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  • GLP-1 Drugs Like Ozempic Are Showing a 47 Percent Reduction in Breast Cancer Risk in a Major New Study — and Weight Loss May Not Explain It

    GLP-1 Drugs Like Ozempic Are Showing a 47 Percent Reduction in Breast Cancer Risk in a Major New Study — and Weight Loss May Not Explain It

    The list of conditions that GLP-1 receptor agonists appear to protect against keeps getting longer. These drugs — which include semaglutide (Ozempic, Wegovy), tirzepatide (Mounjaro, Zepbound), and the newly approved orforglipron (Foundayo) — were originally developed for type 2 diabetes before emerging as transformative obesity medications. Then cardiovascular outcome trials showed they reduce heart attacks and strokes. Then the sleep apnea approval added obstructive sleep apnea to the indication list. Then studies suggested reductions in kidney disease progression, non-alcoholic fatty liver disease, and alcohol dependence.

    And now, a major study presented at the American Society of Clinical Oncology Annual Meeting in Chicago in early June 2026 and reported widely on June 10, 2026 has added breast cancer to the rapidly expanding list of conditions that GLP-1 drugs appear to protect against — with an effect magnitude that has stunned the oncology community.

    The study, which analyzed real-world data from a large cohort of women with type 2 diabetes or obesity who were treated with GLP-1 receptor agonists, found that GLP-1 drug use was associated with a 30 to 47 percent lower risk of developing breast cancer compared to women who did not use these medications. The lower end of that range (30 percent) emerged from analyses adjusted for body mass index and weight change — meaning even when researchers accounted for the weight loss that GLP-1 drugs produce, a significant protective signal remained. This finding strongly suggests that GLP-1 drugs may be protecting against breast cancer through mechanisms that go beyond simply reducing body fat — mechanisms that may include direct anti-tumor effects, reduced insulin resistance and associated growth factor signaling, or anti-inflammatory pathways.

    Why This Finding Is Biologically Plausible

    The biological connection between metabolic dysfunction, obesity, insulin resistance, and breast cancer risk is well established. Adipose tissue (fat) produces estrogen through a process called aromatization, making obesity a direct driver of estrogen-dependent breast cancers. Hyperinsulinemia — the elevated insulin levels that accompany insulin resistance in type 2 diabetes and obesity — activates the insulin-like growth factor (IGF-1) pathway, which promotes cancer cell proliferation and survival. Chronic inflammation from adipose tissue dysfunction activates oncogenic pathways that promote tumor growth.

    GLP-1 receptor agonists address multiple of these pathways simultaneously. They reduce body fat (reducing aromatization and adipose inflammation), improve insulin sensitivity (reducing hyperinsulinemia and IGF-1 signaling), and have direct anti-inflammatory effects. Preclinical studies have also documented direct GLP-1 receptor agonist activity on cancer cell lines, suggesting GLP-1 receptors may be expressed in breast cancer tissue and may mediate direct anti-proliferative effects when activated.

    The study’s finding that the protective signal persists even after adjustment for weight and BMI is the most provocative result, because it suggests the drug’s biological effects — beyond simple caloric restriction and fat mass reduction — are contributing to cancer protection.

    What This Means for the 15 Million Americans on GLP-1 Drugs

    Approximately 15 million Americans are currently prescribed GLP-1 receptor agonists. The vast majority are taking them for type 2 diabetes or weight management. If the breast cancer protective signal seen in this study is confirmed in larger prospective trials and in controlled analyses, it would represent an additional major health benefit of these medications — one that could influence prescribing decisions, insurance coverage arguments, and cancer prevention discussions.

    The researchers caution that this is observational data from a real-world cohort, not a randomized controlled trial. Confounding variables — the possibility that GLP-1 drug users differ from non-users in ways that independently affect breast cancer risk — must be accounted for before these findings can be considered definitive. Prospective studies and potential randomized trials with cancer outcomes as endpoints are now being planned. The Phase 3 ORCA trial of semaglutide in high-risk cancer prevention populations is one ongoing effort that will provide higher-quality evidence.

    For women currently taking GLP-1 drugs for any indication, this study is not a recommendation to take them as cancer prevention without diabetes or obesity indication — rather, it is an important signal that the health benefits of these medications may be broader than previously understood.

    Frequently Asked Questions

    Q: What did the new GLP-1 and breast cancer study find?

    A: A real-world cohort study presented at ASCO 2026 found that women with type 2 diabetes or obesity who used GLP-1 receptor agonists had a 30–47% lower breast cancer risk compared to non-users. The effect persisted after adjustment for weight loss.

    Q: Does this mean women should take GLP-1 drugs specifically to prevent breast cancer?

    A: No. This is observational data, not a randomized trial. The finding is a promising signal that warrants further research, not a clinical recommendation for GLP-1 drugs as cancer prevention outside of established indications.

    Q: Why might GLP-1 drugs protect against breast cancer beyond weight loss?

