DISEASE MODELS
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We recently built a new mouse model that combines early genetic alterations with disease-relevant dietary carcinogens to study gastric premalignancy. Using this model, we learned that early TP53 alterations ultimately lead to premalignant lesions that have a selective pressure to alter a cell cycle regulator. Although this second alteration enabled disease progression, it also yielded a therapeutic vulnerability.
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After realizing that hypoxia transcriptional programs may be heightened in p53 mutant gastric and esophageal adenocarcinomas, we designed an in vivo system to measure hypoxia activity in real-time during xenograft tumor growth. Using this system, we were able to identify a new dependency in these deadly cancers. |
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We have designed a genetically engineered mouse model to characterize the functional and clinical significance of SOX9 alterations in colorectal cancer. Phenotypic evaluation, histopathological analyses, and molecular studies (e.g. single-cell RNA-sequencing) of this model will enable a thorough understanding of the genome stable subtype of colorectal cancer.
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