Fighting Breast Cancer

Thirty-seven Years ago, in 1987, University of Osaka researchers noticed a strange pattern of DNA sequences in Escherichia coli, a prokaryotic organism. They saw five short repeating DNA segments, with identical sequences. These were separated by short non-repeating DNA segments with unique individual sequences. It was the first time microbiologists observed such a pattern, yet, when it became recurring, they started calling it the Clustered Regularly Interspaced Short Palindromic Repeat, CRISPR, mechanism. Years later, Dutch scientists found that a protein, composed of genes coding for enzymes to cut DNA, always accompanied CRISPR. This sequence was labeled Cas (WiB, 2024). With time, UC Berkeley scientists discovered that CRISPR-Cas9 systems could be cultivated as tools to cut any extracted DNA strands, and multiple laboratories began publishing papers demonstrating how the CRISPR-Cas 9 system could be used to edit genomes in human cells (Wib, 2022). Somewhere in between the story of CRISPR-Cas9, in 1994, French activists launched the Pink October movement, a month-long campaign fighting the leading cause of death in women: Breast cancer (Cécile, 2024). A high number of all breast cancers are triple negative breast cancers, TNBCs, which are thought to be the result of a faulty BRCA1 gene. This gene is inherited from both parents, and if properly functioning, prevents the development of cancer. Yet, a BRCA1 gene mutation causes body cells to generate genetic alterations, which can lead to various forms of breast and ovarian cancer (Moffit, N.d.). In advocacy for Pink October, this paper will focus on gene editing through CRISPR-Cas 9, and how it can be used to edit carrier cells of breast cancer to prevent one of the major causes of mortality worldwide.

To begin, breast cancer in itself often occurs due to BRCA1 gene mutation. This trait provides instructions for making a protein that acts as a tumor suppressor, which prevents cells from growing and dividing too rapidly or in an uncontrolled way. It commonly interacts with other proteins to mend breaks in DNA, so plays a critical role in a cell’s environmental wellbeing and development (Medline Plus, N.d.). With this, comes the medical research on Homology-Directed Repair, which can be used to acquire the desired editing outcome in genomes. HDR recognizes when two strands of DNA are mutated, and activates a repair process. It seeks out an identical (homologous) sequence, to invade the broken DNA strand, and align its sequence with the complementary template strand. The cell’s repair machinery then copies the correct sequence, and repairs the break, for the defective gene to be restored. 

Thus, the germline mutations in the BRCA1 gene could be overcome through HDR, which would resist cancer development. This would follow specific steps: Designing a synthetic Guide RNA, specific to the mutated BRCA1 sequence, to guide Cas9 to the exact location in the gene where the mutation exists. Then, Cas 9 would cut the gene where needed, and using Homology-Directed Repair, a template of an efficient BRCA1 gene would be introduced, thus replacing the mutation with the normal sequence (ScienceDirect, 2021). This would prevent the frequent development of breast cancer in women who are prone to evolving the illness due to their genetic composition. 

However, medical ethics are an important issue to address. Some advantages of genetic modification are to do with its precision in gene editing, as well as its development of the quaternary research sector in developing regenerative medicine. Some disadvantages relate to its high cost, the risk of unintended consequences (it’s very new), the unequal distribution for its use (where only the wealthy might have access to it), and its unknown, long term impacts ( Li, Wei, et al., 2024).

To conclude, CRISPR-Cas 9 can be used to genetically modify human genes, in order to fight illnesses such as breast cancer, a battle during Pink October month. This technology can edit BRCA1 genes that are ineffective in suppressing cancer mutations, though like any other medical advancements, this technology holds ethical implications. The question remains: Will future generations, 20 years from now, still celebrate Pink October? Or will the world have evolved in such a way that CRISPR-Cas 9 will have advanced to genetically engineer all humans in being immune to illnesses, and Pink October will only remain as a memory?

Works Cited

Ayadi, Wissem, et al. “A Combination of EGFR-Targeted Therapy and a New Tri-Therapy Strategy Inhibits TNBC Progression in a Preclinical Study.” ScienceDirect. Infectious Diseases Now, vol. 51, no. 8, 2021, pp. 673–684. ScienceDirect, doi:10.1016/j.idnow.2021.07.010.

BRCA1 Gene: “BRCA1 Gene.” MedlinePlus Genetics, U.S. National Library of Medicine, September 2023, medlineplus.gov/genetics/gene/brca1/.

Cécile. “Pink October: Origins and Significance of This Month-Long Fight Against Breast Cancer.” Sortir à Paris, 2024, www.sortiraparis.com/en/news/in-paris/articles/281872-pink-october-origins-and-significance-of-this-month-long-fight-against-breast-cancer.

“CRISPR: A Game-Changing Genetic Engineering Technique.” What is Biotechnology, 2024, www.whatisbiotechnology.org/index.php/science/summary/crispr.

“Jennifer Doudna.” What is Biotechnology, 2022, www.whatisbiotechnology.org/index.php/people/summary/doudna.

 Li, Wei, et al. “Comprehensive Analysis of BRCA1 Mutation and Its Association with Tumor-Infiltrating Lymphocytes in Triple-Negative Breast Cancer.” Cancer Cell International, vol. 22, no. 27, 2022, doi:10.1186/s12935-022-02654-3.

“What Causes Triple-Negative Breast Cancer?” Moffitt Cancer Center, www.moffitt.org/cancers/triple-negative-breast-cancer/diagnosis/causes.