TP53 deletion

TP53-D is common in systemic ALK-negative ALCL and is associated with leukemic disease and p53 overexpression. TP53-D did not directly affect survival, but it negated the favorable impact of low IPI and DUSP22-R on PFS, suggesting its potential value as an adverse prognostic marker.

A diagnosis of statin-associated anti-HMGCR IMNM was established, and treatment with mycophenolate mofetil and intravenous immunoglobulin resulted in partial biochemical improvement...Further evaluation revealed mantle cell lymphoma with bone marrow involvement, IGH::CCND1 rearrangement, and TP53 deletion, consistent with high-risk disease. In this context, continued clinical and laboratory monitoring is appropriate in inflammatory myopathy, and new hematologic abnormalities warrant further evaluation.

P3, N=382, Active, not recruiting, University of Arkansas | Trial completion date: Sep 2027 --> Sep 2028 | Trial primary completion date: Sep 2026 --> Sep 2027

Notably, brusatol increased normal leukocyte and platelet counts while reducing leukemic infiltration in both bone marrow and extramedullary sites. These findings provide mechanistic insight into the synergistic effects of the brusatol-venetoclax combination, supporting further evaluation of this therapeutic strategy in myeloid leukemias.

P1/2, N=33, Active, not recruiting, Fundacio Sant Joan De Deu | Recruiting --> Active, not recruiting

She was started on azacitidine and venetoclax. In resource-limited setting, this case underscores urgent need for heightened clinical vigilance. Likewise, it highlights the urgent need for a more risk-adapted approach to persistent isolated neutropenia and compels us to confront a critical question: how many patients are we failing to diagnose in time, and how many windows for potentially life-altering intervention are we silently allowing to close?

Survival differed significantly among the three etiological groups (χ2=11.53, P=0.003). AEL is a subtype of acute myeloid leukemia with extremely poor prognosis that is highly associated with TP53 gene abnormalities.

This case suggests that the combination of cladribine and low-dose rituximab may be an effective therapeutic strategy for classical HCL with TP53 abnormality, enabling deep molecular response and reversal of associated bone marrow fibrosis. Further prospective studies are warranted to validate these findings.

The patient exhibited vascular endothelial growth factor receptor amplification, mutations in CHEK1, ERCC3, and TP53, deletion of CD274 (gene of PD-L1), and microsatellite stability. These findings suggest that immunotherapy may be beneficial to URCS patients with low PD-L1 expression and microsatellite stability, when accompanied by immunotherapy-associated genetic alterations.

P1, N=32, Not yet recruiting, Northside Hospital, Inc.

However, a subset of aged mice with mutated Rps15 eventually develop B-cell leukemia (37% penetrance), which exhibits increased Myc activity with strong pro-survival and proliferation signatures. Mutant RPS15 thus induces both hypo- and hyper-proliferative signals, initially weighted towards cell cycle arrest; and that through translational rewiring, oxidative stress, DNA damage response defects and genomic instability set the stage for the acquisition of additional driving mutations, such as TP53 deletion, that can overcome this cell cycle block to trigger tumorigenesis.

The median overall survival of 5 patients with available follow-up was 11 months. We conclude that the reciprocal translocation t(5;12)(q32;p13) requires a careful and step-wise diagnostic work-up to differentiate between an underlying ETV6::PDGFRB fusion gene with associated excellent prognosis on imatinib and an ETV6::ACSL6 fusion gene, for which the prognosis is poor and alloHCT appears to be a promising therapeutic option.