Radically different
President Trump has reportedly signed off on a plan to dismiss Food and Drug Administration Commissioner Marty Makary. It would be the latest high-profile departure to hit Robert F. Kennedy Jr.’s health department.
Makary has served in the role for a little over a year. His tenure was ambitious, filled with the announcements of dozens of new initiatives, including efforts to shorten drug review timelines, crack down on misleading ads, and pressure the food industry to remove chemical dyes.
Scientists from the German Cancer Research Center and HI-STEM have uncovered a major reason why acute myeloid leukemia (AML) frequently returns after treatment. Their findings, published in Cell Stem Cell, reveal that leukemia stem cells, the rare but critical cells that sustain the disease, exist in multiple biologically distinct forms, each with different vulnerabilities and resistance mechanisms.
The discovery helps explain why venetoclax, one of the most important targeted therapies in AML, often loses effectiveness over time. More importantly, it provides a framework for designing personalized combination therapies that could prevent relapse by targeting resistant stem cell populations before they expand.
Acute myeloid leukemia is an aggressive blood cancer characterized by the rapid accumulation of abnormal myeloid cells in the bone marrow. Although newer targeted therapies have improved outcomes, relapse remains the central clinical challenge.
One of the most transformative advances in AML treatment has been the introduction of venetoclax, a selective inhibitor of the anti-apoptotic protein BCL-2. Combined with hypomethylating agents or low-dose chemotherapy, venetoclax has substantially improved responses, particularly in older patients who are unable to tolerate intensive chemotherapy.
Yet despite these advances, most patients eventually relapse.
Researchers have long suspected that leukemia stem cells are responsible. These rare cells possess the ability to self-renew indefinitely and survive therapeutic pressure, allowing the disease to regenerate even after apparently successful treatment.
In the new study, researchers analyzed samples from more than 150 AML patients to better understand how leukemia stem cells respond to therapy.
Their findings challenge the idea that AML stem cells represent a single uniform population. Instead, the team identified at least four distinct leukemia stem cell subtypes, each resembling different developmental stages of normal blood cell formation.
This developmental identity turned out to be critically important because it determined which survival pathways the cells depended on—and therefore how sensitive they were to venetoclax.
Some stem cell subtypes were highly dependent on BCL-2 and responded well to treatment. Others relied on alternative survival programs that rendered them intrinsically less sensitive to the drug.
One of the study’s most significant findings was that leukemia stem cells are not fixed in a single state. Instead, they can dynamically reprogram themselves in response to therapy.
Venetoclax works by blocking BCL-2, a protein that protects leukemia cells from programmed cell death. When BCL-2 is inhibited, susceptible leukemia cells undergo apoptosis.
However, the researchers found that under treatment pressure, many leukemia stem cells transition into more resistant cellular states. Rather than relying on BCL-2, these resistant cells switch to using a related survival protein known as BCL-xL.
This adaptive shift effectively allows the cells to bypass venetoclax and survive treatment.
The findings strengthen a broader principle increasingly recognized across oncology: cancer is not only genetically heterogeneous but also highly plastic. Tumor cells can alter their identity to evade therapeutic pressure, making durable treatment responses difficult to achieve with single-agent therapies.
The study also points toward potential strategies for overcoming this resistance.
By identifying which survival pathways individual leukemia stem cell subtypes depend on, researchers showed that resistant populations could potentially be targeted with rational drug combinations. In particular, combining venetoclax with inhibitors targeting BCL-xL emerged as a promising approach.
In mouse models transplanted with patient-derived leukemia cells, these subtype-specific combination therapies were significantly more effective than current standard approaches.
This suggests that future AML therapy may require simultaneous targeting of multiple stem cell states to prevent resistant populations from emerging during treatment.
Another key advance from the study was the identification of biomarkers capable of distinguishing the different leukemia stem cell subtypes.
These biomarkers could eventually enable clinicians to determine, at the time of diagnosis, which resistance mechanisms are most likely to arise in a particular patient.
