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Indian cancer researchers develop tablet to prevent cancer recurrence

The tablet is also touted to reduce the side effects of treatments like radiation and chemotherapy by a significant 50 per cent

Indian cancer researchers develop tablet to prevent cancer recurrence

The Tata Memorial Centre (TMC) in Mumbai, a leading cancer research and treatment centre in India, claims to have made a groundbreaking discovery in cancer treatment. After a decade of research, scientists and doctors at the institute have developed a tablet that could prevent the recurrence of cancer in patients.

This tablet is also touted to reduce the side effects of treatments like radiation and chemotherapy by a significant 50 per cent. The key focus of this discovery is the understanding of what happens after cancer treatment.


According to the Tata Memorial Centre (TMC) research, dying cancer cells release cell-free chromatin particles (cfChPs), fragments of chromosomes that can turn healthy cells into cancerous ones. Some of these particles may fuse with healthy chromosomes, leading to the formation of new tumours.

To tackle this problem, doctors administered pro-oxidant tablets containing resveratrol and copper (R+Cu) to rats. These tablets generate oxygen radicals that can destroy chromatin particles.

When taken orally, R+Cu produce oxygen radicals in the stomach, which are quickly absorbed into the bloodstream. These radicals then work to destroy cfChPs released in circulation, preventing the movement of cancer cells from one part of the body to another, known as metastases.

Additionally, the researchers claim that R+Cu can help prevent chemotherapy toxicity. The researchers, in their presentation, referred to this breakthrough as the "Magic of R+Cu."

Led by Prof Indraneel Mittra from the Translational Research Laboratory at TMC's Advanced Centre for Treatment, Research, and Education (ACTREC), the study involved implanting human breast cancer cells into mice to induce tumour formation.

After establishing tumours, the mice underwent various treatments, including chemotherapy, radiotherapy, or surgery. Notably, half of the mice received agents designed to deactivate or destroy cfChPs.

The focus on cfChPs arises from their potential role in the spread of cancer. After chemotherapy and radiotherapy, the researchers observed a significant increase in human DNA (cfChPs) and cancer proteins in the mice brains.

However, mice treated with cfChP-deactivating/destroying agents showed minimal presence of human cfChPs or cancer proteins in their brains.

The significance of these findings lies in the suggestion that cfChPs, containing cancer-causing genes, may travel through the bloodstream and enter healthy cells in different organs, contributing to the metastatic spread of cancer.

This challenges the traditional understanding of cancer metastasis and highlights the potential role of these released particles in initiating cancer in previously healthy cells.

Moreover, the study raises concerns about the unintended consequences of current cancer treatment practices. While chemotherapy and radiotherapy aim to eliminate primary tumour cells, the release of cfChPs from dying cells poses a potential threat.

These particles can travel to distant organs, instigating the formation of secondary tumours in otherwise healthy tissues. The researchers propose a shift in the perspective on cancer metastasis, urging clinicians to consider cfChPs as a potential culprit rather than attributing metastasis solely to migrating cancer cells.

This shift has critical implications for developing effective cancer treatment policies. Furthermore, the study advocates for the inclusion of drugs or agents that can deactivate or destroy cfChPs in cancer treatment protocols.

By targeting these particles, the researchers believe it is possible to mitigate the risk of metastatic spread.

This represents a potential breakthrough in enhancing the outcomes of cancer treatment, addressing not only the primary tumour but also the risk of secondary tumours arising from the release of cfChPs.

This cancer treatment breakthrough can be successful for the post-treatment of cancer-cured patients.

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