Minimally invasive surgery (MIS) has improved colorectal cancer (CRC) treatment by reducing recovery time, pain, and infection risk compared to traditional open surgery, though a mini laparotomy is still needed for specimen removal. Natural orifice specimen extraction (NOSE) offers a promising alternative by using natural body openings for extraction, potentially minimizing complications further, yet requires more evidence to confirm its safety and effectiveness over conventional methods.

18p deletion (18p-) syndrome is a rare chromosomal abnormality with a wide range of phenotypes. Its main clinical features are short stature, intellectual disability, and facial dysmorphism, which are rarely accompanied by autoimmune thyroid disease (ATD) or pituitary abnormalities. Herein, we report the first Chinese patient with a de novo 18p deletion who presented with ATD and non-functioning pituitary adenoma.

Cellular senescence plays a significant role in tumorigenesis and tumor progression. Substantial evidence indicates that senescence occurs in cancer-associated fibroblasts (CAFs), the predominant stromal component within the tumor microenvironment (TME), which profoundly impacts tumor biology. However, despite growing evidence of stromal cell involvement in cancer progression, the specific mechanisms and clinical implications of senescent CAFs (SCAFs) in hepatocellular carcinoma (HCC) have not been fully elucidated.

Perivascular epithelioid cell tumor (PEComa) of the pancreas is a rare tumor of pancreatic mesenchymal origin with malignant potential. Critical to appropriate clinical management is determining whether the tumor is benign or malignant. Because of its rarity, morphologic and histologic characteristics and limited patient follow-up of pancreatic PEComa have precluded precise definition of malignancy. However, because malignant pancreatic PEComa appears to be distinctly uncommon, further improvements characterizing its preoperative imaging features could facilitate use of diagnostic endoscopic ultrasound biopsy and perhaps ablative treatment. This paper presents a case of pancreatic PEComa treated at the Affiliated Hospital of North Sichuan Medical College and includes a systematic literature review with special emphasis on the key imaging features of pancreatic PEComa.

Cancer immunotherapy has revolutionized clinical oncology; however, the inherent complexity and heterogeneity of cancer present substantial challenges to achieving broad therapeutic efficacy. Tumor heterogeneity manifests not only among different patients but also within individual tumors, further complicating personalized treatment approaches. Single-cell sequencing technologies encompassing genomics, transcriptomics, epigenomics, proteomics, and spatial omics have significantly enhanced our ability to dissect tumor heterogeneity at single-cell resolution with multi-layered depth. These approaches have illuminated tumor biology, immune escape mechanisms, treatment resistance, and patient-specific immune response mechanisms, thereby substantially advancing precision oncology strategies. This review systematically examines recent advances in single-cell multi-omics technologies across various cancer research areas, emphasizing their transformative impacts on understanding tumor heterogeneity, immunotherapy, minimal residual disease monitoring, and neoantigen discovery. Additionally, we discuss current technical and analytical limitations and unresolved questions associated with single-cell technologies. We anticipate single-cell multi-omics technologies will become central to precision oncology, facilitating truly personalized therapeutic interventions.

Dysgerminoma, a uncommon malignant neoplasm originating from primitive ovarian germ cells, is exceptionally rare during pregnancy. While several studies have documented dysgerminoma diagnosis via peritoneal effusion cytology, no cases identified during pregnancy have been reported to date. This study presents the first reported case of dysgerminoma diagnosed through peritoneal effusion cytology in a pregnant patient.

Digestive system cancers-including gastric, liver, colorectal, esophageal, and pancreatic malignancies-remain leading causes of cancer death, with treatment resistance posing major challenges in advanced disease. Patient-derived cancer organoids (PDCOs), 3D mini-tumors grown from patient biopsies, have revolutionized personalized oncology by faithfully replicating tumor biology and enabling predictive drug testing for chemotherapy, radiotherapy, targeted therapy, and immunotherapy. While demonstrating good predictive accuracy, current limitations include incomplete tumor microenvironments, variable establishment rates, and lengthy processing times. Emerging technologies like AI, organ-on-chip systems, and 3D bioprinting are addressing these challenges, while clinical trials explore applications in neoadjuvant therapy and real-time treatment guidance. This Review highlights key advances in PDCO technology and its transformative potential for treatment decision-making in digestive system cancers, bridging laboratory research with clinical care to enable truly personalized therapeutic strategies tailored to individual tumor biology.

