TP53 deletion

Integrating methylation markers SHOX2, HOXA9, Septin9, and RASSF1A exhibits significant diagnostic potential in pleural effusion lymphoma, especially within DLBCL subgroups. These markers could prove valuable in identifying high-risk subgroups and guiding clinical decision-making.

BAP1, MTAP, and NF2/merlin were retained by immunohistochemistry, but p53 was overexpressed by immunohistochemistry in the flat mesothelioma in situ, papillary mesothelioma in situ, and invasive mesothelioma. Almost all cases of mesothelioma in situ that have been previously described have a BAP1 mutation/deletion; this is the first example of mesothelioma in situ associated with a TP53 mutation, and suggests that staining for p53 may be useful in evaluating potential mesothelioma in situ cases.

Germline genetic testing based solely on MPC had a diagnostic yield comparable to guideline-based testing. MPC could be considered as an independent criterion for genetic testing to improve the identification of a hereditary cancer predisposition.

We herein report a case of the leukemic phase of chronic lymphocytic leukemia (CLL)-type lymphoma that abruptly developed 12 months after the initial diagnosis of autoimmune hemolytic anemia (AIHA), in which retrospective immunohistochemistry and next-generation sequencing (NGS) revealed that (1) lymphoma with a CLL-type immunophenotype underlay the development of secondary AIHA, (2) complete loss of TP53 function by double-hit TP53 abnormalities (TP53 deletion and mutation) was secondarily acquired, and (3) complete loss of TP53 function could have contributed to clinical manifestation of transformed lymphoma. Immunohistochemistry for LEF1 and an NGS analysis may help physicians precisely diagnose CLL-type lymphoproliferation-associated AIHA.

IgH cytogenetic abnormalities indicate aggressive disease and poorer survival in NDMM, especially when accompanied by other high-risk markers. ASCT may mitigate these adverse outcomes, supporting its role in individualized treatment strategies.

This is accompanied by significant reductions in IL-6, MIP-2, and VEGF levels, reprogramming the tumor microenvironment to support CD8 T cell infiltration. In summary, our study demonstrates that PRPK deletion suppresses solar UV-induced photocarcinogenesis by inhibiting PD-L1 expression and enhancing CD8 T cell infiltration, highlighting its potential as a therapeutic target for NMSC.

These Pik3ca-activated tumor cells were more sensitive to alpelisib, a p110α-selective inhibitor approved by the FDA for the treatment of some PIK3CA mutant cancers, compared to Pik3ca WT cells..

These findings suggest that a subset of cases diagnosed as B-PLL based on blood morphology may represent a variant of SMZL with prolymphocytic morphology. The excellent response to Rituximab further supports this hypothesis. Our study reinforces the need for reclassification of such cases within the spectrum of SMZL rather than a separate entity.

The prognosis of EO-CRC is a subject of controversy, with varying trends observed across different age groups at onset, as well as between genders and ethnicities. In this study, we aimed to uncover the potential mechanisms behind the continuous rise in EO-CRC incidence and to provide a basis for optimizing standardized screening and treatment strategies for EO-CRC through a comprehensive analysis of the differences between EO-CRC and LO-CRC.

Data suggest that TP53 patients benefit from treatment if they achieve CR within the first 2 cycles. Discontinuing VEN/AZA in low-risk MRD-negative patients does not appear to worsen overall survival, though long-term outcomes remain to be seen.

Moreover, EphA2 inhibitors dasatinib and ALW II-41-27 remarkably suppress the progression of tumors expressing PLEKHA1-TACC2 in vivo. Functionally, PLEKHA1-TACC2 fusion and Trp53 deletion significantly increases tumor incidence, tumor multiplicity, and mouse mortality in transgenic ESCC mouse model, which could be suppressed by regorafenib, a EphA2 inhibitor approved by FDA in solid tumors. Together, our data indicate that PLEKHA1-TACC2 fusion protein has oncogenic activities and serves as a promising prognosis marker and therapeutic target.