Ancient Proteins Reveal Mysterious Human Relatives in Southwestern China

Denisovans are one of the most elusive branches of the human family tree. Scientists first identified them in 2010, when DNA from a tiny finger bone found in Denisova Cave in Siberia revealed a previously unknown group of ancient humans. Since then, researchers have confirmed only a handful of fossils outside Siberia as Denisovan—two jaws, a rib and a skull.

However, genetic evidence suggests Denisovans traveled widely. People in Southeast Asia and Oceania still carry Denisovan DNA. What was missing was fossil evidence from the region in between: southwestern China. Now, a new study published in Nature could fill that gap.

Continue reading “Ancient Proteins Reveal Mysterious Human Relatives in Southwestern China”

Nitrile Gloves, Not Ribbons

Every October, the noise starts up again: it’s breast cancer’s turn for awareness. I brace for it a little every year. What bothers me isn’t the concept, it’s watching companies race to out-pink each other.

A pink ribbon on a shirt or a car can foster a certain amount of solidarity, but at the corporate level, the awareness noise is genuinely inescapable: a building lit up pink for the night, a pink yogurt lid, or a player running out onto the field in pink cleats. Many companies have run some version of the same campaign, and what actually happens to the profit from pink merchandise varies wildly: modest percentages, hard caps on total donations, or numbers that only recently moved after enough people asked questions.

In addition to the question of money is the question of effect: what does a company’s participation do? If the goal actually is awareness, I’ve never understood who remains unaware. It tends to generate goodwill instead, and the sometimes cynical among us might call that marketing, whether or not that’s the intent.

Here’s a sentence that’s true to me, one most people have their own version of: my sister had breast cancer. One in eight women in the U.S. will hear that diagnosis in her lifetime (though women aren’t the only ones who get it). So we are aware. We have been aware for a long time.

At one point, however, we actually needed awareness, in the literal sense of the word. When the American Cancer Society started its breast cancer awareness campaign in 1985, breast cancer was a disease people didn’t discuss in polite company, self-exams weren’t routine, and mammograms weren’t the norm they are now. Getting people to talk about it, check themselves, and get screened was a real, specific goal, and awareness did its job at the time. Last year marked the campaign’s fortieth anniversary, a point at which even the American Cancer Society’s own retrospective pointedly admitted: awareness alone isn’t enough anymore.

October runs on that word, awareness, as if noticing something were the same as solving it. As if on November 1st, we can dust off our hands, congratulate ourselves, and move on to the next color of the month. But breast cancer research doesn’t run on that calendar. Real, promising work has been happening. Learning about it might not change anything either, not directly, but it’s one step closer to what the American Cancer Society itself is now calling “Turning Awareness Into Action.”

More Than a Pretty Face

This starts, perhaps unexpectedly, with the axolotl, a foot-long Mexican salamander known for its perpetual smile and the feathery gills that fan out from its head like a spray of coral. The most common pet-store variety is also, conveniently for this piece, pale pink. It has become plastered across backpacks, folders, plush toys, and t-shirts. My nine-year-old niece and her friends are obsessed with them.

Continue reading “Nitrile Gloves, Not Ribbons”

Can GLP-1 RAs Help Me Live Longer? Well…

scientist working in a research lab

GLP-1 Receptor Agonists (GLP-RAs) have transformed the treatment of diabetes and obesity and are an important advance in the successful treatment of these and maybe other chronic diseases. These medicines were originally developed to treat diabetes, with Ozempic, a semaglutide, released in 2016. In 2023 these drugs became known more generally because of their off-target effect of stimulating weight loss (1).

GLP-1 stands for “glucagon-like peptide 1”, a peptide hormone that is released from cells in the small intestine in the presence of nutrients. One of its functions is to mediate the secretion of insulin in response to these nutrients by activating the GLP-1 receptor in the pancreas.

What are some of the off-target effects of GLP-1RAs on aging that researchers are uncovering?

