Cancer
HIV research paves way for new ovarian cancer therapies
HIV research has identified a new target for ovarian cancer by selectively blocking a cleft in the retinoblastoma protein that protects tumour-supporting macrophages.
The discovery could make ovarian – and potentially other – cancers more responsive to immunotherapies, treatments that use the body’s immune system to fight disease.
Scientists at the Wistar Institute found that targeting a specific cleft in the retinoblastoma protein removed only tumour-supporting macrophages while sparing those that fight disease.
Macrophages are immune cells that can either attack tumours or shield them from harm.
The work builds on decades of HIV studies led by Dr Luis Montaner, executive vice president of the Wistar Institute and director of its HIV Cure and Viral Diseases Center.
Montaner said: “This target emerged from our work understanding how macrophages survive HIV infection.
“It shows how insights from one field of medicine can inform breakthroughs in another.”
Targeting tumour-protecting macrophages without harming beneficial ones has long been a challenge.
Wistar researchers showed that selectively inhibiting this protein cleft depleted only tumour-supporting macrophages, leaving protective immune cells intact. Animal studies confirmed tumour shrinkage using this approach.
Montaner said: “This is a first-in-kind target against a solid tumour.
“It opens new avenues for therapies that could complement existing immunotherapies.”
The study highlights the value of long-term, cross-disciplinary research. It took more than 10 years from the initial HIV-linked finding to identifying this cancer target.
Next steps include exploring applications in acute myeloid leukaemia, pancreatic cancer and combination therapies.
An experimental cancer drug reduced bone loss and body fat in mice modelling post-menopausal changes, early research suggests.
The compound, CADD522, appeared to strengthen bones and help the animals stay leaner after surgery designed to mimic hormonal changes seen after menopause.
The treatment remains at an early experimental stage and has so far only been tested in animals.
The study, led by the University of East Anglia, investigated CADD522, which was originally developed to block a protein involved in the growth and spread of several cancers.
Mice treated with the compound for eight weeks showed significant improvements in bone health. Scans found increased bone volume and better preservation of the honeycomb-like structures inside bones that are crucial for strength and resilience.
Blood tests suggested the treatment stimulated new bone growth without interfering with the body’s normal process of breaking down and rebuilding bone.
Dr Darrell Green, lead researcher from UEA’s Norwich Medical School, said: “Osteoporosis affects around one in three women over the age of 50, leaving sufferers vulnerable to painful fractures that can seriously impact quality of life.
“Current treatments exist, but many are plagued by side effects, safety concerns or inconvenient dosing schedules that make long-term use difficult.”
The researchers also found that mice receiving CADD522 weighed less than untreated mice despite eating the same amount of food.
They had less body fat and fewer fat deposits in their bone marrow, a process commonly seen after menopause and linked to declining bone health.
The team also examined brain tissue and found that the drug appeared to reverse several menopause-related changes in fatty acids.
Levels of omega-3 fats including DHA remained largely intact, while several other lipid abnormalities shifted back towards healthier patterns.
Green said: “We didn’t directly test for memory or thinking ability, but our work raises questions about whether this drug could one day help address wider menopause-related health problems.”
Safety experiments in mice, rats and dogs found that CADD522 could be taken orally and was well tolerated.
The compound also appeared to be metabolised more slowly in human tissue than in rodents, potentially improving its performance in people.
“This is still in the early stages and has so far only been tested in animals but we hope that the benefits will translate to humans to ultimately reduce fracture rates,” added Green.
The research was led by UEA in collaboration with the University of Maryland, the Scintillon Research Institute in San Diego and the University of Stirling.
Safety testing was funded by The Sir William Coxen Trust as part of the development of CADD522 as a childhood cancer treatment.
The FDA has granted accelerated approval to AstraZeneca drug Etcamah for certain adults with advanced breast cancer carrying an ESR1 mutation.
Etcamah, also known as camizestrant, was approved in combination with a CDK4/6 inhibitor, either abemaciclib, palbociclib or ribociclib.