    A: By reducing hyperinsulinemia, improving insulin sensitivity (lowering IGF-1 signaling), reducing adipose-tissue inflammation, and potentially through direct GLP-1 receptor activity on breast tissue — all mechanisms independent of weight loss.

    Q: Which GLP-1 drugs were included in the study?

    A: The study analyzed GLP-1 receptor agonist use broadly, including semaglutide (Ozempic/Wegovy) and tirzepatide (Mounjaro/Zepbound) among the most commonly used agents. Results were not limited to a specific drug within the class.

    Q: How does this new finding fit with the other cancer data on GLP-1 drugs?

    A: A 2024 Nature Medicine study documented lower incidence of multiple obesity-associated cancers in GLP-1 users. The 2026 ASCO breast cancer study adds specifically to that growing body of evidence suggesting GLP-1 drugs may have broad anti-cancer properties.

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  • GLP-1 agonists: MedlinePlus Medical Encyclopedia

    GLP-1 agonists: MedlinePlus Medical Encyclopedia

    Ahmann AJ, Riddle MC. Therapeutics of type 2 diabetes mellitus. In: Melmed S, Auchus, RJ, Goldfine AB, Rosen CJ, Kopp PA, eds. Williams Textbook of Endocrinology. 15th ed. Philadelphia, PA: Elsevier; 2025:chap 34.

    Dhatariyan KK, Umpierrez GE, Crandall JP. Diabetes mellitus. In: Goldman L, Cooney KA, eds. Goldman-Cecil Medicine. 27th ed. Philadelphia, PA: Elsevier; 2024:chap 210.

    Jensen MD, Bessesen DH. Obesity. In: Goldman L, Cooney KA, eds. Goldman-Cecil Medicine. 27th ed. Philadelphia, PA: Elsevier; 2024:chap 201.

    Moiz A, Filion KB, Tsoukas MA, Yu OH, Peters TM, Eisenberg MJ. Mechanisms of GLP-1 receptor agonist-induced weight loss: a review of central and peripheral pathways in appetite and energy regulation. Am J Med. 2025 Jun;138(6):934-940. Epub 2025 Jan 31. PMID: 39892489.  pubmed.ncbi.nlm.nih.gov/39892489/.

    Moiz A, Filion KB, Tsoukas MA, Yu OHY, Peters TM, Eisenberg MJ. The expanding role of GLP-1 receptor agonists: a narrative review of current evidence and future directions. EClinicalMedicine. 2025 Jul 17;86:103363. PMID: 40727007; PMCID: PMC12303005. pubmed.ncbi.nlm.nih.gov/40727007/.

    Orandi BJ, Aronne LJ. Obesity. In: Chung RT, Rubin DT, Wilcox CM, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 12th ed. Philadelphia, PA: Elsevier; 2026:chap 8.

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  • Chikungunya Outbreaks Are Now Active in Three Different Countries and Territories Simultaneously — and Summer Travelers Are at Risk from the Caribbean to the Indian Ocean

    Chikungunya Outbreaks Are Now Active in Three Different Countries and Territories Simultaneously — and Summer Travelers Are at Risk from the Caribbean to the Indian Ocean

    Summer 2026 has produced an unusual public health picture on the CDC Travel Health Notices page: three simultaneous active travel notices for chikungunya — the mosquito-borne virus known for causing weeks of debilitating joint pain — across three different geographic regions. Suriname, a country on the northeastern coast of South America, has had an active chikungunya outbreak since February 2026. Mayotte, a French territory in the Indian Ocean off the coast of Mozambique, has been under a CDC chikungunya notice since March 10, 2026. And French Guiana, the French overseas territory on the northern coast of South America adjacent to Brazil, received a new CDC travel notice for chikungunya on June 4, 2026 — just 10 days ago.

    Three simultaneous active outbreaks across two continents and the Indian Ocean, all in destinations that receive American travelers during peak summer season, all involving the same virus, and all preventable by a vaccine that most American travelers have never heard of.

    Chikungunya is caused by the chikungunya alphavirus, transmitted primarily by Aedes aegypti and Aedes albopictus mosquitoes — the same species responsible for dengue fever and Zika virus transmission. It cannot spread person to person. It requires a mosquito bite for transmission, which means travelers who effectively prevent mosquito bites can protect themselves. But unlike dengue — for which no reliably effective, widely available vaccine existed in the U.S. until recently — chikungunya now has an FDA-approved single-dose vaccine that provides broad, durable protection.

    The Pattern of These Three Simultaneous Outbreaks

    The geographic distribution of the three current CDC chikungunya notices reflects distinct but parallel epidemiological situations. In Suriname, chikungunya has been circulating since at least February 2026, consistent with the country’s tropical climate that supports year-round Aedes mosquito activity. Suriname borders Guyana to the west, Brazil to the south, and French Guiana to the east — meaning outbreak activity in Suriname creates risk for cross-border spread to adjacent territories, and the French Guiana notice issued June 4 is likely connected to regional transmission dynamics that began in Suriname and Brazil.

