Objective Chemotherapy-induced thrombocytopenia (CIT) is a dose-limiting toxicity that can necessitate chemotherapy delays or dose reductions. This review examines evidence that CIT involves injury to both megakaryocytes (MKs) and the bone marrow microenvironment (BMME) and considers the implications for thrombopoietin receptor agonist (TPO-RA) therapy. Methods PubMed was searched for English-language literature without a publication-date restriction and was comprehensively updated through August 10, 2026. Evidence concerning CIT mechanisms and the mechanistic effects of TPO-RAs was integrated through a predefined narrative thematic framework, with explicit consideration of the directness of evidence for human CIT. Results Available studies suggest that TPO-RAs may have effects beyond platelet production, although evidence for vascular, metabolic, and immune microenvironmental effects derives largely from non-CIT or preclinical settings. Persistent rather than nadir CIT, lower endogenous thrombopoietin, and the absence of marrow infiltration, prior pelvic irradiation, or temozolomide exposure may enrich for response. A 2026 phase 3 trial directly demonstrated that romiplostim reduced CIT-induced chemotherapy dose modifications in persistent CIT, but biomarker-guided selection remains to be validated. Conclusion The “seed and soil” model organizes previously published evidence and should be regarded as hypothesis-generating in human CIT. Prospective studies are needed before microenvironment-directed combinations or CIT-specific biomarker thresholds can be recommended.

Objective: To evaluate the prognostic value of TP53 mutations in patients with diffuse large B-cell lymphoma (DLBCL). Methods: We retrospectively analyzed the clinical data and gene sequencing results of 253 newly diagnosed DLBCL. Survival and correlation analyses were performed. Results: We further revealed significant prognostic heterogeneity among different TP53 hotspot mutations, with mutations at codons G245, R175, R273, and R282 indicating a poorer prognosis. Within the DBD, mutations in exons 5, 7, and 8 were associated with poorer PFS, while mutations in exons 5, 6, and 8 were linked to poorer OS. Additionally, mutations in the Loop-L2, Loop-L3, and LSH motifs within the DBD were all significantly associated with unfavorable PFS and OS. Notably, in the cohort treated with R-CHOP plus novel agents (R-CHOP+X), there were no significant differences in response rates or survival between TP53-mut and TP53-wt patients, suggesting this combination may overcome the adverse prognosis associated with TP53 mutations. Conclusion: TP53 mutation is a crucial adverse prognostic factor in DLBCL. Given the significant prognostic heterogeneity among different TP53 hotspot mutations, a more refined risk stratification based on the TP53 mutational profile is warranted in clinical practice. For patients with high-risk mutations, combining R-CHOP with targeted therapies and exploring novel combination strategies targeting specific pathways are recommended. In contrast, standard R-CHOP may remain an appropriate option for patients with low-risk mutations. Future prospective trials are needed to validate the efficacy of R-CHOP combined with targeted agents in TP53-mutated DLBCL to optimize treatment strategies and improve patient outcomes.