The Download: supercharged scams and studying AI healthcare

This is today’s edition of The Download, our weekday newsletter that provides a daily dose of what’s going on in the world of technology.

We’re in a new era of AI-driven scams

When ChatGPT was released in late 2022, it showed how easily generative AI could create human-like text. This quickly caught the eye of cybercriminals, who began using LLMs to compose malicious emails. Since then, they’ve adopted AI for everything from turbocharged phishing and hyperrealistic deepfakes to automated vulnerability scans.

Many organizations are now struggling to cope with the sheer volume of cyberattacks. AI is making them faster, cheaper, and easier to carry out, a problem set to worsen as more cybercriminals adopt these tools—and their capabilities improve. Read the full story on how AI is reshaping cybercrime.

—Rhiannon Williams

“Supercharged scams” is one of the 10 Things That Matter in AI Right Now, our essential guide to what’s really worth your attention in the field.

Subscribers can watch an exclusive roundtable unveiling the technologies and trends on the list, with analysis from MIT Technology Review’s AI reporter Grace Huckins and executive editors Amy Nordrum and Niall Firth.

Healthcare AI is here. We don’t know if it actually helps patients.

Doctors are using AI to help them with notetaking. AI-based tools are trawling through patient records, flagging people who may require certain support or treatments. They are also used to interpret medical exam results and X-rays.

A growing number of studies suggest that many of these tools can deliver accurate results. But there’s a bigger question here: Does using them actually translate into better health outcomes for patients? We don’t yet have a good answer—here’s why.

—Jessica Hamzelou

The story is from The Checkup, our weekly newsletter that gives you the latest from the worlds of health and biotech. Sign up to receive it in your inbox every Thursday.

The must-reads

I’ve combed the internet to find you today’s most fun/important/scary/fascinating stories about technology.

1 DeepSeek has unveiled its long-awaited new AI model
The Chinese company has just launched preview versions of DeepSeek-V4. (CNN)
+It says V4 is the most powerful open-source platform. (Bloomberg $)
+ And rivals top closed-source models from OpenAI and DeepMind. (SCMP)
+ The model is adapted for Huawei chip technology. (Reuters $)

2 More countries are curbing children’s social media access
Norway is set to enforce the latest ban. (Reuters $)
+ The Philippines could follow soon. (Bloomberg $)
+ Americans are pushing to get AI out of schools. (The New Yorker)

3 The US has accused China of mass AI theft as tensions rise
A White House memo claims Chinese firms are exploiting American models. (BBC)
+ Beijing calls the accusations “slander.” (Ars Technica)

4 OpenAI set itself apart from Anthropic by widely releasing its new model
It’s releasing GPT-5.5 to all ChatGPT users, despite cybersecurity concerns. (NYT $)
+ OpenAI says the new model is better at coding and more efficient. (The Verge)

5 Meta is cutting 10% of jobs to offset AI spending
Roughly 8,000 layoffs are set to be announced on May 20. (QZ)
+ Anti-AI protests are growing. (MIT Technology Review)

6 Palantir is facing a backlash from employees
Thanks to its work with ICE and the Trump administration. (Wired $)
+ Surveillance tech is reshaping the fight for privacy. (MIT Technology Review)

7 The era of free access to advanced AI is coming to an end
AI labs are under mounting pressure to start turning profits. (The Verge)

8 Elon Musk’s feud with Sam Altman is heading to court 
The case has already revealed several unflattering secrets. (WP $)

9 A new movement is encouraging people to ditch their smartphones for a month
“Month Offline” is like a Dry January for smartphones. (The Atlantic)

10 Spotify has revealed its most-streamed music of the last 20 years
Featuring Taylor Swift, Bad Bunny, and The Weeknd. (Gizmodo

Quote of the day

“We want a childhood where children get to be children. Play, friendships, and everyday life must not be taken over by algorithms and screens.” 

—Norwegian Prime Minister Jonas Gahr Store announces age restrictions for social media.

