ObjectiveColorectal cancer (CRC) carries high morbidity and mortality worldwide. IFITM1 serves as a potential independent prognostic factor for CRC metastasis and advanced stages, partly through regulating the Wnt/β-catenin pathway. LncRNA AK093407 is upregulated in CRC and promotes cancer cell proliferation, but its regulatory mechanism remains unclear. This study aimed to investigate the biological function of LncRNA AK093407 in CRC progression and clarify its regulatory mechanism on IFITM1 and the Wnt/β-catenin signaling pathway.MethodsThis in vitro study included clinical tissue samples from 22 CRC patients and human CRC cell lines. Proteomic analysis was applied to screen potential downstream targets of AK093407. The expression levels of AK093407 and IFITM1 in clinical tissues and cell lines were detected by qRT-PCR. Lentiviral infection and siRNA transfection were used to establish overexpression and knockdown models. MTT, colony formation, transwell, wound healing, and flow cytometry assays were performed to assess cell proliferation, migration, invasion, and apoptosis. Western blotting was used to measure key proteins in the Wnt/β-catenin pathway. Subcellular fractionation and RIP assays were used to explore the molecular mechanism.ResultsLncRNA AK093407 and IFITM1 were both significantly highly expressed in CRC tissues and cells. Overexpression of AK093407 or IFITM1 markedly enhanced proliferation, migration, and invasion and inhibited apoptosis. Knockdown of IFITM1 reversed the oncogenic effects induced by AK093407 overexpression, while IFITM1 overexpression rescued the phenotypic changes caused by AK093407 silencing. Mechanistically, IFITM1 activated the Wnt/β-catenin pathway and directly interacted with β-catenin.ConclusionsLncRNA AK093407 promotes CRC malignant progression by upregulating IFITM1 and activating the Wnt/β-catenin signaling pathway, forming a novel AK093407-IFITM1-Wnt/β-catenin regulatory axis. These findings identify a potential diagnostic and therapeutic target for CRC, although further in vivo validation is warranted.

Hepatocellular carcinoma (HCC), the most common primary malignant tumour of the liver, is notorious for its high mortality rate.Alpinia officinarum Hance (A. officinarum) is a perennial medicinal herb used for the management of abdominal pain, vomiting, and gastrointestinal tumours, and is widely applied as a dietary intervention by the Li ethnic group in Hainan, China. Kaempferide, a bioactive flavonoid isolated from this herb, exhibits promising antitumor properties; however, its precise mechanism against HCC remains incompletely understood. In this study, we demonstrated that kaempferide could inhibit proliferation and migration of HCC cells, induce G0/G1 phase cell arrest and promote the accumulation of ROS, while suppressing xenograft tumour growth in nude mice. Further investigations revealed that kaempferide targeted BNIP3L and suppressed mitophagy, evidenced by elevated P62 levels and reduced LC3-II levels. In summary, kaempferide exerts anti-HCC effects by inhibiting mitophagy via the downregulation of BNIP3L, suggesting its potential role as a therapeutic candidate for HCC.

Apoptosis, as the predominant form of programmed cell death, plays a crucial role in maintaining tissue homeostasis. Apoptotic bodies (ABs), which are extracellular vesicles released during the terminal phase of apoptosis, were initially characterized as functionless cellular debris. However, they are now recognized for mediating intercellular communication via biomolecule delivery in both physiological and pathological states. Owing to their diverse biological properties, ABs have emerged as promising therapeutic candidates for treating a wide range of diseases, including cancer, cardiovascular and bone diseases, neurodegenerative disorders, diabetes, and infectious/inflammatory conditions, and have demonstrated potential in promoting tissue regeneration. Furthermore, ABs present in bodily fluids carry abundant disease-related information and offer a dynamic representation of patients' physiological states, rendering them valuable tools for diagnosis and prognosis. This review consolidates progress in ABs research, delineates their pathophysiological roles, and assesses challenges and opportunities for their clinical application.

Small cell carcinoma of esophagus (SCCE), uncommon and aggressive malignancy with a poor prognosis and limited therapeutic consensus, less than 1% of all oesophageal cancers, presents with symptoms of dysphagia and weight loss, leading to diagnosis through endoscopy and histopathological evaluation. This paper presents two case reports of SCCE. Case 1 involves a 70-year-old male with progressive dysphagia, revealing a lobulated mass in mid-esophagus diagnosed as SCCE. Imaging and biopsy confirmed the diagnosis, with positive markers for CAM5.2 and Chromogranin, managed through a multidisciplinary approach, with chemoradiotherapy initiated as primary treatment due to disease's aggressiveness and limited surgical benefit. Case 2 describes a 60-year-old male with multiple comorbidities, demonstrated rapid disease progression and systemic complications associated with SCCE. Current literature supports the use of chemoradiotherapy for locally advanced SCCE, although overall prognosis remains poor, an average survival of approximately 12 months. Further studies are warranted to establish optimal management strategies.

