ews Health Researchers uncover new way to identify patients with high breast cancer risk

Scientists have identified specific structural changes within lymph nodes that could offer a crucial new way to predict the likelihood of breast cancer spreading, potentially guiding more personalised treatment approaches.

A recent study revealed that the intricate network supporting lymph nodes can undergo changes due to the disease, even before cancer cells become visible to doctors.

These structural shifts were found to have significant implications for patient outcomes: some were linked to an improved chance of survival, while others indicated a worse prognosis.

Researchers suggest these findings could be instrumental in informing treatment decisions, helping to tailor therapies more effectively and potentially allowing some individuals to avoid unnecessary interventions.

Lymph nodes are vital components of the immune system, playing a key role in fighting infections and cancer.

In breast cancer, the lymph nodes located in the armpit are frequently the initial site of disease dissemination.

Currently, all patients diagnosed with invasive breast cancer undergo surgery to remove these lymph nodes for cellular examination.

While this is effective, it can lead to long-term side effects like swelling of the arm (lymphoedema) and may be unnecessary for some patients.

The new research, funded by the charity Breast Cancer Now, could therefore help identify people who are at higher or lower risk of breast cancer spreading. 

Dr Simon Vincent, chief scientific officer at Breast Cancer Now, said: “These findings suggest that changes to the structure of the lymph nodes are more than just a consequence of the cancer. They can also play an active role in helping breast cancer progress.

“With one person tragically dying from breast cancer every 45 minutes in the UK, we urgently need research like this so that we can better understand who is most at risk of their cancer progressing and becoming incurable. Only then we can find ways to stop it.

“With a better understanding of how lymph nodes change as breast cancer spreads, we could find new targets for future treatments for types of breast cancer that are harder to treat.”

Dr Amy Llewellyn and Dr Kalnisha Naidoo from King’s College London, together with Professor Sophie Acton at University College London, studied 331 lymph node samples taken from people with different types of breast cancer and compared them to healthy lymph nodes in people free from the disease.

They looked at a unique group of cells within lymph nodes called fibroblastic reticular cells (FRC).

The FRC network provides the structure for the lymph node, controls fluid flow and activates different immune cells.

The team found that the structure of this FRC network can change even before the breast cancer has spread and the changes were different depending on the type of breast cancer, any spread, and whether someone had received chemotherapy.

In the future, these findings could support new treatments, more tailored care and ensure more people avoid unnecessary side-effects.

Dr Llewellyn said: “Until now we have not fully understood how and when lymph nodes become altered in a way that allows cancer to spread.

“As a result, every breast cancer patient currently must have some of their lymph nodes removed for accurate staging and treatment planning.

“While this is effective, it can lead to long-term complications and may be unnecessary for some patients, particularly those with early-stage disease or those whose cancer responds well to treatment.

“There is therefore an urgent need to better understand the biology of the lymph node chain and our study addresses this gap by providing the first large-scale analysis of FRC in human lymph node tissue from breast cancer patients.”

Ruth Smith, 59, from Buckinghamshire, was diagnosed with triple negative breast cancer in January 2023 after discovering a lump in her right breast.

“Going through breast cancer treatment and being told that lymph nodes needed to be removed was daunting, and at the time I just focused on doing whatever was necessary to treat the cancer,” she said.

“Living with lymphoedema afterwards has been a constant reminder of what I went through – it developed on my arm like a series of 10p pieces in April 2024.

“The swelling and discomfort can have a real impact on daily life, and it’s something I now have to manage long-term.

“Research like this is so important because it could help doctors better understand who really needs which treatments, and hopefully reduce the number of people who go on to develop lymphoedema in the future.”

The research is published in the Journal of Pathology.

 

 

 

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Experts Can Soon Predict Cognitive Decline in Alzheimer’s

 Alzheimer’s disease is becoming more common, with over 10 million new dementia cases reported each year globally—that's about one every 3.2 seconds. 

After diagnosis, many patients wonder, "What will happen next?" This is a challenging question for doctors to answer. To help, a team at Amsterdam University Medical Center has created a model that predicts cognitive decline.