Several research studies of GLP-1 RAs have indicated that not only do they have the positive effects of regulating blood glucose and weight, but they have also shown benefits that include reduction of heart, liver and kidney diseases. A study published in Nature in 2026 by Feng and colleagues (2) now presents evidence that these drugs may even affect aging in a mouse model, attenuating age effects and maintaining cognition. The results are promising. The scientists looked at several recognized hallmarks of aging, including stem cell attrition, inflammation, protein folding and stability issues, and genomic stability. For both hematopoietic stem cells (HSCs) and neural stem cells (NSCs), the authors found that treatment with semaglutide increased the regenerative capacity of the respective tissues. Furthermore, they found that in semaglutide treatment increased expression of mitochondria-related genes and the oxidative-stress response genes, increased ATP content, and reduced levels of reactive oxygen species.

Continue reading “Can GLP-1 RAs Help Me Live Longer? Well…”

A New Human Neuron Model for Tau-Targeted Drug Screening

Every neuron relies on a protein called tau to keep its internal skeleton, the microtubule network, working properly. In a group of brain diseases known as “tauopathies,” tau stops doing its job. It misfolds, clumps together, and eventually contributes to the neuron loss that causes memory changes and shifts in behavior. Scientists studying these diseases have long wanted to watch this process unfold from its earliest moments in living human neurons. However, this has been surprisingly difficult.

Continue reading “A New Human Neuron Model for Tau-Targeted Drug Screening”

ADC Development: The Questions Running in the Background

You’ve had food stuck in your teeth at some point during a conversation you thought was going well. Or toilet paper trailing from the back of your shoe on a day you felt particularly put together. Maybe you’ve even forgotten to color in your very blonde eyebrows and spent the rest of the day looking like someone erased the top half of your face. But you had no idea. You’re walking around with the quiet, complete confidence of someone operating on incomplete information.

You weren’t wrong about anything you could see. You just couldn’t see everything, which is a different problem than getting a bad result. A bad result tells you something is wrong, but this doesn’t. This happens in the lab too. The number is clean, the program is advancing, and somewhere in the data, something is happening that your readout has no way to show you.

Antibody-drug conjugate (ADC) development has a version of this problem. The cytotoxicity readout is real, reliable, and correct. It’s also an aggregate, and an aggregate compresses everything that happened into a single number. That number can’t tell you which mechanisms produced it, which ones are underperforming, or what to change if the program stops working. It just tells you cells died, or they didn’t. You’re walking around with the quiet, complete confidence of someone operating on incomplete information.

Cytotoxicity: Where Every Program Begins

Cell viability assays were built to answer one question: did the cells die? Increase the dose, more cells die. Decrease it, fewer do. The curve is clean, the data is reliable, and the payload is doing what it was designed to do. For cytotoxicity, it’s the right question to ask.

That question has an established platform with consistent, reproducible data: our CellTiter-Glo® and RealTime-Glo™ Assays.

For most ADC programs, this is where the measurement work starts and stops, but it should only be where it starts. The question they answer well is only one of several your ADC is raising. The number means what it says, but the question it answers has a boundary, and the boundary leaves you with an incomplete picture.

Continue reading “ADC Development: The Questions Running in the Background”

Time Capsules in the Language of Science

In elementary school, I spent an art class layering greens. Jungle green fabric with a subtle coordinating stripe, delicate spring green tissue paper so translucent you could see through it, pieces of chunky emerald felt cut into the shape of leaves, sparkling seafoam and teal glitter, all of it pressed and glued onto a piece of tagboard in what my teacher called a monochromatic collage. All shades of one color. Mono: one. Chroma: color. I didn’t think about the word at the time because I was too busy glittering.

That same week, I took a science quiz on monocots and dicots and got the answer wrong. I couldn’t remember which plants had one seed leaf and which had two. When I got the test back and saw my error, it clicked. Of course a monocot has one seed leaf. I’d been using mono in art class while missing it on a science quiz down the hall. The root moved between rooms, but I hadn’t learned yet that it could.

