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GENE:

MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)

i
Other names: MLLT10, MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor, AF10, Myeloid/Lymphoid Or Mixed-Lineage Leukemia; Translocated To, 10, ALL1-Fused Gene From Chromosome 10 Protein, Protein AF-10, Myeloid/Lymphoid Or Mixed-Lineage Leukemia (Trithorax (Drosophila) Homolog); Translocated To, 10, Myeloid/Lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila); Translocated To, 10, Type III AF10 Protein, Type IV AF10 Protein, Type I AF10 Protein
Associations
10d
Impact of Fusion Partners and Transplantation Benefit in Intensively Treated KMT2A-Rearranged Acute Myeloid Leukemia. (PubMed, Cancers (Basel))
Our study revealed the heterogeneous outcomes of KMT2A-rearranged AML patients and clarified the impact of HSCT across different age groups.
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KMT2A (Lysine Methyltransferase 2A) • MLLT3 (MLLT3 Super Elongation Complex Subunit) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
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KMT2A rearrangement
28d
Clonal Evolution and Lineage Switch from T-Cell Acute Lymphoblastic Leukemia to Acute Myeloid Leukemia in Therapy-Resistant PICALM::MLLT10 Leukemia. (PubMed, EJHaem)
The sequential acquisition of cooperating genetic lesions supports clonal evolution and highlights the need for molecular monitoring and novel therapeutic strategies. The authors have confirmed clinical trial registration is not needed for this submission.
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NF1 (Neurofibromin 1) • PHF6 (PHD Finger Protein 6) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor) • SMC1A (Structural Maintenance Of Chromosomes 1A)
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EZH2 mutation • Chr del(5q)
1m
Precursor B-Cell Acute Lymphoblastic Leukemia With PICALM∶∶MLLT10 Fusion Gene Positivity:Report of One Case and Literature Review. (PubMed, Zhongguo Yi Xue Ke Xue Yuan Xue Bao)
PICALM∶∶MLLT10 fusion gene-positive precursor B-cell acute lymphoblastic leukemia(pro-B-ALL)is clinically rare.This article reports the case of a 29-year-old female patient who presented a mediastinal mass.Diagnostic investigations confirmed PICALM∶∶MLLT10 fusion gene-positive pro-B-ALL.The patient sequentially received radiotherapy and multiple lines of chemotherapy but developed short-term drug resistance and lineage change,progressing to mixed-phenotype acute leukemia.A review of relevant literature was conducted to analyze its pathogenesis and molecular characteristics,aiming to provide references for clinical diagnosis and treatment.
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MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
1m
PICALM::MLLT10 translocated leukemia. (PubMed, FEBS Lett)
This approach is demonstrated in the recent promising results achieved utilizing venetoclax, a BCL2 inhibitor, in patients with PICALM::MLLT10 acute leukemia. Herein, we provide updates on the pathophysiology, clinical presentation, prognosis, and treatment of PICALM::MLLT10 acute leukemia.
Review • Journal • IO biomarker
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MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
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Venclexta (venetoclax)
1m
Endometriosis: From Genes to Global Burden. (PubMed, Int J Mol Sci)
The identified genetic markers related to pain provide a biological basis for the profound physical suffering. At the same time, the robust DALYs and YLDs data quantify the devastating impact on mental health, particularly highlighting the significant burden of depression and anxiety.
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SIRT1 (Sirtuin 1) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor) • TEAD3 (TEA Domain Transcription Factor 3)
2ms
Genetic landscape of pediatric acute myeloid leukemia in Taiwan. (PubMed, Sci Rep)
Patients with RUNX1 mutations had inferior 5 year OS in multivariable analysis (p-value = 0.009). These findings suggest specific genomic alterations that may refine risk stratification and guide future therapeutic protocols in Taiwanese pediatric patients with AML.
Journal
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FLT3 (Fms-related tyrosine kinase 3) • RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
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RUNX1 mutation
2ms
Adult Acute Myeloid Leukaemia With DDX3X::MLLT10: A Rare Entity With Significant Unmet Clinical Needs. (PubMed, EJHaem)
Collectively, these cases highlight the genomic heterogeneity of this rare entity, as well as significant unmet clinical needs due to the poor prognosis and chemoresistance observed. These findings may inform future iterations of AML classification and prognostication in adults.
Journal
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DDX3X (DEAD-Box Helicase 3 X-Linked) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
3ms
Journal
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MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
3ms
Allogeneic hematopoietic stem cell transplantation for pediatric acute leukemia harboring the PICALM-MLLT10 fusion in two cases (PubMed, Zhongguo Dang Dai Er Ke Za Zhi)
At the latest follow-up, both patients were alive and in good clinical condition. These observations suggest that proceeding to hematopoietic stem cell transplantation after venetoclax-based chemotherapy may improve the long-term survival of children with PICALM-MLLT10-positive leukemia.
Journal
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MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
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Venclexta (venetoclax)
4ms
Detection of Fusion Genes Using RNA Sequencing in Acute Leukemia. (PubMed, Ann Lab Med)
This was the first study to evaluate the performance of whole RNA-seq in fusion detection in patients with acute leukemia in Korea. Incorporating RNA-seq into diagnostic workflows may facilitate earlier and more precise therapeutic decisions and improve prognostic assessment in patients with acute leukemia.
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RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • ETV6 (ETS Variant Transcription Factor 6) • FUS (FUS RNA Binding Protein) • USP42 (Ubiquitin Specific Peptidase 42) • HNRNPH1 (Heterogeneous Nuclear Ribonucleoprotein H1) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor) • NCOA2 (Nuclear Receptor Coactivator 2)
5ms
Upfront Menin-inhibitor resistance in multiply pretreated leukemias. (PubMed, Exp Hematol)
Future studies will need to clarify more broadly which genomic/epigenomic alterations drive upfront resistance. Regardless of mechanism, our data supports using Menin-inhibitors upfront or in early lines of therapy before substantial genomic or epigenomic evolution has occurred.
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TP53 (Tumor protein P53) • KMT2A (Lysine Methyltransferase 2A) • KMT2C (Lysine Methyltransferase 2C) • AFF1 (AF4/FMR2 Family Member 1) • AFDN (Afadin, Adherens Junction Formation Factor) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
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TP53 mutation
5ms
Evaluation of the cytomorphology, immunophenotype, and molecular genetics of lymphoblastic lymphoma/leukemia in serous effusion. (PubMed, Acta Cytol)
The integration of clinical manifestations, cytological evaluation, and gene expression profiles is instrumental in achieving accurate diagnosis, sub-classification, and prognosis of LBL/ALL within the context of SE.
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CD20 (Membrane Spanning 4-Domains A1) • ARID1A (AT-rich interaction domain 1A) • NOTCH1 (Notch 1) • NF1 (Neurofibromin 1) • TET2 (Tet Methylcytosine Dioxygenase 2) • WT1 (WT1 Transcription Factor) • BCOR (BCL6 Corepressor) • PAX5 (Paired Box 5) • SETD2 (SET Domain Containing 2, Histone Lysine Methyltransferase) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • JAK3 (Janus Kinase 3) • ARID2 (AT-Rich Interaction Domain 2) • CD5 (CD5 Molecule) • CD79A (CD79a Molecule) • MME (Membrane Metalloendopeptidase) • CD7 (CD7 Molecule) • CD2 (CD2 Molecule) • CD99 (CD99 Molecule) • SPN (Sialophorin) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
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ARID1A mutation