Isabel English

ORCID: 0000-0002-0566-9585
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About
Contact & Profiles
Research Areas
  • Acute Myeloid Leukemia Research
  • Fibroblast Growth Factor Research
  • Pancreatic and Hepatic Oncology Research
  • Chronic Myeloid Leukemia Treatments
  • Epigenetics and DNA Methylation
  • Cancer Cells and Metastasis
  • Eosinophilic Disorders and Syndromes
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Cancer Genomics and Diagnostics
  • Ferroptosis and cancer prognosis
  • Cancer-related gene regulation
  • Kruppel-like factors research
  • Cancer Immunotherapy and Biomarkers
  • Signaling Pathways in Disease
  • Biochemical and Molecular Research
  • Cancer Research and Treatments
  • Protein Degradation and Inhibitors
  • DNA Repair Mechanisms
  • Extracellular vesicles in disease
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • 3D Printing in Biomedical Research
  • Cancer-related Molecular Pathways
  • Ubiquitin and proteasome pathways
  • Angiogenesis and VEGF in Cancer
  • Proteoglycans and glycosaminoglycans research

Oregon Health & Science University
2016-2025

Fred Hutch Cancer Center
2025

University of Portland
2022-2023

Centre Interdisciplinaire de Recherche en Biologie
2016

Inserm
2016

Collège de France
2016

Paris Cardiovascular Research Center
2016

Yale University
2016

OHSU Knight Cancer Institute
2014

Cancer Institute (WIA)
2014

10.1038/s41586-018-0623-z article EN Nature 2018-10-01

Acute myeloid leukemia (AML) is a cancer of myeloid-lineage cells with limited therapeutic options. We previously combined ex vivo drug sensitivity genomic, transcriptomic, and clinical annotations for large cohort AML patients, which facilitated discovery functional genomic correlates. Here, we present dataset that has been harmonized our initial report to yield cumulative 805 patients (942 specimens). show strong cross-cohort concordance identify features response. Further, deconvoluting...

10.1016/j.ccell.2022.07.002 article EN cc-by-nc-nd Cancer Cell 2022-07-21

Potent FLT3 inhibitors, such as quizartinib (AC220), have shown promise in treating acute myeloid leukemia (AML) containing internal tandem duplication (ITD) mutations. However, responses are not durable and resistance develops within months. In this study, we outline a two-step model of whereby extrinsic microenvironmental proteins ligand (FL) fibroblast growth factor 2 (FGF2) protect FLT3-ITD+ MOLM14 cells from AC220, providing time for subsequent accumulation ligand-independent...

10.1158/0008-5472.can-15-3569 article EN Cancer Research 2016-09-27

Translating the genetic and epigenetic heterogeneity underlying human cancers into therapeutic strategies is an ongoing challenge. Large-scale sequencing efforts have uncovered a spectrum of mutations in many hematologic malignancies, including acute myeloid leukemia (AML), suggesting that combinations agents will be required to treat these diseases effectively. Combinatorial approaches also critical for combating emergence genetically heterogeneous subclones, rescue signals...

10.1073/pnas.1703094114 article EN Proceedings of the National Academy of Sciences 2017-08-07

Protective signaling from the leukemia microenvironment leads to cell persistence, development of resistance, and disease relapse. Here, we demonstrate that fibroblast growth factor 2 (FGF2) bone marrow stromal cells is secreted in exosomes, which are subsequently endocytosed by cells, protect tyrosine kinase inhibitors (TKIs). Expression FGF2 its receptor, FGFR1, both increased a subset lines primary AML stroma; FGF2/FGFR1 associated with exosome secretion. FGFR inhibition (or gene...

10.7554/elife.40033 article EN cc-by eLife 2019-02-05

Abstract Pancreatic ductal adenocarcinoma (PDAC) is classified into two distinct subtypes, classical and basal. Basal PDACs (∼25% of PDACs) have the worst overall survival are only class to act as an independent poor prognostic factor. Therefore, there urgent need understand basal PDAC development, identify biomarkers find its unique vulnerabilities. We found high expression chromatin architectural protein, HMGA2 in subtype pancreatic cancer. This was across patient-derived cell lines,...