Cisplatin resistance in ovarian cancer, particularly in ovarian clear cell carcinoma, involves intricate mechanisms related to oxidative stress, deoxyribonucleic acid repair, and cell cycle. Resistance in ovarian clear cell carcinoma is associated with genes, such as pyruvate dehydrogenase kinase-2 and hepatocyte nuclear factor 1 beta, which enhance glycolysis and reduce reactive oxygen species that would normally facilitate cisplatin induced deoxyribonucleic acid damage. Additionally, nuclear factor erythroid 2-related factor-2 and superoxide dismutase-2 play pivotal roles in regulating reactive oxygen species levels, thereby safeguarding ovarian clear cell carcinoma cells from oxidative damage. The postsynaptic density protein 95/discs large/zona occludens-1 (PDZ)-binding motif-angiopoietin-like 4 nicotinamide adenine dinucleotide phosphate oxidase-2 axis plays a crucial role in modulating ferroptosis, presenting potential therapeutic targets. A deeper understanding of these mechanisms offers promising strategies to overcome cisplatin resistance, particularly in ovarian clear cell carcinoma. These insights could pave the way for targetted therapies aimed at improving ovarian cancer outcomes, especially for ovarian clear cell carcinoma subtypes.

BACKGROUND Neuroendocrine breast tumors represent an uncommon subtype of breast cancer, accounting for less than 1% of all breast malignancies and fewer than 0.1% of all neuroendocrine tumors. Their histological and immunophenotypic features closely resemble neuroendocrine neoplasms of other organs, and diagnosis requires careful exclusion of extramammary primaries. CASE REPORT We present the case of a 75-year-old woman diagnosed with primary small cell neuroendocrine breast carcinoma following an incidental detection of a right breast mass. She underwent a simple mastectomy with sentinel lymph node biopsy, followed by adjuvant carboplatin-etoposide chemotherapy. One year later, she developed a solitary hepatic metastasis, which was successfully treated with metastasectomy and repeat adjuvant chemotherapy. Despite initial responses, subsequent surveillance imaging demonstrated progressive hepatic metastatic disease. This case underscores the aggressive clinical behavior and diagnostic challenges associated with high-grade neuroendocrine breast tumors. The 2019 WHO classification highlights the importance of distinguishing neuroendocrine carcinoma subtypes due to differing prognostic and therapeutic implications. Although multiple treatment modalities exist, outcomes remain poor in high-grade or advanced disease. CONCLUSIONS Neuroendocrine breast tumors remain insufficiently understood because of their rarity. This report highlights the importance of thorough histopathological evaluation, meticulous exclusion of extramammary primaries, and close longitudinal follow-up. Additional research is needed to establish standardized diagnostic and therapeutic guidelines.

Recently, a standardized reporting system for soft tissue cytopathology was introduced. The aim is to evaluate the diagnostic utility of FNA in the diagnosis of bone and soft tissue lesions by comparing the cytological and histopathological diagnoses in a large group of cases and to determine the risk of malignancy (ROM) rates according to the World Health Organization (WHO) Reporting System for Soft Tissue Cytopathology.

The pathology databases were searched for cases that underwent FNA for bone and soft tissue lesions between 2020 and 2023. Only cases that had available histological follow-up were included. The FNAs are categorized as nondiagnostic (ND), benign, atypical, soft tissue neoplasm of uncertain malignant potential (STNUMP), suspicious for malignancy (SM), malignant (primary/metastatic) according to WHO Reporting System for Soft Tissue Cytopathology. The risk of malignancy (ROM) was calculated for each group.

The study consisted of 427 cases, including 30 ND (7%), 322 benign (75.4%), 19 atypical (4.5%), 7 STNUMP (1.6%), 5 SM (1.2%), and 44 malignant (10.3%). The ROM rates were 16.6%, 1.8%, 57.9%, 28.5%, 80%, and 100% for the groups: ND, benign, atypical, STNUMP, SM, and malignant, respectively. The diagnostic accuracy, sensitivity, and specificity of FNA in all bone and soft tissue lesions were 98.6%, 92.3%, and 100%, respectively.

