Author: Elise Johnson

Before the First Dose

Posted on by Elise Johnson

Kierkegaard observed that one of humanity’s enduring tensions is that while life can only be understood backwards, it must be lived forwards. It’s a truth medicine knows intimately: in the treatment that worked until it didn’t, the resistance that arrived without warning, the moment a doctor has to tell a patient that the drug that was helping has stopped. Not because anyone made a mistake, but because the critical knowledge that would have mattered arrived too late, if at all.

A recent paper from the National Cancer Institute is, in a small but meaningful way, science’s pursuit of that elusive foresight: an understanding that emerges early enough, for once, to change what happens next.

The Elegant Idea

For decades, chemotherapy has worked by brute force, flooding the body with toxins designed to kill rapidly dividing cells. The problem is that rapid division isn’t unique to cancer. Hair follicle cells, gut lining cells and immune cells also divide rapidly, which is why patients lose hair, lose energy and become susceptible to infection. Chemotherapy targets a behavior, but the drug has no way to tell a healthy cell from a cancerous one.

Antibody-drug conjugates (ADCs) change that. Instead of targeting what cancer cells do, they target what cancer cells are. Cancer cells tend to display certain proteins on their surface in far greater numbers than healthy cells do. The antibody is engineered to seek out those proteins specifically. It navigates to its target, binds and waits for the cell to do what cells routinely do: pull it inside. Once there, the cell’s own digestive machinery (the lysosome) breaks down the chemical tether holding the toxin to the antibody, releasing the toxin to kill the cell from within. More than a dozen ADCs have received FDA approval in recent years, and the field is evolving fast.

What the Cell Does Next

But cancer cells don’t simply accept their fate. Even when an ADC delivers its payload perfectly—the antibody finds its target, the cell pulls it inside, the lysosome cuts the tether—a pump embedded in the cell membrane can grab the released toxin and throw it back out before it causes damage.

The delivery worked. The package got ejected anyway.

These pumps—ATP-binding cassette transporters, or more plainly, efflux pumps—are a normal feature of cell biology. Their job is cellular housekeeping, clearing out unwanted or toxic substances before they cause damage. Under the pressure of drug treatment, cancer cells do what life has always done under pressure: the ones best equipped to survive do. The same mechanism that has shaped living things for billions of years now works against the treatment. Not all cancer cells are identical, and the ones that happen to produce more pumps survive while others don’t, gradually shifting the tumor toward resistance.

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Light Has a Favorite Color, But It’s Complicated

Posted on by Elise Johnson

Last spring, my niece and I made a trip to a home improvement store to put together a Mother’s Day planter for my sister. My niece had a clear vision: my sister’s favorite color is blue, so we were going to buy blue flowers. We walked every aisle of the garden center. We checked the annuals, the perennials, and the hanging baskets then left with purple, red, and a grumpy 7-year-old.

It turns out we were not up against a bad selection. We were up against biology.

The Problem with Blue

Blue is one of the rarest colors in the natural world. The food industry is currently finding that out the hard way. There is a good chance you have eaten something blue today. Maybe it was the frosting on a birthday cake, the coating on some M&M’s® candies, or the sports drink in your refrigerator. That blue almost certainly came from a petroleum-based synthetic dye, and for the first time in decades, the food industry is being asked to find something better.

The FDA banned Red Dye No. 3 in January 2025, and pressure has been building around the remaining synthetic dyes ever since, including Blue No. 1 and Blue No. 2. Major food brands have begun announcing plans to reformulate.

There is just one problem. Blue is genuinely, stubbornly hard to make in nature. It turns out that blue has almost nothing to do with color, and almost everything to do with light.

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More Than Beer and Cheese: Why Wisconsin Has Always Been Good Ground for Science 

Posted on by Elise Johnson

Challenging Assumptions About Innovation

When people talk about places where science and technology tend to flourish, a few names surface almost immediately. Silicon Valley, Boston, Seattle, Houston. Cities associated with density, competition and speed.

For many people outside the state, Wisconsin still collapses into a short list of associations: beer, cheese, cold winters, maybe a football team. Biotechnology rarely makes that list.

That hesitation usually has less to do with science itself and more to do with assumptions about where innovation is supposed to live. National Wisconsin Day, celebrated February 15, is a good moment to look past those assumptions and consider what Wisconsin has quietly offered for a long time: an environment and culture that is well-suited for scientific advances.

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The Breakthrough Was There All Along

Posted on by Elise Johnson

If you’ve ever played The New York Times game Connections, you know the feeling. You’re staring at a grid of words, knowing the solution is there, but unable to see how the pieces fit together. All you can do is work with the words in front of you. There are no extra clues, no new information coming. The only option is to shuffle, to look at the same information in a different arrangement until patterns begin to appear.

Nothing about the problem changes. Then something about how you see it does.

In 2014, a third-year medical student named David Fajgenbaum checked himself into the emergency room mid-exam. He felt off. By the time anyone understood why, he was in the ICU with multiple organ failure from a disease so rare it wasn’t taught in medical school: Castleman disease. The only approved drug didn’t work. A priest came to his bedside and read him his last rites. He was 25.

Fajgenbaum survived that relapse, and four more after it. As he recounted in a recent episode of NPR’s Radiolab, he understood that chemotherapy was keeping him alive without curing him, and that waiting for a new drug to be developed (a process that typically takes 10 to 15 years and billions of dollars) wasn’t an option he had. So he did something unusual. He started asking his doctors to save his blood samples, and he ran experiments on himself.

What he found was that a specific signaling pathway in his immune system, mTOR, was in overdrive. When he searched the existing pharmacological literature for something that could block it, he found an answer that had been sitting in pharmacies for 25 years. Sirolimus, a drug approved in 1999 to prevent organ transplant rejection, had never been used for Castleman disease. The biology of his disease hadn’t changed. The drug had always existed. The connection simply hadn’t been made.

He took it. It worked. He has been in remission for over a decade.

The detail worth holding onto isn’t the drug or the disease. It’s the instinct. Fajgenbaum didn’t wait for new knowledge to arrive. He looked differently at what already existed.

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