A5025034336- Bladder and Urothelial Cancer Treatments
- Acute Lymphoblastic Leukemia research
- DNA Repair Mechanisms
- Urinary and Genital Oncology Studies
- Epigenetics and DNA Methylation
- BRCA gene mutations in cancer
- interferon and immune responses
- CRISPR and Genetic Engineering
- CAR-T cell therapy research
- RNA modifications and cancer
- Acute Myeloid Leukemia Research
- Polyamine Metabolism and Applications
University of Michigan–Ann Arbor
2023-2025
University of Washington
1996
Over 100 distinct disease-associated mutations have been identified in the breast-ovarian cancer susceptibility gene BRCA1. Loss of wild-type allele > 90% tumors from patients with inherited BRCA1 indicates tumor suppressive function. The low incidence somatic suggests that inactivation sporadic occurs by alternative mechanisms, such as interstitial chromosomal deletion or reduced transcription. To identify possible features genomic region may contribute to instability well potential...
While the mutational landscape across early T-cell precursor acute lymphoblastic leukemia (ETP-ALL) and ETP-like is known, establishing a unified framework that activates stem cell genes characteristic of these tumors remains elusive. Using complementary mouse human models, chromatin mapping, enhancer profiling, we show coactivator ZMIZ1 promotes normal malignant ETP population growth by inducing transcription factor MYB in feedforward circuits to convergently activate oncogenes (MEF2C,...
Abstract Background: Bladder cancer patient treatment and outcomes are determined by the tumor’s ability to invade metastasize. Our previous work has shown that TRIM29, also known as ATDC, is regulated TP63 in basal bladder cancers, where it promotes invasion metastasis. We observe TRIM29 predominately localizes intermediate filaments invasive cells. Hypothesis: progression of regulating K14-containing focal adhesions. Methods: To test this hypothesis, we utilized cell culture models cancer,...
Abstract Background: Treatment of muscle-invasive bladder cancer remains challenging and, BCG, one the few treatments that prevents progression high-risk non-muscle invasive tumors to metastatic disease, is difficult obtain. Thus, development new treatment approaches block muscle disease essential. We find TRIM29 (tripartite motif containing 29, also known as ATDC), drives through modulation focal adhesions FAK and c-Src (Src). Despite this, literature has reported conflicting effects Src...
Abstract Bladder cancer is a common malignancy whose lethality determined by invasive potential. We have previously shown that TRIM29 , also known as ATDC transcriptionally regulated TP63 in basal bladder cancers where it promotes progression and metastasis, but the molecular events which promote invasion metastasis downstream of remained poorly understood. Here we identify stimulation migration specific role during invasion. show physically interacts with K14 + intermediate filaments turn...