Acute myeloid leukemia (AML) is a highly heterogeneous malignant hematological neoplasm. Although standard diagnostic procedures have been established, traditional methods still face limitations with regard to efficiency, accuracy, and standardization. In recent years, artificial intelligence (AI) has demonstrated notable advantages in medical image analysis, flow cytometry interpretation, and genetic data modeling, offering new approaches for adjunctive diagnosis of AML. This review systematically summarizes recent research advances in adjunctive diagnosis of AML, categorizing current AI-based approaches based on data modality into three groups: blood smear image analysis, flow cytometry data interpretation, and genetic data modeling. We focus on the application strategies, diagnostic performance, and limitations of these approaches. Studies have shown that AI not only enhances diagnostic efficiency and reduces subjective bias, but also holds promise in identifying novel biomarkers. Nevertheless, current models still suffer from limited generalizability and insufficient clinical interpretability. Future efforts should prioritize data standardization, improve model transparency, and facilitate the seamless integration of AI systems into clinical workflows to support precision diagnosis and treatment of AML.

We have little knowledge about the synchronous occurrence of gastrointestinal stromal tumors (GISTs) and other types of histologic tumors. This association is very rare.

We describe a case of synchronous stromal tumor and adenocarcinoma of the left side colonic localization. Immunohistochemistry identified c-Kit expression. The discovery of colonic adenocarcinoma was on operative specimen after histologic examination. The patient underwent left oncologic colectomy with stoma. Follow-up at one year postoperatively did not detect tumor recurrence.

Clinical implications of the association between these two neoplasms are not clearly described. Treatment depends on the the most aggressive histologic type or obviously highest stage. Knowledge of the genetic data of this association offers opportunity of treatment with the new targeted-therapy molecules. Surgical resection, may remain the curative treatment.

Synchronous adenocarcinoma and GIST has been more commonly described in the stomach.  The pathogeneses of tumorigenesis may not be the same for the two tumors. More studies seem be necessary to clarify a potential role of different genes in the development of adenocarcinomas. And therefore, above all their therapeutic implications.

Early immune reconstitution following autologous hematopoietic stem cell transplantation (autoHSCT) is associated with improved outcome in various cancers. Natural killer (NK) cells are the first lymphocyte subset to recover post-autoHSCT and play a crucial role in antitumor immunity. In this study, we have performed an in-depth characterization of NK cells in adult patients with different hematological malignancies. Our results revealed that, immediately after autoHSCT, NK cells transiently acquired a decidual-like phenotype, displayed a more immature and activated state, and exhibited an upregulation of inhibitory receptors and a downregulation of activating receptors. This decidual-like and activated phenotype was characterized by increased expression of CD56, CD9, CD49a, CD151, CD38 and HLA-DR. Additionally, we assessed plasma cytokine levels and identified associations between cytokine concentrations and NK cell phenotypic changes. In vitro experiments suggested that these phenotype alterations could modulate NK cell function. Finally, in patients with non-Hodgkin lymphoma (NHL), we observed a correlation between NK cell maturation status and progression-free survival. Collectively, our findings provide valuable insights into NK cell dynamics during immune reconstitution following autoHSCT and may inform of strategies for improving patients' management.

Pineal parenchymal tumors are rare central nervous system neoplasms, accounting for less than 1 % of all CNS tumors. We conducted a bibliometric analysis of the 100 most cited articles on pineal parenchymal tumors to identify research trends and highlight influential contributions. Tumor types analyzed included pineocytoma, pineal parenchymal tumor of intermediate differentiation (PPTID), pineoblastoma, and papillary tumor of the pineal region (PTPR), along with the recently classified desmoplastic myxoid tumor, SMARCB1-mutant. To our knowledge, this is the first bibliometric analysis dedicated to pineal parenchymal tumors.

Articles were identified through the Web of Science database without time restriction, screened by title, keyword, and abstract. Tumor categorization followed the WHO 5th edition for CNS tumors. Articles discussing non-parenchymal pineal region tumors were excluded. Citation count determined article selection. Data collected included publication year, authorship, journal source, study category, pathology focus, and article type. Data collection and analysis was performed using Microsoft Excel and Google Sheets.

A total of 573 articles were retrieved; the top 100 were analyzed, totaling 3845 citations. These articles were published in 42 journals from 16 countries and 74 institutions. The oldest article was published in 1970 and the most recent in 2021. Acta Neuropathologica contributed the most publications (14). The United States accounted for the highest number of articles (34) and citations (1,326). Histopathology was the most studied category (36 %), and case reports and series were the predominant article types. The papillary tumor of the pineal region was the most frequently discussed pathology.