“This means that in the future, it may be possible to determine at the time of diagnosis which patient will benefit most from which therapy,” said Alexander Waclawiczek, PhD, first author of the study.
Such an approach would represent a major shift away from treating AML as a largely uniform disease and toward truly individualized therapy guided by stem cell biology.
The findings also reinforce the growing importance of cancer stem cell biology in therapeutic design. Rather than focusing exclusively on eliminating bulk tumor cells, future strategies may increasingly aim to eradicate the specific stem cell populations capable of regenerating disease after therapy.
“The results should help to align AML therapy in the future more closely with the biological characteristics of individual AML cases and, in particular, their leukemia stem cells, rather than treating all patients according to a similar protocol,” said Andreas Trumpp, PhD, who led the study.
The next major step will be translating these findings into clinical trials testing personalized combination therapies tailored to leukemia stem cell subtype composition.
The post Leukemia Stem Cell Diversity Drives Treatment Resistance in AML appeared first on Inside Precision Medicine.
Capricor Therapeutics accused Nippon Shinyaku and its U.S. subsidiary of failing to follow through on marketing plans for a Duchenne muscular dystrophy treatment, and refusing to fix a pricing glitch that was belatedly discovered in their exclusive distribution agreement.
A key issue is a “fatal flaw” in a pricing formula that would make it “economically impracticable” for the therapy to reach patients covered by Medicare, Medicaid, and private insurers, according to a lawsuit filed in a New Jersey state court on Thursday. Nippon Shinyaku and NS Pharma, the subsidiary, disclosed the problem in March 2025.
Basically, the formula ties Medicare reimbursement to the price that Capricor would charge NS Pharma, since it would be the only U.S. buyer. But as it stands, the lawsuit indicated that health care providers would get reimbursed less than they would pay to cover the cost of acquiring and administering the medicine, which is called deramiocel.
Researchers at the Johns Hopkins Kimmel Cancer Center and the Telomere Clinic at Johns Hopkins have identified an inherited cancer predisposition syndrome that results in unusually long telomeres that allow lymphocytes to stay in a biologically more youthful state for extended periods, increasing the risk of lymphoid malignancies. The findings, published the journal Blood, showed that inherited loss-of-function mutations in the POT1 gene disrupt normal telomere regulation and alter the aging dynamics of immune cells. The investigators found that because of this longer cellular lifespan cancer-associated mutations are persistent and expand over time, creating favorable conditions for the development of lymphoma and related blood cancers.
“The spectrum of lymphoid cancers was striking,” said senior author Mary Armanios, MD, a professor of medicine at Johns Hopkins. “Family members developed childhood leukemia, multiple forms of lymphoma, and adult-onset chronic lymphocytic leukemia—cancers often considered biologically distinct and associated with different inherited risks. Yet within the same families, multiple lymphoid malignancies appeared across generations. Some individuals developed melanoma before lymphoma, while others developed as many as five cancers over a lifetime. The good news is the cancers tended to be slow-growing and usually curable.”
Telomeres are protective caps at the ends of chromosomes that normally shorten with age and as a result of cell division, which limits the lifespan of cells that accumulate damage. POT1, or protection of telomeres 1, normally regulates telomere length by binding single-stranded telomeric DNA and restricting telomerase-mediated elongation. The researchers said that “POT1 binds single-stranded telomeric DNA and is essential for telomere protection, but POT1 heterozygous loss of function is permissive of telomerase elongation in the absence of a detectable DNA damage response.”
For their initial research the investigators focused on 51 people from 24 families that were know to carry mutant POT1 variants. The surveyed the participants to evaluate family cancer histories and collected biological samples to define the range of cancers associated with the mutations with the aim of examining how telomeres influenced lymphocyte aging. The data showed that among this small cohort, hematologic malignancies were the second most common cancers after melanoma, occurring in 27% of participants, with lymphoid cancers accounting for approximately three-quarters of blood malignancies found.