One More Thing

""

NASA/JPL-CALTECH VIA WIKIMEDIA COMMONS; CRAFT NASA/JPL-CALTECH/SWRI/MSSS; IMAGE PROCESSING: KEVIN M. GILL


The search for extraterrestrial life is targeting Jupiter’s icy moon Europa

As astronomers have discovered more about Europa over the past few decades, Jupiter’s fourth-largest moon has excited planetary scientists interested in the geophysics of alien worlds.

 All that water and energy—and hints of elements essential for building organic molecules —point to an extraordinary possibility. In the depths of its ocean, or perhaps crowded in subsurface lakes or below icy surface vents, Jupiter’s big, bright moon could host life. 

To find further evidence, NASA is now searching for signs of alien existence on Europa. Read the full story on the mission.


—Stephen Ornes

We can still have nice things

A place for comfort, fun and distraction to brighten up your day. (Got any ideas? Drop me a line.)

+ Here’s a fun look at the secret collaborations of pop history.
+ Meet the mannequins showing how the “ideal” body has evolved.
+ A photographer has cataloged all 12,795 objects in her home into an archive of a life.
+ Slime molds are unexpectedly beautiful when viewed through these high-detail macro shots.

Japanese Pharma Companies Turning to CDMOs Earlier in Product Life Cycle

Japanese pharmaceutical companies are engaging CDMOs earlier in the development cycle, as increasing complexity in peptide programs places greater strain on in-house capabilities, according to officials at Neuland Laboratories, which is attending CPHI Japan this week. The company says it has seen a notable shift in demand over the past 12–24 months, with more early-stage programs seeking external support.

This trend is being driven in part by growing activity from venture-backed biotech companies and spinouts emerging from large pharmaceutical R&D organizations, reports a Neuland spokesperson, who adds that as these programs advance into clinical development, demand for specialized CDMO capabilities is increasing.

Neuland has observed a rise in peptide-related engagements from Japanese companies, particularly at the preclinical and early clinical stages, where technical requirements are more demanding, notes Sharadsrikar Kotturi, PhD, CSO at Hyderabad, India-based Neuland Labs.

Peptide development presents several challenges compared with traditional small molecules, explains Kotturi. Analytical complexity remains a key issue, with structural characteristics making characterization, impurity detection, and purity assessment more difficult, he continues. Scaleup is also constrained by the availability and quality of protected amino acids, which can affect manufacturing timelines, cost, and overall success rates.

Regulatory expectations further add to the burden, points out Kotturi. Demonstrating purity, consistency, and process control to authorities such as Japan’s Pharmaceuticals and Medical Devices Agency requires extensive data, while shifting requirements introduce additional hurdles during development and approval. Simultaneously, pricing and regulatory pressures in Japan are increasing the operational load on drug developers, he states. Frequent drug price revisions are pushing companies to improve cost efficiency, reinforcing the case for outsourcing.

“The bottleneck isn’t discovery anymore. It’s execution,” says Kotturi. “In peptides, programs are running into challenges around analytical complexity, scaleup, and the availability of key raw materials such as protected amino acids.”

 

 

 

The post Japanese Pharma Companies Turning to CDMOs Earlier in Product Life Cycle appeared first on GEN – Genetic Engineering and Biotechnology News.

Health-care AI is here. We don’t know if it actually helps patients.

I don’t need to tell you that AI is everywhere.

Or that it is being used, increasingly, in hospitals. Doctors are using AI to help them with notetaking. AI-based tools are trawling through patient records, flagging people who may require certain support or treatments. They are also used to interpret medical exam results and X-rays.

A growing number of studies suggest that many of these tools can deliver accurate results. But there’s a bigger question here: Does using them actually translate into better health outcomes for patients?

We don’t yet have a good answer.

That’s what Jenna Wiens, a computer scientist at the University of Michigan, and Anna Goldenberg of the University of Toronto, argue in a paper published in the journal Nature Medicine this week.

Wiens tells me she has spent years investigating how AI might benefit health care. For the first decade of her career she tried to pitch the technology to clinicians. Over the last few years, she says, it’s as though “a switch flipped.” Health-care providers not only appear much more interested in the promise of these technologies, they have also begun rapidly deploying them.

The problem is that many providers aren’t rigorously assessing how well they actually work.

