Arturo Orlacchio
Biochemistry, Genetics and Molecular Biology · The Ohio State University
Publications
59
Citations
319
Est. group size
~4
Recurring co-author estimate
Active years
13
Publishing since 2014
This researcher studies the molecular biology of cancer, with a particular focus on pancreatic cancer and cell signaling pathways such as PI3K/AKT/SGK1 that drive tumor growth. Recent work also explores epigenetic therapies (drugs that alter gene activity without changing DNA sequence) and how combining these with immunotherapy might improve treatment outcomes in pancreatic cancer. The work spans laboratory studies of cancer biology as well as clinical and case-based cancer research.
Publication output has fluctuated over the past decade, with a notable spike in 2023 followed by a return to a moderate, steady pace of about 5-6 papers per year.
Generated by claude-sonnet-5 from public bibliographic data · Jul 20, 2026
- Abstract 2451: Dual-function platform for chemotherapy prediction and mutation detection in pancreatic cancer by <i>tCAM-seq</i>
Cancer Research · 2026
- Abstract P2-08-09: Predictors of inadequate ovarian function suppression (OFS) in premenopausal women with hormone receptor (HR)-positive breast cancer receiving a gonadotropin-releasing hormone (GnRH) agonist in combination with endocrine therapy
Clinical Cancer Research · 2025
- Continuous Regression of Metastatic Pancreatic Adenocarcinoma after Suspending Chemotherapy: A Case Report
Case Reports in Oncology · 2025
- 312 LOW DOSE DOUBLE EPIGENETIC THERAPY IMPROVES IMMUNOTHERAPY RESPONSE AND PROLONGS SURVIVAL IN PANCREATIC CANCER.
Gastroenterology · 2024
- Epigenetic therapeutic strategies in pancreatic cancer
International review of cell and molecular biology · 2024
- Abstract B043: Dual epigenetic therapy combined with anti-PD1 rescues HMA-induced suppressive myeloid phenotype and reduces tumor growth in a PDAC model
Cancer Research · 2024
- Abstract B062: Low dose dual epigenetic therapy utilizing hypomethylating agents and HDAC inhibitors prolong survival in an orthotopic PDAC model and alter the tumor microenvironment
Cancer Research · 2024
- Data from SGK1 Is a Critical Component of an AKT-Independent Pathway Essential for PI3K-Mediated Tumor Development and Maintenance
2023
- Suppl. Fig. Legends from SGK1 Is a Critical Component of an AKT-Independent Pathway Essential for PI3K-Mediated Tumor Development and Maintenance
2023
- Figure S1 from SGK1 Is a Critical Component of an AKT-Independent Pathway Essential for PI3K-Mediated Tumor Development and Maintenance
2023
- Figure S4 from SGK1 Is a Critical Component of an AKT-Independent Pathway Essential for PI3K-Mediated Tumor Development and Maintenance
2023
- Figure S2 from SGK1 Is a Critical Component of an AKT-Independent Pathway Essential for PI3K-Mediated Tumor Development and Maintenance
2023
- Figure S3 from SGK1 Is a Critical Component of an AKT-Independent Pathway Essential for PI3K-Mediated Tumor Development and Maintenance
2023
- Figure S5 from SGK1 Is a Critical Component of an AKT-Independent Pathway Essential for PI3K-Mediated Tumor Development and Maintenance
2023
- Figure S1 from SGK1 Is a Critical Component of an AKT-Independent Pathway Essential for PI3K-Mediated Tumor Development and Maintenance
2023
- Cancer Research×14
- bioRxiv (Cold Spring Harbor Laboratory)×3
- Nature Communications×2
- Communications Biology×2
- Cancer Immunology Research×2
- Shimaa Soliman
Biochemistry, Genetics and Molecular Biology · The Ohio State University
- Kotaro Nakanishi
Biochemistry, Genetics and Molecular Biology · The Ohio State University
- Anita K. Hopper
Biochemistry, Genetics and Molecular Biology · The Ohio State University
- Chao Cai
Biochemistry, Genetics and Molecular Biology · Purdue University West Lafayette
- Michael G. Kearse
Biochemistry, Genetics and Molecular Biology · The Ohio State University
This profile was generated automatically from public scholarly data (OpenAlex). Group size and activity levels are estimates derived from co-authorship patterns.
Last updated Jul 19, 2026.
Claim or correct this profile