Publication Date

2026

Keywords

breast cancer, microbiome

Abstract

Breast cancer remains one of the most prevalent cancers worldwide, affecting approximately one in eight women in the United States1. Recent advances in microbiome research have highlighted the microbiome’s essential role in maintaining health and influencing disease progression. Increasing attention has been directed toward understanding how microbial communities contribute to cancer development, particularly through effects on immune function, metabolism, and cellular signaling pathways. While most existing research has examined the gut microbiome and its relationship to breast cancer focusing on the gut–breast axis, microbial translocation, and their contributions to tumor progression, there is a growing need to characterize the breast tissue–specific microbiome itself. Such work may reveal patterns of dysbiosis directly associated with breast carcinogenesis2. To complement the literature, we analyzed publicly available RNA sequence data from the National Center for Biotechnology Information (NCBI) biosamples SAMN20520696 and SAMN20520701, to evaluate taxonomic profiles associated with normal and malignant breast tissues. This analysis is ongoing; so far, we have observed that breast cancer tissues demonstrate reduced microbial diversity and enrichment of specific taxa. Understanding these microbial shifts may offer important insights into the role of dysbiosis in breast cancer progression and identify potential microbial biomarkers for future diagnostic or therapeutic applications.

This Research has been presented

Florida Undergraduate Research Conference, Jacksonville, FL March 2026

Share

COinS
 
 

To view the content in your browser, please download Adobe Reader or, alternately,
you may Download the file to your hard drive.

NOTE: The latest versions of Adobe Reader do not support viewing PDF files within Firefox on Mac OS and if you are using a modern (Intel) Mac, there is no official plugin for viewing PDF files within the browser window.