    Mayotte’s chikungunya outbreak is separate in origin — the island’s subtropical Indian Ocean climate creates independent conditions for Aedes activity, and chikungunya has a well-documented history of large outbreak cycles in Indian Ocean territories, including the catastrophic 2005–2006 outbreak in La Réunion that infected nearly one-third of the island’s population.

    What these three outbreaks share is the presence of Aedes aegypti or Aedes albopictus at epidemic transmission levels, a population of susceptible individuals without prior immunity, and the current arrival of the summer travel season, which increases the probability of importation to the United States via returning travelers.

    What Chikungunya Does to the Human Body

    The word chikungunya comes from the Makonde language of Tanzania, meaning “that which bends up” — a reference to the stooped posture that patients adopt in response to severe joint pain. The description is medically accurate and experientially unforgettable. After an incubation period of 2 to 12 days following a mosquito bite, patients develop sudden high fever — often above 103°F — accompanied by polyarthralgia, the simultaneous severe painful inflammation of multiple joints. The hands, wrists, ankles, and feet are most commonly affected, and the pain is frequently described by patients as worse than anything they have experienced. Many cannot walk, dress, or grip a cup.

    The acute phase typically lasts 7 to 10 days. Most patients recover. But approximately 25 to 50 percent of people infected with chikungunya develop chronic post-chikungunya arthritis — persistent joint pain that continues for months to years after the initial infection has resolved. This is the longest-lasting and most debilitating consequence of chikungunya, and it disproportionately affects older adults and those with pre-existing joint disease.

    The Vaccine That Travelers Are Not Getting

    The FDA approved Ixchiq (chikungunya vaccine) in November 2023 for adults 18 and older at increased risk of chikungunya exposure. Ixchiq is a live-attenuated, single-dose vaccine that requires no booster and has demonstrated strong immunogenicity and an acceptable safety profile in clinical trials. It is available through travel medicine clinics and many primary care providers.

    Despite its approval, Ixchiq remains significantly underutilized among American travelers to chikungunya-endemic and outbreak-affected regions. Awareness of the vaccine’s existence is low among both patients and some general practitioners who do not specialize in travel medicine. Travelers heading to Suriname, French Guiana, Mayotte, or any of the many Caribbean and South American destinations currently experiencing elevated chikungunya activity should specifically ask about Ixchiq at their travel medicine consultation.

    The vaccine requires at least 28 days to induce full protection, so travelers should plan accordingly — those departing within 28 days should be advised to rely on intensive mosquito bite prevention while the vaccine becomes effective, or may not benefit from vaccination for their current trip. As with all mosquito-borne disease prevention, repellent use, protective clothing, air conditioning, and bed nets remain essential complements to vaccination.

    Frequently Asked Questions

    Q: Where are the current chikungunya outbreaks with CDC travel notices?

    A: As of June 2026, active CDC chikungunya travel notices cover Suriname (February 2026), Mayotte, a French Indian Ocean territory (March 10, 2026), and French Guiana (June 4, 2026).

    Q: What are the symptoms of chikungunya?

    A: Sudden high fever and severe polyarthralgia — simultaneous joint pain in multiple joints, especially the hands, wrists, ankles, and feet — beginning 2 to 12 days after a mosquito bite. The pain is frequently described as the worst the patient has ever experienced. Most cases resolve within 7 to 10 days, but 25–50% develop chronic joint pain lasting months to years.

    Q: Is there a vaccine for chikungunya?

    A: Yes. Ixchiq is an FDA-approved single-dose live-attenuated vaccine for adults 18 and older. It was approved November 2023 and is available at travel medicine clinics. It requires approximately 28 days to become fully effective.

    Q: Who should get vaccinated against chikungunya before travel?

    A: Adults 18 and older traveling to areas with active chikungunya transmission who will have outdoor exposure to mosquitoes. This currently includes travelers to Suriname, French Guiana, Mayotte, and other active outbreak areas.

    Q: How is chikungunya different from dengue fever?

    A: Both are transmitted by Aedes mosquitoes and cause fever. Chikungunya is distinguished by the severe arthralgia (joint pain) that dominates its clinical picture and can persist for months to years. Dengue more commonly causes a characteristic rash, severe headache, and potentially hemorrhagic complications.

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  • Vagus nerve stimulation: MedlinePlus Medical Encyclopedia

    Vagus nerve stimulation: MedlinePlus Medical Encyclopedia

    After the surgery, you may stay overnight or go home on the same day. You will have two wound dressings, on your chest and on the left side of your neck.

    You may have pain for a few days and feel a slight bump where the device was placed. Your provider may prescribe pain medicines. If you have been given antibiotics, take them as instructed.

    Do not take baths, swim, or use a hot tub until your provider approves. You may be allowed to have sponge baths with your incision covered.