This bibliometric analysis reveals a dominance of histopathological studies and reveals critical gaps in clinical studies, surgical management, and patient outcomes. Targeted future research in these areas is needed to improve diagnosis, management, and patient care.

While RTP4 is known to regulate odorant receptor trafficking, its role in colorectal cancer (CRC) remains unclear. This study investigates the clinical relevance and functional mechanisms of RTP4 in CRC. Comprehensive analyses revealed significant downregulation of RTP4 expression in CRC tissues, correlating with poor patient prognosis. RTP4 expression showed strong associations with immune-related genes, biological processes and anti-tumour immune cell infiltration. Mechanistic studies demonstrated that RTP4 upregulates MHC-I expression, which enhances CD8⁺ T cell recruitment and strengthens anti-tumour immunity in both cellular and animal models. Furthermore, RTP4 overexpression markedly improved the efficacy of immune checkpoint blockade therapy. All in all, our findings establish RTP4 as a dual-functional biomarker for prognosis prediction and a potential target to enhance immunotherapy responsiveness in CRC.

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide, with limited effective therapies and poor prognosis. Although sorafenib and lenvatinib are approved for advanced HCC, their clinical efficacy is often compromised by drug resistance and adverse effects. Bruceine D (BD) has shown antitumor potential in several cancers, but its mechanisms in HCC remain poorly defined.

The effects of BD on HCC cell proliferation, apoptosis, and migration were assessed by MTT, colony formation, EdU incorporation, flow cytometry, wound healing, and transwell assays. Differentially expressed genes were identified by RNA sequencing and validated by RT-qPCR, with particular focus on Hsp70 family members. Protein expression and interactions were analyzed using Western blotting, co-immunoprecipitation (Co-IP), and Cellular Thermal Shift Assay (CETSA). Molecular docking was performed to predict BD binding sites on Hsp70. The antitumor efficacy and safety of BD were further evaluated in BALB/c nude mouse xenograft models.

BD significantly inhibited HCC cell growth, induced apoptosis, and suppressed migration in a dose-dependent manner in vitro study. Transcriptomic profiling revealed downregulation of Hsp70 family members (HspA1A, HspA1B, HspA8), confirmed by RT-qPCR and Western blotting. Molecular docking suggested hydrogen bond interactions of BD with multiple residues in the Hsp70 domain. Co-IP assays demonstrated that Hsp70 binds STAT3, and BD disrupted this interaction, resulting in reduced STAT3 phosphorylation and suppression of downstream effectors (MCL-1, survivin). CETSA proved BD protected HSP70 at various temperature gradients in HCC cells. In vivo, BD markedly reduced tumor volume without affecting body weight or causing histopathological abnormalities in major organs.

This study demonstrates that BD exerts potent antitumor effects against HCC by inhibiting proliferation, inducing apoptosis, and suppressing migration, primarily through disruption of the Hsp70/STAT3 signaling axis. With its favorable safety profile, BD represents a promising candidate for further development as a therapeutic agent in HCC.

This study aims to analyze the expression patterns, clinical relevance, and biological functions of SLC16A4 across multiple cancer types, with a focus on liver hepatocellular carcinoma (LIHC) in silico analysis.

We conducted a pan-cancer analysis using data from TCGA and GTEx databases to evaluate SLC16A4 expression in various cancer types. The LIHC cohort was stratified based on SLC16A4 expression levels for further clinicopathological and survival analysis. Functional enrichment, immune infiltration, and RNA modification correlations were explored using bioinformatics tools, including GO, KEGG, GSEA, and ssGSEA.

In LIHC, SLC16A4 was markedly downregulated in tumor tissues compared to normal tissues, and its low expression correlated with advanced pathologic stages and poor histologic grades. Survival analysis revealed that high SLC16A4 expression was associated with improved overall survival and disease-specific survival in LIHC, with multivariate analysis confirming its role as an independent prognostic factor. Functional enrichment analysis linked SLC16A4 to key metabolic pathways. In addition, SLC16A4 expression was correlated with RNA modification genes and mismatch repair genes, suggesting its involvement in post-transcriptional regulation and genomic stability. Immune infiltration analysis revealed that high SLC16A4 expression was associated with increased infiltration of immune cells and regulating immune-related molecules, indicating its potential role in modulating the tumor immune microenvironment.

SLC16A4 exhibits cancer-specific expression patterns and plays a multifaceted role in tumor progression, metabolism, and immune regulation. Its potential as a diagnostic and prognostic biomarker, particularly in LIHC, warrants further investigation. These findings highlight SLC16A4 as a promising target for future cancer research and therapy.