As a result, the researchers noted that “our data identify extended cellular longevity due to long TL as an inherited risk factor for lymphoma, explaining its syndromic association with solid tumors and, in some cases, myeloproliferative neoplasms.”
The investigators also found that telomeres responded differently that is typically observed as people aga. In those people with the POT1 mutation telomere length remained stable over time and in some cases lengthened rather than shortening with age. The findings indicated that lymphocytes retained prolonged replicative capacity, allowing cells with oncogenic mutations to survive instead of being eliminated through senescence.
To find out whether these findings extended beyond the studied families, the researchers then analyzed data from 210 adults with POT1 variants enrolled in the UK Biobank and found that people carrying pathogenic POT1 variants had an eightfold increased risk of lymphoma, and 45% developed lymphoid malignancies by age 80.
The research also examined asymptomatic POT1 mutation carriers to understand how lymphoma develops before clinical diagnosis. Among carriers without lymphoma, 12 of 20 had evidence of B-cell or T-cell clonality, a precursor state associated with lymphoma development. After age 65, all studied carriers showed detectable clonality. Sequencing and cytogenetic analyses revealed lymphoma-associated mutations in nearly all mutation carriers older than 60 years.
The study was prompted by earlier research which has shown evidence linking long telomeres to tumor development. Work in animal models had shown that long telomere length can bypass cellular senescence checkpoints and increase tumor incidence. Other research had also found POT1 mutations in melanoma, papillary thyroid cancer, glioma, sarcoma, and chronic lymphocytic leukemia. But, the prevalence and natural history of these mutations across hematologic malignancies had remained uncertain.
The findings may influence future approaches to cancer surveillance and genetic evaluation in individuals with POT1 variants. The researchers said that ultralong lymphocyte telomere length could help identify pathogenic variants and distinguish variants of uncertain significance. They noted, however, that telomere length testing may have limitations because advanced clonality can interview with the ability to accurately measure baseline telomeres.
“Our data suggest that, for now, telomere length clinical testing should be reserved for individuals with variants in the gene that have unclear significance,” Armanios said.
The post Lymphoid Cancer Risk Linked to Long Telomeres and <i>POT1</i> Mutations appeared first on Inside Precision Medicine.
You may have a memory of being separated from a parent when you were a child, even just for a few minutes. Maybe you lost them in a crowd or wandered a little too far at the store and felt panicked and afraid.
A moment like this might be among your earliest memories because the feeling was so intense, says Caitlyn Downie, LCSW, the Director of Trauma and Resilience at the Child Mind Institute. That offers some insight into the fear of a child of any age who is separated from a parent or caregiver in a more serious way. The effects of this stress are so powerful they can actually change the way a child develops.
A toddler whose mother goes to prison. A kindergartener whose father is detained and deported. A teen who is placed in foster care. These are a few examples of what experts call traumatic separation, a clinical concept based on the importance of the parent-child bond and the profound effects that can result from breaking it.
Traumatic separation isn’t a clinical diagnosis, but research shows that it can be profoundly harmful to kids. What makes it traumatic (as opposed to routine partings, like when an adult regularly leaves their child to go to work) is the character of the separation: ones that are sudden, unexpected, or confusing, or those that come about through larger distressing events, like a natural disaster or war. It’s not defined by the time spent apart — both short and long-term separations can be harmful.
Some common examples of separation that can become traumatic include:
Separating from a parent or primary caregiver can be distressing to a child even when it’s deemed necessary for their safety, as in cases where the parent they have been separated from has abused them, says Kimberly Alexander, PsyD, a psychologist at the Child Mind Institute. “There’s still a natural attachment that occurs. And the separation disrupts that relationship, even if it’s for the support and care of the child.”
More than eight decades of research has shown the profound developmental importance of the parent-child bond. This is the guiding principle of attachment theory, which was pioneered by a British psychologist who studied children who were evacuated during the Blitz, the aerial bombardment of London in World War II.
