Introduction

Breast cancer ranks second among the leading causes of cancer-related deaths in women, following lung cancer. Unfortunately, it is the primary cause of death for Hispanic women. Basal (triple-negative) subtypes account for approximately 10-20% of breast cancers, and they pose a challenge to treat due to the lack of specific targets. Triple-negative breast cancer is a highly aggressive and deadly tumor type, especially among Hispanic women, with a poor prognosis compared to other breast cancer subtypes. Therefore, it is vital to identify new molecules with therapeutic and prognostic value to treat this evolving disease. Multiple studies have shown that genes associated with chromosome X are linked to cancer. Although these genes are tightly regulated and expressed only in immune-privileged organs, many of them become abnormally expressed in tumors.

Methods

Through genomic analysis, we have identified that newly identified X-linked genes once thought to be located in the gene deserts in the human genome actually harbor tumor-specific genes belonging to the family of antigenic cancer testis-antigens (CT genes). However, there is limited information available on their expression and function in triple-negative breast cancer. To address this gap, we utilized an integrated genomic approach to identify specific CT genes that are differentially expressed in this type of breast cancer. Furthermore, employing an integrated genomic approach found a highly immunogenic CT gene.

Results

Using a variety of molecular in vitro and in vivo assays, we have determined that this CT gene plays a critical role in regulating pathways related to triple-negative breast cancer. 

Conclusion

This could potentially identify a new diagnostic and therapeutic target for this type of breast cancer.

S.S.G. is a CPRIT Scholar in Cancer Research. S.S.G. is supported by a First-time Faculty Recruitment Award from the Cancer Prevention and Research Institute of Texas (CPRIT; RR170020). S.S.G. is also supported by grants from a) Lizanell and Colbert Coldwell Foundation; b) The Edward N. and Margaret G. Marsh Foundation; c) The American Cancer Society - RSG-22-170-01-RMC, d) NIH grant 1R01AI175837-01.