Take “ambient AI” tools, for example. Also known as AI scribes, they “listen” to conversations between doctors and patients, then transcribe and summarize them. Multiple tools are available, and they are already being widely adopted by health-care providers.

A few months ago, a staffer at a major New York medical center who develops AI tools for doctors told me that, anecdotally, medics are “overjoyed” by the technology—it allows them to focus all their attention on their patients during appointments, and it saves them from a lot of time-consuming paperwork. Early studies support these anecdotes and suggest that the tools can reduce clinician burnout.

That’s all well and good. But what about patient health outcomes? “[Researchers] have evaluated provider or clinician and patient satisfaction, but not really how these tools are affecting clinical decision-making,” says Wiens. “We just don’t know.”

The same holds true for other AI-based technologies used in health-care settings. Some are used to predict patients’ health trajectories, others to recommend treatments. They are designed to make health care more effective and efficient.

But even a tool that is “accurate” won’t necessarily improve health outcomes. AI might speed up the interpretation of a chest X-ray, for example. But how much will a doctor rely on its analysis? How will that tool affect the way a doctor interacts with patients or recommends treatment? And ultimately: What will this mean for those patients?

The answers to those questions might vary between hospitals or departments and could depend on clinical workflows, says Wiens. They might also differ between doctors at various stages of their careers.

Take the AI scribes, as another example. Some research on AI use in education suggests that such tools can impact the way people cognitively process information. Could they affect the way a doctor processes a patient’s information? Will the tools affect the way medical students think about patient data in a way that impacts care? These questions need to be explored, says Wiens. “We like things that save us time, but we have to think about the unintended consequences of this,” she says.

In a study published in January 2025, Paige Nong at the University of Minnesota and her colleagues found that around 65% of US hospitals used AI-assisted predictive tools. Only two-thirds of those hospitals evaluated their accuracy. Even fewer assessed them for bias.

The number of hospitals using these tools has probably increased since then, says Wiens. Those hospitals, or entities other than the companies developing the tools, need to evaluate how much they help in specific settings. There’s a possibility that they could leave patients worse off, although it’s more likely that AI tools just aren’t as beneficial as health-care providers might assume they are, says Wiens.

“I do believe in the potential of AI to really improve clinical care,” says Wiens, who stresses that she doesn’t want to stop the adoption of AI tools in health care. She just wants more information about how they are affecting people. “I have to believe that in the future it’s not all AI or no AI,” she says. “It’s somewhere in between.”

This article first appeared in The Checkup, MIT Technology Review’s weekly biotech newsletter. To receive it in your inbox every Thursday, and read articles like this first, sign up here.
 

A CAR-T biotech’s dramatic turnaround, and drugmakers’ tactics to drive more scripts

How did a biotech company that almost ran out of money three times get acquired for over $3 billion? Will the M&A streak continue? And why are drugmakers working with a telehealth company called Prescribery?

We discuss all that and more on this week’s episode of “The Readout LOUD,” STAT’s weekly biotech podcast. Venture capitalist Bryan Roberts joins us to discuss his firm’s investment in Kelonia Therapeutics, the CAR-T biotech that Eli Lilly just said it would buy for $3.25 billion.

Read the rest…

Enabling In Vivo Lentiviral Therapies: Manufacturing Strategies to Improve Purity, Scalability, and Clinical Readiness

Lentiviral vectors are gaining momentum not just as ex vivo tools but as potential in vivo therapeutic platforms. But with that shift comes a number of manufacturing challenges, including higher doses, tighter control of impurities, greater batch consistency, and scalable processes to meet both clinical and commercial needs.

In this GEN Podcast, two experts from SK pharmteco, a global CMO, address these challenges and lay out some best practices that guide the manufacture of lentiviral vectors with the requisite purity, robustness, and economic feasibility required for widespread clinical adoption..

 

Podcast Guests:

Tatiana Nanda

Tatiana Nanda, PhD
CTO, Cell and Gene Therapy
SK pharmteco

Mardhani Aparajithan

Mardhani Aparajithan
Director of Manufacturing,
Science and Technology
SK pharmteco


Produced with support from:

skpharmteco logo

The post Enabling <i>In Vivo</i> Lentiviral Therapies: Manufacturing Strategies to Improve Purity, Scalability, and Clinical Readiness appeared first on GEN – Genetic Engineering and Biotechnology News.

