New Atlas Reveals Glioma’s Hidden Complexity

Researchers have created the most detailed spatial multiomic atlas to date of glioma tumour microenvironments, shedding new light on why these aggressive brain cancers are so difficult to treat. By combining spatial proteomics, transcriptomics and glycomics, the team analysed 670 tumour lesions from 310 adult and paediatric patients, generating a rich, open-source dataset for the cancer research community.

Gliomas are among the deadliest cancers, with survival often measured in months for the most aggressive forms such as glioblastoma (GBM). The new study helps explain why: tumour cells within the same lesion can vary dramatically in their expression of so-called “targetable” antigens.

Why Targeted Therapies Fail

Single-cell analyses revealed that even widely studied targets such as B7H3 and EGFR are inconsistently expressed. While GBM and pleomorphic xanthoastrocytoma showed a high prevalence of B7H3-positive tumour cells, most gliomas – including many childhood tumours – expressed candidate tumour antigens in fewer than half of their cancer cells.

This variability means that therapies designed to attack a single antigen may leave large portions of the tumour untouched, allowing cancer cells to survive and regrow. The findings provide a biological explanation for why promising immunotherapy and targeted therapy trials have often failed to deliver lasting benefits.

The study also examined paired samples from patients with isocitrate dehydrogenase (IDH)-mutant gliomas, comparing tumours before and after recurrence. Rather than being driven solely by genetic changes in cancer cells, recurrence was linked to a profound spatial reorganisation of the tumour microenvironment.

Immune Signals Predict Survival

In initial tumours, immune niches rich in T cells and vasculature-associated myeloid cells were common. At recurrence, these niches gave way to tumours dominated by microglia and CD206-positive macrophages, suggesting that immune remodelling plays a central role in disease progression and treatment resistance.

By integrating multiple data layers, the researchers identified N-glycosylation patterns as the strongest classifier of tumour grade. Meanwhile, immune-related gene expression programmes emerged as the most powerful predictor of survival in glioblastoma, outperforming traditional clinical and molecular markers.

Beyond its scientific findings, the atlas is being released as a community resource, offering a baseline map of glioma tumour microenvironments across all stages of disease. Researchers say it provides a new framework for glioma classification, outcome prediction and the rational design of future therapies that account for the full complexity of glioma biology.

 

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Study discovers targeted therapy to help adolescents with deadly nerve cancer

A targeted therapy has been discovered to treat adolescent patients who suffer from a deadly paediatric nerve cancer called neuroblastoma, a recent study has stated.


Neuroblastoma is one of the most common and aggressive paediatric nervous system tumours and generally has a poor prognosis, particularly when it advances in older children.

Treatment success for the disease varies, but is exponentially less in adolescent patients, particularly because the disease lacks effective targeted therapies.

The Mount Sinai researchers found that neuroblastoma in older children and adolescents harbouring deletions within a gene called ATRX may be responsive to a targeted therapy called tazemetostat.

Tazemetostat disables an enzyme called EZH2 that inhibits genes that promote normal neuron development, in turn killing neuroblastoma cells. Neuroblastoma arises in immature nerve cells of the adrenal glands and portions of the spine during the development of the sympathetic nervous system, which controls the body's "flight or fight" response to stress.

EZH2 inhibitors are already being tested in phase I and phase II clinical trials for other cancers, including lymphomas, sarcomas, and other solid tumours, with some favourable results.

"We hypothesised that mutant ATRX proteins contribute to aggressive neuroblastoma," said a Professor of Oncological Sciences and senior corresponding author.

"In this study, we aimed to decipher the underlying biology of these altered proteins in neuroblastoma, a tumor for which effective therapeutic strategies remain obscure, and to exploit identified dependencies," added the Prof.

Mount Sinai scientists continue to expand this research into the role of the mutant ATRX protein in the laboratory and hope to eventually open a clinical trial with collaborating institutions.

Based on this research, they believe that EZH2 inhibitors could also be effective in other ATRX mutant cancers, such as pediatric glioblastoma, multiforme and osteosarcoma.

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How to fight head and neck cancer

April 7-14 is celebrated as Global Head and Neck Cancer Awareness Week. In the wake of this, an oncologist tells us how we can be better prepared to fight this disease.