    Avoid wearing tight clothes that could rub on your incision. Change your dressing as advised. Wash your hands with soap for at least 20 seconds before and after changing your dressings.

    Check your incision for any signs of infection, such as redness, swelling, increased pain, warmness, or pus.

    Your stitches will be absorbed on their own.

    Ask your surgeon if you need to avoid driving or using any machinery.

    You will have a follow-up visit to program the device in 2 to 4 weeks. The device is set to deliver stimulation at a certain frequency for a specific time at regular intervals. The device is usually set at low levels at first to see how your symptoms respond.

    You will be given a handheld magnet to use at home:

    • Sweeping the magnet over the device delivers extra stimulation.
    • Removing the magnet makes the device resume the programmed stimulation cycle.
    • This allows you to control the device as needed.

    For example, if you have epilepsy, and a seizure is about to happen, you can swipe the magnet to send an extra burst of stimulation.

    You will need regular checkups so your device can be monitored. Your provider will check:

    • That the device is in the correct position and working properly
    • The number of stimulations delivered
    • If the programming needs to be adjusted
    • How much power is left in the batteries

    Check with your provider before having any imaging, such as an MRI, as it may interfere with the device.

    Be sure to go to all of your follow-up visits as long as you have the device.

    Side effects can occur due to nerve stimulation and are temporary. When you first start using VNS, you may notice:

    • Hoarseness or a change in your voice
    • Mild coughing
    • A tickling sensation in your throat
    • Shortness of breath
    • Pain in your neck or throat
    • Nausea, vomiting
    • Difficulty swallowing or speaking
    • Tingling or prickling sensation in the skin
    • Headaches
    • Difficulty sleeping or worsening of sleep apnea

    These side effects usually improve with time.

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  • First-in-Class Drug Targeting Treatment-Resistant High Blood Pressure Wins FDA Approval — and Works Like No Existing Drug

    First-in-Class Drug Targeting Treatment-Resistant High Blood Pressure Wins FDA Approval — and Works Like No Existing Drug

    High blood pressure — hypertension — is the single most treatable risk factor for cardiovascular disease and stroke, the two leading causes of death in the United States. There are already more than a dozen classes of antihypertensive medications. For most patients, combining two or three of these drugs in appropriate doses achieves adequate blood pressure control and dramatically reduces the risk of heart attack, stroke, kidney failure, and premature death.

    But for a significant subset — estimated at 10 to 15 percent of all hypertensive patients — blood pressure remains uncontrolled despite taking two, three, or even four medications at maximum tolerated doses. This is called resistant hypertension, and it represents one of the most clinically frustrating situations in internal medicine: a patient taking a handful of pills every day, experiencing their side effects, and still not achieving the blood pressure target that determines their future risk of cardiovascular catastrophe.

    For these patients, the FDA’s May 18, 2026 approval of baxdrostat (Baxfendy) — developed by AstraZeneca — represents the arrival of a fundamentally new therapeutic option built on a mechanism of action that no previously approved drug has ever targeted in this indication.

    “We have been waiting for an innovative medication like BAXFENDY for hypertension for many years,” said Bryan Williams, MD, Chair of Medicine at University College London and a primary investigator for the pivotal BaxHTN trial. “Its novel way of lowering blood pressure has the potential to transform clinical practice by targeting a root cause of persistently uncontrolled hypertension.”

    The Aldosterone Problem and Why Existing Drugs Miss It

    Aldosterone is a steroid hormone produced by the adrenal glands that regulates sodium and water retention in the kidneys. When aldosterone levels are excessive — whether due to a benign adrenal tumor (primary aldosteronism), stress-related overproduction, or other dysregulation — the kidneys retain too much sodium and water, blood volume rises, and blood pressure increases in a way that does not respond well to most standard antihypertensive mechanisms.

    The renin-angiotensin-aldosterone system (RAAS) is already a major target of existing hypertension drugs: ACE inhibitors, ARBs, and direct renin inhibitors all interfere with the pathway that leads to aldosterone production. But these drugs do not directly target aldosterone synthase — the specific enzyme, encoded by the CYP11B2 gene, that is the final step in aldosterone manufacturing in the adrenal gland. Blocking earlier steps in the RAAS leaves aldosterone synthase activity largely intact, allowing it to produce aldosterone through compensatory mechanisms.

    Baxdrostat is a selective aldosterone synthase inhibitor — a small-molecule oral drug that directly and selectively inhibits CYP11B2, preventing aldosterone from being synthesized in the first place. This selectivity is critical: the enzyme CYP11B1, which produces cortisol and sits in a closely adjacent biochemical pathway, is not significantly affected by baxdrostat at therapeutic doses. This means baxdrostat lowers aldosterone — and therefore blood pressure — without disrupting the cortisol axis that regulates the stress response, immune function, and metabolism. AstraZeneca confirmed in clinical trials that baxdrostat lowered aldosterone levels without affecting cortisol levels.

