Putting the brakes on tumor stealth

December 6, 2018, Monash University
Putting the brakes on tumor stealth
Dr. Richard Berry with lab members Dr. Gabby Watson, Zhihui Fu and Felix Deuss. Credit: Monash University

New research undertaken at Monash University has shed new light on how some cancers are able to escape our immune system.

The findings have significant implications for the burgeoning field of immunotherapy, an approach that is focused on harnessing the remarkable power of our own to seek out and destroy cancer.

The research, led by Dr. Rich Berry from the Monash Biomedicine Discovery Institute (BDI) and ARC Centre of Excellence in Advanced Molecular Imaging, was published today in the journal Structure.

"The immune system is complex and highly regulated, comprising a number of accelerators and brakes," explained Dr. Berry.

"While the accelerators activate the immune system, the brakes are critical to maintain the balance and prevent the immune system attacking the body's own healthy tissues."

However, many tumours exploit this mechanism by expressing markers on their surface that engage the brakes, in order to restrict the immune system.

"One method of immunotherapy, termed 'checkpoint inhibition' involves blocking the immune brakes in order to unleash the formidable power of the immune system on the tumour," Dr. Berry said.

So far, two such brakes, PD-1 and CTLA-4, have been effectively targeted in the clinic. However, despite some positive results, many patients do not respond to these treatments. Scientists are on the hunt for new immune brakes to target.

Using high intensity X-rays at the state-of-the-art Australian Synchrotron, the team from Monash determined the 3-D of a new immune , termed CD96. The structure reveals the precise molecular details of how CD96 binds to tumours.

"This is really exciting because studies using mouse models indicate that blocking CD96 might be even more effective at controlling tumour spread than the currently available treatments," Dr. Berry said.

These studies could pave the way for future experiments aimed at further interrogating the role of CD96 in tumour control, and ultimately aid in the development of novel agents for the treatment of a range of cancers.

The paper in Structure is titled Structural basis for CD96 immune receptor recognition of nectin-like protein-5 (CD155).

Explore further: Tumour immune cells could aid cancer therapies, study shows

More information: Structural basis for CD96 immune receptor recognition of nectin-like protein-5 (CD155), Structure, DOI: 10.1016/j.str.2018.10.023

Related Stories

Tumour immune cells could aid cancer therapies, study shows

November 7, 2018
A pioneering technique designed to spot differences between immune cells in tumours could speed the development of cancer treatments, research suggests.

Nobel-winning therapy weaponises immune system against cancer

October 1, 2018
A revolutionary cancer treatment pioneered by the winners of the 2018 Nobel Prize for Medicine has been hailed as the future of fighting the disease—and it has fewer devastating side effects than chemotherapy.

Gene signature discovery may predict response to immune therapy

November 8, 2018
Scientists led by Dr. Daniel De Carvalho at Princess Margaret Cancer Centre have discovered a gene signature biomarker that may predict which patients will respond—or not—to immune therapy.

Cancer cells play hide-and-seek with immune system

June 29, 2016
When the immune system attacks cancer, the tumour modifies itself to escape the immune reaction. Researchers at LUMC published on this subject in Nature on 28 June.

Cancer-causing mutation suppresses immune system around tumours

December 12, 2017
Mutations in 'Ras' genes, which drive 25% of human cancers by causing tumour cells to grow, multiply and spread, can also protect cancer cells from the immune system, finds a new study from the Francis Crick Institute and ...

Immune cells the missing ingredient in new bladder cancer treatment

July 24, 2017
New research offers a possible explanation for why a new type of cancer treatment hasn't been working as expected against bladder cancer.

Recommended for you

Pushing closer to a new cancer-fighting strategy

December 11, 2018
A molecular pathway that's frequently mutated in many different forms of cancer becomes active when cells push parts of their membranes outward into bulging protrusions, Johns Hopkins researchers report in a new study. The ...

Scientists have identified and modelled a distinct biology for paediatric AML

December 11, 2018
Scientists have identified and modelled a distinct biology for paediatric acute myeloid leukaemia, one of the major causes of death in children.

HER2 mutations can cause treatment resistance in metastatic ER-positive breast cancer

December 11, 2018
Metastatic breast cancers treated with hormone therapy can become treatment-resistant when they acquire mutations in the human epidermal growth factor receptor 2 (HER2) that were not present in the original tumor, reports ...

Loss of two genes drives a deadly form of colorectal cancer, reveals a potential treatment

December 11, 2018
Colorectal cancers arise from earlier growths, called polyps, found on the inner surface of the colon. Scientists are now learning that polyps use two distinct molecular pathways as they progress to cancer, called the "conventional" ...

Taking uncertainty out of cancer prognosis

December 11, 2018
A cancer diagnosis tells you that you have cancer, but how that cancer will progress is a terrifying uncertainty for most patients. Researchers at Cold Spring Harbor Laboratory (CSHL) have now identified a specific class ...

Successful anti-PD-1 therapy requires interaction between CD8+ T cells and dendritic cells

December 11, 2018
A team led by a Massachusetts General Hospital (MGH) investigator has found that successful cancer immunotherapy targeting the PD-1 molecule requires interaction between cytotoxic CD8+ T cells, which have been considered ...

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.