Javascript must be enabled to continue!
Figure 1 from The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal Adenocarcinoma
View through CrossRef
<p>KDM4C is differentially upregulated in pancreatic cancer and correlates with poor prognosis. <b>A,</b> Western blots show human PDAC cell lines overexpress KDM4C compared with the noncancerous pancreatic epithelial cell line HPNE. <b>B,</b> Representative photomicrographs of KDM4C expression by IHC on TMAs of archival PDAC samples demonstrates upregulation of KDM4C in neoplastic cells compared with matched nonneoplastic pancreatic tissues. <b>C,</b> Bar graph showing the mean and distribution of the immunoscores of KDM4C expression in 187 cases of PDAC and matched normal pancreas. The score difference between the groups was assessed for statistical significance via paired <i>t</i> test; ****, <i>P</i> ≤ 0.0001. <b>D,</b> Kaplan–Meier survival plot showing increased survival of patients with low-KDM4C expressing PDAC (<i>n</i> = 96) compared with high-expressing tumors (<i>n</i> = 90) from the TMA dataset (<i>P</i> = 0.03). To determine KDM4C expression, we used PDAC TMAs, comprised of 187 PDAC cases. From each case, two punches (1.5 mm) from separate tumor areas (T1 and T2) and one punch (1.5 mm) from the normal pancreas (N) were included. After IHC staining with anti-KDM4C antibody, the samples were evaluated by a pathologist for both the intensity and percentage of stained cells in a semi-quantitative way. Intensity: 0: no staining/1: weak/2: moderate/3: strong. Proportion: 1: less than 10%/2: 10% to 50%/3: 50% to 75%/4: more than 75%. The final immunoscore was calculated by adding the intensity score to the proportion score according to the Allred method. The average immunoscore score from the tumor area was divided by the immunoscore from the matched normal area for each case. The log<sub>2</sub> ratio was then used for survival analysis, with a threshold log<sub>2</sub> ratio of 0.32.</p>
American Association for Cancer Research (AACR)
Title: Figure 1 from The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal Adenocarcinoma
Description:
<p>KDM4C is differentially upregulated in pancreatic cancer and correlates with poor prognosis.
<b>A,</b> Western blots show human PDAC cell lines overexpress KDM4C compared with the noncancerous pancreatic epithelial cell line HPNE.
<b>B,</b> Representative photomicrographs of KDM4C expression by IHC on TMAs of archival PDAC samples demonstrates upregulation of KDM4C in neoplastic cells compared with matched nonneoplastic pancreatic tissues.
<b>C,</b> Bar graph showing the mean and distribution of the immunoscores of KDM4C expression in 187 cases of PDAC and matched normal pancreas.
The score difference between the groups was assessed for statistical significance via paired <i>t</i> test; ****, <i>P</i> ≤ 0.
0001.
<b>D,</b> Kaplan–Meier survival plot showing increased survival of patients with low-KDM4C expressing PDAC (<i>n</i> = 96) compared with high-expressing tumors (<i>n</i> = 90) from the TMA dataset (<i>P</i> = 0.
03).
To determine KDM4C expression, we used PDAC TMAs, comprised of 187 PDAC cases.
From each case, two punches (1.
5 mm) from separate tumor areas (T1 and T2) and one punch (1.
5 mm) from the normal pancreas (N) were included.
After IHC staining with anti-KDM4C antibody, the samples were evaluated by a pathologist for both the intensity and percentage of stained cells in a semi-quantitative way.
Intensity: 0: no staining/1: weak/2: moderate/3: strong.
Proportion: 1: less than 10%/2: 10% to 50%/3: 50% to 75%/4: more than 75%.
The final immunoscore was calculated by adding the intensity score to the proportion score according to the Allred method.
The average immunoscore score from the tumor area was divided by the immunoscore from the matched normal area for each case.
The log<sub>2</sub> ratio was then used for survival analysis, with a threshold log<sub>2</sub> ratio of 0.
32.
</p>.
Related Results
Figure 6 from The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal Adenocarcinoma
Figure 6 from The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal Adenocarcinoma
<p>Proximity labeling identifies histone acetylase SIRT1 as a direct KDM4C nuclear interactor and a novel KDM4C–SIRT1–DUSP2 axis regulating ERK activity in PDAC. <b>A,&...
Abstract C081: The lysine demethylase KDM4C is an oncogenic driver in pancreatic ductal adenocarcinoma
Abstract C081: The lysine demethylase KDM4C is an oncogenic driver in pancreatic ductal adenocarcinoma
Abstract
Deregulation of proteins involved in chromatin regulation is common in pancreatic ductal adenocarcinoma (PDAC), occurring via both genomic and non-genomic m...
Data from The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal Adenocarcinoma
Data from The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal Adenocarcinoma
<div>Abstract<p>Deregulation of proteins involved in chromatin regulation is common in pancreatic ductal adenocarcinoma (PDAC). Lysine demethylase 4C (KDM4C) is one of ...
Figure 4 from The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal Adenocarcinoma
Figure 4 from The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal Adenocarcinoma
<p>Compensatory upregulation of KDM4A restores cell-intrinsic ERK signaling in <i>KDM4C</i>-null cells but not immune surveillance. <b>A,</b> Western ...
Figure 2 from The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal Adenocarcinoma
Figure 2 from The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal Adenocarcinoma
<p>CRISPR-mediated <i>KDM4C</i> deletion attenuates PDAC growth <i>in vitro</i> and <i>in vivo</i>. <b>A,</b> Western blot sho...
Abstract 5735: Novel KRAS G12D degrader ASP3082 demonstrates in vivo, dose-dependent KRAS degradation, KRAS pathway inhibition, and antitumor efficacy in multiple KRAS G12D-mutated cancer models
Abstract 5735: Novel KRAS G12D degrader ASP3082 demonstrates in vivo, dose-dependent KRAS degradation, KRAS pathway inhibition, and antitumor efficacy in multiple KRAS G12D-mutated cancer models
Abstract
KRAS is one of the most frequently mutated oncogenes in various cancers. Among KRAS mutations, KRAS G12D is the most frequent driver mutation and is found i...
Kras Plays An Important Role In Generating Differentiated Blood Cells
Kras Plays An Important Role In Generating Differentiated Blood Cells
Abstract
Background
Kras is a small GTPase essential for mouse embryonic development. Although Kras-/- fetal liver cells reconst...
The molecular mechanism underlying KRAS regulation on STK31 expression in Pancreatic ductal adenocarcinoma
The molecular mechanism underlying KRAS regulation on STK31 expression in Pancreatic ductal adenocarcinoma
Abstract
KRAS mutations are common in pancreatic ductal adenocarcinoma (PDAC) but targeting mutant KRAS is still challenging. Kinase inhibitors are ideal targeted therapeut...