CRISPR Base Editing Repairs Hard-to-Treat Cystic Fibrosis Mutation in Cell Models

Affecting an estimated 100,000 people globally, cystic fibrosis (CF) cases stem from mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) protein. In the past several decades, scientists have successfully engineered various small-molecule therapies that lessen the severity of the disease. However there are still treatment challenges. Now, data from a new study in a cell model demonstrates that a gene therapy can successfully repair an “untreatable” mutation associated with a particularly severe form of the disease. Details of the potential therapy are published in a new Science Translational Medicine paper titled “Functional correction of the untreatable CFTR 1717-IG>A mutation through mRNA- and sgRNA-optimized base editing.” 

Many current therapies benefit patients with the most common disease-associated mutation, F508del. However they often have little effect on patients who harbor other types of mutations. For example, some patients have a mutation named 1717-1G>A, which is relatively common but doesn’t have any approved therapies due to being a splicing mutation that results in little to no protein production. In fact, “about 10% of people with CF do not qualify for any of the available CFTR modulator therapies, particularly those people with severe splicing mutations that result in frameshifts and the formation of premature termination codons.”

The 1717-1G>A mutation is the target of the therapy described in the paper, which was written by scientists from the University of Trento and their collaborators elsewhere. Specifically, the team developed an “adenine base editing strategy to efficiently correct the 1717-1G>A mutation,” they wrote in Science Translational Medicine. “By harnessing the SpRY-­ ABE9 system, which we delivered as optimized RNAs for both the base editor and single guide RNA (sgRNA), we achieved functional correction in patient-derived models.” 

Furthermore, the scientists note that they opted to use base editing rather than strategies like base editing because it has the advantage of “typically higher nucleotide modification efficiencies and a streamlined system requiring only the editor and an sgRNA” and because it has been used in other CF studies. 

Using their ABE9 base editor and modified CRISPR-Cas9 tool, the scientists report successfully editing up to 30% of target DNA in human embryonic kidney cell lines and patient-derived airway epithelial cells with minimal off-target effects. It also corrected the mutation in intestinal organoids derived from CF patients as evidenced by restored CFTR activity. 

Additional studies are needed, especially in animals, to fully assess the effectiveness of potential therapy but early results are promising. Overall, the approach achieved an editing efficiency of 13%. Prior studies showed that 10% efficiency may be enough for functional recovery. The results suggest that the therapy could benefit the subset of patients whose disease is caused by 1717-1G>A.

The post CRISPR Base Editing Repairs Hard-to-Treat Cystic Fibrosis Mutation in Cell Models appeared first on GEN – Genetic Engineering and Biotechnology News.

Heart’s Constant Beating Suppresses Tumor Growth in Cardiac Tissues

The results of a study by researchers at the International Centre for Genetic Engineering and Biotechnology (ICGEB) suggest that the heart’s constant beating may actively suppress tumor growth in cardiac tissues. The collective findings from the team’s research in mouse models and in engineered heart tissues (EHT) suggests that this is because cellular pathways in these tissues alter gene regulation in cancer cells to keep them from proliferating.

Headed by Giulio Ciucci, PhD, and Serena Zacchigna, MD, PhD, at the ICGEB Cardiovascular Biology Laboratory, the scientists say the findings shed light on the role of mechanical forces in protecting the heart from cancer and may pave the way to new cancer therapies based on mechanical stimulation. First author Ciucci, together with senior author Zacchigna and colleagues reported on their findings in Science, in a paper titled “Mechanical load inhibits cancer growth in mouse and human hearts.” In their report the authors concluded “Collectively, the data presented in this work provide evidence that mechanical load in the heart inhibits cancer cell proliferation, likely explaining the low incidence of cardiac tumors.”