The treatment is for adults with hormone receptor-positive, HER2-negative, locally advanced or metastatic breast cancer when an estrogen receptor-1 (ESR1) mutation is detected during aromatase inhibitor and CDK4/6 inhibitor therapy using an FDA-authorised test.
ESR1 mutations are acquired resistance mutations that tumours may develop during treatment with aromatase inhibitors, a type of endocrine therapy commonly used as a front-line treatment for locally advanced or metastatic breast cancer.
Fewer than 5 per cent of patients have the mutation when HR-positive metastatic breast cancer is diagnosed, according to the FDA. After disease progression on an aromatase inhibitor, nearly 40 per cent have the mutation.
Acting FDA commissioner Kyle Diamantas said: “Women living with metastatic breast cancer face an uphill battle as their tumors continuously evolve to escape treatment.
“We owe them every weapon in our arsenal.
“Today’s approval delivers a win to these patients by granting them a targeted therapy designed specifically to overcome resistance, giving them more time before their disease progresses.”
The accelerated approval programme allows earlier approval of drugs that treat serious conditions and fill an unmet medical need based on surrogate or intermediate endpoints.
For Etcamah, approval was based on how long patients lived without their disease worsening, measured from when the resistance mutation was first detected in their blood.
The FDA said it has not yet been confirmed whether intervening when the mutation is detected, rather than waiting until disease progression is confirmed, results in a clinically meaningful benefit. Confirmatory studies are therefore required to verify and describe clinical benefit.
Angelo de Claro, director of the FDA’s Oncology Center of Excellence, said: “I commend both the FDA and the sponsor for their commitment to advancing cancer care and securing this accelerated approval.
“This marks the first FDA approval of a cancer therapy guided by the detection of a resistance mutation in circulating tumor DNA (ctDNA) before imaging tests show that the disease is progressing.
“But additional evidence is needed to confirm clinical benefit.”
Circulating tumour DNA, or ctDNA, consists of small pieces of tumour DNA released into the blood and can allow earlier molecular detection of resistance mutations.
The FDA also authorised the Guardant360 CDx assay as a companion diagnostic to identify patients with breast cancer who have ESR1 mutations for treatment with camizestrant.
Efficacy was assessed in a clinical trial comparing a switch to Etcamah plus a CDK4/6 inhibitor with continued treatment using an aromatase inhibitor plus a CDK4/6 inhibitor.
Estimated median progression-free survival was 16 months in the Etcamah group, compared with 9.2 months in the aromatase inhibitor group.
Etcamah’s prescribing information includes a boxed warning about the risk of irregular heart rhythm when taken with certain other medicines. It also includes warnings about an abnormally slow heart rate and potential harm to an unborn baby.
The FDA convened its Oncologic Drugs Advisory Committee for the application on 30 April 2026.
Scotland has launched a review of NHS IVF access, including whether treatment should extend to single women and couples with children from previous relationships.
The national review will assess how fertility services can better reflect modern family structures while maintaining fair and consistent access across Scotland.
It will also examine access to fertility preservation services, particularly for women who have undergone cancer treatment, and ways to cut waiting times for patients who need donor eggs or sperm.
Scotland currently offers the most comprehensive nationwide NHS IVF provision in the UK. Eligible patients can access up to three full cycles of IVF treatment through the NHS, subject to existing eligibility criteria.
Ministers will also consider updated clinical guidance from the National Institute for Health and Care Excellence.
The revised recommendations suggest patients who have not achieved a successful pregnancy after three IVF cycles could benefit from up to three additional NHS-funded treatment cycles.
The review is part of the Scottish Government’s commitment to examining how fertility services are delivered and whether they meet patients’ needs across Scotland.
Scottish health secretary Angela Constance said: “Access to NHS IVF treatment should be fair, timely and reflect the way people’s lives and families look today, and delivering this review is one of our key 100 day commitments.
“The review will look closely at the current system, including waiting times for those who need donor eggs or sperm for their treatment.
“This work builds on annual Scottish Government funding, which has supported the expansion of NHS IVF treatment over the past ten years.”
Healthcare leaders and fertility specialists will be watching closely as the review progresses, with any future changes potentially broadening access to treatment and addressing long-standing concerns around equity, consistency and waiting times.
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