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Effect of treating AKPS organoids with either single agent KRAS G12C inhibition or APC restoration, or combination on chromatin accessibility.

ABSTRACT: We show that single agent treatment with either divarasib (KRAS G12Ci) or APC restoration, results in cell plasticity.

ORGANISM(S): Mus musculus

PROVIDER: GSE301559 | GEO | 2026/04/05

REPOSITORIES: GEO

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Effect of treating AKPS organoids with either single agent KRAS G12C inhibition, TEAD inhibiton or APC restoration, or dual and triple combination on gene expression.

Project description:We have previously shown that single agent treatment with either divarasib (KRAS G12Ci) or APC restoration, results in cell plasticity. Here, we aim to evaluate the effects on combination treatment and if gene expression changes can be enhanced with TEAD inhbiiton.

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Effect of treating DLD1 organoids with either single agent MEK (cobimetinib) inhibition or APC restoration on chromatin accessibility.

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Effect of treating AKPS organoids with either single agent KRAS G12C inhibition or APC restoration, or combination on chromatin accessibility.

Project description:Effect of treating AKPS organoids with either single agent KRAS G12C inhibition or APC restoration, or combination on chromatin accessibility.

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Effect of treating AKPS organoids with either single agent KRAS G12C inhibition, TEAD inhibiton or APC restoration, or dual and triple combination on gene expression.

Project description:Effect of treating AKPS organoids with either single agent KRAS G12C inhibition, TEAD inhibiton or APC restoration, or dual and triple combination on gene expression.

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Apc restoration promotes cellular differentiation and reestablishes crypt homeostasis in colorectal cancer

Project description:The Adenomatous Polyposis Coli (APC) tumor suppressor is mutated in the vast majority of human colorectal cancers (CRC) and leads to deregulated Wnt signaling. To determine whether Apc disruption is required for tumor maintenance, we developed a mouse model of CRC whereby Apc can be conditionally suppressed using a doxycycline-regulated shRNA. Apc suppression produces adenomas in both the small intestine and colon that, in the presence of Kras and p53 mutations, can progress to invasive carcinoma. In established tumors, Apc restoration drives rapid and widespread tumor-cell differentiation and sustained regression without relapse. Tumor regression is accompanied by the re-establishment of normal crypt-villus homeostasis, such that once aberrantly proliferating cells reacquire self-renewal and multi-lineage differentiation capability. Our study reveals that CRC cells can revert to functioning normal cells given appropriate signals, and provide compelling in vivo validation of the Wnt pathway as a therapeutic target for treatment of CRC Analysis of RNA isolated from colon polyps that presented in shAPC or shAPC/Kras mice as compared to shRenilla (neutral) mouse colon mucosa

2015-06-18 | E-GEOD-67186 | biostudies-arrayexpress

Apc restoration promotes cellular differentiation and reestablishes crypt homeostasis in colorectal cancer

2015-06-18 | GSE67186 | GEO

Effect of treating DLD1 organoids with either single agent MEK (cobimetinib) inhibition or APC restoration on chromatin accessibility.

Project description:Effect of treating DLD1 organoids with either single agent MEK (cobimetinib) inhibition or APC restoration on chromatin accessibility.

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SMALL MOLECULE IMAGING AGENT FOR MUTANT KRAS G12C.

Project description:Multiple potent covalent inhibitors for mutant KRAS G12C have been described and some are in clinical trials. These small molecule inhibitors potentially allow for companion imaging probe development, thereby expanding the chemical biology toolkit to investigate mutant KRAS biology. Herein, we synthesized and tested a series of fluorescent companion imaging drugs (CID) for KRAS G12C, using two scaffolds, ARS-1323 and AMG-510. We created four fluorescent derivatives of each by attaching BODIPY dyes. We found that two fluorescent derivatives (BODIPY FL and BODIPY TMR) of ARS-1323 bind mutant KRAS and can be used for biochemical binding screens. Unfortunately, these drugs could not be used as direct imaging agents in cells, likely because of non-specific membrane labeling. To circumvent this challenge, we then used a two step procedure in cancer cells where an ARS-1323 alkyne is used for target binding followed by fluorescence imaging after in situ click chemsitry with picolyl azide Alexa Fluor 647. We show that this approach can be used to image mutant KRAS G12C directly in cells. Given the current lack of mutant KRAS G12C specific antibodies, these reagents could be useful for specific fluorescence imaging.

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Apc, Kras, and Trp53 mutations

Project description:Apc, Kras, and Trp53 mutations

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Differential RNA-seq analysis comparing APC-defective and APC-restored SW480 colorectal cancer cells

Project description:Identify genes that are differentially regulated as a consequence of restoration of full-length functional APC in a colorectal cancer cell lines.

2016-02-01 | GSE76307 | GEO

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