Andrew J. Aguirre

This study shows that KRASG12C inhibitors alter the surface proteome of lung cancer cells, revealing FOLR1 as a new target when combined with an antibody drug conjugate.

This study identifies ALPP/ALPPL2 as a targetable vulnerability in pancreatic cancer by analyzing proteomic changes induced by KRAS inhibition and developing an antibody drug conjugate.

The paper identifies combinatorial KRAS/FGFR dependence in pancreatic cancer through genetic interaction mapping and shows that combined inhibition overcomes resistance.

This study designs protease-activatable cytokine prodrugs to reduce toxicity while maintaining antitumor efficacy in tumor models.

This paper develops LIME, a bacterial platform that engagers T and NK cells to target tumors, showing enhanced cytotoxicity and immune response in preclinical models.

This study identifies Glis3 as a key transcription factor driving metastasis in PDAC by promoting a neural-like progenitor cell state.

This study identifies KEAP1 loss as a resistance mechanism to KRAS inhibitors in pancreatic and lung cancer and shows that combining glutamine inhibition with KRAS inhibitors can overcome this resistance.

APEX infers cancer gene expression from plasma cfChIP-seq data, outperforming existing methods and enabling subtype classification and biomarker identification.

This study identifies that cancers limit p53 neoantigen display on MHC molecules, evading T cell detection through immune selection and ERAP1-mediated destruction.

This paper identifies VEGFA-VEGFR2 signaling driven by PI3Kγ activation as a mechanism of acquired resistance to KRAS G12D inhibitors and shows that blocking this pathway restores drug sensitivity in resistant cancer models.

This study identifies that combining DHODH inhibition with BCL-XL targeting synergistically induces apoptosis in pancreatic cancer, offering a new combination therapy strategy.

The paper analyzes multiomic data from primary and metastatic esophageal adenocarcinoma tumors to identify cell states and their spatial interactions, linking them to clinical outcomes.

This study uses deep mutational scanning to analyze KRAS variants, identifying gain- and loss-of-function mechanisms and their impact on oncogenic activity.

This study evaluates the therapeutic potential of RMC-7977, a broad-spectrum RAS inhibitor, in pancreatic ductal adenocarcinoma models, showing strong anti-tumor effects with minimal impact on normal tissues.

The paper introduces a method to screen large variant libraries with mutations across wide regions using improved mutant detection software, enabling accurate variant calling and counting from sequencing data.

The paper uses Perturb-seq to assess the phenotypic impact of somatic variants in cancer, revealing a continuum of gain-of-function KRAS variants.

This study uses single-nucleus and spatial transcriptomics to analyze pancreatic cancer before and after neoadjuvant treatment, revealing changes in cell states and immune infiltration that may inform therapy.

The paper profiles the enteric nervous system of human and mouse colon at single-cell resolution, revealing diverse neuron subsets and shared transcriptional programs between species.