TP53 (Tumor protein P53)

Upfront CTx only regimens used were classified into three groups to reflect disease treatment conventions: standard-dose, high-dose (intensified regimens of sufficient dosage to require stem cell support) and those including intraventricular methotrexate (IVT-MTX)...With outcomes established, clinical trials are now encouraged to focus on quality-of-life following different intensified approaches to identify the kindest curative strategies. Cancer Research UK, Children with Cancer UK, Children's Cancer North, Star for Harris, JGW Patterson Foundation, Little Hero and Blue Skye Thinking.

The 5‑index risk model demonstrated robust predictive ability in a real‑world setting, providing a reliable basis for personalized treatment decisions in Chinese DLBCL patients undergoing CAR‑T. Future work will focus on further optimizing the model and conducting multi‑regional validation.

Using B-ALL cell lines and patient-derived xenografts, we show that FATP2-expressing TP53-mutant B-ALL resistance to CAR-T is dependent on exogenous lipid uptake to fuel fatty acid oxidation (FAO) and cell survival, which can be pharmacologically targeted through inhibition of neutral lipolysis and CPT1. These findings identify FATP2-mediated fatty acid uptake and downstream FAO as a potential target to improve existing CAR-T efficacy in human B-ALL.

Nanopore sequencing enables rapid, accurate, multidimensional molecular classification of diagnostically intractable CNS tumors using routine FFPE and frozen tissue, achieving high diagnostic resolution in comparison with reference methods while drastically reducing turnaround time and cost, making precision neuropathology feasible beyond quaternary centers.

Herein, we report the first documented case of phenotypic conversion to SCLC in a patient with advanced pulmonary sarcomatoid carcinoma (PSC) who received pemetrexed, carboplatin, and camrelizumab only, with no targeted agents administered. TP53 and RET mutations may be implicated in this phenotypic transition. This case provides new insights into the biological mechanism underlying the evolution of PSC to SCLC.

Proteomics analysis revealed a strategic mechanism to resist TMZ-induced apoptosis by upregulating exosomal proteins associated with biogenesis, chemoresistance, and therapeutic adaption. This finding revealed a considerable TMZ resistance mechanism and provided a new inspiration for preventing exosome biogenesis to resensitise TMZ cytotoxicity towards GBM.

SBAs display genomic heterogeneity. The novel HGC stratifies these tumors based on homology to foregut or hindgut alterations and may be superior to anatomic location for characterizing pathology. Additional studies are needed to validate and further explore these findings.

Sonrotoclax demonstrated rapid, durable responses and manageable safety in heavily pretreated patients with R/R MCL, including high-risk subgroups, supporting its further clinical evaluation as an oral therapy for R/R MCL.

Despite histologic similarity, anogenital BCC demonstrates a distinct molecular profile, suggesting an alternative pathogenesis. Further genomic studies are warranted.

ZR-CHOP demonstrates encouraging activity and acceptable safety in molecularly selected high-risk DLBCL, particularly in the MCD-like subgroup. (ClinicalTrials.gov number, NCT05290337).

Clinically, elevated LFPM expression correlates with poorer survival, specifically in p53R175H-mutant cancers. Our work unveils a pivotal mechanism for mutant p53 stabilization and nominates the LFPM-p53R175H axis as a promising therapeutic target.

Reduced mTOR and p70S6K expression was associated with suppression of cell proliferation and survival signaling. Overall, these findings suggest that MSN-based delivery may enhance the anticancer effects of PTU, highlighting its potential as a therapeutic strategy in cancer research.