ArticleACS synthetic biology2026
Oncogenic Alterations in PI3K Signaling Emulated Optogenetically Recapitulate Some Phenotypic Changes in Mammary Epithelia.
Keith A Gagnon, Veronica W Hui, Terry Ching, Amy E Stoddard, Esther Koh, Jeroen Eyckmans, Ahmad S Khalil, Christopher S Chen
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In one paragraphArticle in ACS synthetic biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 · Who and what moneyAuthors and funding
8 authors.
Keith A GagnonDepartment of Biomedical Engineering, Boston University, Boston, Massachusetts 02215, United States.ORCID 0000-0002-8898-9372 Veronica W HuiDepartment of Biomedical Engineering, Boston University, Boston, Massachusetts 02215, United States.
Terry ChingDepartment of Biomedical Engineering, Boston University, Boston, Massachusetts 02215, United States.
Amy E StoddardBiological Design Center, Boston University, Boston, Massachusetts 02215, United States.
Esther KohBiological Design Center, Boston University, Boston, Massachusetts 02215, United States.
Jeroen EyckmansDepartment of Biomedical Engineering, Boston University, Boston, Massachusetts 02215, United States.
Ahmad S KhalilDepartment of Biomedical Engineering, Boston University, Boston, Massachusetts 02215, United States.ORCID 0000-0002-8214-0546 Christopher S ChenDepartment of Biomedical Engineering, Boston University, Boston, Massachusetts 02215, United States.ORCID 0000-0003-2445-8449 Funding
BIOLOGY OF THE LUNG--MULTIDISCIPLINARY PROGRAMT32HL007035 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI Darrell N. Kotton, JOSEPH P MIZGERD · 1985 to 2026
$24.3MSynthetic toolkit for precision gene expression control and signal processing in mammalian cellsR01EB029483 · NIBIB · HARVARD UNIVERSITY · PI Ahmad Samir Khalil · 2020 to 2026
$5.0MSynthetic vascularization and regeneration in engineered tissuesR01EB033821 · NIBIB · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI SANGEETA N. BHATIA, CHRISTOPHER S CHEN · 2023 to 2026
$2.2MNational Science Foundation CMMI-1548571NIBIB NIH HHS R01 EB029483NIBIB NIH HHS R01 EB033821NIH HHS T32HL007035
6 · The paper itselfAbstract
Cancer is known to be a disease of altered cellular signaling; however, the relationship between mutation-specific changes to signal transduction and the phenotypic consequences produced remains poorly understood. Here, we investigate two common breast cancer driver mutations, the
Indexed as
Class I Phosphatidylinositol 3-KinasesMammary Glands, HumanOptogeneticsPhosphatidylinositol 3-KinasesSignal TransductionBreast NeoplasmsCell Line, TumorEpithelial CellsEpithelial-Mesenchymal TransitionErb-b2 Receptor Tyrosine KinasesFemaleHumansMutationPhenotypeClass I Phosphatidylinositol 3-KinasesERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesPhosphatidylinositol 3-KinasesPIK3CA protein, humanbreast cancerEMToptogeneticsPI3K-signalingsignaling dynamicstemporal dynamics
Identifiers
PMID41554087
PMCPMC13022691
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