Adenocarcinomas originating at stoma sites are extremely rare. While many cases are associated with colorectal cancer or inflammatory bowel disease, instances without such predisposing factors are even rarer.

A 39-year-old man with a history of Hirschsprung's disease presented with tumor growth at his permanent stoma site, which had been established 27 years earlier. A biopsy confirmed adenocarcinoma. Preoperative imaging, including CT, MRI, and PET-CT, showed no evidence of lymph node or distant metastasis. Immunohistochemical staining (CK7+, CK20+, CDX2+) was consistent with a primary tumor of the small bowel. Based on the preoperative diagnosis of localized disease and the clinical goal of preserving intestinal function, local resection was performed with negative margins. Histopathological examination confirmed a primary ileal adenocarcinoma. The patient remains recurrence-free 30 months postoperatively without adjuvant chemotherapy.

This report presents a rare case of stoma-site adenocarcinoma arising 27 years after surgery for Hirschsprung's disease. In long-term survivors of pediatric stoma surgery, chronic physical and chemical irritation may contribute to malignancy even in the absence of a predisposing malignant background. Malignancy at the stoma site can be discovered by patients through self-examination; therefore, both patients and clinicians must recognize the potential risk for early detection.

It is estimated that 5%-10% of patients who develop breast cancer have a causative inherited pathogenic or likely pathogenic variant (P/LP variant). In 2020, the UK National Test Directory published criteria for mainstream genetic testing for breast cancer patients (R208) and, subsequently, eligibility criteria to determine which patients are eligible for gene testing and PARP inhibitor treatment (R444.1).

Using the clearly defined criteria from NHS genomics, eligibility for testing under R208/R444.1 was determined for all patients diagnosed with breast cancer between March 2021 and March 2025. Eligible patients were offered genetic testing. Incidence of P/LP variants and impact on treatment were examined.

A total of 1812 patients had new DCIS/invasive breast cancer diagnoses, 255 were eligible for testing and 196 consented. Of these, 28 patients (14.3%) had a P/LP variant. Eight of these patients were eligible only using family history criteria. Twenty-one patients were eligible for breast conservation surgery. Preoperative genetic results were available for 13: eight patients opted for bilateral mastectomy rather than breast conservation. Where results were available postoperatively, three of eight patients who had breast conservation are planning bilateral risk reducing surgery. Three women newly diagnosed with a BRCA variant received a PARP inhibitor. Eligibility assessment for testing was time-consuming for trained clinicians.

14.3% of patients eligible and tested for a breast cancer-related hereditary P/LP variant were positive, which aligns with the expected number predicted by Genomics England. Family history scoring is an important element. Positive results were associated with changes in surgical decision-making for 14 women and enabled 3 patients to receive a PARP inhibitor.

Radiation therapy (RT) is a mainstay of treatment for a myriad of cancers, often utilized for tumors that are unable to be resected, as well as an adjunct to surgery and chemotherapy. Unfortunately, many cancers are resistant to RT-induced damage and subsequent cell death. This has spurred the pursuit of novel radiation sensitizers that could potentiate the effects of this widely used and important treatment modality. Since its discovery as a regulated cell death mechanism in 2012, ferroptosis has been studied for its connection to cancer and other known oxidative pathways. With this, the interplay between RT and ferroptosis in cancer has recently begun to be explored. Radiation increases reactive oxygen species (ROS), facilitates lipid peroxidation, and releases free ferrous iron, all of which directly impact the ferroptotic pathway. In conjunction, RT has been shown to induce the expression of ferroptosis-related molecules (e.g., SLC7A11, GPX4) through the P62-KEAP1-NRF2 pathway, thereby preventing cell death via ferroptosis. The use of ferroptosis inducers (FINs) to block these antioxidant mechanisms is a promising area of study as pharmacological radiosensitizers to improve the efficacy of RT and patient outcomes. In this comprehensive narrative review, the molecular connections between ferroptosis, cancer, and radiation will be discussed, the preponderance of existing literature investigating the potential of FINs as radiosensitizers will be presented, and possible areas of future study will be offered.

Driven by changes in lifestyle and environmental factors, the global incidence of cancer is steadily increasing, which has established it as a leading cause of mortality worldwide. The current paradigm for cancer diagnosis and treatment relies on conventional methods, such as imaging, endoscopy, and tissue biopsy, which present significant limitations regarding sensitivity in early screening, diagnostic specificity, and personalized treatment. Consequently, the development of more efficient and accurate technologies remains a major objective in modern oncology research, and artificial intelligence (AI) has emerged as a particularly promising solution. Through machine learning and deep learning algorithms, AI is reshaping cancer care by enabling automated detection of minute lesions during screening and quantitative analysis of pathological features for diagnosis. It may also advance tumor theranostics through multimodal data integration for treatment stratification, response prediction, and image-guided or targeted therapeutic decision-making, whereas providing data-driven recommendations for personalized treatment. Despite these prospects, medical AI development faces several key issues, including data bias, model explainability, clinical reliability and generalizability, emerging limitations of foundation models and generative AI, and regulatory and ethical issues that need to be addressed. By reviewing recent advances in AI across screening, diagnosis, theranostics, and treatment, we aim to clarify where these methods are already useful, where evidence remains limited, and why closer collaboration among clinicians, engineers, and data scientists is needed for clinical translation. We hope this review serves as a practical reference for researchers and clinicians evaluating how AI may be integrated into oncology in a more standardized, clinically responsible way.

