Fu-Ju Chou
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Research Interests
Fu-Ju Chou has a total of 37 co-authors. Here are the top co-authors by number of shared publications:
- Chunzhang Yang
Neuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, USA
31 shared publications - Fengchao Lang
Neuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland
31 shared publications - Kareem A. Zaghloul
Surgical Neurology Branch, NINDS, National Institutes of Health , Bethesda, MD 20892
30 shared publications - Dionne L. Davis
Neuro-Oncology Branch, National Cancer Institute, Center for Cancer Research, National Cancer Institute, National Institutes of Health; Bethesda, MD, 20892, USA
29 shared publications - Hua Song
Neuro-Oncology Branch, National Cancer Institute, Center for Cancer Research, National Cancer Institute, National Institutes of Health; Bethesda, MD, 20892, USA
29 shared publications - Mark R. Gilbert
Neuro-Oncology Branch, National Cancer Institute, Center for Cancer Research, National Cancer Institute, National Institutes of Health; Bethesda, MD, 20892, USA
29 shared publications
Latest Publications
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S2 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
(A) Gene expression profiling showed the expression of GPX4 and SLC7A11 in IDH-mutated NHA cells (B) ROS-Glo assay measured the oxidative stress in IDH1WT and IDH1Mut NHA cells in response to ipatasertib (Ipa, 1 mM) treatment. (C) GSH, and GSSG level was measured in IDHWT and IDH1Mut NHA cells in response to Ipa (1 mM) treatment. GSH/GSSG ratio was calculated. (D) Immunoblotting analysis evaluated cleaved PARP in IDH1WT and IDH1Mut NHA cells with TMZ (200 mM) and/or Ipa (1mM) treatment. b-actin was used as an internal control. (E) Cell viability analysis on NHA IDHWT cells under TMZ (200 mM) and Ipa (1mM) treatment. **p < 0.01.
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S2 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
(A) Gene expression profiling showed the expression of GPX4 and SLC7A11 in IDH-mutated NHA cells (B) ROS-Glo assay measured the oxidative stress in IDH1WT and IDH1Mut NHA cells in response to ipatasertib (Ipa, 1 mM) treatment. (C) GSH, and GSSG level was measured in IDHWT and IDH1Mut NHA cells in response to Ipa (1 mM) treatment. GSH/GSSG ratio was calculated. (D) Immunoblotting analysis evaluated cleaved PARP in IDH1WT and IDH1Mut NHA cells with TMZ (200 mM) and/or Ipa (1mM) treatment. b-actin was used as an internal control. (E) Cell viability analysis on NHA IDHWT cells under TMZ (200 mM) and Ipa (1mM) treatment. **p < 0.01.
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S3 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
(A) Phase contrast images showed the cytotoxicity of TMZ (400 mM)/ipatasertib (Ipa, 2 mM) combination treatment in the brain tumor-initiating cells (BTICs). A ferroptosis inhibitor, Ferrstain-1 (Ferr-1, 5 mM), was used to rescue the ferroptotic cell death. Bar = 100 mM. (B) Representative flow cytometric analysis of live/dead staining in BTICs in response to TMZ/Ipa treatment. (C) Statistical analysis of dead/live cell ratio in BTICs. (D) The limiting dilution assay evaluated the frequency of generating spheres in GSC827 and TSC603 after receiving TMZ/Ipa treatment. **p < 0.01.
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S3 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
(A) Phase contrast images showed the cytotoxicity of TMZ (400 mM)/ipatasertib (Ipa, 2 mM) combination treatment in the brain tumor-initiating cells (BTICs). A ferroptosis inhibitor, Ferrstain-1 (Ferr-1, 5 mM), was used to rescue the ferroptotic cell death. Bar = 100 mM. (B) Representative flow cytometric analysis of live/dead staining in BTICs in response to TMZ/Ipa treatment. (C) Statistical analysis of dead/live cell ratio in BTICs. (D) The limiting dilution assay evaluated the frequency of generating spheres in GSC827 and TSC603 after receiving TMZ/Ipa treatment. **p < 0.01.
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Table S1 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S1 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S4 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
(A) Heatmap of gene expression profile for glioma specimen. The leading edge of the KEGG_MTOR_SIGNALING_PATHWAY geneset was shown. (B) Dose-response curve measured the cell viability in IDH1WT NHA cells in response to TMZ/Ipa combination treatment. (C) isobologram analysis showed the synergistic effect of TMZ and Ipa in IDH1WT NHA cells. (D) The combination index (C.I.) was calculated to show the additive effect of TMZ and Ipa.
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S4 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
(A) Heatmap of gene expression profile for glioma specimen. The leading edge of the KEGG_MTOR_SIGNALING_PATHWAY geneset was shown. (B) Dose-response curve measured the cell viability in IDH1WT NHA cells in response to TMZ/Ipa combination treatment. (C) isobologram analysis showed the synergistic effect of TMZ and Ipa in IDH1WT NHA cells. (D) The combination index (C.I.) was calculated to show the additive effect of TMZ and Ipa.
