How bladder cancer originates and progresses has been illuminated as never before in a study led by researchers at Weill Cornell Medicine and the New York Genome Center.
Weill Cornell Medicine Oct 9 2024 The researchers found that antiviral enzymes that mutate the DNA of normal and cancer cells are key promoters of early bladder cancer development, and that standard chemotherapy is also a potent source of mutations. The researchers also discovered that overactive genes within abnormal circular DNA structures in tumor cells genes drive bladder cancer resistance to therapy.
Dr. Nicolas Robine, director of computational biology at the New York Genome Center, and Dr. Olivier Elemento, director of the Englander Institute for Precision Medicine and a professor of physiology and biophysics at Weill Cornell Medicine, also led the study with Dr. Faltas. The co-first authors were Duy Nguyen, a technician in the Faltas Laboratory ; William Hooper, a bioinformatics scientist at the New York Genome Center; and Dr. Weisi Liu, an instructor in the Faltas Laboratory.
"The exact role of APOBEC3-induced mutations in cancer initiation hasn't been clear," said Dr. Faltas, who is also the chief research officer at the Englander Institute for Precision Medicine and a member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine. "But we found that these mutations appear early in urothelial cancer, occurring even in pre-malignant urothelial tissue." In his lab, Dr.
Related StoriesThis prompted the team to experimentally model an ecDNA version of one of these genes, called CCND1, a master regulator of the cell cycle in the laboratory. The results of these experiments confirmed that CCND1 in this extrachromosomal configuration drives treatment resistance.
Bladder Cancer Cancer DNA Carcinoma Cell Chemotherapy Evolution Gene Genes Genome Laboratory Malignant Medicine Precision Medicine Research Tumor Urethra
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