Hepatocellular carcinoma (HCC) remains a leading cause of cancer death worldwide. Sonodynamic therapy (SDT) offers a non-invasive, deep-penetrating approach by using ultrasound to activate sonosensitizers and generate cytotoxic reactive oxygen species (ROS). Yet poor intratumoral delivery and low ROS quantum yields of existing agents have stalled clinical translation. Here, we present a synergistic SDT platform that overcomes these barriers by combining transient vasodilation of tumor microvessels with the clinically widely used Antianginal drug isosorbide mononitrate and an acceptor-donor-acceptor-donor-acceptor type organic nanosonosensitizer (BTz) engineered for a narrow bandgap and enhanced ultrasound responsiveness. Isosorbide mononitrate increases nanosonosensitizer accumulation by ~ 1.8-fold. Under ultrasound irradiation, nanosonosensitizer produced high ROS generation, resulting in 78% tumor growth inhibition in murine HCC models-nearly double that of SDT alone-without detectable systemic toxicity. Crucially, the near-infrared fluorescence of nanosonosensitizer enabled real-time, image-guided tracking of sonosensitizer uptake and therapeutic response. By repurposing a safe vasodilator and integrating it with a high-performance organic sonosensitizer, this work establishes a readily translatable, minimally invasive paradigm for precise SDT of localized, inoperable or metastatic HCC.

Bladder cancer is characterized by its heterogeneous nature and high propensity for recurrence and progression. The absence of reliable diagnostic and prognostic biomarkers to accurately identify high-risk patients further complicates the clinical management of the disease. MOC-31, an antibody that targets epithelial cell adhesion molecule (EpCAM), is utilized to distinguish between mesothelioma and metastatic cancer, but its clinical utility, prognostic value and functional dynamics in bladder cancer have yet to be verified.

The global incidence of thyroid cancer, particularly papillary thyroid carcinoma (PTC), is rising due to more frequent incidental findings. Despite a high 10-year survival rate of 93%, up to 28% of PTC patients experience locoregional recurrence. Postoperative monitoring typically relies on serum thyroglobulin (Tg), but the presence of anti-thyroglobulin antibodies (TgAb) interferes with Tg measurement, necessitating reliable detection methods. This study aimed to assess the predictive value of postoperative TgAb levels for PTC recurrence and establish a TgAb threshold as a prognostic marker.

Mantle cell lymphoma (MCL) is a rare B-cell Non-Hodgkin-lymphoma that predominantly affects elderly patients. While younger and fit patients receive an intensive first-line treatment, older or comorbid patients have limited options of chemo-immunotherapy (CIT) alone followed by anti-CD20-antibody maintenance. Targeted oral agents as Bruton`s tyrosine kinase inhibitors (BTKi, e.g. ibrutinib) - and B-cell lymphoma 2 (Bcl2) - inhibitors (e.g. venetoclax) have revolutionized the treatment especially for relapsed patients, with apparent synergistic effects. The MCL elderly III trial of the European MCL Network is an international phase II trial evaluating the efficacy of the combination of ibrutinib, venetoclax and rituximab as well as the CIT bendamustine and rituximab in combination with ibrutinib in elderly patients with untreated MCL.

In this paper, the tumor-host interaction is modeled using a Lotka-Volterra framework. The critical parameters that define the possible dynamical regimes are identified through linear stability analysis. The effects of both constant and periodic perturbations are examined, along with their clinical implications. The treatment dose required to drive the system to a desired state is determined. It is also shown that aggressive tumors evolve toward a limit cycle when the host is under the action of low-frequency periodic treatment. As the frequency increases, a transition to a non-chaotic attractor occurs. This transition narrows as the frequency of the external periodic perturbation increases. No chaotic behavior is observed, even at higher values of both perturbation strength and frequency, as the maximum Lyapunov exponent remains negative. These results suggest that although aggressive tumors may not be completely eradicated by conventional anticancer therapies, they could potentially be controlled through external low-frequency periodic treatments that target directly only the host, such as immunotherapy.