Here’s what the research tells us about the harms of traumatic separation:
Think of secure attachment as a “fundamental sense of security and safety” that a child feels with a parent or caregiver, says Dylan Gee, PhD, a psychologist at Yale University who studies how early-life stress affects children’s development.
“Attachment is the lens through which children come to know what they can expect from the world around them,” she explains. “Is this going to be a safe place or a dangerous place? This is foundational to a child’s sense of their ability to navigate the world. Traumatic separation can shatter that sense of safety.”
Children’s brains are especially plastic, says Dr. Gee, constantly learning to understand their environment and how to deal with stress. “Trauma that occurs in childhood can be even more consequential than trauma that occurs later in life,” she says, and experiencing these disruptions in childhood can affect the way your brain and body are primed to react to stress later on.
But heightened plasticity is a paradox, she adds. “It confers more vulnerability, but it also confers more potential for resilience — children have heightened potential for supportive intervention and for healing and recovery.”
There are acute and short-term effects that are common across kids of all ages:
Sleep problems: “It’s often one of the first things that we see: nightmares, trouble falling asleep, or a lot of crying as kids are trying to fall asleep,” Dr. Gee says.
Separation anxiety: This might look like distraction, withdrawal, or clinginess because of fear of being separated from their new caregivers, Dr. Alexander says.
But signs may take weeks or months to show up. Dr. Alexander advises caregivers to consider the child’s baseline — their typical patterns of eating, sleeping, or engaging with others. “If they’re having more trouble with sleep, they’re eating more, eating less, they’re withdrawing or expressing a lot of worried thoughts three or four months later — that’s something worth getting looked at by a clinician,” she says.
“Sometimes people ask, ‘Well, when is separation the most harmful?’ It can be extremely harmful at any age,” Dr. Gee emphasizes. But there are specific signs at different developmental stages:
Babies may not be as consciously aware of being separated from a parent as older children, “but they’re fundamentally aware that their primary source of regulation and safety is missing,” Dr. Gee says. Because infants are so reliant on caregivers for nurturing and sustenance, the separation “can be experienced as a threat to their survival.” That might look like “crying a lot or becoming withdrawn,” she says. “And at any age we can see intense fear.”
Toddlers and young children might become extra clingy with new caregivers or show regressive behaviors like bedwetting or baby talk. Regressive behaviors happen when kids are overwhelmed by stress and can’t express themselves another way, Downie says. “It’s like your nervous system goes kind of haywire,” she explains, “so it uses the body to signal that something is wrong.”
Similarly, kids at this age might act out more, throwing more tantrums, or withdraw. They might develop selective mutism, a condition where kids are too anxious or distressed to speak, even when they want to, in certain situations or with certain people.
School-age children might act out or experience separation anxiety. They may also struggle to understand the meaning of the separation, why it happened, or who is at fault for it. Thus, kids at this age are more prone to magical or distorted thinking and feelings of guilt, thinking or saying things like, “I’m the one that caused this” or “This is my fault.”
The weight of these distorted thoughts or other worries, Dr. Alexander says, might make it appear as though a child is struggling to concentrate or that they’re disengaged or distracted. They might withdraw in a group or be averse to stepping outside of their comfort zone.
Children who are school age or older can also experience emotional desensitization — a kind of emptiness of feeling — Downie says, which can look like spikes in irritability, a lack of empathy, not smiling or expressing positive emotions, or an inability to relate to others.
“I’ve seen teenagers have a lot of mistrust with systems and be very oppositional,” says Downie. “Like, ‘I don’t trust you. I don’t trust my teacher. I don’t trust this child services worker.’” It might make sense that, say, a teen in foster care would be wary of the foster care system. But Downie says it’s often a larger instinct for anger and mistrust, one that extends beyond any specific entity or person.
The teenage years are also when kids are forming their identity, and traumatic separation can fundamentally alter that process. For example, a teen with younger siblings may step into a parent role, taking on new worries and responsibilities. Conversely, teens may become more reckless in a caregiver’s absence, putting them at risk for substance abuse or incarceration.