    What the BaxHTN Phase 3 Trial Found

    The BaxHTN trial enrolled 796 patients with uncontrolled or resistant hypertension — all already on at least two antihypertensive agents, including a diuretic — and randomized them 1:1:1 to receive baxdrostat 2 mg once daily, baxdrostat 1 mg once daily, or placebo in addition to their background therapy, for 12 weeks.

    At week 12:

    • Patients on baxdrostat 2 mg had a 15.7 mmHg reduction in seated systolic blood pressure from baseline — a 9.8 mmHg placebo-adjusted reduction.
    • Patients on baxdrostat 1 mg had a 14.5 mmHg reduction — an 8.7 mmHg placebo-adjusted reduction.
    • The placebo group had a 5.8 mmHg reduction from baseline.

    Both doses met the primary endpoint of statistically significant systolic blood pressure reduction. The findings were consistent in patients with both uncontrolled hypertension (not at goal despite two or more drugs) and truly resistant hypertension (not at goal despite three or more drugs, including a diuretic). Results were also supported by a separate Phase 3 Lancet-published Bax24 trial using ambulatory blood pressure monitoring, confirming the effect on 24-hour blood pressure rather than only the clinic reading.

    A 9.8 mmHg reduction in systolic blood pressure is not a cosmetic number. Systematic reviews of blood pressure interventions consistently show that each 5 mmHg reduction in systolic blood pressure reduces the risk of major cardiovascular events by approximately 10 percent. For patients whose blood pressure has been inadequately controlled despite multiple medications — meaning they have been living with elevated cardiovascular risk despite treatment — a nearly 10 mmHg additional reduction is clinically meaningful and potentially life-extending.

    Who Will Benefit and What Comes Next

    Baxfendy is approved as an add-on oral treatment for adults with hypertension not adequately controlled on other medications. It is taken once daily in 1 mg or 2 mg doses. The key safety considerations identified in trials are hyperkalemia (elevated blood potassium), which requires periodic monitoring, and hyponatremia (low sodium) in some patients. Neither was dose-limiting in the vast majority of trial participants.

    The drug received Fast Track and Breakthrough Therapy designations from the FDA during development, signaling the agency’s recognition of the unmet need it addresses. AstraZeneca is also studying baxdrostat in additional conditions where aldosterone excess plays a mechanistic role, including chronic kidney disease and heart failure — conditions that frequently co-occur with resistant hypertension.

    Frequently Asked Questions

    Q: What is baxdrostat (Baxfendy) and who is it for?

    A: Baxdrostat is the first-ever oral aldosterone synthase inhibitor, FDA-approved May 18, 2026 as an add-on treatment for adults with hypertension not adequately controlled on other antihypertensive medications.

    Q: How does baxdrostat work differently from other blood pressure drugs?

    A: It directly and selectively inhibits aldosterone synthase (the CYP11B2 enzyme), preventing aldosterone production at its source. No previously approved drug has targeted this specific enzyme. Existing RAAS drugs act earlier in the pathway and leave aldosterone synthase partially active.

    Q: How much does baxdrostat lower blood pressure?

    A: In the BaxHTN Phase 3 trial, baxdrostat 2 mg added to background therapy produced a 9.8 mmHg placebo-adjusted reduction in systolic blood pressure at 12 weeks. The 1 mg dose achieved an 8.7 mmHg reduction.

    Q: Does baxdrostat affect cortisol levels?

    A: No. Baxdrostat selectively inhibits CYP11B2 (aldosterone synthase) without significantly affecting CYP11B1 (cortisol synthesis). Clinical trials confirmed aldosterone reductions without changes in cortisol.

    Q: What are the main side effects of baxdrostat?

    A: Hyperkalemia (elevated potassium) and hyponatremia (low sodium) are the primary safety considerations, both requiring periodic monitoring. Neither was dose-limiting in most trial participants.

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  • CRISPR Gene Editing Achieves a Functional Cure for Sickle Cell Disease in 96 Percent of Patients — RUBY Trial Results in the New England Journal of Medicine Are Historic

    CRISPR Gene Editing Achieves a Functional Cure for Sickle Cell Disease in 96 Percent of Patients — RUBY Trial Results in the New England Journal of Medicine Are Historic

    The phrase “functional cure” is used carefully in medicine — it describes an outcome in which a disease’s effects are so effectively suppressed that the patient lives as though they do not have it, even if the underlying genetic cause remains. For sickle cell disease, a condition that has caused lifelong suffering, organ damage, and premature death for 100,000 Americans and millions globally, achieving a functional cure through gene editing is one of the most profound accomplishments medicine has produced in years.