Head and neck cancer is the sixth most common cancer in the world. In central Asia, it is the most common one.

Smoking, consumption of alcohol, and chewing of tobacco are the main causes. Human Papilloma Virus (HPV) infection is also a risk factor.

Persistent mouth ulcers, painful ulcerative lesion on the lip, a hoarse voice, dysphagia, and lump in the throat are the major symptoms.

The disease can be diagnosed by clinical examination, CT scan, MRI, and biopsy. After the diagnosis and staging of the disease, head and neck cancer is treated through surgery, radiotherapy, and chemotherapy.

In the early stages, the disease is mainly treated by surgery. In certain clinical situations, radiotherapy is the treatment of choice. Bulky tumours are generally best treated with a combination of surgery and radiotherapy. More than 60% of head and neck cancers are advanced locoregional diseases. 

The use of radiotherapy with concurrent chemotherapy has been demonstrated to be associated with survival advantage over radiotherapy alone.

Although platinum-based chemotherapy is a preferred choice of treatment for fit patients, targeted therapies for platinum-unfit patients come with good survival advantages. 

Recently, targeted therapies and immune-oncology drugs have also shown promising results in relapsed cases. 

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Genetics variants associated with obesity identified

Researchers have identified genetic variants associated with obesity that is central to developing targeted interventions to reduce the risk of chronic illnesses like hypertension, Type-2 diabetes and heart disease. The team found genetic sites that affect the human body's size and shape, including height and obesity. The findings will help understand how genes can predispose certain individuals to obesity.

In the study, researchers found 24 coding loci (or positions) -- 15 common and nine rare -- along chromosomes of individuals that predispose to higher waist-to-hip ratio. Higher values of the waist-to-hip ratio are associated with more incidence of diseases associated with obesity. 

"For the first time, we were able to examine, on a large scale, how low-frequency and rare variants influence body fat distribution," said a researcher. 

"A better understanding of the genetic underpinnings of body fat distribution may lead to better treatments for obesity and other downstream diseases obesity also impacts, for example, Type-2 diabetes and heart disease," he suggested.

Further analysis revealed pathways and gene sets that influenced not only metabolism but also regulation of body fat tissue, bone growth and adiponectin, a hormone that controls glucose levels and breaks down fat. Performing functional studies across other organisms, the team also identified two genes that were associated with a significant increase in triglyceride and body fat across species.

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Breast cancer drugs may help treat resistant lung cancers

A class of drugs used to treat certain breast cancers could help fight lung cancers that have become resistant to targeted therapies, according to a study conducted in mice.

The study, und that lung tumours in mice caused by mutations in a gene called EGFR shrunk sig protein called p110a was blocked.

Drugs to block p110a are currently showing promise in clinical trials against certain breast cancers, so could be approved for clinical use in the near future, said researchers.

The new findings suggest that these drugs could potentially benefit patients with EGFR-mutant lung cancers whose tumours have become resistant to treatment.

"At the moment, patients with EGFR-mutant lung cancers are given targeted treatments that are very effective for the first few years," said a Prof. 

"These drugs are improving, but unfortunately after a couple of years the cancer usually becomes resistant and starts to grow and spread again," the Prof. said.

The second line of treatment is currently conventional chemotherapy, which is not targeted and has substantial side-effects, researchers said.

It would be worth investigating whether p110a inhibitors could be used as second-line therapy, they said.

The team targeted a specific interaction between the RAS protein and p110a.

The RAS gene is mutated in around one in five cancers, causing uncontrolled growth, and is a key focus of the study.

When the researchers blocked this interaction in genetically modified mice with EGFR mutations, their tumours shrank significantly.

Before the intervention, the tumours filled around two thirds of the space inside the lung.

When the interaction between RAS and p110a was genetically blocked, this shrank significantly to about a tenth of the space inside the lung.

The intervention also had very few side-effects.

"As we wanted to pinpoint the specific interaction responsible, we used a genetic technique that would not be practical in a patient treatment," said the Prof.

"We're looking to develop ways to do this with drugs, as blocking this specific pathway would significantly reduce side-effects, but this work is many years from the clinic," the Prof. said.

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