Naing Lin Shan
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
Naing Lin Shan has a total of 86 co-authors. Here are the top co-authors by number of shared publications:
- Lajos Pusztai
Yale Cancer Center, Yale School of Medicine, New Haven, CT
66 shared publications - Kim R. M. Blenman
Yale University
64 shared publications - Michal Marczyk
Department of Data Science and Engineering Silesian University of Technology Gliwice Poland
64 shared publications - Sheila Umlauf
Yale University 6 Yale Center for Molecular Discovery West Haven, Connecticut
63 shared publications - Julia Foldi
Women’s Cancer Research Center, UPMC Hillman Cancer Center, Pittsburgh, Pennsylvania
38 shared publications Christos Hatzis
37 shared publications
Latest Publications
- Open Access
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S7 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Cell viability assessment in parental BT-474 cells, trastuzumab-resistant BT474 clones (BT-TR1 and BT-TR2) and trastuzumab and pertuzumab-resistant BT474 clones (BT-TPR1 and BT-TPR2) treated with PF-05175157
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S7 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Cell viability assessment in parental BT-474 cells, trastuzumab-resistant BT474 clones (BT-TR1 and BT-TR2) and trastuzumab and pertuzumab-resistant BT474 clones (BT-TPR1 and BT-TPR2) treated with PF-05175157
- Open Access
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S8 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
ACC1 (ACACA) and ACC2 (ACACB) protein levels in breast cancer cell lines
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S8 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
ACC1 (ACACA) and ACC2 (ACACB) protein levels in breast cancer cell lines
- Open Access
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figure S9 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Heatmap of inhibit delta of top 10 drugs across 10 breast cancer cell lines
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure S9 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Heatmap of inhibit delta of top 10 drugs across 10 breast cancer cell lines
- Open Access
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Supplementary File S1 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Results of a high-throughput cell proliferation screen of 385 human cancer cell lines treated with PF-05175157, identifying sensitive multiple myeloma, breast, ovarian, and lung cancer cell lines.
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary File S1 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Results of a high-throughput cell proliferation screen of 385 human cancer cell lines treated with PF-05175157, identifying sensitive multiple myeloma, breast, ovarian, and lung cancer cell lines.
- Open Access
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S1 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Cell lines with IC50 concentrations below 10 mmol/L threshold that was readily achievable in human serum, in Phase I/II clinical trials with PF-05175157
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S1 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Cell lines with IC50 concentrations below 10 mmol/L threshold that was readily achievable in human serum, in Phase I/II clinical trials with PF-05175157
- Open Access
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Supplementary File S4 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Significantly upregulated genes associated with metabolic repair and recovery pathways identified following PF-05175157 treatment.
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary File S4 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Significantly upregulated genes associated with metabolic repair and recovery pathways identified following PF-05175157 treatment.
- Open Access
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Supplementary File S3 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Lipidomic results: PF-05175157 effect on cellular lipid composition
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary File S3 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Lipidomic results: PF-05175157 effect on cellular lipid composition
- Open Access
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S2 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
MRNA expression levels endoplasmic reticulum stress related genes at baseline and after 24 hours exposure to PF-05175157 in MDA-MB-468 cells
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S2 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
MRNA expression levels endoplasmic reticulum stress related genes at baseline and after 24 hours exposure to PF-05175157 in MDA-MB-468 cells
- Open Access
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Supplementary File S2 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Synergy analysis of PF-05175157 combinations across multiple drug classes in human cancer cell lines.
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary File S2 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Synergy analysis of PF-05175157 combinations across multiple drug classes in human cancer cell lines.
- Open Access
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S3 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Log fold change in endoplasmic reticulum stress related genes from single cell RNAseq of MDA-MB-468 cells
- 15 October 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S3 from Inhibition of Acetyl-CoA Carboxylase Induces Endoplasmic Reticulum Stress and Augments the Efficacy of Anticancer Therapies
Log fold change in endoplasmic reticulum stress related genes from single cell RNAseq of MDA-MB-468 cells