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Cancer cells can metastasize throughout the body by various mechanisms, including the lymphatic system, resulting in tumor‐induced lymphangiogenesis that can profoundly affect patient survival. The aim of the present study was to examine the role of lymphangiogenesis in the metastasis of pancreatic cancer to the peripheral nerve plexus. Immunohistochemistry was performed to analyze specimens obtained from 70 ductal adenocarcinoma patients. The markers used included lymphangiogenic factor vascular endothelial growth factor (VEGF)‐C, the lymphatic‐specific marker D2‐40, and cytokeratin 19, an independent prognostic factor for pancreatic tumors. The relationship between survival rate and invasion of both the lymphatic vessels and peripancreatic nerve plexus (PNP) was evaluated, with clearly elevated lymphatic vessel density (LVD) in tissues adjacent to the cancer tissues. In fact, LVD levels were higher in adjacent tissues than in localized cancer tissues, and lymphatic vessel invasion into tissues adjacent to the tumor was significantly correlated with both PNP invasion (P = 0.005) and lymph node metastasis (P = 0.010). Correspondingly, LVD in tissues adjacent to the tumor was correlated with both invasion of lymphatic vessels surrounding the tumor (P = 0.024) and VEGF‐C expression (P = 0.031); in addition, VEGF‐C expression was correlated with invasion of lymphatic vessels around the tumor (P = 0.004). Survival rates were significantly lower in patients in whom there was peritumor lymphatic vessel invasion (P < 0.001), extrapancreatic nerve plexus invasion (P = 0.001), and/or lymph node metastasis (P < 0.001). Based on these results, lymphatic invasion associated with adjacent tumor growth likely contributes to the development of metastatic tumors that invade the PNP.

Background Cancer remains a leading global cause of mortality, making early detection crucial for improving survival outcomes. The study aims to develop a machine learning-enabled blood-derived exosomal RNA profiling platform for multi-cancer detection and localization. Methods In this multi-phase, multi-center study, we analyzed RNA from exosomes derived from peripheral blood plasma in 818 participants across eight cancer types during the discovery phase. Machine learning techniques were applied to identify potential pan-cancer biomarkers. During the screening and model validation phases, the sample size was progressively expanded to 1,385 participants in two steps, while the candidate biomarkers were refined into a set of 12 exosomal tumor RNA signatures (ETR.sig). In the subsequent model construction phase, diagnostic models were developed using the expanded cohort and ETR.sig. Statistical analyses included the calculation of receiver operating characteristic (ROC) curves and AUC values to assess the models' ability to distinguish cancer cases from controls and determine tumor origins. To further validate and explore the biological relevance of the identified biomarkers, we integrated tissue RNA-seq, single-cell data, and clinical information. Results Machine learning analysis initially identified 33 candidate biomarkers, which were narrowed down to 20 ETR.sig in the screening phase and 12 ETR.sig in the validation phase. In the model construction phase, a diagnostic model based on ETR.sig, built using the Random Forest (RF) algorithm, showed excellent performance with an AUC of 0.915 for distinguishing pan-cancer from controls. The multi-class classification model also demonstrated strong classification power, with macro-average and micro-average AUCs of 0.983 and 0.985, respectively, for differentiating between eight cancer types. Additionally, tumor origin classification using the RF-based diagnostic models achieved high AUC values: BRCA 0.976, COAD 0.98, KIRC 0.947, LIHC 0.967, LUAD 0.853, OV 0.972, PAAD 0.977, and PRAD 0.898. Integration of tissue RNA-seq, single-cell data, and clinical information revealed key associations between ETR.sig-related genes and tumor development. Conclusions The study demonstrates the robust potential of exosomal RNA as a minimally invasive biomarker resource for cancer detection. The developed ETR.sig platform offers a promising tool for precision oncology and broad-spectrum cancer screening, integrating advanced computational models with nanoscale vesicle biology for accurate and rapid diagnosis.

Diabetes mellitus (DM) has been reported to be associated with an increased risk of several types of cancers. However, its relationship with cholangiocarcinoma (CC), which includes intrahepatic cholangiocarcinoma (ICC) and extrahepatic cholangiocarcinoma (ECC), remains unclear. We conducted a meta-analysis to assess the association between diabetes and the risk of CC (including ICC and ECC). We identified studies by a literature search of Medline (from 1 January 1966) and Embase (from 1 January 1974), through 30 November 2010, and by searching the reference lists of pertinent articles. Summary relative risks (RRs) with corresponding 95% confidence intervals (CIs) were calculated with a random-effects model. A total of 15 articles (10 case–control and five cohort studies) were included in this study. The number of reports on DM and risk of specific cancer were as follows: CC (n = 5), ECC (n = 9), and ICC (n = 9). Compared with those without diabetes, individuals with diabetes had an increased risk of CC (summary RRs, 1.60; 95% CI, 1.38–1.87; P = 0.992 for heterogeneity), ECC (summary RRs, 1.63; 95% CIs, 1.29–2.05; P = 0.005 for heterogeneity), and ICC (summary RRs, 1.97; 95% CIs, 1.57–2.46; P = 0.025 for heterogeneity). The funnel plot revealed no evidence for publication bias concerning diabetes and the risk of CC (including ICC and ECC). These findings strongly support the positive link between DM and the increased risk of CC (including ICC and ECC).

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies, with a marked potential for invasion and metastasis. Emerging evidence has suggested that dysregulation of long non-coding RNAs (lncRNAs) is associated with the development of multiple types of cancer. However, the function of lncRNAs in PDAC is poorly known. In the present study, a microarray assay was used to screen for differently expressed lncRNAs in PDAC and it was identified that cancer upregulated drug resistance (CUDR) was upregulated in PDAC. CUDR increased PDAC cell proliferation, migration and invasion, inhibited apoptosis, and promoted drug resistance; it also regulated the PDAC cell epithelial-mesenchymal transition. The CUDR-induced PDAC malignant phenotypes is via the protein kinase B and extracellular-signal-regulated kinase signaling pathways. Downregulation of CUDR may be a novel therapeutic strategy to prevent PDAC development and drug resistance in the future.

