ZRSR2

Last update 08 May 2025

Basic Info

Synonyms

CCCH type zinc finger, RNA-binding motif and serine/arginine rich protein 2, Renal carcinoma antigen NY-REN-20, U2 small nuclear ribonucleoprotein auxiliary factor 35 kDa subunit-related protein 2

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Introduction

Pre-mRNA-binding protein required for splicing of both U2- and U12-type introns. Selectively interacts with the 3'-splice site of U2- and U12-type pre-mRNAs and promotes different steps in U2 and U12 intron splicing. Recruited to U12 pre-mRNAs in an ATP-dependent manner and is required for assembly of the pre-spliceosome, a precursor to other spliceosomal complexes. For U2-type introns, it is selectively and specifically required for the second step of splicing.

100 Clinical Results associated with ZRSR2

100 Translational Medicine associated with ZRSR2

0 Patents (Medical) associated with ZRSR2

169

Literatures (Medical) associated with ZRSR2

25 Mar 2025·Blood Advances

Validation of the revised 2022 European LeukemiaNet risk stratification in adult patients with acute myeloid leukemia

Article

Author: Brümmendorf, Tim ; Hanoun, Maher ; Steffen, Björn ; Jost, Edgar ; Fransecky, Lars ; Kiani, Alexander ; Kaufmann, Martin ; Blau, Wolfgang ; Thiede, Christian ; Schäfer-Eckart, Kerstin ; Kraus, Sabrina ; Niemann, Dirk ; Zukunft, Sven ; Morgner, Anke ; Schaich, Markus ; Bornhäuser, Martin ; Schliemann, Christoph ; Hochhaus, Andreas ; Eckardt, Jan-Niklas ; Schroeder, Thomas ; Baldus, Claudia D. ; Bill, Marius ; Serve, Hubert ; Ruhnke, Leo ; Sauer, Tim ; Kaiser, Ulrich ; Krause, Stefan W. ; Middeke, Jan Moritz ; Mikesch, Jan-Henrik ; Stasik, Sebastian ; Seggewiss-Bernhardt, Ruth ; Giagounidis, Aristoteles ; Platzbecker, Uwe ; Kullmer, Johannes ; Meinhardt, Achim ; Krug, Utz ; Schäfer, Silvia ; Müller-Tidow, Carsten ; Wurm, Alexander A. ; Stölzel, Friedrich ; Repp, Roland ; Grigoleit, Götz Ulrich ; Neubauer, Andreas ; Scholl, Sebastian ; Röllig, Christoph ; Schetelig, Johannes ; Altmann, Heidi ; Hänel, Mathias

AbstractIn 2022, the European LeukemiaNet (ELN) risk stratification for patients with acute myeloid leukemia (AML) has been updated. We aimed to validate the prognostic value of the 2022 ELN classification (ELN22) by evaluating 1570 patients with newly diagnosed AML (median age, 56 years) treated with cytarabine-based intensive chemotherapy regimens. Compared with 2017 ELN classification (ELN17), which allocated 595 (38%), 413 (26%), and 562 patients (36%) to the favorable-, intermediate-, and adverse-risk categories, ELN22 classified 575 (37%), 410 (26%), and 585 patients (37%) as favorable, intermediate, and adverse risk, respectively. Risk group allocation was revised in 340 patients (22%). Most patients were reclassified into the ELN22 intermediate- or ELN22 adverse-risk group. The allocation of patients according to the ELN22 risk categories resulted in a significantly distinct event-free survival (EFS), relapse-free survival, and overall survival (OS). Compared with ELN17, reallocation according to the ELN22 recommendations resulted in a significantly improved prognostic discrimination for OS (3-year area under the curve, 0.71 vs 0.67). In patients with ELN22 favorable-risk AML, co-occurring myelodysplasia-related (MR) gene mutations did not significantly affect outcomes. Within the ELN22 adverse-risk group, we observed marked survival differences across mutational groups (5-year OS rate of 21% and 3% in patients with MR gene mutations and TP53 mutations, respectively). In patients harboring MR gene mutations, EZH2-, STAG2-, and ZRSR2-mutated patients showed an intermediate-like OS. In patients with secondary AML and those who underwent allogeneic hematopoietic cell transplantation, EFS and OS significantly differed between ELN22 risk groups, whereas the prognostic abilities of ELN17 and ELN22 classifications were similar. In conclusion, ELN22 improves prognostic discrimination in a large cohort of intensively treated patients with AML. Given the heterogeneous outcome in patients with MR gene alterations, ranging between those of intermediate and adverse risk patients, we suggest re-evaluation of risk allocation in these patients.