Pathological diagnosis of colorectal malignant polyps is a core component guiding clinical treatment and subsequent management. Precise diagnosis and risk stratification of malignant polyps by pathologists serve as the fundamental basis for clinicians to formulate individualized treatment plans (including endoscopic resection or additional surgical resection). Accordingly, this article systematically elaborates on the key diagnostic points for malignant polyps, including the Paris endoscopic classification of colorectal polyps and its clinical significance, the histological definition of malignant polyps, assessment systems for submucosal invasion depth (such as Haggitt grading and Kikuchi SM grading), as well as the interpretation of critical high-risk histological features including poor differentiation, lymphovascular invasion, and tumor budding. In addition, diagnostic and differential diagnostic points for special lesion types, such as poorly differentiated intramucosal carcinoma and composite adenoma with microcarcinoid, are also summarized. Collectively, this review aims to provide comprehensive references for pathologists and clinicians, thereby promoting standardized management of colorectal malignant polyps.

Objective: To explore the gross morphology and variation characteristics of the left gastric vein (LGV) by means of cadaveric anatomical measurement and three-dimensional imaging reconstruction. Methods: A total of 39 adult cadaver specimens fixed with 4% formaldehyde solution from Zhongshan School of Medicine, Sun Yat-sen University, and 40 cases of abdominal contrast-enhanced CT imaging data of patients with gastric cancer admitted to the Seventh Affiliated Hospital of Sun Yat-sen University between January 2023 and December 2024 were included in this study. Specimens with obvious decomposition, tissue deformation, structural damage, or a history of upper abdominal surgery were excluded; patients with pathologically confirmed gastric cancer and CT images suitable for three-dimensional vascular reconstruction were selected, while those complicated with liver cirrhosis, portal hypertension, or a history of major upper abdominal surgery were excluded. The perigastric and perihepatic vessels were exposed in cadaver specimens to observe the morphology and course of the LGV and measure related anatomical parameters; the imaging data were scanned with dual-source CT using standardized parameters, and three-dimensional vascular reconstruction was performed on a post-processing workstation. The LGV was classified according to the Lee criteria. Results: Cadaveric dissection showed that the LGV originated from the middle of the lesser curvature of the stomach, coursed leftward along the lesser curvature, received 2-3 esophageal veins at the inferior margin of the esophageal hiatus, and then obliquely descended rightward to drain into the hepatic portal vein. Both cadaveric dissection and imaging detected three drainage sites of the LGV: the hepatic portal vein, the portal vein angle, and the splenic vein. CT angiography (coronal plane) and cadaver specimens both showed that the proportion of drainage into the hepatic portal vein was the highest [52.5% (21/40) vs. 53.8% (21/39)], followed by the splenic vein [35.0% (14/40) vs. 41.0% (16/ 39)], and the least common was drainage into the portal vein angle [12.5% (5/40) vs. 5.1% (2/39)]. The length of the LGV was (40.3±7.4) mm in cadaver specimens and (48.4±11.9) mm on imaging; the distance from the drainage site to the portal vein angle was (13.8±8.1) mm in cadaver specimens and (13.1±8.2) mm on imaging. In both the imaging group and the cadaver group, the type Ip accounted for the highest proportion of LGV classification, at 40.0% (16/40) and 41.0% (16/39), respectively, and no type IV was detected in either group. The proportion of type II in the imaging group was 22.5% (9/40), which was higher than that in the cadaver group (7.7%, 3/39); the proportion of type Ia in the cadaver group was 25.6% (10/39), which was higher than that in the imaging group (15.0%, 6/40); the proportions of type IIIa (20.0% in the imaging group vs. 20.5% in the cadaver group) and type IIIp (2.5% in the imaging group vs. 5.1% in the cadaver group) were similar between the two groups. Conclusions: There are certain variations in the anatomical course and diameter of the LGV. The LGV most commonly drains into the hepatic portal vein, and is mainly classified as type I.