Heart cancer is very rare in mammals, but as the authors noted, “The mechanisms that protect the heart remain elusive.” The adult human heart in addition has a limited capacity for self-renewal, with cardiomyocytes regenerating at roughly 1% per year. “This suggests that the same mechanisms that halt the proliferation of cardiac cells could also inhibit the growth of cancer cells in the adult heart,” the authors continued. One proposed explanation for this loss of cardiomyocyte proliferative capacity lies in the intense mechanical demands placed on heart tissues, which must continuously pump blood against significant resistance. “We hypothesized that it could similarly hamper the proliferation of cancer cells in the heart,” the investigators reported.

Using a genetically engineered mouse model, Ciucci et al. first showed that the heart is remarkably resistant to cancer-causing mutations, even when potent oncogenic changes were introduced. To understand why, the authors developed a transplantation model in which the heart’s mechanical workload could be reduced. By grafting a donor heart into the neck of a compatible mouse, they created a “mechanically unloaded” organ, one that remained perfused with blood but did not bear physiological strain. “To assess the contribution of mechanical load to the low incidence and growth of cancer in the heart, we used a model of in vivo cardiac unloading by heterotopically transplanting a donor heart into the neck of a recipient syngeneic mouse,” they explained.

Image of lung cancer cells (in green) growing in a heart, in which cardiomyocytes are stained in red. Nuclei are stained in blue. [Ciucci et al., Science 2026]
Image of lung cancer cells (in green) growing in a heart, in which cardiomyocytes are stained in red. Nuclei are stained in blue. [Ciucci et al., Science 2026]

After injecting human cancer cells directly into the heart muscle, they compared tumor behavior in the unloaded transplanted heart versus the animal’s native, mechanically active heart. Across their experiments, Ciucci et al. found that mechanical load consistently suppressed the growth of various cancer types, while unloading the heart promoted tumor cell proliferation within cardiac tissue.

According to the study findings, mechanical forces within the tissue reshape the cancer cell genome’s regulatory landscape, influencing whether cells can proliferate. Central to this process is Nesprin-2, a protein that transmits mechanical signals from the cell surface to the nucleus. “Nesprin-2, a protein known to mediate mechanotransduction from the cytoplasm to the nucleus, emerged as a key molecule sensing mechanical forces operating in beating hearts and translating them into reduced cell proliferation,” the scientists reported.

Nesprin-2, a component of the LINC complex, senses the mechanical microenvironment of the heart and functionally alters chromatin structure and histone methylation, reducing gene activity linked to tumor cell proliferation. When Nesprin-2 was silenced in cancer cells, those cells regained the ability to grow in the mechanically active environment of the heart, forming tumors. “Silencing of Nesprin-2 in lung cancer cells prior to their implantation in the heart in vivo restored the capacity of the cells to proliferate in the presence of physiological mechanical load, resulting in the formation of large tumors,” the authors stated.

The team noted that their collective results shed light on the role of mechanical forces in protecting the heart from cancer and may pave the way to new approaches to cancer therapy. “This offers fundamental insights into the biology of cell proliferation within the myocardium, and additionally, the mechanical stimuli that operate in a beating heart could be exploited for the development of a mechanical therapy for cancer.”

The post Heart’s Constant Beating Suppresses Tumor Growth in Cardiac Tissues appeared first on GEN – Genetic Engineering and Biotechnology News.

AACR 2026 Video Update: Cancer Research Edges Toward an AI-Driven Era

SAN DIEGO – At the American Association for Cancer Research (AACR) Annual Meeting 2026, the conversation around AI-driven cancer research has moved decisively past theory. Now the focus is on what’s being deployed and how to gain researchers’ and clinicians’ trust.

Fay Lin, PhD, senior editor, technology at GEN, and Jonathan D. Grinstein, PhD, North American editor at Inside Precision Medicine, discuss how AI is increasingly embedded across cancer research areas, from organoid models to pathology. Yet challenges such as data integration, longitudinal patient tracking, and clinician confidence continue to hinder its impact on patient outcomes.

Watch the full discussion below for a clearer view of the trends, tensions, and inflection points in AI shaping the future of cancer research:

 

The post AACR 2026 Video Update: Cancer Research Edges Toward an AI-Driven Era appeared first on GEN – Genetic Engineering and Biotechnology News.

