BACKGROUND Minimally invasive surgery (MIS) and anterior (ALIF), transforaminal (TLIF), or lateral lumbar interbody fusion (LLIF) often require percutaneous pedicle screw fixation (PSF) to achieve circumferential fusion. Robotic guidance technology may augment workflow to improve screw placement and decrease operative time. OBJECTIVE To report surgical experience with robotically assisted percutaneous screw placement following LLIF. METHODS Data from fusions with robotically assisted PSF in prone or lateral decubitus positions was reviewed. A CT-guided robotic guidance arm was used for screw placement (Excelsius GPS™, Globus Medical Inc, Audubon, Pennsylvania). Postoperative CT imaging facilitated screw localization. 3-dimensional and 2-dimensional coordinates of the screw tip and tail were calculated and compared with a target trajectory to calculate targeting errors. Breach was defined as a violation of the lateral or medial pedicle wall. RESULTS Robotic-guided screw placement was successful in 28/31 patients. In those patients, 116/116 screws were successfully implanted. The breach rate was 3.4% (4/116). Across 17 patients (70 screws), mean 3-D accuracy was 5.0 ± 2.4 mm, mean 2-D accuracy was 2.6 ± 1.1 mm, and mean angular offset was 5.6 ± 4.3° with corresponding intraclass correlation coefficients (ICC) of 0.775 and 0.693. 3-dimensional accuracy correlated with age (R = 0.306, P = .011) and BMI (R = 0.252, P = .038). Accuracy did not significantly differ among vertebral body levels (P > .22). Mean operative time for MIS-TLIF and percutaneous screws was 277 ± 52 and 183 ± 54 min, respectively. Operative time did not significantly decrease across either group (P > .187). CONCLUSION The Excelsius GPS™ robotic guidance system allows accurate PSF in most cases with 2 mm 2-D accuracy. Future studies are needed to demonstrate the utility of this novel guidance system and workflow improvement.
Studies of tumors from human familial adenomatous polyposis, sporadic colon cancer, and mouse and rat models of intestinal cancer indicate that the majority of early adenomas develop through loss of normal function of the Adenomatous polyposis coli (APC) gene. In murine models of familial adenomatous polyposis, specifically the multiple intestinal neoplasia mouse (Min) and the polyposis in the rat colon (Pirc) rat, most adenomas have lost their WT copy of the Apc gene through loss of heterozygosity by homologous somatic recombination. We report that large colonic adenomas in the Pirc rat have no detectable copy number losses or gains in genomic material and that most tumors lose heterozygosity only on the short arm of chromosome 18. Examination of early mouse and rat tumors indicates that a substantial subset of tumors shows maintenance of heterozygosity of Apc in genomic DNA, apparently violating Knudson's two-hit hypothesis. Sequencing of the Apc gene in a sampling of rat tumors failed to find secondary mutations in the majority of tumors that maintained heterozygosity of Apc in genomic DNA. Using quantitative allele-specific assays of Apc cDNA, we discovered two neoplastic pathways. One class of tumors maintains heterozygosity of Apc Min/+ or Apc Pirc/+ RNA expression and may involve haploinsufficiency for Apc function. Another class of tumors exhibits highly biased monoallelic expression of the mutant Apc allele, providing evidence for a stochastic or random process of monoallelic epigenetic silencing of the tumor suppressor gene Apc.epigenetics | genomic stability | loss of imprinting | X-inactivation
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