While the predictions aren't completely certain, they offer a general idea of the disease's progression over five years. Currently, a prototype app is being used for research purposes, with plans to develop a more user-friendly version involving input from patients, families, and healthcare providers.

Cognitive decline happens at different rates for everyone, and many people want to know what to expect for themselves or their family members. This means there's a real need for improved prediction models, says Pieter J. van der Veere, M.D., from Amsterdam University Medical Center, Netherlands.

 

This research is published in the journal Neurology. It also explored the potential of new drugs to lessen the decline in patients with the disease.

 

How researchers developed the model

The researchers developed models to estimate how quickly people's scores on thinking and memory tests would decrease over time. They then compared these predictions with actual test results from participants. The study involved 961 individuals with an average age of 65; 310 had mild cognitive impairment, while 651 had mild dementia. All participants had amyloid-beta plaques in their brains, which are early indicators of Alzheimer's disease and are the focus of new medications. 

 

The cognitive test scores range from zero to 30. A score of 25 or higher suggests no dementia, 21 to 24 indicates mild dementia, 10 to 20 represents moderate dementia, and scores below 10 suggest severe dementia. 

 

After five years, people with mild cognitive impairment showed a drop in their test scores from 26.4 at the beginning of the study to 21.0 at the end. Those with mild dementia had their scores decrease from 22.4 to 7.8 over the same period. 

 

While the models were useful for predicting cognitive decline, they also highlighted some uncertainty, according to van der Veere. In half of the cases involving mild cognitive impairment, the actual scores were within two points of the predicted scores. For those with mild dementia, the scores were within three points of the prediction for half of the participants.

The researchers found that a person with mild cognitive impairment, who had a test score of 28 and a specific level of amyloid plaques, would be expected to progress to moderate dementia (score of 20) in six years. If a treatment reduces the decline by 30%, this person would take 8.6 years to reach moderate dementia. Meanwhile, for someone with mild dementia starting at a score of 21, reaching a score of 15 was predicted to take 2.3 years, extending to 3.3 years if the decline was reduced by 30%. 

 

Cognitive decline happens at different rates for everyone, and many people want to know what to expect for themselves or their family members. This means there's a real need for improved prediction models, according to Van der Veere.

One limitation of the study was that the cognitive tests were not always conducted at the same time of day. People with cognitive decline may score lower later in the day when they feel more fatigued.

 

Providing patients with an app that helps them customize treatments and forecasts

The researchers have not only created the predictive model but also designed a prototype app for clinicians, according to the study's authors. 

 

The tool, which is currently being developed, includes a communication sheet explaining the predictions for clinicians to share with patients and caregivers. Additionally, the app provides information for patients about the disease, diagnosis, and prognosis.

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Nox4 protein can be used as a marker to predict untreatable kidney cancer

A team of researchers from The University of Texas Health Science Center at San Antonio confirmed the role of a certain protein in the development of high-grade kidney cancer. The researchers also showed that a higher level of the protein can be used as a marker to predict which tumors will develop treatment resistance and progress more rapidly.

Dharam Kaushik, MD, led the study published May 31 in the journal Translational Research.
Dr. Kaushik is an associate professor of urology in the Long School of Medicine at the university, also called UT Health San Antonio. He also is a genitourinary oncologic surgeon at the Mays Cancer Center, home to UT Health San Antonio MD Anderson.

About 30% of patients with kidney cancer are not diagnosed until their cancer has spread to other parts of the body. Metastatic disease is notoriously resistant to current targeted therapies. In 2018, there were about 403,262 new cases of kidney cancer and 175,098 related deaths worldwide. 

"Therefore, there is an urgent unmet need for developing new tools to predict which cancers will develop into high grade that are resistant to treatment."
Dr. Dharam Kaushik, Associate Professor of Urology, Long School of Medicine, UT Health San Antonio

In previous preclinical and animal studies the researchers proved that the protein -- nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-4 (Nox4) -- often called Nox4, was involved in promoting the more serious cancer.

In the current study, the researchers studied the treatment records of 350 patients who had kidney cancer between January 2013 and June 2016. Their results showed that Nox4 also concentrates in the nucleus of human kidney cancer cells. The findings were bolstered by a series of statistical analyses using clinical data of patients who survived or died from kidney cancer. The combined results suggest that nuclear Nox4 expression may be an independent marker of disease progression and poor survival in patients with high-grade, advanced-stage kidney cancer.

