A study is examining where delays occur in diagnosing endometriosis  – a condition that can take seven to twelve years to diagnose.

Endometriosis affects an estimated 1.5 million women and people in the UK, but there is currently no consistent way of measuring where and why diagnostic delays happen.

The research aims to develop the first standardised framework for understanding the diagnostic journey and identifying points where interventions could improve care.

The international project involves researchers from the University of Sheffield, University of Liverpool, University of Oxford, Aarhus University in Denmark and the University of Edinburgh, alongside Endometriosis UK.

Dr Rebecca Mawson, NIHR clinical lecturer in primary care at the University of Sheffield, is part of the research team.

She said: “Our project asks: where exactly are people getting lost or let down on their journey to diagnosis, and how can we map those points in a systematic way to identify where interventions could make a real difference.”

The project is led by Dr Babu Karavadra, NIHR academic clinical fellow in general practice at the University of Liverpool, who has been awarded a World Endometriosis Society Early Career Investigator Award as lead principal investigator at the University of Liverpool.

Researchers will review existing evidence, gather experiences from people living with endometriosis and bring together an international panel to map the diagnostic pathway and agree common definitions for key points along the journey.

The work will focus particularly on people whose experiences are often missing from research, including Black women, people living in rural or deprived areas, LGBTQ+ communities and disabled people.

Primary care will also be central to the research because it is often where people first seek help with symptoms.

Mawson said: “Primary care needs to be at the heart of this work. Primary care is often where people first seek help with their symptoms, so it has a crucial role in understanding diagnostic delay.

“If we only look at what happens once someone reaches specialist gynaecology, we risk missing some of the barriers that shape the journey long before that point.”

Unlike cancer research, where internationally recognised standards exist for studying diagnostic delays, endometriosis research has been more fragmented, with studies measuring different parts of the diagnostic journey in different ways.

The researchers hope to create an ‘Endometriosis Diagnostic Pathway Framework’ to help identify where people are falling through the gaps and where healthcare could be improved.

They will also develop a ‘Snakes and Ladders’ style visual representation showing how systemic barriers, chance and individual experiences can influence whether someone reaches a diagnosis.

The project forms part of the PEARL network, Primary care Endometriosis and Adenomyosis Research and Learning, an international collaboration of primary care and community researchers and clinicians.

Mawson said: “Endometriosis diagnostic delay isn’t inevitable. If we can understand where and why people are experiencing barriers, we have a much better chance of designing interventions that actually make a difference.

“The scale of the problem demands that we look at the whole journey, listen to the people experiencing it and build an evidence base that can lead to real change.”

The framework could provide the foundations for future research, clinical guideline development, healthcare professional training and NHS service improvements, with potential applications to related conditions such as adenomyosis and chronic pelvic pain.

A drug targeting a key regulator in triple-negative breast cancer reduced tumour growth and cancer stem cell viability in laboratory models.

Triple-negative breast cancer is an aggressive subtype that disproportionately affects women under 40 and accounts for about 15 to 20 per cent of breast cancers.

The disease lacks receptors for oestrogen, progesterone and the HER2 protein, which are targeted by several cancer drugs, making it particularly difficult to treat.

Researchers from the National University of Singapore’s Yong Loo Lin School of Medicine investigated mechanisms that allow triple-negative breast cancer cells to spread and resist treatment.

They examined regulators of Wnt signalling, a pathway involved in processes including cell growth and movement, and identified a master regulator called DP103.

DP103 is a gene that controls a major biological process. The researchers found it creates a cycle in which cancer cells continue to grow and spread while resisting treatment and maintaining cancer stem cells linked to disease recurrence.

The team then investigated whether a targeted drug known as Supinoxin, or RX-5902, could block DP103 and its effects in triple-negative breast cancer.

Analysis of 21 samples, including patient tumour tissue, laboratory-grown breast cancer cells and organoids derived from local cancer patients, found that the drug reduced cancer stem cell viability by 40 to 60 per cent.

Tumour growth in laboratory-grown tumour models fell by about 50 per cent.

In laboratory models, treatment also reduced tumour size by around 90 per cent while largely sparing healthy cells.

It also extended survival, with half of the treated laboratory models reaching 70 days and beyond, compared with none in the untreated group.

DP103 had previously been identified as a biomarker for triple-negative breast cancer by a team led by Alan Prem Kumar, an assistant professor with the NUS Centre for Cancer Research and principal investigator for the new study.

RX-5902 is already being studied as a treatment for breast cancer, and Kumar said the findings could help identify patients who may be more likely to benefit.

“Our findings suggest that DP103 could potentially serve as a diagnostic biomarker to identify the patients most likely to benefit from RX-5902 treatment, paving the way for a more precise, personalised approach to treating triple-negative breast cancer,” he said.

“Instead of treating all patients the same, future clinical trials could focus on those whose tumours have high levels of DP103, where the therapy is expected to have the greatest impact,” said Kumar.

First author Cai Wanpei said RX-5902 could prevent beta-catenin, a protein whose mutation is associated with various cancers, from entering the nucleus of human cells and switching off genes that drive cancer growth and spread.

“This slows tumour progression and triggers apoptosis – the natural death of cancer cells,” said Cai, who was a PhD student at the NUS Centre for Cancer Research and NUS Medicine’s pharmacology department during the research.

Study co-author Celestial T. Yap said triple-negative breast cancer remains particularly difficult to treat because conventional treatments such as surgery, chemotherapy and immunotherapy may not work for all patients.

She said DP103 could represent a “biological vulnerability” in the disease.

“This discovery offers new insights that could support more precise patient selection and open the door to better targeted strategies for durable disease control and improved clinical outcomes,” said Yap, an associate professor with the NUS Centre for Cancer Research and NUS Medicine’s physiology department.

The researchers said abnormal Wnt signalling also drives several other cancers, meaning the findings could offer avenues for treating other aggressive cancers.

Their next steps include validating DP103 as a predictive biomarker in larger patient groups and further developing therapies targeting the regulator for clinical testing.

The team will also investigate combining RX-5902 with existing therapies to further improve treatment outcomes.