In younger, fit patients with acute myeloid leukemia (AML), intensive chemotherapy (IC) followed by consolidation or allogeneic hematopoietic stem cell transplantation (HSCT) is the standard approach. The authors performed a systematic review and meta-analysis to evaluate younger patients with AML treated with hypomethylating agents (HMA) plus venetoclax.

The patient was a 7-year-old boy admitted with facial edema. Ultrasound indicated moderate pericardial effusion and pleural effusion. Contrast-enhanced chest computed tomography showed indistinct mediastinal structures with mild-to-moderate enhancement, suggestive of a mediastinal space-occupying lesion. Further evaluation with whole-body PET-CT, pathological biopsy of the mediastinal lesion, cytological examination of pleural and pericardial effusions, and immunohistochemistry led to the final diagnosis of isolated myeloid sarcoma. Pathological examination is the gold standard for clinical diagnosis; however, limited sampling sites can result in missed or incorrect diagnoses. Multiple and multi-site sampling should be undertaken according to the clinical context, combined with flow cytometry and immunohistochemistry to assist diagnosis and reduce missed diagnoses and misdiagnoses.

Hepatic metastases are a leading cause of mortality in gastrointestinal cancers, often exacerbated by the limited efficacy of conventional chemotherapeutics. Biobran/MGN-3, a rice bran-derived arabinoxylan, has shown promise in sensitizing cancer cells to paclitaxel.

This study is aimed at distinguishing the phenotypes of low-grade gliomas based on the P53 signaling pathway gene set, revealing the transcriptomic changes in different phenotypes, screening phenotype-related feature genes, constructing a TP53 score, quantitatively describing TP53-related phenotypes, and predicting the response of glioma patients to chemotherapy.

To develop a deep learning (DL)-based automated segmentation model for rectal cancer on T2-weighted (T2W) magnetic resonance (MR) images.

There is a lack of consensus and data validating lower cell counts for sample adequacy of thyroid fine-needle aspiration (FNA). We investigated less stringent adequacy thresholds under the Bethesda System for Reporting Thyroid Cytopathology (TBSRTC) and evaluated malignancy risks for "nondiagnostic" nodules by ultrasound features.

N7-methylguanosine (m7G) is an important RNA modification involved in the regulation of gene expression during transcription. While its roles in mRNAs and tRNAs are increasingly understood, the distribution and function of m7G in long non-coding RNAs (lncRNAs), particularly in oral squamous cell carcinoma (OSCC), remain poorly understood. This study aimed to systematically characterize the m7G methylation landscape of lncRNAs in OSCC and investigate the oncogenic function and regulatory mechanism of the m7G-modified lncRNA DPY19L1P1.

Developing therapy resistance and exhibiting high invasiveness are significant challenges in treating aggressive cancers, such as glioblastoma, where intercellular communication plays a crucial role in cellular organization, survival, and resistance to treatment. Tunneling nanotubes (TNTs), nanometer-sized membranous channels that connect distant cells, have emerged as an efficient form of intercellular communication that may enable cancer cells to evade therapeutic interventions.

Breast cancer is the most prevalent malignant tumor among women worldwide. Its progression is driven, in part, by mitochondrial metabolic dysregulation, which can also contribute to therapeutic resistance. Although targeting mitochondrial metabolism offers new opportunities for treatment, significant therapeutic challenges remain. These include metabolic heterogeneity among subtypes and individual patients, drug resistance arising from metabolic plasticity, and suboptimal clinical translation of metabolic therapies. This review systematically synthesizes the mitochondrial metabolic mechanisms underlying different breast cancer subtypes, emphasizing the spatial network regulatory functions of mitochondrial metabolism. It further critically evaluates combined therapeutic strategies targeting metabolic vulnerabilities. By integrating current research limitations with emerging breakthroughs, we outline novel therapeutic frameworks to advance the development of precision medicine approaches focused on mitochondrial metabolism.

Acute myeloid leukemia (AML) is an aggressive and molecularly diverse hematologic malignancy with unfavorable clinical outcomes and limited options for targeted therapy. This study investigated whether polypyrimidine tract-binding protein 1 (PTBP1), an RNA-binding protein (RBP), affects AML progression by binding to WNK lysine-deficient protein kinase 1 (WNK1).

Centromere protein A (CENPA) is a histone H3 variant essential for centromere function and has been implicated in tumorigenesis in several cancers. However, its clinical significance and biological role in endometrial cancer (EC) remain poorly characterized. This study aimed to elucidate the oncogenic function and underlying mechanisms of CENPA in EC progression.

Collagen type XI alpha 1 (COL11A1) is overexpressed in pancreatic cancer and is often associated with poor survival, chemoresistance, and tumor recurrence. However, the role of COL11A1 in pancreatic cancer remains poorly understood.

