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Expression of Transgenes in Native Bladder Urothelium Using Adenovirus-Mediated Transduction

Expression of Transgenes in Native Bladder Urothelium Using Adenovirus-Mediated Transduction

Published on: October 6, 2022

Macroscopic somatic clonal expansion in morphologically normal human urothelium.

Ruoyan Li¹, Yiqing Du², Zhanghua Chen¹

¹Biomedical Pioneering Innovation Center (BIOPIC), School of Life Sciences, Peking University, Beijing, China.

Science (New York, N.Y.)

|October 2, 2020

Summary

Somatic mutations in normal human urothelium were studied. Aristolochic acid exposure dramatically accelerated mutation accumulation and clonal expansion in bladder epithelium.

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Area of Science:

Oncology
Genetics
Cell Biology

Background:

Understanding somatic mutation accumulation in normal cells is crucial for cancer research.
Morphologically normal human urothelium (MNU) is a key area for studying early cancer development.
Limited knowledge exists regarding clonal expansions and mutational landscapes in normal urothelial tissues.

Purpose of the Study:

To investigate somatic clonal events and expansion in morphologically normal human urothelium.
To identify the role of specific mutagens, such as Aristolochic acid (AA), in driving somatic mutations.
To characterize the mutational spectrum and genomic alterations in normal urothelial cells.

Main Methods:

Analysis of somatic mutations and clonal events in morphologically normal human urothelium.
Investigation of the impact of Aristolochic acid (AA) exposure on mutation accumulation and clonal expansion.
Genomic profiling to identify mutations in specific genes and copy number alterations.

Main Results:

Macroscopic clonal expansions were identified in normal human urothelium.
Aristolochic acid (AA) was identified as a major mutagenic factor, accelerating mutation accumulation and clonal expansion.
Mutations were frequently observed in chromatin remodeling genes (e.g., KMT2D, KDM6A), with rare occurrences in TP53, PIK3CA, and FGFR3. KMT2D mutations were common irrespective of mutagen exposure.
Copy number alterations were infrequent, and single AA-associated clones expanded significantly.

Conclusions:

Aristolochic acid significantly drives somatic mutation and clonal expansion in normal urothelium.
Chromatin remodeling genes are frequently mutated in normal urothelial cells, indicating their role in early neoplastic development.
Somatic mutations and clonal expansions in normal tissues are critical for understanding cancer initiation and evolution.