- Open Access
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S1 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
(A) Immunoblotting analysis evaluated the siRNA knockdown efficiency of AKT in U87 cells. (B) Phase contrast imaging showed the cytotoxicity of ipatasertib (Ipa) in IDH1WT and IDH1Mut NHA cells. Bar = 100 mM. (C) Representative flow cytometric analysis of live/dead staining in IDH1WT and IDH1Mut NHA cells in response to Ipa (0, 1, and 2 mM) treatment. (D) Statistical analysis of dead/live cell ratio in IDH1WT and IDHMut NHA cells after Ipa treatment. **p < 0.01.
- 25 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S1 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
(A) Immunoblotting analysis evaluated the siRNA knockdown efficiency of AKT in U87 cells. (B) Phase contrast imaging showed the cytotoxicity of ipatasertib (Ipa) in IDH1WT and IDH1Mut NHA cells. Bar = 100 mM. (C) Representative flow cytometric analysis of live/dead staining in IDH1WT and IDH1Mut NHA cells in response to Ipa (0, 1, and 2 mM) treatment. (D) Statistical analysis of dead/live cell ratio in IDH1WT and IDHMut NHA cells after Ipa treatment. **p < 0.01.
- Open Access
- 3 April 2023
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S4 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
(A) Heatmap of gene expression profile for glioma specimen. The leading edge of the KEGG_MTOR_SIGNALING_PATHWAY geneset was shown. (B) Dose-response curve measured the cell viability in IDH1WT NHA cells in response to TMZ/Ipa combination treatment. (C) isobologram analysis showed the synergistic effect of TMZ and Ipa in IDH1WT NHA cells. (D) The combination index (C.I.) was calculated to show the additive effect of TMZ and Ipa.
- 3 April 2023
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S4 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
(A) Heatmap of gene expression profile for glioma specimen. The leading edge of the KEGG_MTOR_SIGNALING_PATHWAY geneset was shown. (B) Dose-response curve measured the cell viability in IDH1WT NHA cells in response to TMZ/Ipa combination treatment. (C) isobologram analysis showed the synergistic effect of TMZ and Ipa in IDH1WT NHA cells. (D) The combination index (C.I.) was calculated to show the additive effect of TMZ and Ipa.
- Open Access
- 3 April 2023
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S3 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
(A) Phase contrast images showed the cytotoxicity of TMZ (400 mM)/ipatasertib (Ipa, 2 mM) combination treatment in the brain tumor-initiating cells (BTICs). A ferroptosis inhibitor, Ferrstain-1 (Ferr-1, 5 mM), was used to rescue the ferroptotic cell death. Bar = 100 mM. (B) Representative flow cytometric analysis of live/dead staining in BTICs in response to TMZ/Ipa treatment. (C) Statistical analysis of dead/live cell ratio in BTICs. (D) The limiting dilution assay evaluated the frequency of generating spheres in GSC827 and TSC603 after receiving TMZ/Ipa treatment. **p < 0.01.
- 3 April 2023
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S3 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
(A) Phase contrast images showed the cytotoxicity of TMZ (400 mM)/ipatasertib (Ipa, 2 mM) combination treatment in the brain tumor-initiating cells (BTICs). A ferroptosis inhibitor, Ferrstain-1 (Ferr-1, 5 mM), was used to rescue the ferroptotic cell death. Bar = 100 mM. (B) Representative flow cytometric analysis of live/dead staining in BTICs in response to TMZ/Ipa treatment. (C) Statistical analysis of dead/live cell ratio in BTICs. (D) The limiting dilution assay evaluated the frequency of generating spheres in GSC827 and TSC603 after receiving TMZ/Ipa treatment. **p < 0.01.
- Open Access
- 3 April 2023
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S2 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
(A) Gene expression profiling showed the expression of GPX4 and SLC7A11 in IDH-mutated NHA cells (B) ROS-Glo assay measured the oxidative stress in IDH1WT and IDH1Mut NHA cells in response to ipatasertib (Ipa, 1 mM) treatment. (C) GSH, and GSSG level was measured in IDHWT and IDH1Mut NHA cells in response to Ipa (1 mM) treatment. GSH/GSSG ratio was calculated. (D) Immunoblotting analysis evaluated cleaved PARP in IDH1WT and IDH1Mut NHA cells with TMZ (200 mM) and/or Ipa (1mM) treatment. b-actin was used as an internal control. (E) Cell viability analysis on NHA IDHWT cells under TMZ (200 mM) and Ipa (1mM) treatment. **p < 0.01.
- 3 April 2023
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S2 from Protein Kinase B (PKB/AKT) Protects IDH-Mutated Glioma from Ferroptosis via Nrf2
(A) Gene expression profiling showed the expression of GPX4 and SLC7A11 in IDH-mutated NHA cells (B) ROS-Glo assay measured the oxidative stress in IDH1WT and IDH1Mut NHA cells in response to ipatasertib (Ipa, 1 mM) treatment. (C) GSH, and GSSG level was measured in IDHWT and IDH1Mut NHA cells in response to Ipa (1 mM) treatment. GSH/GSSG ratio was calculated. (D) Immunoblotting analysis evaluated cleaved PARP in IDH1WT and IDH1Mut NHA cells with TMZ (200 mM) and/or Ipa (1mM) treatment. b-actin was used as an internal control. (E) Cell viability analysis on NHA IDHWT cells under TMZ (200 mM) and Ipa (1mM) treatment. **p < 0.01.