Gastric cancer (GC) is among the most frequently diagnosed malignancies worldwide. Identifying novel therapeutic targets is of great significance.

Thyroid collision tumors (TCTs) are rare thyroid malignancies characterized by the coexistence of distinct tumor types. We investigated the histopathology, immunohistochemistry, and gene mutations to comprehensively characterize the heterogeneity of TCTs.

Melanoma, an aggressive cancer with a poor prognosis, is difficult for early diagnosis, and there are limited drug treatments. Biologically active molecules, especially polyphenols and flavonoids, have a great therapeutic potential; however, their applications are limited by low aqueous solubility and bioavailability.

Multiple myeloma (MM) is a malignancy of plasma cells whose excessive immunoglobulin production elevates reactive oxygen species (ROS), promoting pathogenesis. Active compounds from Traditional Chinese Medicine, such as celastrol, can exert antitumour effects by further increasing ROS levels to toxic levels, thereby inducing apoptosis. Our previous study has demonstrated that pyridoxine-5'-phosphate oxidase (PNPO) is the specific target of celastrol. In this study, we discovered that PNPO, a key enzyme involved in vitamin B6 coenzyme metabolism, is highly expressed in various cancers, including MM. Increased PNPO levels correlated with MM disease progression, promoting cell proliferation and inducing osteoclast differentiation via exosomes. Concurrently, through a structure-based virtual screening workflow targeting critical PNPO residues (R95 and K117), we identified Hetrombopag as a potential PNPO inhibitor. Hetrombopag simultaneously inhibited MM cell proliferation and osteoclast differentiation. Preliminary data from clinical trials also supported the idea that hetrombopag treatment can prolong survival in MM patients. Our research highlights the significant role of PNPO in MM progression and suggests hetrombopag as a promising therapeutic option for MM treatment.

Prostate cancer comprises biologically distinct subtypes. Ki67 reflects tumour proliferation, while prostate-specific antigen immunostaining (PSA-IHC) indicates differentiation, with low PSA-IHC suggesting dedifferentiation. The prognostic role of these markers in de novo metastatic hormone-sensitive prostate cancer (mHSPC) remains unclear.

Although radical perineal prostatectomy is performed less frequently, it represents a minimally invasive open approach that avoids the retropubic space and extensive pelvic dissection. Its longterm oncologic and functional equivalence to standard retropubic prostatectomy has not been adequately evaluated in randomized cohorts.

Inflammatory myofibroblastic tumors (IMTs), originating from mesenchymal cells, are rare neoplasms with intermediate biological potential. Despite being predominantly benign, they can progress to locally aggressive disease and may recur over time. IMTs are predominantly seen in the pediatric population, making our case of IMT in an older adult even rarer. A 67-year-old female with a 42-pack-year smoking history presented with cough, fever, and progressively worsening exertional dyspnea. Imaging studies, including chest X-ray followed by chest computed tomography, identified a right lower lobe lung nodule without evidence of metastasis. Subsequent evaluation with robotic bronchoscopy and endobronchial ultrasound revealed densely cellular reactive lung tissue on lymph node biopsy. Ultimately, the patient underwent a robotic-assisted right lower lobectomy. Final pathology confirmed the diagnosis of an IMT. IMTs are characterized by the presence of spindle cells associated with dense monomorphic inflammatory cells. It has been found that IMT arises from chromosomal rearrangements that aberrantly activate various kinase signaling pathways. This understanding of the molecular mechanisms underlying IMT development has elucidated the neoplastic nature of the disease and has also been pivotal in distinguishing IMT from other inflammatory pseudotumors. Surgical resection remains the cornerstone of treatment, with targeted therapies offering promising results for unresectable or advanced cases. IMTs pose a multifaceted challenge in clinical practice due to their diverse clinical manifestations, histopathological variability, and unclear etiopathogenesis, underscoring the need for continued research and a multidisciplinary approach to optimize patient outcomes.

Neuroblastoma (NB) is the most common extracranial solid tumor among pediatric cancers and accounts for approximately 15% of childhood cancer-related deaths. Neurotrophic receptor tyrosine kinases (NTRKs) are genes that play critical roles in the development and function of the nervous system. Therefore, elucidating the role of NTRKs in NB is important for both understanding basic biological mechanisms and developing novel therapeutic approaches. Specifically, NTRK fusions are being investigated as potential biomarkers and therapeutic targets for targeted therapy strategies. The tumor-agnostic TRK inhibitors larotrectinib and entrectinib are used to treat advanced or metastatic solid tumors with NTRK gene fusions. Accordingly, this study aimed to investigate the clinical significance of NTRK1, NTRK2, and NTRK3 point mutations, gene fusions, and protein expression, and to assess the effectiveness of these in guiding targeted therapy decisions in NB.