Adults caring for a child who has been separated from a parent — family members, foster parents, teachers — “can play a profound role in supporting their mental health and resilience,” says Dr. Gee.
One of the most important things caregivers can do is be present as a child reacts to their experiences, especially if and when scary feelings come up. But be careful not to lead kids or assume they feel a certain way. “You don’t want to make something more distressing to a child if it’s not presenting itself,” says Downie.
If a child expresses guilt, or says something like, “This is my fault,” there are still ways to validate the feeling without endorsing the statement, says Dr. Alexander. You might say something like: “I can understand why that thought comes to mind and how difficult it is to feel that way. When you’re ready, let’s think about other possibilities to this situation.”
One of the hardest things about traumatic separation is the uncertainty — Where did they go? When will they come back? What is happening? Giving kids some sense of consistency and stability can help them feel safe despite the unknowns. So as much as possible, help them stick to any routines: going to school, seeing friends, doing activities they enjoy.
Dr. Alexander advises focusing on things you can control — for example, shielding kids from potentially worrying discussions in a family where a parent has been deported.
“There would likely be a lot of conversations in the home about the situation, maybe a lot of watching the news, maybe making a lot of phone calls to attorneys,” she explains. “So where are you having those conversations, and can you have them in an area or at a time of day where your kid isn’t overhearing the discussions out of context?”
For young kids, it might be as simple as asking them to play in their room. For teens, it might be better to have certain conversations when they are out of the house and invite them to participate directly in others.
Caregivers might not have all the answers — like knowing when a child’s parent is coming back — but they can create a sense of consistency and stability in how they respond to kids’ questions, too.
Avoid undue reassurance (“Everything is going to be fine”) or over-promising (“They’ll be back in two weeks”) by focusing on what kids can expect, says Dr. Gee. For example: “What I can tell you is that I’m here for you, and I’m going to be with you until he’s back,” or “You’re safe with me, and I’m going to stay with you through this really hard time.”
Children are sensitive to tone, Dr. Alexander says. “So, if you’re having really big emotions that are out of context for a child, the child is looking at these emotions and trying to understand what’s happening. ‘Am I in danger in this specific moment?’”
She says it helps to have conversations about these moments, especially with younger kids. “Like, ‘I know you noticed mommy crying. We’re feeling really big feelings, and this is how we’re going to deal with those big feelings. I’m going to take a break. I’m going to get a sip of water. Whenever you’re having big feelings, I want you to let me know so that I can help you try doing the same things,’” Dr. Alexander says, explaining the importance of naming the emotion and then teaching kids that there are ways of dealing with it.
The effects of traumatic separation can persist even after a child and their caregiver are reunited. Traumatic separation, like other adverse childhood experiences, puts kids at risk for a host of long-term medical and mental health conditions, including depression, anxiety, attention issues, and post-traumatic stress disorder (PTSD).
But Downie notes that not everyone who experiences traumatic separation develops PTSD. “Just because someone’s experiencing trauma now doesn’t mean that it’s going to become a PTSD diagnosis,” she says. “A lot of the behaviors that we’re talking about are normal and expected. There’s an adjustment period when a separation happens.” But if symptoms persist or escalate over several months, a child may need more serious support.
While not every child who experiences a separation may receive a trauma diagnosis or require treatment, cognitive behavioral therapy (CBT) — and the more specific trauma-focused cognitive behavioral therapy (TF-CBT) — is the “gold standard,” says Downie. TF-CBT is specifically for children experiencing trauma-related symptoms. An important component of TF-CBT is creating a trauma narrative, where kids create a story about what happened to help them process it. “But if you have a child who is not ready to process and integrate that trauma, you can’t force the pacing of the treatment,” she says.
In short, a good clinician will follow a child’s lead — even if that means just sitting in the same room with them to build trust. “People really need to feel like they’re being heard and that they can trust someone,” Downie says. Which is why a supportive caregiver or trusted adult can make a big difference.
