S. P. Gorantla

发表

Activating JAK-mutations confer resistance to FLT3 kinase inhibitors in FLT3-ITD positive AML in vitro and in vivo

K. Döhner, T. Haferlach, J. Duyster, 2020, Leukemia.

The IL-3, IL-5, and GM-CSF common receptor beta chain mediates oncogenic activity of FLT3-ITD-positive AML

M. Reth, Kathrin Kläsener, C. Miething, 2021, Leukemia.

Oncogenic JAK2V617F causes PD-L1 expression, mediating immune escape in myeloproliferative neoplasms

M. Boerries, H. Busch, N. Kröger, 2018, Science Translational Medicine.

NIPA (Nuclear Interaction Partner of ALK) Is Crucial for Effective NPM-ALK Mediated Lymphomagenesis

C. Miething, J. Duyster, S. P. Gorantla, 2022, Frontiers in Oncology.

The systemic mastocytosis-specific activating cKit mutation D816V can be inhibited by the tyrosine kinase inhibitor AMN107

F. Lordick, C. Peschel, J. Duyster, 2005, Leukemia.

F604S exchange in FIP1L1-PDGFRA enhances FIP1L1-PDGFRA protein stability via SHP-2 and SRC: a novel mode of kinase inhibitor resistance

A. Reiter, J. Duyster, K. Zirlik, 2015, Leukemia.

The FIP1L1-PDGFRA T674I mutation can be inhibited by the tyrosine kinase inhibitor AMN107 (nilotinib).

C. Peschel, J. Duyster, N. von Bubnoff, 2006, Blood.

The low frequency of clinical resistance to PDGFR inhibitors in myeloid neoplasms with abnormalities of PDGFRA might be related to the limited repertoire of possible PDGFRA kinase domain mutations in vitro

R. Engh, C. Peschel, J. Duyster, 2011, Oncogene.

Studies on the functional domains in oncogenic JAK2 and identification of drug resistant mutations in FIP1L1-PDGFRa

S. P. Gorantla, 2011 .

Establishment and Molecular Characterization of Two Patient-Derived Pancreatic Ductal Adenocarcinoma Cell Lines as Preclinical Models for Treatment Response

M. Spielmann, M. Drenckhan, A. Künstner, 2023, Cells.

Oncogenic JAK2V617F requires an intact SH2-like domain for constitutive activation and induction of a myeloproliferative disease in mice.

C. Peschel, J. Duyster, M. Kremer, 2010, Blood.

Role of SH2 Domain in JAK2-V617F Mediated Transformation.

C. Peschel, J. Duyster, T. Dechow, 2006 .

Phosphorylation of BECLIN-1 by BCR-ABL suppresses autophagy in chronic myeloid leukemia

J. Duyster, C. Albers, Z. Yue, 2019, Haematologica.

NPM1c alters FLT3-D835Y localization and signaling in acute myeloid leukemia.

A. Bradley, P. Paschka, G. Vassiliou, 2019, Blood.

Platelets regulate ischemia-induced revascularization and angiogenesis by secretion of growth factor–modulating factors

Ying Sun, T. Geisler, C. Kleinschnitz, 2023, Blood advances.

Molecular biomarkers of leukemia: convergence-based drug resistance mechanisms in chronic myeloid leukemia and myeloproliferative neoplasms

N. von Bubnoff, S. P. Gorantla, Meike Kaehler, 2024, Frontiers in pharmacology.

A newly identified 45‐kDa JAK2 variant with an altered kinase domain structure represents a novel mode of JAK2 kinase inhibitor resistance

J. Duyster, N. von Bubnoff, S. P. Gorantla, 2023, Molecular oncology.

Type II mode of JAK2 inhibition and destabilization are potential therapeutic approaches against the ruxolitinib resistance driven myeloproliferative neoplasms

J. Duyster, Dhurvas Chandrasekaran Dinesh, N. von Bubnoff, 2024, Frontiers in oncology.

Targeting cancer-derived extracellular vesicles by combining CD147 inhibition with tissue factor pathway inhibitor for the management of urothelial cancer cells

N. von Bubnoff, S. P. Gorantla, Piet Zamzow, 2024, Cell communication and signaling : CCS.

Ruxolitinib Mediated Paradox JAK2 Hyperphosphorylation Is Due To The Protection Of Activation Loop Phosphotyrosines From Phosphatases

C. Peschel, J. Duyster, S. P. Gorantla, 2013 .