Cancer
Ovarian cancer vaccine project advances
A UK project to develop the world’s first ovarian cancer prevention vaccine is gathering pace.
A new study will see researchers funded by the charity Cancer Research UK initially establish the targets for the vaccine.
They will investigate which proteins on the surface of early-stage ovarian cancer cells are most strongly recognised by the immune system and how effectively the vaccine kills mini-models of ovarian cancer called organoids.
If this research is successful, work will then begin on clinical trials of the vaccine. The hope is that in the future, women could be offered this vaccine to prevent ovarian cancer in the first place.
There are around 7,500 new ovarian cancer cases every year in the UK, and it is the 6th most common cancer in women.
There is no current screening programme for the disease and some women with inherited copies of altered genes are at higher risk.
Ovarian cancer risk is up to 65% higher in women with altered BRCA1 genes, and up to 35% higher in women with altered BRCA2 genes, compared to women without these gene alterations.
Currently, women with BRCA1/2 alterations are recommended to have their ovaries removed by the age of 35, which means that they can’t have children in the future, and they experience early menopause.
Director of the Ovarian Cancer Cell Laboratory, MRC Weatherall Institute of Molecular Medicine at the University of Oxford and lead for the OvarianVax project, Professor Ahmed Ahmed, said: “We need better strategies to prevent ovarian cancer. Currently women with BRCA1/2 mutations, who are at very high risk, are offered surgery which prevents cancer but robs them of the chance to have children afterwards. At the same time, many other cases of ovarian cancer aren’t picked up until they are in a much later stage.
“Teaching the immune system to recognise the very early signs of cancer is a tough challenge. But we now have highly sophisticated tools which give us real insights into how the immune system recognises ovarian cancer.
“OvarianVax could offer the solution to prevent cancer, firstly in women at high risk but also more widely if trials prove successful. Thanks to this funding, our research can take a big step forward towards a viable vaccine for ovarian cancer.”
Previous research by Professor Ahmed and his team at the University of Oxford has found that immune cells from ovarian cancer patients “remember” the tumour.
Building on this research, the scientists will train the immune system to recognise over 100 proteins on the surface of ovarian cancer, known as tumour-associated antigens.
They will find out which of these antigens trigger the immune system to recognise and kill cells which are becoming ovarian cancer.
Tissue samples from the ovaries and fallopian tubes of people with ovarian cancer will be used to recreate the early stages of ovarian cancer in the study.
The researchers will work with patient and public representatives to establish who would be willing to take the vaccine, who could benefit most from it, how it could be administered and how to ensure it is taken up by as many eligible women as possible, if it is successful in future clinical trials.
It will still take many years for the vaccine to reach a point where it is widely available to women at risk of ovarian cancer.
However, this funding is an exciting step towards a world where doctors can prevent ovarian cancer at an early stage, rather than treating it once the disease has already taken hold.
Chief executive of Cancer Research UK, Michelle Mitchell, said: “Projects like OvarianVax are a really important step forward into an exciting future, where cancer is much more preventable. This funding will power crucial discoveries in the lab which will realise our ambitions to improve ovarian cancer survival.
“OvarianVax builds on the exciting developments in vaccine technology during the pandemic. This is one of many projects which we hope will give women longer, better lives, free from the fear of cancer.”
Ovarian cancer cases are rising among younger adults in England, with bowel cancer showing a similar pattern, a new study suggests.
Researchers said excess weight is a key contributor, but is unlikely on its own to explain the pattern.
The authors wrote: “These patterns suggest that while similar risk factors across ages are likely, some cancers may have age-specific exposures, susceptibilities, or differences in screening and detection practices.”
They added: “Although overweight and obesity are linked to 10 of the 11 cancers evaluated and account for a substantial proportion of cancer cases, both BMI-attributable and BMI-non-attributable incidence rates have increased, though the latter more slowly, suggesting other contributors.”
The study analysed cancer incidence, meaning new diagnoses, in England between 2001 and 2019 across more than 20 cancer types, comparing adults aged 20 to 49 with those aged 50 and over.
