By Nancy Lapid
(Reuters) – When prostate cancer patients need therapy to reduce male hormone levels, delivering some of the treatment via a patch on the skin may be just as effective as traditional means of administration with fewer side effects, according to a mid-stage study.
Prostate cancer cells usually require male androgen hormones, such as testosterone, to grow. Androgen deprivation therapy (ADT) employs drugs that block the androgens’ “pathway” to receptor proteins on cancer cells, along with so-called luteinizing hormone-releasing hormone (LHRH) drugs that are injected or implanted to lower the testicles’ production of testosterone.
Side effects of the treatments include hot flashes, fatigue, memory problems, and bone density loss.
In the new trial, being presented at the 2025 ASCO Genitourinary Cancers Symposium in San Francisco, 79 patients with prostate cancer all received androgen receptor pathway inhibitor drugs. In addition, they were randomly assigned to receive either LHRH drugs or a transdermal patch containing estradiol, a form of the female hormone estrogen.
Transdermal estradiol, currently used for menopausal hormone therapy, is a potentially attractive alternative approach to ADT, said study leader Dr. Nick James of the Institute of Cancer Research, The Royal Marsden NHS Foundation Trust, in London.
It suppresses testosterone without estrogen depletion; it increases bone density; it’s inexpensive; and it avoids the blood clot risk associated with oral estrogen, he explained.
Within six months, 61% of patients in each arm were responding well to treatment, as assessed by their blood levels of prostate specific antigen.
Patients using the estradiol patches had a lower rate of hot flashes than those on LHRH drugs – 5% versus 24% – and a lower rate of high blood pressure – 5% compared with 17%.
Enlargement of breast tissue was more common in the estradiol patch group, however.
It will be some time before the researchers can assess whether the patches were non-inferior to the LHRH drugs in terms of metastasis-free survival, or length of time without the disease spreading.
They noted that in two earlier trials, estradiol patches were equivalent to LHRH in rates of androgen suppression, superior at improving metabolic parameters, quality of life, and bone density, and non-inferior to LHRH in achievement of metastasis-free survival among men with locally advanced disease.
Estradiol patches could be particularly attractive to patients who are on an LHRH drug and are troubled by side effects like hot flashes, James said.
They also have appeal from a cost standpoint, he added.
“This sort of repurposing of an older, cheap drug is an important way to improve outcomes, separate from developing new drugs,” he said.
BIOMARKER TEST FINDS ALZHEIMER’S PATHOLOGY EARLIER
Years before clumps of tangled tau proteins show up on brain scans of patients with Alzheimer’s disease, an experimental test can detect small amounts of the clumping protein in cerebrospinal fluid, researchers reported in Nature Medicine.
Patients with Alzheimer’s disease with few or no tau neurofibrillary tangles in the brain gain more from current therapies compared to patients with advanced tau tangles, the researchers noted. Currently approved medicines, Leqembi from Biogen and Eisai and Eli Lilly’s Kisunla, target amyloid plaques in the brain, but tau is widely believed to be a contributor to the disease and a target of much current research.
“Our test identifies very early stages of tau tangle formation – up to a decade before any tau clumps can show up on a brain scan,” study leader Thomas Karikari of the University of Pittsburgh said in a statement.
“Early detection is key to more successful therapies for Alzheimer’s disease since trials show that patients with little-to-no quantifiable insoluble tau tangles are more likely to benefit from new treatments than those with a significant degree of tau brain deposits.”
Karikari’s team identified a core region of the tau protein that is necessary for neurofibrillary tangle formation, and further identified a sequence of amino acids that are characteristic of clumping-prone tau proteins.
In particular, two places on the protein can yield useful clues to the status of early-stage tau aggregation that could potentially be reversed, if appropriate interventions are developed, they said.
“A large percentage of people who have brain amyloid-beta deposits will never develop dementia,” said Karikari.
“Early detection of tangle-prone tau could identify the individuals who are likely to develop Alzheimer’s-associated cognitive decline and could be helped with new generation therapies.”
(Reporting by Nancy Lapid; editing by Bill Berkrot)
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