TP53 mutation

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

We illustrate four use cases of ASHOP: (1) stratification of DUX4-rearranged B-cell leukemias into Early/Multipotent and Committed subgroups with distinct outcomes, (2) characterization of HOXA/HOXB expression patterns in acute myeloid leukemias, (3) correlating mutational burden with mismatch repair deficiency and mutational signatures, (4) investigation of TP53 alteration landscape. ASHOP is an open-access resource to inform genomic and transcriptomic data interpretation for hematologic malignancies, and will expand to support additional diseases and data modalities from the ASH community.

These findings establish a mechanistic link between hormonal signaling, p53 allelic status, and m6A-dependent post-transcriptional regulation. Although further in vivo validation is required, disruption of the ALKBH5-REG1A axis may contribute to heterogeneous endometrial responses to tamoxifen, thereby providing a conceptual framework for biomarker-oriented investigation.

Additionally, we explore the mechanisms underlying TP53 mutations in the leukemic transformation of MPNs, including clonal evolution to multihit status and the role of inflammation and therapy. Finally, recent findings on the clinical impact of multihit TP53 mutations and potential strategies for targeting the p53 pathway in MPNs and sAML are presented.

This review synthesizes current knowledge on the unique tumor biology of breast cancer in young women, highlighting the need for precision oncology approaches that account for age-related tumor behavior. Enhanced characterization of this population may ultimately improve survival outcomes and quality of life for young women affected by breast cancer.

Malignant EAML can invade atypical venous routes such as the lumbar vein. Comprehensive imaging, multidisciplinary evaluation, and long-term follow-up are crucial for successful management.

Our study highlights the complementary diagnostic value of p53 and Smad4 IHC relative to molecular testing in PDAC, especially when tissue is limited, as commonly encountered in FNB specimens. The newly established Smad4 IHC classification system, which integrates an intermediate expression category into the conventional two-tier framework, demonstrates superior clinical utility and enhances predictive accuracy for SMAD4 genomic alterations.

The mutational patterns affecting homologous recombination repair differ across gynecologic and breast cancers. Further research into cancer-specific HRD mechanisms is warranted.

We conducted a single-center retrospective study of 69 patients treated with Tisagenlecleucel, to evaluate the prognostic impact of TP53 alterations (TP53Alt), including mutations and/or deletions...These findings identify TP53 alterations as a strong adverse prognostic factor in patients with r/r B-ALL treated with CAR-T therapy. Screening for TP53Alt may guide risk-adapted strategies, including early consolidation with hematopoietic stem cell transplantation or alternative therapies.

This study offers a comprehensive molecular characterization of AC, comparing distinct oncogenic pathway signatures between primary and metastatic disease. The identification of pathway-specific alterations offers valuable insights into the molecular heterogeneity of AC and highlights opportunities for pathway-targeted therapies. These findings emphasize the importance of integrative molecular profiling to advance precision oncology and improve outcomes for patients with this rare malignancy.

These results demonstrate that LLQ-45 activates the antitumor function of p53 Y220C via covalent modification, thereby suppressing tumor cell growth. This study provides a framework for targeting neomorphic pockets and advances targeted cancer therapies.

Fusion transcript analysis identified 91 recurrent fusions, including novel partners with ERBB2, MED1, and CDK12, suggesting the possibility of unique molecular events. Interpretation and conclusions This study demonstrates that Indian breast cancer patients exhibit molecular subtypes and actionable mutations comparable to Caucasian cohorts.