Among younger women, cases of 16 out of 22 cancers increased significantly over the period, while among younger men, 11 out of 21 cancers increased significantly.
In particular, there was a significant rise in 11 cancers with known behavioural risk factors among adults under 50. These were thyroid, multiple myeloma, liver, kidney, gallbladder, bowel, pancreatic, endometrial, mouth, breast and ovarian cancers.
Rates of all 11 also rose significantly among adults aged 50 and over, with the notable exceptions of bowel and ovarian cancer.
Five cancers, endometrial, kidney, pancreatic, multiple myeloma and thyroid cancer, increased significantly faster in younger than in older women, while multiple myeloma increased faster in younger than in older men.
The researchers looked at established risk factors including smoking, alcohol intake, diet, physical inactivity and body mass index, a measure used to assess whether someone is underweight, a healthy weight, overweight or obese.
With the exception of mouth cancer, all 11 cancers were associated with obesity. Six, liver, bowel, mouth, pancreatic, kidney and ovarian, were also linked to smoking.
Four, liver, bowel, mouth and breast, were associated with alcohol intake. Three, bowel, breast and endometrial, were linked to physical inactivity, and one, bowel, was associated with dietary factors.
But apart from excess weight, trends in those risk factors over the past one to two decades were stable or improving among younger adults.
That suggests other factors may also play a part, including reproductive history, early-life or prenatal exposures, and changes in diagnosis and detection.
The study noted that red meat consumption fell among younger adults, while fibre intake remained stable or slightly improved in both sexes between 2009 and 2019, although more than 90 per cent of younger adults were still not eating enough fibre in 2018.
Established behavioural risk factors accounted for a substantial share of cancer cases.
Excess weight was the risk factor associated with most cancers in 2019, ranging from 5 per cent for ovarian cancer to 37 per cent for endometrial cancer.
The researchers said the findings were based on observational data, meaning the study could identify patterns but could not prove cause and effect.
They also noted there were no consistent long-term national data for several risk factors, that the analysis was limited to England rather than the UK, and that cancer remains far more common overall in older adults despite the rise in cases among younger people.
An AI tool could help spot breast cancer risk by analysing how individual breast cells behave when squeezed under stress, research suggests.
Researchers at City of Hope and the University of California, Berkeley, created a microfluidic platform that assesses women’s breast cancer risk at the cellular level.
The platform squeezes individual breast epithelial cells, which line breast tissue, to measure how they deform, recover and behave under stress.
Because more than 90 per cent of women do not have a known genetic predisposition to breast cancer or a family history of the disease, the researchers said the approach could help fill a key gap in risk assessment.
Mark LaBarge, professor in the department of population sciences at City of Hope, said: “For women with a known genetic risk factor for breast cancer, there are things you can do like follow a higher-risk screening protocol. For everybody else, you’re left wondering, ‘Am I at high risk?’
“By translating physical changes in cells into quantifiable data, this tool gives women something tangible to discuss with their doctors, not just risk estimates, but evidence drawn directly from their own cells.”
The researchers developed a machine learning algorithm that identifies and measures cells showing signs of accelerated ageing, generating an individual breast cancer risk score.
They said the platform uses simple electronics that could be easy and affordable to replicate on a large scale.
Lydia Sohn, chair in mechanical engineering at UC Berkeley, said: “Our team isn’t the first to measure the mechanical properties of cells; however, other approaches require advanced imaging technology that’s expensive, cumbersome and has limited availability.
“In contrast, MechanoAge uses computer chips that are simpler than an Apple Watch and ‘RadioShack parts’ that are cheap and easy to assemble, potentially making the device highly scalable.”
About 6 per cent of women who develop breast cancer carry known genetic mutations.
For women outside this group, risk is usually estimated indirectly using population models or measures such as breast density, which can both overestimate and underestimate individual risk.
The researchers said there is currently no non-genetic test that can identify women at higher risk of breast cancer.
Screening mammograms can detect cancer only once it has started to grow, but the MechanoAge platform aims to assess risk earlier by looking for physical changes in individual cells.