New ADC Yields Encouraging Clinical Benefit in Platinum-Resistant Ovarian Cancer

Patients with advanced platinum-resistant ovarian cancer whose disease had progressed on standard therapy experienced clinical benefit when treated with the investigational antibody-drug conjugate (ADC) QLS5132.

This finding is according to results from a Phase I clinical trial presented at the American Association for Cancer Research (AACR) Annual Meeting 2026, held in San Diego.

Patients diagnosed with platinum-resistant ovarian cancer face both a poor prognosis and limited treatment options, explained Tao Zhu, MD, chief physician and vice president of Zhejiang Cancer Hospital in China, who presented the study.

Zhu and collaborators tested an investigational ADC, QLS5132, which targets the protein CLDN6. QLS5132 combines a CLDN6-targeting monoclonal antibody with a cytotoxic payload, topoisomerase-1 inhibitor, at a drug-to-antibody ratio of 8:1. CLDN6, Zhu said, makes an ideal target as a protein with very high expression on the surface of ovarian cancer cells and minimal cell-surface expression in healthy tissues.

“The primary purpose of this first-in-human study was to evaluate the safety, tolerability, and pharmacokinetic profile of QLS5132 in patients with platinum-resistant ovarian cancer and determine the recommended Phase II dose for future clinical development,” Zhu said. “Additionally, we aimed to assess preliminary antitumor activity to establish an early signal of clinical benefit in this heavily pretreated population with limited options.”

The Phase I, single-arm, dose-escalation trial enrolled 28 patients with a median age of 57.5 who had been diagnosed with advanced platinum-resistant ovarian cancer and who had experienced progression while on standard therapy. The research team administered QLS5132 as an intravenous infusion every three weeks at dose levels of 1.6 mg/kg, 3.2 mg/kg, 4.8 mg/kg, 5.6 mg/kg, and 6.4 mg/kg.

Treatment-related adverse events (TRAEs) occurred in 26 (92.9%) patients, with nausea, anorexia, anemia, and weakness occurring most frequently. Nine (32.1%) patients experienced TRAEs of grade 3 or higher, and of those grade ≥3 TRAEs, seven were instances of hematological toxicity. No TRAEs led to treatment discontinuation or death, and no patients experienced interstitial lung disease, ocular toxicity, or febrile neutropenia, Zhu said.

After a median follow-up of 2.2 months, nine patients had a partial response at various dose levels. Two of these partial responses occurred in patients who had no detectable CLDN6 expression.

Across all dose levels, 18 evaluable patients experienced an objective response rate of 50% and a disease control rate of 94.4%. When calculated for the 17 evaluable patients who had received dose levels ≥3.2 mg/kg, the objective response rate and disease control rate rose to 52.9% and 100%, respectively. These responses to QLS5132 occurred irrespective of patients’ CLDN6 expression levels at baseline.

“The most encouraging finding from our study was that QLS5132 demonstrated compelling antitumor activity in patients with platinum-resistant ovarian cancer, with an objective response rate exceeding 50%,” said Zhu. “Equally important, at the potential recommended Phase II dose, we observed a favorable safety profile with no reported cases of interstitial lung disease, ocular toxicity, oral mucositis, or febrile neutropenia.”

Zhu also noted that, though more research would be needed to confirm, preliminary data indicated antitumor activity from QLS5132 regardless of CLDN6 expression levels—which, he said, could expand its potential as a treatment option to a broad cohort of patients with platinum-resistant ovarian cancer.

Zhu acknowledged that further research would be needed to fully understand why QLS5132 can have anticancer effects in patients with undetectable CLDN6 tumoral expression. But he suggested the phenomenon may have a few explanations, including tumor heterogeneity, as well as a potent bystander effect resulting in antitumor efficacy even in cells with low or no CLDN6 expression.

“These findings support the advancement of QLS5132 into Phase III studies, with the goal of providing a much-needed new treatment option for these patients,” said Zhu.

Some limitations of this study include a small sample size and an exploratory single-arm design.

This study was funded by Qilu Pharmaceutical. Zhu discloses no conflicts of interest.

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