heresy: *what if the tumor doesn't need to die?* In a study led by Professor Kwang-Hyun Cho of the Department of Bio and Brain Engineering, published in Advanced Science ("Control of Cellular Differentiation Trajectories for Cancer Reversion," DOI 10.1002/advs.202402132), researchers took colon cancer cells and — without poisoning, irradiating, or cutting them — turned them back into normal cells. Not dead. Not damaged. Just normal again. The tumors, grown in mice, shrank dramatically. The surrounding tissue was left intact, because there was never an attack to survive. This is early research — cell lines and animal models, no human trials, real obstacles still unsolved. But the conceptual break is the story. For the first time, cancer treatment has a second verb. Not just destroy. Also: convert. The digital twin of a cell The KAIST team's insight begins with a redefinition of what cancer is. The conventional view treats cancer as a pile of broken machinery: mutations accumulate, checkpoints fail, cells proliferate. Cho's group looked at the same evidence and saw something different — a trajectory. During oncogenesis, they observed, normal cells don't just break. They regress, sliding backward along the differentiation path they followed when they matured. A colon cell becomes, in effect, a confused stem cell: immature, proliferative, lost. If cancer is a wrong turn on a developmental road, then the treatment question changes. You don't blow up the road. You build a map and find the turn. That map is what the team calls a digital twin — a complete computational model of the gene network governing a cell's differentiation. Using data from 4,252 intestinal cells, they reconstructed a network of 522 interacting components, capturing how genes regulate one another as a cell matures or degrades. Then they did the audacious thing: they asked the simulation which levers, flipped together, would push a cancer cell back down the road toward normalcy. The answer came through a system they built called BENEIN (Boolean Network Inference and Control), which models gene interactions as logical relationships and systematically tests which interventions redirect the network's state. The simulation pointed to three master regulators — the genes MYB, HDAC2, and FOXA2 — acting together as the switch that holds the cancerous state in place. Turn all three off simultaneously, the model predicted, and the cell would stop proliferating and differentiate into something resembling a normal intestinal cell. They tested it, and it worked. In three colon cancer cell lines, suppressing MYB, HDAC2, and FOXA2 together strongly induced differentiation into normal-like cells. The cancer cells began expressing markers of healthy intestinal tissue. Proliferation collapsed — not because the cells died, but because they grew up. In animal models, tumors formed from the reprogrammed cells were dramatically smaller than controls, and under the microscope they looked far more like normal tissue. The signature achievement, and the one that would matter most to any patient reading this: there was no collateral damage. Nothing was poisoned, burned, or irradiated. The healthy tissue never came under fire, because there was no fire. 1 of 25h
    Today's Rank

    #1

    Today's Rank

    #1