We conclude that FNA is a simple and accurate technique for assessment of bone and soft tissue lesions. The WHO Soft Tissue Cytopathology Reporting System could improve communication among pathologists and clinicians, simplify clinical management of patients, and support further research in soft tissue cytology.

Ribeiro and colleagues offer timely evidence that large language models can make oncology imaging reports more accessible to radiologists and patient and public involvement representatives. Their findings also highlight an important distinction between a report that is easier to read and one that patients understand accurately. As the authors acknowledge, the patient-facing assessment included three representatives with previous experience in oncology imaging research and was restricted to reports that had received high factual-correctness scores from radiologists. This approach was suitable for comparing presentation preferences, although it provides limited evidence about comprehension in routine practice, particularly for lower-scoring or clinically ambiguous outputs. Further studies could examine unselected reports in patients with varied health and digital literacy, using outcomes such as comprehension, recognition of uncertainty, emotional response, and intended action. In future adequately powered studies, accounting for ratings clustered by reader and report may provide more precise estimates. Such evidence would help clarify the role of AI-generated explanations in patient-facing oncology care.

Myelofibrosis (MF) is a heterogeneous myeloproliferative neoplasm characterized by splenomegaly, constitutional symptoms, cytopenias, and risk of leukemic transformation. As therapeutic options expand, treatment discontinuation and sequencing are increasingly recognized as clinically relevant determinants of patient outcomes.

A literature search was performed using PubMed/MEDLINE and major hematology conference proceedings (ASH and EHA), covering publications from January 2010 through February 2026. This review discusses mutation-informed risk stratification, current and emerging JAK inhibitor treatment sequencing strategies, and practical approaches to treatment discontinuation and therapeutic transition in MF.

Optimizing outcomes in MF increasingly requires proactive transition management rather than reactive treatment interruption. Early identification of treatment failure, phenotype-guided therapeutic sequencing, and integration of molecular risk assessment may improve long-term disease management and could contribute to better clinical outcomes, although prospective confirmation remains necessary.

Gastric cancer (GC) is a very aggressive cancer with a high potential for metastasis. A naturally occurring flavonoid, luteolin (Lut) has metabolic regulation and anti-cancer properties. This work investigates whether Lut modulates glucose metabolism and targets AKR1B1 to prevent the epithelial-mesenchymal transition (EMT) in GC. Lut was used to treat human GC cell lines that were grown in both normal and high-glucose environments. Western blotting and qPCR were used to assess the expression levels of EMT markers and AKR1B1. The CCK-8 assay, the scratch assay, and the Transwell assay were used to measure cell movement, invasion, and proliferation, respectively. Metabolic flux analysis was used to measure fructose and lactate generation in order to assess glycolytic activity. We carried out AKR1B1 overexpression and knockdown experiments to elucidate the functional involvement of AKR1B1 in the action of Lut. In order to fully assess the anticancer effects of Lut and its underlying mechanisms, a high-glucose paradigm in nude mice was developed for in vivo validation. AKR1B1 expression was markedly elevated in GC cells under high-glucose circumstances, and this was accompanied by increased glycolytic activity. At the same time, the cells showed signs of EMT, including enhanced migratory and invasion capacities. Subsequent research showed that Lut therapy substantially alleviated anomalies in glucose metabolism by drastically suppressing AKR1B1 expression, downregulating important glycolytic enzymes, and reducing the generation of fructose and lactate. Additionally, by boosting E-cadherin expression, lowering vimentin and N-cadherin levels, and preventing cell migration and invasion, luteolin dramatically corrected high-glucose-induced EMT. The inhibitory effects of luteolin on glycolysis and EMT were largely offset by AKR1B1 overexpression, according to functional experiments; on the other hand, inhibition of AKR1B1 considerably reduces AKT pathway activation, which suppresses the malignant phenotype of gastric cancer cells. Together, these findings show how important AKR1B1 is to this regulatory axis. According to these results, luteolin inhibits high-glucose-induced metabolic reprogramming and EMT in gastric cancer cells via acting on AKR1B1, which lowers the cells' capacity for metastasis. Lut may reduce the metabolic dysregulation brought on by hyperglycemia by blocking AKR1B1, which in turn prevents GC cells from undergoing the epithelial-mesenchymal transition. This discovery highlights Lut as a potential metabolic therapeutic drug and offers mechanistic insight into the evolution of gastric cancer caused by hyperglycemia.