Abstract
Over 90% of breast cancer is cured; yet there remain highly aggressive breast cancers that develop rapidly and are extremely difficult to treat, much less prevent. Breast cancers that rapidly develop between breast image screening are called “interval cancers.” The efforts of our team focus on identifying multiscale integrated strategies to identify biologically aggressive precancerous breast lesions. Our goal is to identify spatiotemporal changes that occur prior to development of interval breast cancers. To accomplish this requires integration of new technology. Our team has the ability to perform single cell in situ transcriptional profiling, noncontrast biological imaging, mathematical analysis, and nanoscale evaluation of receptor organization and signaling. These technological innovations allow us to start to identify multidimensional spatial and temporal relationships that drive the transition from biologically aggressive precancer to biologically aggressive interval breast cancer.This article is categorized under:Cancer > Computational ModelsCancer > Molecular and Cellular PhysiologyCancer > Genetics/Genomics/Epigenetics
Highlights
The precursor lesion(s) for biologically aggressive breast cancers are poorly understood
The clinical aggressiveness of a precancerous breast lesion is primarily evaluated based on epithelial cell morphology
Our study provides evidence that morphologically normal breast tissue can express proteins such as Wnt10B/EZH2 that are associated with aggressive breast cancer biology
Summary
Spatiotemporal strategies to identify aggressive biology in precancerous breast biopsies. Frankhauser1 | Tijana Jovanovic-Talisman1 | Lily Lai1 | Lisa D. Wang2 | Ashish Mahabal3 | Joseph Geradts4 | Russell C. Rockne1 | Jerneja Tomsic1 | Veronica Jones1 | Christopher Sistrunk1 | Gustavo Miranda-Carboni5 | Eric C. Dietze1 | Loretta Erhunmwunsee1 | Terry Hyslop6 | Victoria L. Funding information National Cancer Institute, Grant/Award Numbers: 3U01CA189283-S1, P20 CA24619, P30CA033572, R01CA170851, R01CA192914, R01CA220693, T32 CA221709, U01CA189283
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