    The RUBY Trial, published in the New England Journal of Medicine on April 1, 2026, has delivered exactly that result. Of 28 patients with severe sickle cell disease who were treated with renizgamglogene autogedtemcel (reni-cel) — a CRISPR-Cas12a gene editing therapy that modifies patients’ own blood-forming stem cells — 27 (96 percent) had no painful sickle cell crises for up to two years following treatment. Their average hemoglobin levels rose to near-normal levels, effectively restoring the oxygen-carrying capacity that sickle-shaped red blood cells cannot provide.

    “We have seen that a benefit of this CRISPR/Cas12a gene-editing technology is that there is no rejection, so it’s different from traditional bone marrow transplants, which is standard treatment for sickle cell patients currently,” said Dr. Rabi Hanna, lead author and chair of the Pediatric Hematology-Oncology and Blood and Bone Marrow Transplant Division at Cleveland Clinic Children’s, who led the multicenter trial sponsored by Editas Medicine. “Our aim has been to achieve a functional cure to help prevent any future damage caused by sickle cell disease, and these latest results are compelling.”

    How Reni-Cel Works — and Why Cas12a Matters

    Reni-cel uses CRISPR-Cas12a gene editing to target the promoter regions of the HBG1 and HBG2 genes — the switches that normally suppress fetal hemoglobin production after birth. By editing these promoters, reni-cel reactivates the production of fetal hemoglobin (HbF) in adult red blood cells. Since fetal hemoglobin does not sickle, its presence in sufficient quantities effectively dilutes or displaces the dysfunctional sickle hemoglobin, preventing the cell deformation that causes sickle cell crises, organ damage, and shortened life expectancy.

    This approach is distinct from Casgevy (exa-cel) — the first approved CRISPR therapy for sickle cell disease, using CRISPR-Cas9 to target BCL11A, a different suppressor of fetal hemoglobin. Reni-cel uses CRISPR-Cas12a, which has a different molecular structure and cutting mechanism from Cas9, and targets HBG1/HBG2 directly rather than through BCL11A. The two approaches achieve similar biological endpoints — fetal hemoglobin reactivation — through different molecular pathways, meaning they may offer complementary options for patients in whom one approach is less effective.

    The 28 patients — four of whom were treated at Cleveland Clinic Children’s — underwent a procedure in which their stem cells were first collected and taken to a laboratory where the gene editing was performed. They then received chemotherapy to clear their bone marrow, making room for the repaired cells, which were infused back into their bodies. Within weeks of engraftment, fetal hemoglobin levels began rising. Most patients’ hemoglobin reached near-normal values within the first several months — and the patients themselves experienced what the data describe: two years without a painful crisis.

    Access and What Comes Next

    Reni-cel is not yet FDA-approved. The RUBY Trial data represent Phase 1/2 trial results — sufficient to demonstrate safety and early efficacy, but additional confirmatory data and FDA submission will be needed before approval. Editas Medicine, the trial sponsor, is expected to proceed with regulatory submission based on these results. The cost challenge that affects Casgevy — approximately $2.2 million per patient — will also apply to reni-cel, making equitable access a critical policy question for the approximately 100,000 Americans with sickle cell disease, most of whom are Black or Latino, a demographic that has faced persistent underinvestment in sickle cell research and treatment infrastructure for decades.

    Frequently Asked Questions

    Q: What were the RUBY Trial results?

    A: 27 of 28 patients (96%) with severe sickle cell disease had zero painful sickle cell crises for up to two years after treatment with reni-cel. Their average hemoglobin levels rose to near-normal.

    Q: How is reni-cel different from Casgevy?

    A: Reni-cel uses CRISPR-Cas12a to edit the HBG1 and HBG2 fetal hemoglobin promoters directly. Casgevy uses CRISPR-Cas9 to target BCL11A. Both reactivate fetal hemoglobin but through different molecular pathways.

    Q: Is reni-cel FDA-approved?

    A: No. The RUBY Trial is Phase 1/2. FDA submission is expected based on these results. Casgevy is already FDA-approved and represents the current available option.

    Q: How many Americans have sickle cell disease?

    A: Approximately 100,000 Americans, disproportionately African American and Latino.

    Q: Why is gene editing potentially better than bone marrow transplant for sickle cell?

    A: Because patients use their own edited cells, eliminating the need for a matched donor and removing the risk of graft-versus-host disease — the immune attack that is the major complication of donor-based bone marrow transplants.

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  • Neuroblastoma in Children | CureSearch

    Neuroblastoma in Children | CureSearch

    It is a cancer that arises from immature nerve cells called neuroblasts. Neuroblastoma most often begins in the adrenal glands, which are located on top of the kidneys. However, tumors can form anywhere along the sympathetic nervous system, including the chest, neck, abdomen, or pelvis. In some children, the cancer is localized at diagnosis. In others, neuroblastoma has already spread to the lymph nodes, bone marrow, bones or liver.



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  • Which Beans Best Block the Spread of Cancer?

    Which Beans Best Block the Spread of Cancer?