The aim of this study was to investigate the role of miR-208 in the invasion and metastasis of pancreatic cancer cells and the underlying molecular mechanism. miR-208 mimic, miR-208 inhibitor and NC were transfected into pancreatic cancer cell line Bxpc3 using liposome. Transwell invasion and scratch assays were used to test cell migratory and invasive abilities. Western blotting and quantitative PCR methods were used to detect E-cadherin, fibronectin and vimentin protein and mRNA expression in pancreatic cancer cell line BxPC3 after transfection by miR-208 mimic, miR-208 inhibitor and NC. Transwell invasion and scratch assays showed that after overexpressing miR-208, pancreatic cancer cell line BxPC3 exhibited enhanced in vitro migratory and invasive abilities, while after downregulating miR-208 expression, cell migratory and invasive abilities were decreased. Western blotting and quantitative PCR showed that after overexpressing miR-208, expression of E-cadherin, an epithelial cell marker, was decreased and expression of fibronectin and vimentin, interstitial cell markers, was increased in pancreatic cancer cell line BxPC3; however, after inhibiting miR-208, increased E-cadherin expression and decreased fibronectin and vimentin expression were observed in pancreatic cancer cell line BxPC3. After overexpressing miR-208, p-AKT and p-GSK-3β expression was altered by activating AKT/GSK-3β/snail signaling pathway. miR-208 induces epithelial to mesenchymal transition of pancreatic cancer cell line BxPC3 by activating AKT/GSK-3β/snail signaling pathway and thereby promotes cell metastasis and invasion.

Pancreatic cancer (PC) is one of the most common cancers worldwide and a leading cause of cancer-related death. Discovering novel targets is a key for its therapy. Carboxypeptidase E (CPE), a subtype of the pro-protein convertases, has been shown to be upregulated in many types of cancer, yet its function in PC remains elusive. The expressions of CPE in PC cell lines and cancer patients were investigated by Western blot and qRT-PCR. In PC cell line BX-pc-3, CPE was downregulated and its effect on cancer cell proliferation, migration, cisplatin chemosensitivity, and in vivo tumor growth was analyzed by Western blot, proliferation assay, invasion assay, and in vivo transplantation, respectively. The expression of nuclear factor-kappaB (NF-κB), a possible downstream target of CPE was examined by Western blot upon CPE regulation in PC cells, and the effects of inhibiting NF-κB on PC cell invasion and proliferation were examined. CPE was significantly upregulated in PC cell lines and tumor tissues. Proliferation and invasion assays indicated that downregulation of CPE inhibited cancer cell growth and migration and increased chemosensitivity to cisplatin. Inoculation of small interfering RNA (siRNA) transfected BX-pc-3 cells into null mice demonstrated that downregulation of CPE prevented tumor growth in vivo. NF-κB was directly regulated by CPE in pancreatic cancer, and siRNA-mediated inhibition of NF-κB exerted similar anti-tumor effect as downregulating CPE. Taken together, our results demonstrate that CPE plays an important role in pancreatic cancer. Inhibition of CPE may serve as a potential target for PC therapeutics.

Abdominal CT and US examinations showed a well-defined and circumscribed solid mass (4.5 × 5.5 cm) of mixed density with rich blood supply among of portal vein-superior mesenteric vein (PVSMV), spleen vein (SV), superior mesenteric artery (SMA), and inferior vena cava (IVC) without evidence of invasion of surrounding structures or vessels (Fig. 1A-B). In this case, the patient was a 69-year-old woman without any symptoms. Since discovered, the tumor grew slowly and did not invade blood vessels. According to immunocytochemistry, the diagnosis was well-differentiated PNET, and tumor cells may originate from PP cells.

Arsenic （As） contamination has become the environment issue of global concern. In China, large area of farmland and the site soil were contaminated by As, which means that suitable remedying methods were urgently needed. Phytoremediation, as one of environment-friendly soil remediation techniques developed in recent years, shows a bright future for the remediation of As contaminated soils. However, phytoremediation efficiency needs to be enhanced further because of low concentration of bio- available As in the soils. A triangle flask culture experiment was carried out to study the effects of functional species, isolated from As-polluted soils, that could improve As mobility from the soil. These species included two bacilli, B 1 and B2 （Breviba- cillus） and two fungi, F1 （Trichoderma）, F2 （Fusarium）. They could transform the concentration of As fractionation in the soil sterilized by the method of 6~Co-T ray. Through the experiment, the concentrations of non-specifically-sorbed and specifical- ly-sorbed As fractionation, and pH value of culture solution with inoculated treatment were higher than that with the control. Especially, the concentration of non-specifically-sorbed As fractionation in the treatment-inoculated species was 2 to 6 times higher than that of non-inoculation treatment. Moreover, two bacilli and two fungi could produce IAA, which was conducive to the plant survival when they were jointly used in remedying the As-contaminated soil.

S100 proteins are a calcium-binding protein family containing two EF-hand domains exclusively expressed in vertebrates and play roles in many cellular activities. Human S100P gene was first cloned as a 439 bp cDNA in placenta and it was found to be associated with human prostate cancer. Here we describe the cloning of the 1297 bp full-length cDNA, and the characterization of the tissue-specific expression of the human S100P gene. It is abundantly expressed in many tissues including placenta by Northern blot and RT-PCR analysis, unlike the expression pattern of other S100 family genes.