“If people can take anything away from this, it’s that you want to make kids understand that that they’re not responsible for what’s happened and that people do care about them,” Downie says. “Kids are really resilient, and they can adapt in a good-enough environment. They don’t have to have everything to be successful.”
The post What Is Traumatic Separation? appeared first on Child Mind Institute.
MIT Technology Review Explains: Let our writers untangle the complex, messy world of technology to help you understand what’s coming next. You can read more from the series here.
Eight passengers aboard a Dutch-flagged cruise ship have contracted a type of hantavirus, a rare virus transmitted by rats. Three of them have died. As the ship prepares to dock in the Canary Islands, plans are being finalized to let the remaining passengers and crew disembark safely.
The virus in question appears to have a high fatality rate. Read on for answers to the big questions surrounding the outbreak—and to hear why health experts don’t expect a rerun of the covid-19 pandemic.
Hantaviruses are a group of viruses that typically infect rodents but can be transmitted to humans through exposure to the animals or their droppings, urine, or saliva. The viruses don’t seem to cause illness in rodents, but they can make people very unwell. The symptoms can depend on the type of hantavirus a person has been exposed to. Varieties found in the Americas can cause hantavirus cardiopulmonary syndrome, which affects the lungs and heart and has a fatality rate of up to 50%.
That condition made headlines last year when it caused the death of pianist Betsy Arakawa, the wife of actor Gene Hackman.
On April 6, a man aboard the MV Hondius developed respiratory symptoms. He became very unwell and died just five days later. His wife, who left the ship at the island of Saint Helena, also developed symptoms. Her health deteriorated during a flight to Johannesburg, South Africa, and she died the following day, on April 26. South Africa’s National Institute of Communicable Diseases tested samples taken from the woman and confirmed that she had hantavirus.
A third person aboard the ship, who developed symptoms on April 28, died on May 2. Four other passengers who became ill were evacuated—one to South Africa and three to the Netherlands.
An eighth person had disembarked in Saint Helena and reported similar symptoms once he was in Zurich, Switzerland. A team at Geneva University Hospitals confirmed that he had become ill from the Andes virus—a form of hantavirus that can be spread between people.
Health experts don’t believe so. They stress that the situation is nothing like the one the coronavirus that causes covid-19 presented in 2020. For a start, the Andes virus is not a mysterious new virus—scientists already have an understanding of it, and Argentina is sharing diagnostic kits it has already developed.
The virus also doesn’t spread in the same way. Officials at the World Health Organization emphasized that the spread of hantavirus requires close contact—the kind a person might have with a partner, household member, or medical caregiver.
The cruise ship outbreak represents “a specific confined setting where people are interacting in a prolonged close contact,” Abdirahman Mahamud, the alert and response director for the WHO’s health emergency program, said at a press event on Thursday. “With the experience our member states have, and the actions they have taken, we believe that this will not lead to a subsequent chain of transmission.”
All the remaining passengers have been asked to stay in their cabins, which the WHO says are being disinfected. Doctors and health professionals from the WHO and the European Center for Disease Prevention and Control have boarded the ship and are assessing everyone on board.
So far, no one else on board has developed symptoms, Maria Van Kerkhove, WHO acting director for epidemic and pandemic management, said at the press event. That’s “a good sign,” she said, but she added that the Andes virus has a long incubation period (around six weeks). Passengers are being advised to wear a medical mask when they leave their rooms.
At the same event, WHO director general Tedros Adhanom Ghebreyesus said he was in regular contact with the ship’s captain, who was reporting that “morale had increased significantly” since the ship started its journey to the Canary Islands.
The Andes virus is the only hantavirus that is known to be transmitted between people. That transmission seems to rely on prolonged, intimate contact.
There was an Andes virus outbreak in Argentina around eight years ago. Between November 2018 and February 2019, there were 34 confirmed cases of infection, and 11 deaths. That outbreak was triggered when a person with symptoms attended a social gathering, said Tedros. “We are in a similar situation right now,” he said. “A cluster in a confined space with close contact.”