Using the platform, the researchers found that breast cells appear to have a “mechanical age” separate from a person’s chronological age, based on how the cells respond to stress.
They said this is the first time mechanical age has been quantified in biological cells.
Sohn said: “We learned that the older the mechanical age, as determined by how cells respond to being squeezed through our microfluidic device, the higher the risk for breast cancer.”
In this type of mechano-node-pore sensing, an electrical current is measured across a liquid-filled channel.
As cells pass through, they disrupt the current, generating measurements about their size and shape. By narrowing parts of the channel, researchers squeeze the cells and then measure how long each one takes to return to its normal shape.
The team found that cells from older women were stiffer and took longer to bounce back after being squeezed.
They also identified a subset of younger women whose cells behaved more like those from older women. These cells came from women with genetic mutations linked to a higher breast cancer risk.
The researchers then refined the algorithm to assign a risk score based on the cells’ measured mechanical and physical properties. They said it successfully identified women with known genetic risks.
The team then used it to compare cells from healthy women, women with a family history of breast cancer, and cells taken from the healthy breast of women with breast cancer in the other breast.
LaBarge said: “With accuracy, we were able to figure out which women were at high risk of breast cancer and which women didn’t seem to be.”
The work grew out of more than 12 years of collaboration between the two labs, combining engineering with cancer and ageing biology.
Sohn said: “It’s a true collaboration. We’ve learned a lot from each other.
LaBarge added: “In my view, this is what happens when you have a real collaboration that develops over a long time. This result is not what we imagined at the beginning.”
An experimental drug slowed triple-negative breast cancer in mice by flooding tumour cells with toxic fats.
Triple-negative breast cancer lacks three common drug targets, making it one of the hardest-to-treat and most aggressive forms of the disease.
The compound, known as DH20931, appears to push cancer cells past their limits by triggering a surge in ceramides, fat-like molecules that place the cells under intense stress until they self-destruct.
In lab experiments, the drug also made standard chemotherapy more effective. When combined with doxorubicin, researchers were able to reduce the dose needed to kill cancer cells by about fivefold.
The drug targets an enzyme known as CerS2 to sharply increase production of these lipids and stress cancer cells. Healthy cells, by contrast, showed lower sensitivity to the drug in lab tests.
While the early results are promising, further preclinical and clinical trials would still be needed to determine the safety and effectiveness of DH20931 in humans.
Satya Narayan, a professor in the University of Florida’s College of Medicine, led the study with an international group of collaborators.
The researchers published their results on human-derived tumours on 21 April and presented their findings on combination therapy at the annual meeting of the American Association for Cancer Research in San Diego.
Narayan likened the drug’s effects to a home’s electrical system handling a power surge.
While healthy cells act like a properly grounded and installed circuit, cancer cells are more like a jumble of mismatched wires and faulty fuses. DH20931 overwhelms cells not with electricity, but with fats.
He said: “When that surge goes into the cancer cells, they cannot handle the amount of power they are getting. The fuses burn out, the cell can’t handle the surge and it dies.”
The compound was developed at the University of Florida in the lab of Sukwong Hong.
Hong, now a professor at the Gwangju Institute of Science and Technology in South Korea, created DH20931 as one of many drug candidates tested for efficacy in Narayan’s lab.
In the study, researchers implanted human triple-negative breast cancer tumours into mice and treated them with DH20931.
The drug significantly slowed tumour growth without causing noticeable weight loss or signs of toxicity in the animals. In separate lab experiments, it also showed activity against other breast cancer subtypes.
In addition to increasing lipid levels, DH20931 triggers a second stress signal by flooding cells with calcium.
Together, these effects disrupt the mitochondria, the structures that produce a cell’s energy, ultimately leading to cell death.
Narayan said: “It does not just follow one pathway but it goes through multiple pathways. It’s a two-hit hypothesis.
“These pathways are common in all breast cancer types and other solid tumours, so we think this drug can be useful not only in triple-negative breast cancer but potentially other cancers as well.”
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