10.1158/1538-7445.am2025-1438 article EN Cancer Research 2025-04-21

Arterial endothelial cells are morphologically, functionally, and molecularly distinct from those found in veins lymphatic vessels. How arterial fate is acquired during development maintained adult vessels incompletely understood.We set out to identify factors that promote cell vivo.We developed a functional assay, allowing us monitor manipulate vivo, using arteries isolated quails grafted into the coelom of chick embryos. Endothelial migrate artery, their colonization host quantified. Here...

10.1161/circresaha.116.308473 article EN Circulation Research 2016-06-29

Acute myeloid leukemia (AML) is a cancer of myeloid-lineage cells with limited therapeutic options. We previously combined ex vivo drug sensitivity genomic, transcriptomic, and clinical annotations for large cohort AML patients, which facilitated discovery functional genomic correlates. Here, we present new dataset, has been harmonized our initial report to yield cumulative 805 patients (942 specimens). show strong cross-cohort validation identify features response. Further, deconvoluting...

10.2139/ssrn.4041405 article EN SSRN Electronic Journal 2022-01-01

Abstract Despite extensive study, pancreatic ductal adenocarcinoma (PDAC) remains highly lethal resulting in a need for new effective therapies and, particular, combination therapies. Gemcitabine that targets ribonucleotide reductase (RNR) is active PDAC, albeit with modest impacts on long-term outcomes. Inhibition of RNR leads to depletion dNTP pools, provoking replication stress (RS). RS activates the ATR/CHK1/WEE1 S phase DNA damage checkpoint cascade. Our study provides insights into...

10.1158/1538-7445.dnarepair24-b018 article EN Cancer Research 2024-01-09

Abstract Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with median survival time of 10-12 months and an overall 5-year rate 12%. Current treatment includes chemotherapy surgery; however, only 20% patients are eligible for resection due to the majority presenting locally advanced or metastatic disease. Alarmingly, 20-30% who undergo their primary tumor experience rapid liver metastasis within 6 surgery. This “rapid recurrence” (rrPDAc) devastating poorly understood,...

10.1158/1538-7445.panca2023-c102 article EN Cancer Research 2024-01-16

Abstract One of the most aggressive cancers in US is pancreatic ductal adenocarcinoma (PDAc), whose incidence expected to rise coming years. The standard-of-care treatments have improved over past few decades, but they still primarily involve harsh chemotherapy cocktails and only marginally increased overall survival, a 5-year survival rate 12 percent. c-MYC (MYC), potent transcription factor, frequently dysregulated PDAc. In PDAc other cancers, MYC plays significant role tumor progression,...

10.1158/1538-7445.panca2023-a061 article EN Cancer Research 2024-01-16

Abstract Introduction. Head and neck squamous cell carcinomas (HNSCCs) account for nearly 600,000 deaths worldwide annually have limited treatment options. Approximately 20% of HNSCCs harbor amplifications fibroblast growth factor receptor 1 (FGFR1) on chromosome 8p, however FGFR1 amplification by itself does not predict clinical response to FGFR inhibitors. We hypothesized that FGF2, or basic FGF, ligand expression is a better marker activation predictor Results. A tissue micro array (TMA)...

10.1158/1538-7445.am2016-1631 article EN Cancer Research 2016-07-15

Abstract Introduction: Activating mutations in the FLT3 kinase are present ∼25% of newly diagnosed acute myeloid leukemia (FLT3+ AML) patients and confer a poor prognosis. Treatment with inhibitors is initially effective, but residual cells survive bone marrow microenvironment clinical resistance develops within months. We tested proteins from for their ability to protect FLT3-ITD+ MOLM14 AC220, found that ligand (FL) fibroblast growth factor 2 (FGF2) were among most protective. Results:...

10.1158/1538-7445.am2015-984 article EN Cancer Research 2015-08-01
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