A recent study conducted by the Tata Memorial Centre (TMC) sheds light on a troubling phenomenon related to cancer therapies. The study, directed by Prof. Indraneel Mittra of TMC's Advanced Centre for Treatment, Research, and Education in Cancer, found that dying cancer cells produce cell-free chromatin particles (cfChPs) following chemotherapy and radiotherapy, potentially turning healthy cells malignant. This result raises serious concerns about the metastatic spread of cancer after treatment.
The decade-long study investigated the role of standard cancer treatments, such as chemotherapy, radiation, and surgery, in the metastatic spread of cancer. The researchers experimented with grafting human breast cancer cells into immune-deficient animals to create tumours. The mice received a variety of therapies, including medicines targeted to deactivate or kill cfChPs.
The study found a large increase in human DNA (cfChPs) and cancer proteins in mice's brains following chemotherapy and radiotherapy. Mice treated with chemicals that deactivate or destroy cfChPs had little human cfChPs or cancer proteins in their brains. This shows that cfChPs, which contain potential cancer-causing genes, could travel through the circulation, infiltrating healthy cells in multiple organs and starting the metastatic spread of cancer.
Prof. Mittra underscored the importance of these discoveries, citing cancer cells' deadly ability to migrate from the initial site to other sections of the body, a process known as metastasis. This metastatic spread is a serious obstacle in cancer treatment, often resulting in death even after successfully treating the initial tumour.
The study revealed a novel deactivation agent, a nutraceutical discovered in Prof. Mittra's group, that showed promising results in blocking chromosomal fragment invasion into healthy cells. Administering cfChP-deactivating/destroying drugs seems to slow the metastatic progression of malignancy.
This study's findings have important implications for cancer treatment policies. Clinicians are encouraged to explore cfChPs as a possible source of metastatic cancer spread, contradicting the prevalent belief that metastasis is generated by migrating cancer cells. Cancer therapy regimens may need to change, maybe incorporating medications or agents particularly designed to deactivate or eliminate cfChPs.
TMC is collaborating with a nutraceutical business to commercialize chromatin-degrading compounds, which are likely to be released in June or July. This research has shown promise for reducing treatment-related toxicity in human trials across a variety of malignancies. The study's findings are a big step forward in cancer research, encouraging a reconsideration of treatment protocols and bringing hope for better outcomes in cancer care.
As advances in cancer treatment have resulted in many individuals being cured, this study reveals a potential risk connected with current treatment methods. Researchers expect that by addressing the release of cfChPs from dying cells, they may be able to contribute to the creation of more effective and tailored cancer treatments, taking cancer from therapy to cure.
Ultimately, TMC's study sheds light on the complicated interplay between cancer treatments and the potential hazards of metastatic spread after therapy. The exploration of novel techniques, such as cfChP-deactivating drugs, brings up new opportunities to advance cancer care and improve patient outcomes.
Inputs from various sources.
(Rehash/Susmita Bhandary/MSM)