The curative surgical treatment of older patients with oral cavity squamous cell carcinoma (OCSCC) is often personalized by incorporating subjective decisions on age and frailty. We aimed to determine here whether real-world recommended treatment, following official French guidelines only, versus deviation from recommended treatment was beneficial for older patients with OCSCC. To do this, we performed a retrospective evaluation of patients >70 years managed for treatment of p16-negative OCSCC in our tertiary hospital center in France between 2007 and 2017. The association between postoperative morbidity and deviation from recommended treatment was analysed using multivariate logistic regression. Cox Proportional Hazards Regression assessed the associations between deviation from recommended treatment and both the hazard of recurrence and mortality within 5 years. We included 185 patients who were recommended surgical resection of OCSCC: n = 147/185 (79%) patients underwent the recommended treatment and 38/185 (21%) patients underwent deviation from recommended treatment. Patients who underwent deviation from recommended treatment had a significantly lower recurrence-free survival (p = 0.0005) and overall survival (p = 0.008). Deviation from recommended treatment was found independently associated with increased development of 3-month postoperative morbidity (adjusted odds ratio 2.63 [1.23-5.82]; p = 0.02) and increased risk of recurrence within 5 years (adjusted hazard ratio 1.79 [1.14-2.83]; p = 0.01). Deviation from recommended treatment was not found independently associated with increased risk of mortality within 5 years (1.35 [0.82-2.23]; p = 0.2). Overall, deviation from recommended treatment was associated with worse outcomes and so we have identified a decision-making process biased by undocumented and subjective evidence. Preoperative risk models therefore require further validation in older patients with OCSCC to define more appropriate treatment regimens.

Lung cancer (LC) is the leading cause of cancer-related mortality worldwide, accounting for millions of deaths annually. Its major subtypes-lung squamous carcinoma (LUSC), lung adenocarcinoma, and small-cell LC-exhibit distinct risk factors and genetic susceptibilities, necessitating the use of subtype-specific biomarkers. Two-sample Mendelian randomization (MR) analyses were conducted using protein quantitative trait loci from the UK Biobank Pharma Proteomics Project and deCODE datasets. A robust analytical framework, including reverse MR, meta-analysis, summary-data-based MR tests, and colocalization, cisMR-cML, MR.CUE and phenotype scanning analyses were used to identify proteins associated with LC risk. We conducted a systematic review to contextualize our research findings. Follow-up analyses, including pathway enrichment, protein-protein interaction network analysis, and druggability evaluations, were used to explore the mechanisms and therapeutic potential of the identified proteins. Significant proteins were validated using population-level proteomic data from the UK Biobank (UKB). The results showed that twenty-five proteins were significantly associated with LC or its subtypes, including 15 novel findings. 60S ribosomal protein L14 (RPL14) and advanced glycosylation end-product-specific receptor (AGER) emerged as the strongest discovery, demonstrating consistent and significant associations across both MR and population-level analyses. RPL14 exhibited positive associations with overall LC risk (MR_meta: odds ratio [OR]: 2.012, 95% confidence interval [CI]: 1.297-3.119; UKB: OR: 1.509, 95% CI: 1.015-2.244). Similarly, AGER showed significant protective effects against LUSC risk (MR_meta: OR: 0.572, 95%CI: 0.368-0.889; UKB: OR: 0.366, 95% CI: 0.158-0.850). Pathway analysis revealed the involvement of these proteins in immune regulation and tumorigenesis. Among the 13 identified druggable targets, RPL14 and AGER showed therapeutic potential as approved or investigational drugs targeting these proteins. These findings offer new insights into the pathogenesis of LC and potential therapeutic targets.

PD-L1 expression for the prediction of response to immune-checkpoint blockade remains the most broadly utilised clinically validated biomarker in a range of tumour types. In this study, we aimed to assess, in a prospectively collected matched cohort, the impact of sampling technique and both formalin and alcohol fixation on PD-L1 expression and heterogeneity in non-small cell lung carcinoma (NSCLC). Patients undergoing surgical resection for NSCLC were consented. Surgical specimens were received directly from theatre and sampled fresh to produce two sets of core biopsies, two fine-needle aspirates (FNAs) and two whole-block tissue sections from each specimen. A matched biopsy, FNA, and whole-block were placed into formalin or an alcohol-based fixative (Cytolyt™) prior to PD-L1 immunohistochemistry assessment. A total of 114 specimens from 57 patients were included. All whole-block cases (100%), 92% of core biopsies, and 88% of FNAs were adequate for PD-L1 expression analysis. Fixation had no significant impact on adequacy, but cytology specimens fixed in alcohol showed a significant reduction in PD-L1 expression, with 25% of cases placed into different clinically relevant categories of PD-L1 expression. PD-L1 expression by immunochemistry is an exemplar of the challenges of utilising a heterogeneously expressed protein-based predictive biomarker. Regardless of sampling technique, a good quality biopsy or FNA is likely to give a statistically representative PD-L1 expression, although expression ranges close to clinically relevant cut-offs of 1% and 50% remain a source of potential discordance.

