Results 21 to 30 of about 10,998 (173)

Rare SF3B1 R625 mutations in cutaneous melanoma [PDF]

open access: yesMelanoma Research, 2014
RNA splicing is the cellular process that has only recently been found to be an important target for various cancers. Among the spliceosome genes that are involved in cancers, SF3B1 is most frequently mutated. Recurrent mutation in codon 625 has been found in uveal melanoma, but this mutation has not been identified in cutaneous melanoma. We used whole-
Yong, Kong   +2 more
openaire   +2 more sources

SF3B1 promotes tumor malignancy through splicing-independent co-activation of HIF1α [PDF]

open access: yes, 2020
Heterozygous mutations in the splicing factor SF3B1 are frequently occurring in various cancers and drive tumor progression through the activation of cryptic splice sites in multiple genes.
Cortijo, Cédric   +21 more
core   +1 more source

Altered selection of branch sites by sf3b1 mutants.

open access: yes, 2021
(A) Schematic graph for identification of BS by nested lariat RT-PCR and sequencing. cDNA from the intronic lariat is transcribed using an intron-specific antisense primer P1′, and then amplified by two-steps PCRs using primer sets P1′ + P1 and P2′ + P2.
Bei Zhang (428038)   +5 more
core   +1 more source

Interchangeable SF3B1 inhibitors interfere with pre-mRNA splicing at multiple stages [PDF]

open access: yes, 2016
The protein SF3B1 is a core component of the spliceosome, the large ribonucleoprotein complex responsible for pre-mRNA splicing. Interest in SF3B1 intensified when tumor exome sequencing revealed frequent specific SF3B1 mutations in a variety of ...
Effenberger, Kerstin A   +4 more
core   +1 more source

SF3B1 homeostasis is critical for survival and therapeutic response in T cell leukemia [PDF]

open access: yes, 2022
The production of noncanonical mRNA transcripts is associated with cell transformation. Driven by our previous findings on the sensitivity of T cell acute lymphoblastic leukemia (T-ALL) cells to SF3B1 inhibitors, we identified that SF3B1 inhibition ...
Politanska, Yuliya   +25 more
core   +1 more source

Aging Is a Key Driver for Adult Acute Myeloid Leukemia

open access: yesAging and Cancer, EarlyView.
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
wiley   +1 more source

deboever-sf3b1-2014

open access: yes, 2014
Files for replicating SF3B1 study.
Christopher DeBoever (541416)
core   +1 more source

Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance

open access: yesAging and Cancer, EarlyView.
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang   +3 more
wiley   +1 more source

SF3B1 mutations constitute a novel therapeutic target in breast cancer [PDF]

open access: yes, 2015
Mutations in genes encoding proteins involved in RNA splicing have been found to occur at relatively high frequencies in several tumour types including myelodysplastic syndromes, chronic lymphocytic leukaemia, uveal melanoma, and pancreatic cancer, and ...
Wai, P   +19 more
core   +1 more source

Therapeutic Silencing of Tmprss6 Reduces Iron‐Induced Inflammation and Prolongs Survival in MDS Mice

open access: yesAmerican Journal of Hematology, EarlyView.
ABSTRACT Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal hematopoietic disorders characterized by ineffective hematopoiesis, cytopenias, and an increased risk of progression to acute myeloid leukemia (AML). Despite advances in supportive and targeted therapies, disease‐modifying interventions remain limited.
Shahla Vilcassim   +13 more
wiley   +1 more source

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