Bishal Patgiri
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Bishal Patgiri has a total of 3 co-authors. Here are the top co-authors by number of shared publications:
- Anshu Yadav
School of Biotechnology (SBT), Jawaharlal Nehru University (JNU), New Delhi, India, 110067, India
1 shared publication - Jitendra Kumar
Biotechnology Industry Research Assistance Council (BIRAC), New Delhi, India
1 shared publication - Uddalak Das
Developmental Biology and Genetics (DBG), Division of Biological Sciences, Indian Institute of Science (IISc), Bengaluru, India, 560012, India
1 shared publication
Latest Publications
- Open Access
- 20 October 2025
- Published by MDPI AG in Preprints.org
The Taurine-TauT Axis in Hematologic Malignancies: A Review on Redox Homeostasis, Mitochondrial tRNA Stabilization, Leukemic Stem Cell Persistence, and Therapeutic Vulnerabilities
Leukemia encompasses heterogeneous hematologic malignancies characterized by dysregulated hematopoiesis, metabolic reprogramming, and therapy resistance, with relapse driven by persistent leukemic stem cells (LSCs). This comprehensive review delineates the pivotal role of the taurine–TauT (SLC6A6) axis as a metabolic vulnerability across acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), chronic myeloid leukemia (CML), and chronic lymphocytic leukemia (CLL). Taurine, a sulfur-containing β-amino acid, modulates redox homeostasis via taurine chloramine (TauCl) formation, stabilizes mitochondrial tRNA uridine modifications for oxidative phosphorylation (OXPHOS), and regulates calcium fluxes and apoptosis. SLC6A6-mediated taurine uptake is upregulated in leukemic blasts and LSCs, correlating with adverse cytogenetics (e.g., FLT3-ITD, TP53 mutations), chemoresistance to cytarabine, doxorubicin, methotrexate, vincristine, tyrosine kinase inhibitors (TKIs), and BCL2 inhibitors (venetoclax), and minimal residual disease persistence in hypoxic bone marrow niches. Transcriptomic analyses from TCGA, BeatAML, and TARGET cohorts substantiate SLC6A6 as a prognostic biomarker. Therapeutic strategies, including selective SLC6A6 inhibition and chemosensitization, exploit this dependency to amplify ROS-induced apoptosis and eradicate LSCs, potentially enhancing remission durability. Future directions emphasize structure-guided inhibitor development and integrative metabolomic profiling for precision oncology.
- 20 October 2025
- Published by MDPI AG in Preprints.org
Open AccessThe Taurine-TauT Axis in Hematologic Malignancies: A Review on Redox Homeostasis, Mitochondrial tRNA Stabilization, Leukemic Stem Cell Persistence, and Therapeutic Vulnerabilities
Leukemia encompasses heterogeneous hematologic malignancies characterized by dysregulated hematopoiesis, metabolic reprogramming, and therapy resistance, with relapse driven by persistent leukemic stem cells (LSCs). This comprehensive review delineates the pivotal role of the taurine–TauT (SLC6A6) axis as a metabolic vulnerability across acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), chronic myeloid leukemia (CML), and chronic lymphocytic leukemia (CLL). Taurine, a sulfur-containing β-amino acid, modulates redox homeostasis via taurine chloramine (TauCl) formation, stabilizes mitochondrial tRNA uridine modifications for oxidative phosphorylation (OXPHOS), and regulates calcium fluxes and apoptosis. SLC6A6-mediated taurine uptake is upregulated in leukemic blasts and LSCs, correlating with adverse cytogenetics (e.g., FLT3-ITD, TP53 mutations), chemoresistance to cytarabine, doxorubicin, methotrexate, vincristine, tyrosine kinase inhibitors (TKIs), and BCL2 inhibitors (venetoclax), and minimal residual disease persistence in hypoxic bone marrow niches. Transcriptomic analyses from TCGA, BeatAML, and TARGET cohorts substantiate SLC6A6 as a prognostic biomarker. Therapeutic strategies, including selective SLC6A6 inhibition and chemosensitization, exploit this dependency to amplify ROS-induced apoptosis and eradicate LSCs, potentially enhancing remission durability. Future directions emphasize structure-guided inhibitor development and integrative metabolomic profiling for precision oncology.