That stuck with me. Although my formal education is in English and linguistics, my mind naturally sought out scientific connections. Greek and Latin roots were the place where those two interests didn’t have to compete. They had the precision of formulas, a combinatorial logic where twenty roots could unlock hundreds of words, and they worked on both sides of the hallway.

I write about science now, and the roots have remained my constant companion. A few weeks ago I was researching an organism called Rapaza viridis for a blog post on endosymbiosis. I’d never heard of it, but since viridis is Latin for green (the same root that gives us “verdant”), I already guessed this creature had something to do with photosynthesis. It does. R. viridis is a single-celled predator that steals chloroplasts from the algae it hunts and uses them to photosynthesize.

Learning more about the organism, I came across the term “transient chimerism.” Also new to me, but also immediately legible. The trans in “transient” is the same as in “transparent” and “transport”: ‘across,’ ‘through.’ Something passing through. Chimera: the Greek monster stitched together from a lion, a goat, and a serpent. Put together: a temporary state of being made from parts of more than one organism. The roots came through for me once again.

This keeps happening. I’ll hit a term I’ve never seen, and its pieces already feel familiar. I could spend this entire blog walking through terms and showing you their roots, but definitions only stay interesting for so long (and my family already compares me to the father in My Big Fat Greek Wedding). What I’ve become more interested in is something the roots do beyond defining. The roots that end up in a name tend to carry more than a definition. They carry an interpretation, an argument about the thing itself.

For years, I wondered about apoptosis. I knew apo meant ‘away from.’ I could see ptosis maybe shared something with “asymptote,” but I couldn’t figure out what cell death had to do with calculus. In 1972, John Kerr, an Australian pathologist, had been studying a form of cell death that looked nothing like anything he’d seen before. For most of pathology’s history, the only cell death anyone studied was the kind that showed up when something had gone wrong: a cell damaged by injury or infection or toxins, dying violently. That kind of death had a name: necrosis, from the Greek nekros (‘corpse’). The cell swells, ruptures, spills its contents, and triggers inflammation. Studying liver tissue, Kerr noticed a second kind of death happening quietly alongside it, in cells that hadn’t been damaged at all. The cell death he was watching was the opposite. The cell shrank, and its contents condensed. It broke apart into tidy packages that neighboring cells quietly absorbed. No mess. The body had planned this.

Continue reading “Time Capsules in the Language of Science”

AI Identifies the Target. Someone Still Has to Validate It.

Did you see the movie where Spider-Man files his taxes? Or the one where Wonder Woman sits on hold with her insurance company while her pasta water boils over? Or where Captain America finds blight on his tomato plants and drives to the county extension office where he spends fifty minutes with a seventy-four-year-old master gardener named Marlys then leaves with a handwritten note covering his soil composition, his watering schedule, and what Marlys calls “the mulching situation”?

No. Because the ordinary day-to-day doesn’t stand a chance next to the saving of the world.

We spend most of our lives in the ordinary. Not because we’re failing to reach the extraordinary, but because the ordinary is what holds everything together while we get there. It’s not the backdrop but the foundation. It’s what the story depends on, whether or not it gets any credit.

Drug Discovery Has a Storytelling Problem

Drug discovery runs almost entirely on ordinary days, punctuated by the moments that make the news: a new target gets identified, a compound shows promise, a trial produces results. Those moments get the headlines, press releases and keynote slots. What doesn’t get the same attention is the years of work behind those moments: the assays, the failed experiments, the redesigns, the slow accumulation of evidence that either holds up or doesn’t. That work has always been the majority of drug discovery.

Some of the most important work in drug discovery ends in a result nobody publishes, but a dead end isn’t a failure of the program. It’s the program working. The researcher who rules something out has learned something true. That knowledge travels forward even when it doesn’t make the headline because it can redirect the next hypothesis, narrow the next experiment or just quietly move things along. That work moves research forward without anyone announcing it.

