Initial case series experience with robotic-assisted transanal minimally invasive surgery performed with da Vinci single-port system for the excision of rectal cancer.

BACKGROUND: Transanal minimally invasive surgery (TAMIS) is widely used for rectal lesion excision. Robot-assisted TA TAMIS (R-TAMIS) may improve surgical ergonomics. The introduction of the da Vinci Single-Port (SP) robot, designed for endoluminal surgery, has brought new possibilities. Our primary objective herein was to assess the technical and oncological feasibility and efficacy of Single-port robotic TAMIS (SPR-TAMIS) in rectal cancer excision. The secondary objective was to analyze the perioperative outcomes. MATERIALS AND METHODS: We included 14 consecutive patients with rectal cancer who underwent SPR-TAMIS between April 2021 and February 2023. Patient data, surgical details, and clinical outcome data were collected to assess the safety and feasibility of SPR-TAMIS. RESULTS: The median participant age was 72 years, and full-thickness excision was performed without specimen fragmentation in all cases. The median tumor diameter was 2.7 cm, positioned between 10 cm proximally and 7 cm distally from the anal verge. Negative margins were achieved in 93% of cases, with one case requiring further resection. The median operative time was 175 min, and the median hospital stay was 5 days. No intraoperative conversion from SPR-TAMIS to laparoscopic or conventional transanal excision was required. No mortalities or major postoperative complications occurred; however, one patient (7.1%) experienced minor morbidity manifesting as wound dehiscence (Clavien-Dindo grade I). No recurrence was observed during the 24-month follow-up. CONCLUSIONS: In our early experience, SPR-TAMIS is a safe and feasible surgery for selected early stage rectal cancers, offering enhanced visualization and stable maneuverability transanally. This platform may have potential advantages for the excision of larger or more proximal lesions.

Development of a Novel DNA Aptamer Targeting Colorectal Cancer Cell-Derived Small Extracellular Vesicles as a Potential Diagnostic and Therapeutic Agent.

Colorectal cancer (CRC) as the second leading cause of global cancer deaths poses critical challenges in clinical settings. Cancer-derived small extracellular vesicles (sEVs), which are secreted by cancer cells, have been shown to mediate tumor development, invasion, and even metastasis, and have thus received increasing attention for the development of cancer diagnostic or therapeutic platforms. In the present study, the sEV-targeted systematic evolution of ligands by exponential enrichment (E-SELEX) is developed to generate a high-quality aptamer (CCE-10F) that recognizes and binds to CRC-derived sEVs. Via an in-depth investigation, it is confirmed that this novel aptamer possesses high affinity (Kd = 3.41 nm) for CRC-derived sEVs and exhibits a wide linear range (2.0 × 104 -1.0 × 106 particles µL-1 ) with a limit of detection (LOD) of 1.0 × 103 particles µL-1 . Furthermore, the aptamer discriminates CRC cell-derived sEVs from those derived from normal colon cell, human serum, and other cancer cells, showing high specificity for CRC cell-derived sEVs and significantly suppresses the critical processes of metastasis, including cellular migration, invasion, and angiogenesis, which are originally induced by sEVs themselves. These findings are highly encouraging for the potential use of the aptamer in sEV-based diagnostic and therapeutic applications.

In vivo imaging of tumor transduced with bimodal lentiviral vector encoding human ferritin and green fluorescent protein on a 1.5T clinical magnetic resonance scanner.

A combination of reporter genes for magnetic resonance imaging (MRI) and optical imaging can provide an additional level of noninvasive and quantitative information about biological processes occurring in deep tissues. We developed a bimodal lentiviral vector to monitor deep tissue events using MRI to detect myc-tagged human ferritin heavy chain (myc-hFTH) expression and fluorescence imaging to detect green fluorescent protein (GFP) expression. The transgene construct was stably transfected into MCF-7 and F-98 cells. After transplantation of the cells expressing myc-hFTH and GFP into mice or rats, serial MRI and fluorescence imaging were performed with a human wrist coil on a 1.5T MR scanner and optical imaging analyzer for 4 weeks. No cellular toxicity due to overexpression of myc-hFTH and GFP was observed in MTT and trypan blue exclusion assays. Iron accumulation was observed in myc-hFTH cells and tumors by Prussian blue staining and iron binding assays. The myc-hFTH cells and tumors had significantly lower signal intensities in T(2)-weighted MRI than mock-transfected controls (P ≤ 0.05). This is direct evidence that myc-hFTH expression can be visualized noninvasively with a 1.5T clinical MR scanner. This study shows that MRI and fluorescence imaging of transplanted cells at molecular and cellular levels can be performed simultaneously using our bimodal lentiviral vector system. Our techniques can be used to monitor tumor growth, metastasis, and regression during cell and gene-based therapy in deep tissues.

Expression and regulation of latent TGF-beta binding protein-1 transcripts and their splice variants in human glomerular endothelial cells.

Latent transforming growth factor (TGF)-beta-binding protein (LTBP) is required for the assembly, secretion, matrix association, and activation of latent TGF-beta complex. To elucidate the cell specific expression of the genes of LTBP-1 and their splice variants and the factors that regulate the gene expression, we cultured primary human glomerular endothelial cells (HGEC) under different conditions. Basal expression of LTBP-1 mRNA was suppressed in HGEC compared to WI-38 human embryonic lung fibroblasts. High glucose, H(2)O(2), and TGF-beta1 upregulated and vascular endothelial growth factor (VEGF) further downregulated LTBP-1 mRNA in HGEC. RT-PCR with a primer set for LTBP-1S produced many clones but no clone was gained with a primer set for LTBP-1L. Of 12 clones selected randomly, Sca I mapping and DNA sequencing revealed that only one was LTBP-1S and all the others were LTBP-1Sdelta53. TGF-beta1, but not high glucose, H(2)O(2) or VEGF, tended to increase LTBP-1Sdelta53 mRNA. In conclusion, HGEC express LTBP-1 mRNA which is suppressed at basal state but upregulated by high glucose, H(2)O(2), and TGF-beta1 and downregulated by VEGF. Major splice variant of LTBP-1 in HGEC was LTBP-1S 53. Modification of LTBP-1S 53 gene in HGEC may abrogate fibrotic action of TGF-beta1 but this requires confirmation.