Preventing Breast Cancer: Targeting ‘Exhausted’ Immune Cells
Certain immune cells in healthy women can become ‘exhausted,’ making them susceptible for developing breast cancer. Researchers from Cambridge University have identified a pathway involving mutations in the BRCA1 and BRCA2 genes, which are known to increase the risk of breast and ovarian cancer.
The study revealed that immune cells in the breast tissue of women carrying these mutations exhibit signs of malfunction, termed ‘exhaustion.’ These exhausted immune cells are unable to clear damaged breast cells, potentially leading to the development of breast cancer.
Professor Walid Khaled from the University of Cambridge’s Department of Pharmacology highlighted existing drugs capable of reversing this immune cell dysfunction, typically used in late-stage disease. However, employing these drugs preventatively represents a novel approach, offering a non-invasive alternative to breast removal surgery for high-risk individuals.
By analyzing samples from 55 women across various age groups, the researchers created the Human Breast Cell Atlas, providing valuable insights into breast cancer development. Austin Reed, a PhD student involved in the study, emphasized the importance of such resources in understanding breast cancer and improving treatment outcomes.
Breast cancer presents a complex challenge due to its diverse genetic variations and interactions with other risk factors. The study utilized single-cell RNA sequencing to characterize different breast cell types and states, shedding light on how various risk factors contribute to disease development.
Dr. Sara Pensa, a Senior Research Associate at the University of Cambridge’s Department of Pharmacology and a co-author of the study, stressed the significance of prevention in mitigating disease burden and improving outcomes.
Published in Nature Genetics and primarily funded by the Medical Research Council and Cancer Research UK, this research offers promising avenues for preventative breast cancer treatment and underscores the importance of understanding the complex interplay of genetic and environmental factors in disease development.