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Key clinical point: New tumor protein 53 (TP53) mutations could be acquired during acute myeloid leukemia (AML) treatment, particularly after intensive chemotherapy and hematopoietic stem cell transplantation (HSCT), in a proportion of patients with TP53 wild-type AML. Thus, sequential monitoring for emergent TP53 mutations during AML therapy may have clinical relevance.
Major finding: Overall, 15% of patients developed a newly detectable TP53 mutation during AML therapy, with a median variant allele frequency of 15%. Newly detected TP53 mutations were frequent in patients receiving intensive vs low-intensity chemotherapy (23% vs 10%; P = .02) and those who underwent HSCT vs those who did not (36% vs 12%; P = .005).
Study details: Findings are from a retrospective analysis of 200 adult patients with newly diagnosed TP53 wild-type AML who relapsed after or were refractory to frontline therapy.
Disclosures: This study was supported by MD Anderson Cancer Center Support Grant and SPORE. The authors declared no conflict of interests.
Source: Alwash Y et al. Am J Hematol. 2021 Aug 5. doi: 10.1002/ajh.26314.
Key clinical point: New tumor protein 53 (TP53) mutations could be acquired during acute myeloid leukemia (AML) treatment, particularly after intensive chemotherapy and hematopoietic stem cell transplantation (HSCT), in a proportion of patients with TP53 wild-type AML. Thus, sequential monitoring for emergent TP53 mutations during AML therapy may have clinical relevance.
Major finding: Overall, 15% of patients developed a newly detectable TP53 mutation during AML therapy, with a median variant allele frequency of 15%. Newly detected TP53 mutations were frequent in patients receiving intensive vs low-intensity chemotherapy (23% vs 10%; P = .02) and those who underwent HSCT vs those who did not (36% vs 12%; P = .005).
Study details: Findings are from a retrospective analysis of 200 adult patients with newly diagnosed TP53 wild-type AML who relapsed after or were refractory to frontline therapy.
Disclosures: This study was supported by MD Anderson Cancer Center Support Grant and SPORE. The authors declared no conflict of interests.
Source: Alwash Y et al. Am J Hematol. 2021 Aug 5. doi: 10.1002/ajh.26314.
Key clinical point: New tumor protein 53 (TP53) mutations could be acquired during acute myeloid leukemia (AML) treatment, particularly after intensive chemotherapy and hematopoietic stem cell transplantation (HSCT), in a proportion of patients with TP53 wild-type AML. Thus, sequential monitoring for emergent TP53 mutations during AML therapy may have clinical relevance.
Major finding: Overall, 15% of patients developed a newly detectable TP53 mutation during AML therapy, with a median variant allele frequency of 15%. Newly detected TP53 mutations were frequent in patients receiving intensive vs low-intensity chemotherapy (23% vs 10%; P = .02) and those who underwent HSCT vs those who did not (36% vs 12%; P = .005).
Study details: Findings are from a retrospective analysis of 200 adult patients with newly diagnosed TP53 wild-type AML who relapsed after or were refractory to frontline therapy.
Disclosures: This study was supported by MD Anderson Cancer Center Support Grant and SPORE. The authors declared no conflict of interests.
Source: Alwash Y et al. Am J Hematol. 2021 Aug 5. doi: 10.1002/ajh.26314.