We read with interest the meta-analysis by Chen et al. on postoperative acute kidney injury (AKI) following cytoreductive surgery with hyperthermic intraperitoneal chemotherapy (CRS + HIPEC) published in World Journal of Surgical Oncology. In response, we share our institutional experience using a standardized perioperative protocol incorporating goal-directed fluid therapy (GDFT) and epidural analgesia. This approach was intended to support hemodynamic stability and provide effective analgesia. Among 92 patients undergoing CRS + HIPEC, the incidence of postoperative AKI was 2.2%, which was lower than the rates reported in prior studies. However, our cohort had fewer comorbidities and lower perioperative risk profiles than those included in the meta-analysis, representing an important limitation when interpreting these findings. Taken together, our experience suggests that perioperative strategies such as GDFT and epidural analgesia, combined with favorable baseline characteristics, may contribute to reduced AKI risk in this high-risk population. Larger prospective multicenter studies are warranted to validate these observations.

Fms-like tyrosine kinase 3 (FLT3), a class III receptor tyrosine kinase essential for hematopoiesis, is a well-established oncogenic driver in acute myeloid leukemia (AML). Canonical internal tandem duplications (ITD) and tyrosine kinase domain (TKD) mutations inform prognosis and guide targeted therapy. Recent evidence highlights FLT3 as a critical oncogenic hub in acute lymphoblastic leukemia (ALL), where its alterations extend beyond ITD/TKD mutations to include non-canonical mutations with only partially explored functional implications. Moreover, recently discovered regulatory mechanisms, mostly acting on the FLT3 locus, drive FLT3 overexpression in ALL, including transcriptional regulation by rearranged ZNF384, epigenetic modifications, novel circular-RNA URAD::FLT3 fusions, and 13q12.2 deletions leading to enhancer hijacking and topologically associated domain (TAD)-boundary disruptions. The impact of these alterations on leukemogenesis and the possibility to target them in ALL subtypes is discussed here. Data from the Functional Omics Resource of Acute Lymphoblastic Leukemia (FORALL) across B- and T-ALL cell line subtypes drug screening, and from preclinical and clinical evidence reveals a variable efficacy in FLT3-mutated and FLT3-overexpressing ALL subtypes, supporting a molecularly guided treatment approach. Building on the success of FLT3 inhibitors in mutated AML and in light of the emerging results in patients lacking FLT3-ITD and in FLT3-like AML cases, presenting with a gene expression pattern similar to FLT3-mutated ones despite the absence of mutations, we discuss their potential in ALL and we consider novel therapeutic strategies, including new FLT3 inhibitors, antibody-based approaches, FLT3 CAR-T therapy, and synergistic drug combinations, such as FLT3 and BCL2 inhibition. These new insights reviewed here may redefine FLT3 as a pan-leukemic target, with ALL-specific activation mechanisms offering unique therapeutic windows. The implementation of FLT3 expression profiling and full-coding mutation screening in ALL (and in AML) diagnostics could unlock precision medicine approaches. By bridging the AML experience with ALL innovations, this review outlines a roadmap for FLT3-targeted therapies and combination strategies, underscoring the urgency of biomarker-driven clinical trials to optimize FLT3-directed interventions in acute leukemias.

Primary hepatic angiosarcoma (PHA) is an extremely rare malignant tumor originating from vascular endothelial cells, accounting for only 0.1-2% of primary liver malignancies. Kasabach-Merritt syndrome (KMS) is a rare complication characterized by thrombocytopenia, coagulation dysfunction, and microangiopathic hemolytic anemia, seldom reported in adult patients with hepatic angiosarcoma.

We describe a 74-year-old female with a history of vinyl chloride exposure who presented with acute right upper quadrant pain, shock, and multiple ecchymoses, scattered petechiae. Laboratory tests revealed thrombocytopenia and coagulation abnormalities. Imaging demonstrated a large ruptured hepatic mass with hemoperitoneum. The patient underwent emergency right hemihepatectomy, with pathology confirming hepatic angiosarcoma. Postoperatively, the patient's coagulation parameters normalized, confirming resolution of KMS. No recurrence was noted at the 9-month follow-up.

Acute rupture of hepatic angiosarcoma with KMS is a life-threatening condition requiring rapid multidisciplinary intervention. Emergency hepatectomy not only controlled the hemorrhage but also removed the lesion causing KMS. Clinicians should maintain a high index of suspicion for hepatic angiosarcoma in patients presenting with spontaneous hepatic hemorrhage and coagulation abnormalities.