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BIOMARKER:

IDH2 mutation + TP53 mutation

i
Other names: TP53, Tumor Protein P53, Cellular Tumor Antigen P53, Phosphoprotein P53, Tumor Protein P53, Antigen NY-CO-13, Transformation-Related Protein 53, Mutant Tumor Protein 53, P53 Tumor Suppressor, Tumor Suppressor P53, Tumor Protein 53, BMFS5, TRP53, BCC7, LFS1, IDH2, Isocitrate Dehydrogenase (NADP(+)) 2, Isocitrate Dehydrogenase (NADP(+)) 2, Mitochondrial, Isocitrate Dehydrogenase 2 (NADP+), Mitochondrial, Isocitrate Dehydrogenase [NADP], Mitochondrial, Oxalosuccinate Decarboxylase, NADP(+)-Specific ICDH, ICD-M, IDH, IDP, MNADP-IDH, D2HGA2, IDHM, IDPM
Entrez ID:
4ms
A nomogram based on clinical features and molecular abnormalities for predicting the prognosis of patients with acute myeloid leukemia. (PubMed, Transl Cancer Res)
Finally, younger (age <60 years) and elderly (age ≥60 years) patients were each divided into two risk groups with significantly different survival rates. A nomogram consisting of five risk factors was developed for forecasting the prognosis of AML with guaranteed reliability.
Journal
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TP53 (Tumor protein P53) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • DNMT3A (DNA methyltransferase 1)
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TP53 mutation • DNMT3A mutation • IDH2 mutation + TP53 mutation
5ms
Diagnostic Challenges in the Leukemia Phase of Blastic Plasmacytoid Dendritic Cell Neoplasm without Skin Involvement: A Clinical and Pathological Study (ASH 2023)
Only one cycle of decitabine + CAG was given and 5 months later, the disease progressed to the leukemia phase...The latter case had ASXL1 and TET2 mutations detected by NGS analysis, achieved complete remission after receiving venetoclax + azacitidine for one cycle, followed by intermittent venoclax +demethylation agent or low-dose chemotherapy maintenance treatment and live for more than two years now... BPDCN without skin lesions is clinically rare, and its diagnosis is challenging. Comprehensive immunophenotyping and cautious interpretation of immunohistochemistry results such as dim lysozyme expression are crucial. Venetoclax-containing regimens have shown promising therapeutic effects.
Clinical
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TP53 (Tumor protein P53) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • CD20 (Membrane Spanning 4-Domains A1) • CD8 (cluster of differentiation 8) • ASXL1 (ASXL Transcriptional Regulator 1) • TET2 (Tet Methylcytosine Dioxygenase 2) • CD123 (Interleukin 3 Receptor Subunit Alpha) • CD33 (CD33 Molecule) • CD34 (CD34 molecule) • CD36 (thrombospondin receptor) • NCAM1 (Neural cell adhesion molecule 1) • CD5 (CD5 Molecule) • CD14 (CD14 Molecule) • ITGAM (Integrin, alpha M) • MME (Membrane Metalloendopeptidase) • CD7 (CD7 Molecule) • IL3RA (Interleukin 3 Receptor Subunit Alpha) • NRP1 (Neuropilin 1) • SPN (Sialophorin) • TCL1A (TCL1 Family AKT Coactivator A) • ANPEP (Alanyl Aminopeptidase, Membrane) • CLEC4C (C-Type Lectin Domain Family 4 Member C) • MPO (Myeloperoxidase)
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TP53 mutation • ASXL1 mutation • TET2 mutation • CD123 positive • NCAM1 expression • CD123 expression • CD4 expression • IDH2 mutation + TP53 mutation • IL3RA positive • NCAM1 positive
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Venclexta (venetoclax) • azacitidine • decitabine
5ms
Improved Survival with Venetoclax in Patients with Acute Myeloid Leukemia: A Retrospective Single-Center Cohort Study (ASH 2023)
Background: Venetoclax in combination with azacitidine or low-dose cytarabine has become standard treatment for newly diagnosed elderly or unfit patients with acute myeloid leukemia (AML). These real-world data suggested that incorporation of venetoclax combination therapy into existing therapies improved survival in patients with AML. The survival benefit of venetoclax combination therapy was greater in elderly patient and in de novo AML patients than secondary AML patients. Interpretation of the results must be careful because the sample size in the venetoclax group was small.
Retrospective data
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TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NPM1 (Nucleophosmin 1)
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TP53 mutation • NPM1 mutation • IDH1 mutation + TP53 mutation • IDH2 mutation + TP53 mutation
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Venclexta (venetoclax) • cytarabine • azacitidine
5ms
Genetic alterations that deregulate RB and PDGFRA signaling pathways drive tumor progression in IDH2-mutant astrocytoma. (PubMed, Acta Neuropathol Commun)
These findings suggest that gene alterations that activate retinoblastoma (RB) signaling pathways and PDGFR may drive tumor progression and xenograft formation in IDH2-mutant astrocytoma, which is equivalent to progressive IDH1-mutant astrocytoma. Also, our findings suggest that these genomic alterations may represent therapeutic targets in IDH2-mutant astrocytoma.
Journal
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TP53 (Tumor protein P53) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B)
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TP53 mutation • IDH1 mutation • IDH2 mutation • CDKN2A deletion • CDKN2A mutation • CDK4 amplification • IDH2 mutation + TP53 mutation
6ms
Analysis of Treatment Patterns and Outcomes in Patients Ages 60-74 in the Post-Venetoclax Era (ASH 2023)
Low intensity therapy (LIT) regimens included combinations of a hypomethylating agent, low dose cytarabine, venetoclax, cladribine, and/or targeted agents. Intensively-treated patients were younger and more likely to receive HCT but both groups had an OS benefit from HCT. Our data suggest that in the era of novel agents such as venetoclax, less intensive induction strategies may be appropriate for IC-eligible patients between the ages of 60-74.
Clinical
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TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2)
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TP53 mutation • FLT3-ITD mutation • IDH2 mutation + TP53 mutation
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Venclexta (venetoclax) • cytarabine • cladribine