    Which legumes are best at inhibiting the matrix metalloproteinase enzymes that allow cancer to become invasive?

    Although we’re spending billions of dollars on fancy new types of chemotherapy, the overflowing sink that is cancer treatment is expected to rise by about 70% over the next two decades because drugs are being used to merely mop up the mess rather than turn off the faucet. You can’t really give drugs to people to prevent cancer because of the side effects and cost, but there is said to be “overwhelming…evidence that the dietary bioactive compounds found in whole plant-based foods have significant anticancer and chemopreventive [cancer-preventing] properties.”

    I’ve previously talked about the impact of diet and nutrition on the 10 hallmarks of cancer. The bottom line is that evidence points to a diet that includes minimal animal products and, perhaps more importantly, maximal plant foods. Some foods that seem to be especially beneficial include fruits (especially berries), vegetables (especially greens), legumes (beans, split peas, chickpeas, and lentils), nuts and seeds (especially flaxseeds), onions, garlic, mushrooms, herbs and spices (for example, turmeric), and, as a beverage, green tea.

    Chemotherapy may not even be particularly good at mopping up the mess. “Cancer drugs often impair quality of life and fail to extend patient survival.” Let me say that another way: You’re paying for drugs—maybe selling your house to pay for drugs—that may just be making your life worse for no benefit. Some have suggested we demand at least three months of extended life from pharmaceuticals, but if we demand that chemo actually works, would companies give up testing new cancer drugs altogether? On the other hand, by requiring clinically important benefits—what a concept—maybe Big Pharma would reallocate resources toward targeting the more critical cancer processes like metastatic spread, since it’s the tumor metastasis that accounts for 90% of cancer-related deaths. Who cares if some drug shrinks your primary tumor if it’s spreading and cutting your life just as short?

    What about controlling metastatic cancer with some of those natural bioactive compounds in plants? Evidently, “it has been proven that [plant] phytochemicals are able to inhibit nearly every step of the invasion-metastasis cascade,” at least in vitro (in a petri dish). Below is a list of some purported dietary sources of antimetastatic phytochemicals, which you can also see at 2:27 in my video Blocking the Cancer Metastasis Enzyme MMP-9 with Beans and Chickpeas.

    All of these foods are shown to block all sorts of cancer-signaling pathways, but let me focus on one: matrix metalloproteinases (MMPs). Since about 90% of cancer disability and death is due to cancer spreading (metastasis), let’s talk about MMPs, which “actively participate in the whole metastatic journey.” Matrix metalloproteinases are enzymes that allow the cancer to tunnel through the surrounding flesh and invade the lymph or blood vessels, and then enable it to burrow in and grow somewhere else.

    So, Big Pharma developed matrix metalloproteinase inhibitor drugs, which worked great in animal models but caused severe side effects in humans. So, what about using food? There are special proteins in legumes (beans, split peas, chickpeas, and lentils) that reduce MMP activity. But which is the leading legume? Researchers tested eight different kinds: lupin beans, chickpeas, split peas, black-eyed peas, lentils, more common beans (like kidney, black, or pinto), fava beans, and soybeans. Which do you think worked best?

    Without any beans, the matrix metalloproteinase activity churned away at around 100%, and dripping on some protein from split peas didn’t seem to help much, but the black-eyed peas, lentils, common beans, and fava beans cut enzyme activity by more than 50%. Guess what slashed activity by more than 90%? Lupin beans, chickpeas, and soybeans, as you can see below and at 4:08 in my video.

    But does this translate into slowing down the cancer’s spread?

    Researchers plated a layer of human colon cancer cells in a petri dish and then took a razor blade to clear a strip down the middle. Within 48 hours, the cancer quickly converged to fill the gap. But when a little protein from lupin beans, chickpeas, or soybeans was dripped on, it looked like the cancer cells struggled to close the distance, as you can see below and at 4:33 in my video.

    Okay, but they used raw beans. You don’t know if these anti-cancer proteins are destroyed by cooking until you put it to the test. Researchers found that the matrix metalloproteinase inhibitors in soybeans, at least, did remain active after cooking.

    So, maybe it’s no wonder that eating legumes reduces the risk of colorectal cancer. Yes, but colon cancer, which sprouts from the inner lining of the colon, could potentially come in contact with some of these bean proteins. Presumably, they wouldn’t get into the bloodstream.

    Those eating a vegetarian diet do seem to have significantly lower levels of matrix metalloproteinases, but this is just thought to be due to their lower levels of inflammation, similar to the way non-smokers also have lower MMP levels. This is good because this enzyme isn’t just a cancer biomarker, but also may be involved in autoimmune diseases and cardiovascular disease. The machete-type nature of this enzyme can hack through the inflamed, cholesterol-filled atherosclerotic lesions lining diseased arteries and cause the plaque to rupture. People know that those eating a more plant-based diet tend to have less heart disease, but may not realize they harbor significantly less cancer risk, too, particularly among those eating strictly plant-based diets.

