Tanner C. Dalton

ORCID: 0000-0003-0229-9950
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About
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Research Areas
  • Circular RNAs in diseases
  • MicroRNA in disease regulation
  • Glutathione Transferases and Polymorphisms
  • Heat shock proteins research
  • Pancreatic and Hepatic Oncology Research
  • Prostate Cancer Treatment and Research
  • Epigenetics and DNA Methylation
  • Ubiquitin and proteasome pathways
  • Cancer, Hypoxia, and Metabolism
  • Cancer Research and Treatments
  • Kruppel-like factors research
  • Extracellular vesicles in disease
  • Angiogenesis and VEGF in Cancer
  • Lymphoma Diagnosis and Treatment
  • Immune Cell Function and Interaction
  • Biological Research and Disease Studies
  • Cancer Research and Treatment
  • Cancer Immunotherapy and Biomarkers
  • Biochemical and Molecular Research
  • ATP Synthase and ATPases Research
  • Hedgehog Signaling Pathway Studies
  • Genomics, phytochemicals, and oxidative stress
  • Amino Acid Enzymes and Metabolism
  • Cancer Genomics and Diagnostics
  • Immune cells in cancer

National Center on Addiction and Substance Abuse at Columbia University
2025

Columbia University
2023-2024

Columbia University Irving Medical Center
2021-2024

Cornell University
2017-2021

Weill Cornell Medicine
2021

New York University
2020

Abstract Broad-spectrum RAS inhibition has the potential to benefit roughly a quarter of human patients with cancer whose tumours are driven by mutations 1,2 . RMC-7977 is highly selective inhibitor active GTP-bound forms KRAS, HRAS and NRAS, affinity for both mutant wild-type variants 3 More than 90% cases pancreatic ductal adenocarcinoma (PDAC) activating in KRAS 4 Here we assessed therapeutic comprehensive range PDAC models. We observed broad pronounced anti-tumour activity across models...

10.1038/s41586-024-07379-z article EN cc-by Nature 2024-04-08

Hsp90 is a molecular chaperone that protects proteins, including oncogenic signaling complexes, from proteolytic degradation. PU-H71 next-generation inhibitor preferentially targets the functionally distinct pool of present in tumor cells. Tumors are driven by MYC oncoprotein may be particularly sensitive to due essential role epichaperome, which maintains malignant phenotype setting MYC. Burkitt lymphoma (BL) an aggressive B-cell characterized dysregulation. In this study, we evaluated as...

10.1158/1535-7163.mct-16-0848 article EN Molecular Cancer Therapeutics 2017-06-16

Abstract Sensitivity to therapeutic agents is impacted both by genetic heterogeneity between patients or among clones within a tumor and of epigenetic cell states. Prior work demonstrates that human pancreatic tumors comprise malignant cells in mixture multiple states with distinct dependencies, leading reservoir chemoresistance across the tumor; targeting just one two insufficient achieve durable responses. One approach overcome this challenge identify efficacy against However, absence...

10.1158/1538-7445.genfunc25-ia016 article EN Cancer Research 2025-03-11

Abstract The sparse vascularity of pancreatic ductal adenocarcinoma (PDAC) presents a mystery: What prevents this aggressive malignancy from undergoing neoangiogenesis to counteract hypoxia and better support growth? An incidental finding prior work on paracrine communication between malignant PDAC cells fibroblasts revealed that inhibition the Hedgehog (HH) pathway partially relieved angiosuppression, increasing tumor through unknown mechanisms. Initial efforts study phenotype were hindered...

10.1158/2159-8290.cd-23-0240 article EN Cancer Discovery 2023-11-14

Summary Broad-spectrum RAS inhibition holds the potential to benefit roughly a quarter of human cancer patients whose tumors are driven by mutations. However, impact inhibiting functions in normal tissues is not known. RMC-7977 highly selective inhibitor active (GTP-bound) forms KRAS, HRAS, and NRAS, with affinity for both mutant wild type (WT) variants. As >90% pancreatic ductal adenocarcinoma (PDAC) cases activating mutations KRAS , we assessed therapeutic comprehensive range PDAC...

10.1101/2023.12.03.569791 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-12-04

Abstract The sparse vascularity of Pancreatic Ductal Adenocarcinoma (PDAC) presents a mystery: what prevents this aggressive malignancy from undergoing neoangiogenesis to counteract hypoxia and better support growth? An incidental finding prior work on paracrine communication between malignant PDAC cells fibroblasts revealed that inhibition the Hedgehog (HH) pathway partially relieved angiosuppression, increasing tumor through unknown mechanisms. Initial efforts study phenotype were hindered...

10.1101/2023.03.02.529724 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-03-02

Abstract Sensitivity to therapeutic agents is impacted both by genetic heterogeneity between patients or among clones within a tumor and of epigenetic cell states. Prior work demonstrates that human pancreatic tumors comprise malignant cells in mixture multiple states with distinct dependencies, leading reservoir chemoresistance across the tumor; targeting just one two insufficient achieve durable responses. One approach overcome this challenge identify efficacy against However, absence...

10.1158/1538-7445.am2024-934 article EN Cancer Research 2024-03-22

Abstract The advent of Ras inhibitors has revolutionized the treatment paradigm for pancreatic ductal adenocarcinoma (PDAC). However, preclinical models and early clinical results have shown that inhibitor monotherapy is insufficient to produce durable anti-tumor responses. Thus, there a great need design rational combination therapies can increase effect inhibitors. Oncogenic K-Ras known drive profoundly immunosuppressive tumor immune microenvironment (TIME) characteristic PDAC tumors....

10.1158/2326-6074.tumimm24-b014 article EN Cancer Immunology Research 2024-10-18

<div>Abstract<p>The sparse vascularity of pancreatic ductal adenocarcinoma (PDAC) presents a mystery: What prevents this aggressive malignancy from undergoing neoangiogenesis to counteract hypoxia and better support growth? An incidental finding prior work on paracrine communication between malignant PDAC cells fibroblasts revealed that inhibition the Hedgehog (HH) pathway partially relieved angiosuppression, increasing tumor through unknown mechanisms. Initial efforts study...

10.1158/2159-8290.c.7065322 preprint EN 2024-02-08

<div>Abstract<p>The sparse vascularity of pancreatic ductal adenocarcinoma (PDAC) presents a mystery: What prevents this aggressive malignancy from undergoing neoangiogenesis to counteract hypoxia and better support growth? An incidental finding prior work on paracrine communication between malignant PDAC cells fibroblasts revealed that inhibition the Hedgehog (HH) pathway partially relieved angiosuppression, increasing tumor through unknown mechanisms. Initial efforts study...

10.1158/2159-8290.c.7065322.v1 preprint EN 2024-02-08
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