Article

<i>TP53</i> mutations drive therapy resistance via post-mitochondrial caspase blockade

2025-08-31

Abstract excerpt

<h4>ABSTRACT</h4> Acute myeloid leukemia (AML) is a heterogeneous disease characterized by a broad spectrum of molecular alterations that influence clinical outcomes. TP53 mutations define one of the most lethal subtypes of acute myeloid leukemia (AML), driving resistance to nearly all available treatment modalities, including venetoclax plus azacitidine (VenAza). Yet, the molecular basis of this resistance, bey...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work: 55bd94c1-9d6d-5b93-84b6-9bf0226d56ee
DOI: 10.1101/2025.08.28.672283

Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest

<i>TP53</i> mutations drive therapy resistance via post-mitochondrial caspase blockadeDOI 10.1101/2025.08.28.672283Read

The TP53 Apoptotic Network Is a Primary Mediator of Resistance to BCL2 Inhibition in AML CellsSemantic proximity Read

Combined inhibition of BCL-2 and MCL-1 overcomes BAX deficiency-mediated resistance of TP53-mutant acute myeloid leukemia to individual BH3 mimeticsSemantic proximity Read

Targeting TP53-Mutated Acute Myeloid Leukemia: Research and Clinical DevelopmentsSemantic proximity Read

What have we learned about TP53-mutated acute myeloid leukemia?Semantic proximity Read

TP53-mutated acute myeloid leukemia and myelodysplastic syndrome: biology, treatment challenges, and upcoming approaches.Semantic proximity Read

Immune recovery in tumor microenvironment of<i>TP53</i>-mutated AML following venetoclax combination therapySemantic proximity Read

Mitochondrial determinants of response and resistance to venetoclax <i>plus</i> cytarabine duplet therapy in acute myeloid leukemiaSemantic proximity Read

Unraveling Venetoclax Resistance: Navigating the Future of HMA/Venetoclax-Refractory AML in the Molecular EraSemantic proximity Read

<i>BIRC5</i> dependency defines a targetable vulnerability in <i>TP53</i> mutant acute myeloid leukemiaSemantic proximity Read

<i>TP53</i> Inactivation Confers Resistance to the Menin Inhibitor Revumenib in Acute Myeloid LeukemiaSemantic proximity Read

Intact TP-53 function is essential for sustaining durable responses to BH3-mimetic drugs in leukemiasSemantic proximity Read

TP53 signal pathway confers potential therapy target in acute myeloid leukemia.Semantic proximity Read