01 Mar 2025·Journal of Cellular and Molecular Medicine

Rapid Development of Unclassified Myeloid Lineage Acute Leukaemia With Trisomy 6 and U2AF1 Mutation

Article

Author: Lewandowski, Krzysztof ; Kopacz, Agnieszka ; Blajer‐Olszewska, Beata ; Wojtaszewska, Marzena ; Dudycz, Dominika ; Markiewicz, Miroslaw ; Warzybok, Katarzyna ; Szarawarska, Marta ; Moskwa, Monika ; Schwarz, Ewa ; Kosior, Katarzyna ; Mazur, Malwina

ABSTRACTWe present a case of acute clonal bone marrow 98% infiltration of atypical myeloid cells with borderline hypogranular/agranular promyelocytes/myelocytes and occasional blast cells maturity, which also formed extramedullary tumours in the chest wall, with isolated trisomy of chromosome 6 and pathogenic variant U2AF1 (S34F) that escapes established acute myeloid leukaemia (AML) diagnostic criteria according to the World Health Organization (WHO) classification. Following standard daunorubicin and cytarabine induction therapy, the disease progressed with the appearance of a previously undetected clone of leukaemic cells with a distinct immunophenotype demonstrating monocytoid differentiation and clonal evolution to a hypo‐tetraploid karyotype with an average number of 84 chromosomes and new pathogenic NRAS and ZRSR2 mutations. The patient reactivated refractory disseminated intravascular coagulation (DIC) leading to a progressive supratentorial hematoma and finally cardiac arrest. In conclusion, our report shows that atypical clonal myelocytes can massively infiltrate the bone marrow and form extramedullary tumours, justifying the diagnosis and treatment of acute leukaemia, although they did not fit the current classification.

01 Feb 2025·IUBMB Life

Possible new mechanisms of primary drug resistance in NSCLC with EGFR mutation treated with Osimertinib

Article

Author: Zhang, Xinyu ; Li, Qi ; Dong, Chunyan ; Shao, Lujing ; Li, Tong ; Jia, Xinyan

AbstractIn this study, a patient with lung adenocarcinoma harboring an EGFR mutation exhibited primary resistance to the targeted EGFR inhibitor Osimertinib after 2 months of treatment. As the disease advanced, further genetic analysis revealed the emergence of additional mutations in ARID1A, NTRK1, and ZRSR2, alongside the existing EGFR mutation. Subsequent treatment with Pemetrexed resulted in a significant reduction in liver metastases. Protein mass spectrometry sequencing and immunohistochemical analysis collectively indicated that the PI3K/mTOR pathway mediates the mechanism through which these gene mutations confer primary drug resistance. Evidence demonstrates that the co‐occurrence of EGFR and ARID1A mutations diminishes the efficacy of EGFR tyrosine kinase inhibitors (EGFR TKIs). Consequently, it is hypothesized that mutations in NTRK1 and ZRSR2, which are implicated in the PI3K/mTOR pathway, contribute to the primary resistance observed with Osimertinib treatment. In this case, the illness was effectively managed through prompt adjustments to the treatment regimen and the rapid administration of chemotherapy drugs. This finding also constitutes the first evidence that mutations in NTRK1 and ZRSR2 are pivotal in the development of primary resistance to Osimertinib. Consequently, it is imperative to conduct genetic testing at the earliest opportunity and modify the treatment plan accordingly.

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ZRSR2

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