Clinical T2N0 (cT2N0) esophageal squamous cell carcinoma (ESCC) represents a clinical grey zone between early-stage and locally advanced disease, and remains one of the most controversial scenarios in esophageal cancer management. The choice between upfront surgery and neoadjuvant therapy continues to vary across clinical guidelines and real-world practice. With the release of the 2026 International Society for Diseases of the Esophagus (ISDE) guidelines, this issue has once again drawn considerable attention. However, the existing controversy is not merely driven by differences in treatment strategies, but rather reflects the limited accuracy of pretreatment staging and the marked biological heterogeneity within the cT2N0 population. In this article, we review current evidence and international guidelines to analyze the underlying causes of these discrepancies, discuss the appropriate boundaries between upfront surgery and neoadjuvant therapy, and highlight future directions. We propose that the management paradigm for cT2N0 ESCC should shift from uniform treatment strategies toward precision risk stratification based on multidimensional clinical and biological information, thereby enabling more rational and individualized decision-making.

Oligometastatic disease (OMD) is considered an intermediate state between localized disease and widely metastatic disease, offering selected patients with metastatic esophageal cancer the possibility of long-term survival and even potential cure. In recent years, substantial progress has been made in oligometastatic esophageal cancer with advances in local treatment modalities, the widespread application of immunotherapy, and the development of precision medicine. In particular, randomized controlled evidence represented by the ESO-Shanghai 13 trial has, for the first time, demonstrated that local intervention combined with systemic therapy can provide significant survival benefits for patients with oligometastatic esophageal squamous cell carcinoma (ESCC), thereby promoting a shift in treatment strategy from purely palliative care to active multidisciplinary intervention. Meanwhile, the launch of the Oligometastatic Esophageal Squamous Cell Carcinoma (OMESQ) international consensus project marks the transition of oligometastatic ESCC research from borrowing experience from other tumor types toward disease-specific development. However, radiologically defined oligometastatic disease is not equivalent to biologically defined oligometastatic disease, and patient selection may be more important than the treatment modality itself. Based on recent advances in oligometastatic esophageal cancer, this commentary discusses the evolution of concepts, key clinical evidence, current controversies, and future directions. The author believes that research on oligometastatic esophageal cancer is moving from the exploratory stage of determining "whether local treatment is effective" toward a new stage of determining "how to precisely identify patients who are most likely to benefit." Establishing an ESCC-specific treatment framework based on tumor biological characteristics will become an important future direction in this field.

The incidence of early-onset colorectal cancer (EOCRC) has been rising globally in recent years, with an especially rapid increase in disease burden in China. Compared with late-onset colorectal cancer, EOCRC is more often diagnosed following symptomatic presentation, with greater diagnostic delay and more aggressive biological behavior. Patients are typically at critical life stages regarding career development and family building, and have urgent needs for fertility and sexual function preservation, and long-term quality of life. However, current domestic and international guidelines mostly target the general colorectal cancer population, and a systematic management framework tailored to the specific characteristics of early-onset patients is lacking. Therefore, the Hereditary Cancer Committee of the China Anti-Cancer Association organized a multidisciplinary expert panel-including specialists in colorectal surgery, medical oncology, radiation oncology, pathology, genetic medicine, reproductive medicine, psycho-oncology, and specialized nursing-to develop the Chinese Expert Consensus on the Diagnosis and Whole-Course Management of Early-Onset Colorectal Cancer (2026 version), based on evidence-based medicine and Chinese clinical practice. This consensus covers clinical issues such as the definition, epidemiological characteristics, screening and diagnosis, comprehensive treatment strategies, fertility and sexual function preservation, psychosocial support, and long-term follow-up of EOCRC, and presents 18 relevant recommendations. It aims to establish a multidisciplinary team-based whole-course management model that emphasizes both tumor control and long-term quality of life, providing a reference for the standardized diagnosis and treatment of EOCRC.

Pheochromocytoma and paraganglioma (PPGL) are rare neuroendocrine tumors characterized by remarkable clinical heterogeneity and genetic complexity. Conventional diagnostic and therapeutic strategies have largely relied on catecholamine assessment, anatomical imaging, and surgical resection; however, these approaches exhibit substantial limitations in metastatic risk stratification and personalized management for metastatic PPGL. Advances in genomics have enabled the establishment of the molecular cluster classification for PPGL, including pseudohypoxic, kinase-signaling, and Wnt-altered clusters, and corresponding strategies for precise nuclear medicine imaging and tumor surveillance. Recently, the refined application of nuclear medicine molecular imaging, the publication of international consensus guidelines on the management of patients with SDHB and SDHD mutations, and the approval of the hypoxia-inducible factor-2α (HIF-2α) inhibitor belzutifan, collectively have marked the entry of PPGL management into the era of precision medicine. Nonetheless, molecular cluster-guided targeted therapies for metastatic PPGL have not yet been incorporated into clinical guidelines, due to poorly characterized molecular mechanisms, a lack of patient-derived preclinical models, and the absence of cluster-specific, head-to-head clinical trials. Looking forward, the precision medicine in PPGL will move toward refined molecular subtyping, individualized treatment, integrated theranostic approaches, and multicenter collaboration.