Immune cells 'betray' body to aid breast cancer spread, finds new study

The review highlights how changes in immune cells inside tumours may speed up breast cancer spread and could shape future treatment strategies

The immune system is designed to patrol the body and eliminate danger, yet in breast cancer, some of its most important cells can be persuaded to switch sides. A review by Indian researchers explains how macrophages are reprogrammed within the tumour microenvironment and how this shift enables cancer cells to migrate, invade surrounding tissue and eventually spread to distant organs. 

The review, titled “Common Pathways Regulating Macrophage Differentiation and Breast Cancer Metastasis”, was published in Breast Global Journal. It was led by scientists from Nagaland University and Banasthali Vidyapith and examines how immune system cells called macrophages can be manipulated by breast tumours to accelerate disease progression. By highlighting how tumours manipulate the body’s own defences, the study questions our current understanding of cancer progression and opens new avenues for treatments that target not only the cancer cells themselves but also the ecosystem that allows them to thrive.

 

Understanding the immune system’s role in cancer

Our immune system is designed to protect us by spotting and destroying threats, including abnormal cells that could become cancerous. Macrophages are one such defence cell and normally help clear infections and damaged cells. However, these cells can be persuaded by cancer cells to stop defending and start assisting. 

In healthy tissue, macrophages can exist in two broad states -

• M1 macrophages, which are inflammatory and help destroy tumour cells
• M2 macrophages, which calm inflammation and promote tissue repair

While this balance is essential for normal healing, tumours can disrupt it by altering how these cells behave. Within the tumour microenvironment, macrophages are reprogrammed by cancer-derived signals and pushed towards a pro-tumour form. In this altered state, M2-like macrophages are referred to as tumour-associated macrophages or TAMs. Instead of attacking the tumour, these modified cells begin to support cancer growth, survival and spread.  ALSO READ | Can AI catch breast cancer earlier? New Lancet study shows promising results

How tumours turn defenders into allies

The review makes it clear that breast tumours do not simply grow on their own. Instead, they actively recruit and reprogramme macrophages through a cascade of signals.

• Tumour cells release signalling molecules such as colony-stimulating factors and chemokines
• These signals attract circulating immune cells into the tumour microenvironment
• Once inside, the tumour environment shifts macrophages towards the M2 state
• M2-like macrophages then suppress normal immune responses and encourage tumour growth

This switch is not trivial. Once macrophages switch to the pro-tumour mode, they -

• Stimulate new blood vessel formation (angiogenesis), which feeds the growing tumour
• Release chemicals that inhibit T cells, reducing immune attack on tumour cells
• Secrete enzymes that remodel tissue and enable cancer cells to invade neighbouring tissue and enter the bloodstream

These changes transform macrophages from defenders to accomplices, creating a microenvironment that is favourable for cancer progression.  ALSO READ | What myths about breast cancer could be putting your life at risk?

What this means for breast cancer

Breast cancer remains the most commonly diagnosed cancer among women worldwide and is also the leading cause of cancer-related deaths, accounting for nearly 15 per cent of female cancer fatalities. In India, the burden is particularly significant as the disease makes up around 27 per cent of all cancers affecting women, underscoring the urgent need for a deeper understanding and more effective interventions. 

While early detection and new therapies have improved outcomes in some cases, metastasis (spreading of cancer cells to distant organs) remains the largest barrier to long-term survival. 

The review emphasises that understanding how immune cells are co-opted by tumours is vital. “The downregulation or reprogramming of M2 macrophage differentiation could emerge as a viable strategy for reducing breast cancer progression and metastasis. Such approaches may support the development of targeted immunotherapies that complement existing treatment modalities, offering more precise and less toxic options for patients,” said Prof. Ranjit Kumar of Nagaland University’s Department of Zoology.

Future directions: Reclaiming the immune system

Dr Pranay Punj Pankaj from the Department of Zoology at Nagaland University said, “Our study also outlines future research directions aimed at translating these biological insights into clinical solutions. These include identifying molecular markers for macrophage polarisation, developing therapeutic agents that inhibit tumour-promoting immune signals, and designing diagnostic tools to assess tumour microenvironment profiles for personalised treatment planning.” 

Although these approaches are still in development, they represent a shift in how breast cancer may be treated in the future. Rather than fighting the disease on a single front, scientists are exploring ways to dismantle the support system that allows tumours to thrive, which could ultimately make therapies more precise and personalised. 

 

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This report is for informational purposes only and is not a substitute for professional medical advice.