Molecular targeted therapy and immunotherapy have shown promise in managing gastric adenocarcinoma. The amplified expression of Human epidermal growth factor receptor-2 (HER-2) and microsatellite stable (MSI) status serve as indicators of response to targeted therapy and immunotherapy, respectively.

Brain metastasis represents the most prevalent form of brain tumors in adults, with a rising incidence resulting from significant advancements in cancer detection and therapeutic interventions. Current treatment protocols advocate for whole brain radiotherapy (WBRT) for patients who are not candidates for either surgical resection or stereotactic irradiation. However, cognitive decline remains a major side effect of this treatment modality. Hippocampal-sparing WBRT (HA-WBRT) has been shown to decrease brain toxicity, with the main concern being the probability of developing new brain metastasis in the hippocampal avoidance region.

Recent evidence suggests that EpCAM and CD44 could serve as diagnosis or prognosis markers in pancreatic cancer (PC). In this meta-analysis, we evaluated their associations with clinicopathologic features. Specifically, we compared immunohistochemical-positive and -negative PC patients for T stage (T3-T4 vs. T1-T2), N stage (N1 vs. N0), M stage (M1 vs. M0), tumor grade (well/moderately vs. poorly differentiated), UICC Stage (III, IV vs. I, II), and overall survival (OS). The diagnostic meta-analysis was performed analysing the pooled sensitivity and specificity and evaluating overall accuracy to indicate the diagnostic efficacy of the markers. The protocol of this systematic review and meta-analysis was registered on the PROSPERO website under the registration number of CRD42024568390. A systematic search of PubMed, Scopus, and ISI Web of Science was conducted on January 30th, 2025. The statistical analysis was performed using the Review Manager 5.4 software and R language (R package Mada and Metafor). The quality of the studies included was assessed using the Newcastle-Ottawa scale and the QUADAS-2 tool. Data from relevant studies were independently screened and extracted using Rayyan, by at least two authors. A total of 19 studies were eligible (9 studies for EpCAM, 9 studies for CD44, and 2 studies for both EpCAM and CD44), comprising a total of 1370 patients. The diagnostic meta-analysis demonstrated moderate accuracy for EpCAM (AUC, 95% CI of 0.802, 0.69-0.96). A statistically significant association was found for CD44 expression and T-status (OR = 2.04, 95%CI = 1.18-3.51), or N-stage (OR = 2.68, 95%CI = 1.86-3.85), or TNM stage (OR = 3.79, 95%CI = 2.14-6.71). CD44v6 overexpression predicted worse OS (HR = 2.33, p < 0.00001), while EpCAM + CD44 + co-expression was prognostic (HR = 2.02, p = 0.02). Heterogeneity was not observed among the studies included, but further research is warranted to better understand the clinical implications of these markers' positivity in PC diagnosis and prognosis.

The Greatwall kinase inhibits PP2A-B55 phosphatase activity during mitosis to stabilise critical Cdk1-driven mitotic phosphorylation. Although Greatwall represents a potential oncogene and prospective therapeutic target, our understanding of the cellular and molecular consequences of chemical Greatwall inactivation remains limited. To address this, we introduce C-604, a highly selective Greatwall inhibitor, and characterise both immediate and long-term cellular responses to the chemical attenuation of Greatwall activity. We demonstrate that Greatwall inhibition causes systemic destabilisation of the mitotic phosphoproteome, premature mitotic exit and pleiotropic cellular pathologies. Importantly, we show that the cellular and molecular abnormalities associated with reduced Greatwall activity are specifically dependent on the B55α isoform, rather than other B55 variants, underscoring PP2A-B55α phosphatases as key mediators of the cytotoxic effects of Greatwall-targeting agents in human cells. Additionally, we establish that sensitivity to Greatwall inhibition varies in different cell line models and that dependency on Greatwall activity reflects the balance between Greatwall and B55α expression levels. Our findings highlight Greatwall dependency as a cell-specific vulnerability and propose the B55α-to-Greatwall expression ratio as a predictive biomarker of cellular responses to Greatwall-targeted therapeutics.

Epithelial ovarian cancer (EOC) remains one of the most lethal gynecological malignancies. Although treatment options for newly diagnosed advanced EOC include primary debulking surgery (PDS) or neoadjuvant chemotherapy (NACT) followed by interval debulking surgery (IDS), the comparative effectiveness of these strategies remains uncertain across different disease stages.