A groundbreaking study led by Ramya Ganesan of Emory University, US, and published in the journal PLoS Biology, has unveiled a surprising aspect of cancer treatment, particularly chemotherapy.
The research reveals how a standard chemotherapy drug, while targeting cancer cells, inadvertently damages surrounding healthy cells.
This damage can awaken dormant cancer cells, leading to the growth and potential recurrence of the disease.
Chemotherapy has been a cornerstone in the fight against cancer, significantly reducing mortality rates, including in breast cancer patients.
However, a notable challenge has been cancer recurrence, experienced by up to 23% of breast cancer patients within five years of treatment.
A key reason for this recurrence is the presence of dormant cancer cells – cells that stop dividing and don’t respond to chemotherapy but can later re-awaken and proliferate.
The study aimed to understand how chemotherapy might inadvertently trigger these dormant cells to become active again. Ganesan and her team used both a cell model and a mouse model of breast cancer for their research.
They focused on the interaction between cancer cells and stromal cells, which are non-cancerous connective tissue cells present in various organs.
Upon administering the chemotherapy drug docetaxel, the researchers observed a startling outcome. Even at low doses, the drug harmed the stromal cells but not the cancer cells.
This injury to the stromal cells led to the release of two critical cell signaling molecules, granulocyte colony stimulating factor (G-CSF) and interleukin-6 (IL-6). These molecules were found to stimulate the dormant cancer cells, encouraging their growth.
This discovery provides crucial insights into cancer recurrence. It underscores the role of the tumor environment, especially the non-cancerous cells, in how cancer responds to chemotherapy.
Additionally, it sheds light on why high levels of IL-6 in the blood are linked to early recurrence in breast cancer patients undergoing chemotherapy. This could enhance the use of IL-6 as a biomarker for treatment planning.
Furthermore, the study opens new avenues for cancer treatment.
By targeting G-CSF or IL-6 or blocking their signals in cancer cells, it might be possible to prevent the re-awakening of dormant cells during chemotherapy. This approach could significantly reduce the risk of cancer recurrence.
In summary, this research not only adds a critical piece to the puzzle of how cancer recurs but also points to potential strategies for preventing it.
As Dr. Ganesan and Dr. Sukhatme noted, a temporary blockade of these cytokine signals during chemotherapy could be a key to preventing tumor relapse.
This study is a reminder of the complex nature of cancer and the ongoing need to refine and improve treatment strategies for this challenging disease.
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The research findings can be found in PLoS Biology.
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