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• W2890961237 abstract "11611 Background: Necroptosis is a type of necrotic cell death involving several genes transcription and activation of molecular mechanisms as death receptors, interferon, toll-like receptors, intracellular RNA and DNA sensors.The process is leading by the family of receptor-interacting protein kinase ( RIPK3, RIPK2, RIPK1) and the MLKL substrate. Losses of RIPK3 or MLKL, as well as deficiency in apoptosis, could allow tumor cells to escape the immunomediated cells death (ICD). Methods: We performed SNP Arrays (Cytoscan HD and SNP 6.0, Affymetrix) on a cohort of 300 non-M3 AML patients at diagnosis and we analyzed the Overall Survival (OS) of our patients with deficiency on necroptosis pathways. Survival was analyzed with Kaplan-Mayer method and Log-Rank test. We further analyze the relevance of different prognostic factors by the use of COX-Hazard Ratio statistical analysis. Results: We find that 18 patients presented a loss of RIPK1 or MLKL (nobody presented losses in RIPK3/RIPK2) and 13/18 patients were older than 65 years old. The Overall Survival (OS) of patients with alterations in these genes is significantly lower than control group, with a median OS of 3 vs 6 month respectively (p<.0.001). With Fisher Exact Test we further demonstrate that copy number loss of RIPK1 or MLKL are associate to loss of TP53 or FANCAgenes, complex karyotype and advanced age. COXHR model with RIPK1 or MLKL loss, BRACA1 loss, TP53 mutation, FANCA loss, secondary disease and diagnosis karyotype considered as categorical variable shows that necroptosis deficiency (HR 1.98, CI 95% 1.04-3.78), TP53mutation , and secondary AML are independent negative prognostic factors in an optimal model. Conclusions: Our study shows that losses in necroptosis pathways are an uncommon alteration in AML, prevalent in old population. Moreover, we hypothesize that the loss of genes involved in necroptosis could be a real mechanism of tumor immune-escape and could be a rational to select patients that have high probability to be resistant at chemotherapy promoting ICD mechanism. Acknowledgment: ELN,AIL,AIRC, progetto Regione-Università 2010-12, FP7 NGS-PTL project,HARMONY." @default.
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• W2890961237 date "2017-05-20" @default.
• W2890961237 modified "2023-10-16" @default.
• W2890961237 title "Deficient necroptosis pathway as a negative prognostic factor in acute myeloid leukemia." @default.
• W2890961237 doi "https://doi.org/10.1200/jco.2017.35.15_suppl.11611" @default.
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