    Doctor’s Note

    The video I mentioned is Fighting the Ten Hallmarks of Cancer with Diet.

    For other videos on cancer metastasis, check the related posts.



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  • HHS Asks the Public What Works for Addiction Treatment in New Federal Request for Comment — Here Is Why It Matters

    HHS Asks the Public What Works for Addiction Treatment in New Federal Request for Comment — Here Is Why It Matters

    The U.S. Department of Health and Human Services published a Request for Information in the Federal Register on June 10, 2026, inviting public comment on which research, programs, and policies have been most successful in treating addiction, improving mental health outcomes, and supporting long-term recovery. The comment period runs through July 5, 2026, and is framed as part of HHS Secretary Robert F. Kennedy Jr.’s broader initiative, the administration has called the “Great American Recovery.”

    The RFI arrives at a sobering moment for American public health. Opioid overdose deaths have remained above 70,000 annually since 2017 and exceeded 80,000 in 2024, making drug overdose one of the leading causes of death among Americans under age 55. Fentanyl and other synthetic opioids now account for the vast majority of these deaths. The toll extends far beyond mortality statistics — addiction devastates families, communities, workforce participation, and the children of people with substance use disorders.

    The notice explicitly invites input from patients, people with lived experience of addiction and recovery, healthcare providers, community organizations, and researchers. The framing reflects a genuine uncertainty about the best path forward at the federal level — and, depending on how the administration responds to the comments received, could foreshadow significant shifts in federal drug and mental health policy.

    What the Science Says About Addiction Treatment

    The research base for addiction treatment has expanded substantially over the past two decades, and several evidence-based approaches have demonstrated consistent results. Medication-assisted treatment (MAT) for opioid use disorder — using buprenorphine (Suboxone), methadone, or naltrexone (Vivitrol) — remains the most extensively studied and most effective approach for reducing overdose deaths and helping patients maintain recovery. A landmark 2023 study in the New England Journal of Medicine found that patients receiving buprenorphine had significantly lower rates of overdose death than those who did not.

    Despite this evidence, access to MAT remains severely limited. Fewer than 20 percent of people with opioid use disorder receive it, partly due to stigma, provider reluctance to prescribe, geographic disparities, and insurance barriers. Advocacy groups and harm reduction organizations have consistently pushed for more accessible prescribing, expanded availability in emergency departments, and removal of administrative barriers to buprenorphine.

    Residential treatment, peer support specialists, contingency management (which uses positive reinforcement to promote drug-free behavior and is especially effective for stimulant use disorders), and community-based case management have all shown benefit in specific contexts. Mental health co-treatment is also increasingly recognized as essential, given that the majority of people with substance use disorders have co-occurring anxiety, depression, trauma, or other psychiatric conditions.

    Harm reduction strategies — needle exchange programs, naloxone distribution, fentanyl test strips, supervised consumption sites — have a strong evidence base for reducing overdose deaths and HIV transmission, though they remain politically controversial and are not universally available.

    What Advocates Want the Administration to Hear

    Public health advocates are watching this comment process closely. Many are hoping the RFI signals a genuine commitment to expanding evidence-based treatment access rather than a pivot toward approaches that lack a strong scientific foundation. Questions about how the Kennedy-led HHS will address the scientific consensus on MAT, harm reduction, and the role of abstinence-only models will shape the federal response for years.

    The comment process is open to all members of the public at federalregister.gov. Comments submitted by the July 5, 2026 deadline will inform HHS policy development.

    Frequently Asked Questions

    Q: What is the HHS asking for in this public comment request?

    A: HHS is seeking input on which addiction treatment programs, policies, and research approaches have been most successful — to guide future federal policy and funding priorities.

    Q: What are the most effective treatments for opioid use disorder?

    A: Medication-assisted treatment (MAT) using buprenorphine, methadone, or naltrexone has the strongest evidence base. Combined with counseling and support services, MAT significantly reduces overdose deaths.

    Q: How many Americans die of opioid overdoses each year?

    A: Opioid overdose deaths exceeded 80,000 in 2024. Fentanyl and synthetic opioids now account for the vast majority of these deaths.

    Q: How can I submit comments to the HHS RFI?

    A: Comments can be submitted at federalregister.gov by the July 5, 2026 deadline.

    Q: What is harm reduction and why is it controversial?

    A: Harm reduction includes strategies like naloxone distribution, needle exchanges, and fentanyl test strips that reduce the risks of drug use without requiring abstinence. Evidence strongly supports their effectiveness, but they remain politically controversial in some settings.

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  • What Is Breast Cancer? – NCI

    What Is Breast Cancer? – NCI

    The female breast contains lobes, lobules, and ducts that produce and transport milk to the nipple. Fatty tissue gives the breast its shape, while muscles and the chest wall provide support. The lymphatic system, including lymph nodes, filter lymph and store white blood cells that help fight infection and disease.

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