The Shiniest Thing in the Room

Artificial intelligence is drug discovery’s latest extraordinary announcement, and the fanfare is legitimate. Most of the druggable proteome has never been touched. Of approximately 4,500 human proteins considered druggable, all approved drugs to date work through only 716 distinct targets. Drug hunters knew there was more biology to address but lacked a way to find and prioritize candidates at scale. AI is changing that. By scanning genetic evidence, biological networks and scientific literature at a scale no human team can match, AI is surfacing targets that were previously out of reach and ranking them by the strength of the evidence behind them.

Continue reading “AI Identifies the Target. Someone Still Has to Validate It.”

Another Crack in the RAS Code: The Measurement Story Behind Daraxonrasib

In late May 2026, a clinical trial result landed in the New England Journal of Medicine and immediately rewrote what oncologists believed was possible for patients with metastatic pancreatic cancer. Before the paper was published, people in the field were already calling it “transformative.” The data, when it came, agreed. In a disease where most second-line treatments offer months at best, a drug called daraxonrasib nearly doubled how long patients lived compared to those who received chemotherapy.1 It was approved by the FDA in August 2026 as RASONQUE, six months ahead of schedule.2

RAS proteins, which regulate cell growth and are mutated in more than a third of all human cancers,3 had spent forty years resisting every attempt to drug them. The protein’s surface offered no obvious foothold for a small molecule. Once the word “undruggable” attached itself to the RAS protein family, most of the field moved on to more cooperative targets.

Some researchers stayed. And Promega stayed committed to the question that never goes away: does this new compound work inside a living cell? When the next chapter of the RAS story arrived, the tools were ready. Daraxonrasib is one culmination of a much longer story, one that matters for every researcher pursuing a target the field has written off.

The First Answer

To understand what daraxonrasib represents, it helps to see how an earlier chapter of the RAS story faced the same fundamental measurement challenge.

Continue reading “Another Crack in the RAS Code: The Measurement Story Behind Daraxonrasib”

The Hidden Switch That Controls Lysosome Function

This image was generated by AI.

Your cells are constantly juggling two opposing needs: breaking things down and building things up. At the heart of that balancing act are lysosomes—tiny, acid-filled compartments that digest worn-out proteins, recycle cellular debris, and help cells decide whether it’s time to grow or conserve energy.

When lysosomes malfunction, the consequences can be serious. Lysosomal storage diseases, neurodegeneration, and metabolic disorders have all been linked to disrupted lysosome function. A new study published in Nature Communications has uncovered a key part of the control system that keeps lysosomes functioning properly.

Continue reading “The Hidden Switch That Controls Lysosome Function”

Tiny Edits, Big Harvests: How a Massive Mutation Screen Could Transform Crop Engineering

What if we could boost crop yields—not by adding foreign genes, but by tweaking the plant’s own DNA in just the right places?

For decades, plant scientists have known that the noncoding DNA flanking a gene—its promoter and regulatory regions—acts like a volume dial, controlling how much protein the gene produces. Adjusting that dial is the premise behind an approach called quantitative trait engineering (QTE), where CRISPR is used to make small, precise changes to these regulatory sequences instead of inserting entire transgenes. The appeal is enormous: nontransgenic edits face fewer regulatory hurdles and are more likely to gain public acceptance.

The problem? We don’t really understand the rules governing plant promoter architecture. Which nucleotides matter? Where can you cut, insert, or swap bases to crank expression up—or dial it down? Previous attempts to answer these questions have been limited in scale and have rarely uncovered gain-of-function mutations that increase gene expression. Now, however, a new study published in Nature Biotechnology suggests we’re closer to that reality than ever before.

Continue reading “Tiny Edits, Big Harvests: How a Massive Mutation Screen Could Transform Crop Engineering”