The fact that the 2018 outbreak was limited to 34 cases should be somewhat reassuring, he implied. “We believe this will be a limited outbreak if the public health measures are implemented and solidarity is shown across all countries,” he said.
Unfortunately, we don’t have any specific antiviral treatments or vaccines for hantavirus. The WHO recommends early intensive care for people who develop symptoms. “This can save lives,” Anaïs Legand, WHO technical lead on viral hemorrhagic fevers, said on Thursday.
We don’t yet have an answer to that. But we do know that the couple who died had traveled through Argentina, Chile, and Uruguay on a birdwatching trip before they boarded the ship. That trip included visits to areas where species of rats that carry the Andes virus are known to live. The WHO is working with authorities in Argentina to try to retrace the couple’s movements on that trip.
We don’t yet know for sure. The WHO is receiving reports of “potential suspect cases,” Van Kerkhove said at the Thursday briefing. Some of them have links to the ship or its passengers. Each “alert” will be followed up by health authorities in the relevant country, she said.
Five US states have said they are monitoring US nationals who have disembarked from the ship. WHO officials are stressing that they are still sharing technical information with the US Centers for Disease Control and Prevention. “Things are … as they used to be,” Tedros said. “WHO’s mission is to help the world to be safe … and we want the American people to be safe as well.”
But it’s worth noting that cuts made by the Trump administration aren’t exactly putting the US in a good position for events like these. Last year, all full-time employees in the CDC’s Vessel Sanitation Program—which helps prevent and control illness outbreaks on cruise ships—were laid off. Further cuts to the CDC have left public health experts worried about how ill prepared the US is to deal with future disease outbreaks.
Any suspected cases will be monitored by health authorities. Passengers are due to disembark in Tenerife in the Canary Islands on Sunday, May 10, and the WHO has said it will work with the Spanish government to ensure that the risk to residents remains low and that the passengers are treated with dignity and respect.
In the meantime, scientists are working to fully sequence the genome of the virus from patient samples. They want to find out if it is different from the viruses involved in the previous cases. “So far, we haven’t seen anything unusual,” said Van Kerkhove.
J. Craig Venter, PhD recently passed away at the age of 79 from complications following a cancer diagnosis. He was well known in both science and industry and was an integral part of sequencing the human genome in the late 90s, competing with the government organized Human Genome Project. Throughout his career, he made many other important contributions in microbiology, with the “minimal cell,” in synthetic biology, and in personalized medicine. GEN editors share anecdotes of their experiences with him, reflect on the impact that his work has had on various fields in biology, in biotech, and in how the world has responded to the disruptions caused by Venter.
Listed below are links to the GEN stories referenced in this episode of Touching Base:
Genomics Pioneer and Life Sciences Entrepreneur J. Craig Venter Dies at 79
GEN, April 30, 2026
J. Craig Venter Describes a Human Genomics Revolution Still In Progress
By J. Craig Venter, PhD, GEN, June 13, 2025
Lessons from the Minimal Cell
By Hana El-Samad, PhD, GEN, August 21, 2023
From Sequencing to Sailing: Three Decades of Adventure with Craig Venter
By Fay Lin, PhD, GEN, March 8, 2023
“Cracking the Genome”
By Kevin Davies, PhD
Touching Base Podcast
Hosted by Corinna Singleman, PhD
Behind the Breakthroughs
Hosted by Jonathan D. Grinstein, PhD
The post Remembering J. Craig Venter, PhD appeared first on GEN – Genetic Engineering and Biotechnology News.
I learned about hantavirus misinformation this week in the same way I now learn about most public health misinformation: My followers sent it to me.
Within hours of the first headlines about a hantavirus outbreak linked to the expedition cruise ship MV Hondius, my DMs started filling with screenshots. One was from the account of a Texas doctor who became well known during Covid for promoting ivermectin. She was already telling followers that ivermectin would work against hantavirus, too.