"Our analysis showed that a high level of nuclear Nox4 is an important marker predicting resistance to targeted therapy. To our knowledge, this is first report of nuclear Nox4 localization and the correlation with disease progression, poor survival and development of resistance to targeted/immune therapy in kidney cancer," he said.

During the study, the researchers also identified a smaller group of patients with high levels of nuclear Nox4 who had rapid disease progression or died within six months of surgery. "These patients would be ideal candidates for a future study of survival outcomes using adjuvant targeted therapy that includes a Nox4 inhibitor." Dr. Kaushik said.

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Celiac disease shares many genetic factors with T1Diabetes

NIDDK study continues to look at possible factors that lead to the development of the diseases in children.

 New results and information surrounding potential "triggers" of the autoimmune process leading to type 1 diabetes (T1D) and how they interact with genetic factors in children at-risk for developing the disease were highlighted in the "Update from the TEDDY Study" symposium today at the American Diabetes Association's® (ADA's) 80th Virtual Scientific Sessions. Similar evidence for celiac disease is also being accumulated through the large international study program. The data The Environmental Determinants of Diabetes in the Young (TEDDY) study has collected prospectively since 2004 will be utilized in new clinical trials to prevent these autoimmune diseases that jointly affect more than 3% of the general population.

TEDDY is an international multi-center trial researching the potential causes T1D in children. The study is funded by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). T1D occurs when the beta cells of the pancreas that normally make insulin are destroyed by the body's own immune system. When the beta cells are destroyed, the body cannot make insulin and maintain normal blood sugar levels.

Children who have T1D have certain types of genes, but not all children who have those genes develop diabetes. Something from the environment "triggers" the immune destruction of the beta cells. TEDDY is aiming to discover viruses and nutritional factors that interact with genes to "trigger" immune destruction of the beta cells, marked by the appearance of islet autoantibodies. The study enrolls infants identified as "at-risk" for developing T1D and follows them for 15 years to look for the appearance of various beta-cell autoantibodies and diabetes. TEDDY has also studied biomarkers that can predict faster or slower progression to diabetes after the autoimmune destruction has begun.

"An interesting finding from TEDDY has been how early the autoimmune destruction of insulin-producing cells begins – often in the initial two years of life," said study TEDDY co-chair Marian Rewers, MD, PhD, a professor of pediatrics and medicine and executive director of the Barbara Davis Center for Diabetes at the University of Colorado School of Medicine. "There appear to be two subtypes of T1D that differ by genetic factors and immune phenotypes. Metabolomic biomarkers may offer clues to the subtypes and whether a child develops T1D. Interestingly, HbA1c has very different predictive characteristics for progression to clinical diabetes in children with islet autoantibodies, compared to adults with risk factors for type 1 diabetes."

 Additional key updates from the study group include:

 Persistent presence of enterovirus B species in a child's stool predicts development of islet autoimmunity, especially the earlier subtype characterized by the presence of autoantibodies to insulin. 

There are also subtle differences in the composition and function of gut microbiome in children who develop islet autoantibodies, compared to controls. Early use of probiotics may decrease the risk, while use of antibiotics was not related to islet or celiac autoimmunity. 

TEDDY has also found potentially beneficial effects of vitamin D, vitamin C, or a diet rich in polyunsaturated fatty acids, though these observations need to be confirmed in randomized clinical trials. 

Celiac disease, another autoimmune condition, shares many genetic factors with T1D, noted Dr. Rewers. TEDDY investigators follow study participants for both T1D and celiac disease in an attempt to determine why some children with high-risk genes develop T1D or celiac disease, while most remain disease-free. This information will be used to try to prevent both diabetes and celiac disease in children. Recently reported TEDDY research showed an association between gluten consumption in the early years of childhood and an increased risk of celiac disease among genetically predisposed children.

 "While T1D and celiac disease share a lot of genetic 

characteristics, there are intriguing differences in the ways these 

diseases develop and progress," added Dr. Rewers. "TEDDY is 

contributing exciting clues for design of future trials to prevent 

both T1D and celiac disease."

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