Karen J. Dunbar
YOU?
Author Swipe
View article: HMMR/RHAMM recruits SACK1D/FAM83D-CK1α complex at the mitotic spindle to control spindle alignment
HMMR/RHAMM recruits SACK1D/FAM83D-CK1α complex at the mitotic spindle to control spindle alignment Open
The SACK1D/FAM83D-CK1α complex assembles at the mitotic spindle to orchestrate proper spindle positioning and error-free progression through mitosis. The full molecular picture of how this complex assembles and disassembles over the cell d…
View article: The contribution of native protein complexes to targeted protein degradation
The contribution of native protein complexes to targeted protein degradation Open
Targeted protein degradation (TPD) destroys proteins of interest (POIs) by hijacking the cellular proteolytic machinery. Most proteins in cells exist and function as part of multi-protein or macromolecular complexes, thereby allowing a sin…
View article: Single-Cell RNA Sequencing and Inferred Protein Activity Analysis Reveal a Distinct Tumor Phenotype in Early-Onset Colorectal Cancer Patients
Single-Cell RNA Sequencing and Inferred Protein Activity Analysis Reveal a Distinct Tumor Phenotype in Early-Onset Colorectal Cancer Patients Open
Colorectal cancer (CRC) diagnosed before age 50 years (early-onset CRC, EO-CRC) is rising at an alarming rate, yet its molecular and microenvironmental drivers remain poorly understood. EO-CRC is highly heterogeneous, and while subtle diff…
View article: A Cell Marker Atlas to Distinguish Metaplastic Transitions in Human Esophagus and Stomach
A Cell Marker Atlas to Distinguish Metaplastic Transitions in Human Esophagus and Stomach Open
Metaplasia is an adaptative response to injury and inflammation and can be a precursor to dysplasia and cancer. Metaplasia in the esophagus, termed Barrett's esophagus, is the replacement of the stratified squamous epithelium by glandular …
View article: Lactate Suppresses Growth of Esophageal Adenocarcinoma Patient-Derived Organoids through Alterations in Tumor NADH/NAD+ Redox State
Lactate Suppresses Growth of Esophageal Adenocarcinoma Patient-Derived Organoids through Alterations in Tumor NADH/NAD+ Redox State Open
Barrett’s esophagus (BE) is a common precancerous lesion that can progress to esophageal adenocarcinoma (EAC). There are significant alterations in the esophageal microbiome in the progression from healthy esophagus to BE to EAC, including…
View article: Supplementary Figure 1 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma
Supplementary Figure 1 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma Open
Confirmation of CCL5 knockout clones.
View article: Supplementary Figure Legends from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma
Supplementary Figure Legends from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma Open
Supplementary Figure Legends 1-4
View article: Supplementary Figure Legends from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma
Supplementary Figure Legends from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma Open
Supplementary Figure Legends 1-4
View article: Supplementary Figure 1 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma
Supplementary Figure 1 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma Open
Confirmation of CCL5 knockout clones.
View article: Supplementary Figure 2 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma
Supplementary Figure 2 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma Open
Loss of tumor-derived CCL5 reduces tumor cell proliferation in TE-1 cells.
View article: Supplementary Figure 4 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma
Supplementary Figure 4 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma Open
Targeted CCR5 inhibition replicates CCL5 loss with reduced tumor cell proliferation in vitro and in vivo.
View article: Supplementary Figure 4 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma
Supplementary Figure 4 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma Open
Targeted CCR5 inhibition replicates CCL5 loss with reduced tumor cell proliferation in vitro and in vivo.
View article: Supplementary Figure 3 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma
Supplementary Figure 3 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma Open
ERK1/2 signaling pathway in CCL5 knockout cells.
View article: Supplementary Figure 3 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma
Supplementary Figure 3 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma Open
ERK1/2 signaling pathway in CCL5 knockout cells.
View article: Data from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma
Data from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma Open
Cancer-associated fibroblasts (CAFs) can promote tumor growth, metastasis and therapeutic resistance in esophageal squamous cell carcinoma (ESCC), but the mechanisms of action remain elusive. Our objective was to identify secreted factor(s…
View article: Supplementary Figure 2 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma
Supplementary Figure 2 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma Open
Loss of tumor-derived CCL5 reduces tumor cell proliferation in TE-1 cells.
View article: Cancer-Associated Fibroblasts in Esophageal Cancer
Cancer-Associated Fibroblasts in Esophageal Cancer Open
Cancer-associated fibroblasts (CAFs), a heterogenous population, can promote cancer cell proliferation, migration, invasion, immunosuppression, and therapeutic resistance in solid tumors. These effects are mediated through secretion of cyt…
View article: TOC
TOC Open
Review of how fibroblasts affect esophageal cancer (squamous cell carcinoma and adenocarcinoma) progression including their role in preneoplastic conditions, primary tumor growth, metastasis, and therapeutic resistance.While addressing the…
View article: Supplementary Table S3 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression
Supplementary Table S3 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression Open
Supplementary Table S3. Statistics of aligned reads from the CUT&RUN-seq analysis of H3K27ac in ESCC cells with Trp53R172H/- (n=3) and Trp53+/+ (n=2).
View article: Supplementary Figure S6 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression
Supplementary Figure S6 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression Open
Supplementary Figure S6. Graphical abstract depicting the pro-metastatic role and mechanism of Trp53R172H-dependent Csf-1/Csf-1r signaling.
View article: Supplementary Figure S3 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression
Supplementary Figure S3 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression Open
Supplementary Figure S3. Stat3 and EMT pathways are enriched in Trp53R172H- dependent metastasis.
View article: Supplementary Figure S5 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression
Supplementary Figure S5 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression Open
Supplementary Figure S5. CSF-1/CSF-1R signaling associates positively with clinical outcomes, and leukocyte infiltration ESCC.
View article: Supplementary Figure S1 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression
Supplementary Figure S1 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression Open
Supplementary Figure S1. Characterization of the primary and metastatic mouse ESCC cell lines.
View article: Supplementary Table S1 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression
Supplementary Table S1 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression Open
Supplementary Table S1. List of oligonucleotides used in the study.
View article: Supplementary Figure S1 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression
Supplementary Figure S1 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression Open
Supplementary Figure S1. Characterization of the primary and metastatic mouse ESCC cell lines.
View article: Supplementary Table S1 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression
Supplementary Table S1 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression Open
Supplementary Table S1. List of oligonucleotides used in the study.
View article: Supplementary Figure S2 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression
Supplementary Figure S2 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression Open
Supplementary Figure S2. Trp53R172H-dependent Csf-1/Csf-1r signaling promotes metastasis only in the presence of p53-R172H, but not p53 null or wild-type p53.
View article: Supplementary Figure S4 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression
Supplementary Figure S4 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression Open
Supplementary Figure S4. Depletion of Brd4 reduces Csf1 secretion and ESCC tumor cell invasion.
View article: Supplementary Figure S6 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression
Supplementary Figure S6 from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression Open
Supplementary Figure S6. Graphical abstract depicting the pro-metastatic role and mechanism of Trp53R172H-dependent Csf-1/Csf-1r signaling.
View article: Data from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression
Data from p53 Gain-of-Function Mutation Induces Metastasis via BRD4-Dependent CSF-1 Expression Open
TP53 mutations are frequent in esophageal squamous cell carcinoma (ESCC) and other SCCs and are associated with a proclivity for metastasis. Here, we report that colony-stimulating factor-1 (CSF-1) expression is upregulated signific…