Robotic or laparoscopic surgery for rectal cancer - which is the best answer? a comprehensive review of non-oncological outcomes and learning curve

Much effort has been spent evaluating the difference between robotic and laparoscopic surgery platforms for rectal cancer. There is a plethora of literature comparing outcomes for intraoperative events, postoperative complications, long term outcomes, cost, and learning curve. The data are conclusive regarding the higher cost of robotic surgery compared to laparoscopic surgery. This article is a comprehensive review of the available literature regarding intraoperative and postoperative outcomes. For practically all parameters evaluated, there are no significant differences between the two platforms. The ultimate decision on whether to perform robotic vs. laparoscopic surgery should be based on surgeon preference and familiarity with equipment, as well as local resources

SDF-1α is elevated in wound fluid and increases tumor growth.

<p><b>A.</b> SDF-1α levels in wound fluid from BALB/c wildtype (WT) mice were higher than in wound fluid from BALB/c nu/nu mice (nu/nu) or plasma from BALB/c WT animals (cytokine microarray). <b>B.</b> SDF-1α levels in wound fluid from BALB/c WT animals increased during the course of wound healing and were higher in WT wound fluid than in wound fluid from nu/nu animals 9d after wounding (insert). n = 5 samples/time point (0.3d to 5d) and n = 3 samples/time point (5d to 14d); Triangle: mean; filled circle: individual data point. Insert: p = 0.05, n = 3, Mann Whitney test). <b>C, D.</b> Inhibition of SDF-1α/CXCR4 signaling by AMD3100 treatment abolished wound-promoted-tumor growth. <b>C.</b> Experimental design. <b>D.</b> Cumulative tumor volumes. p = 0.0027, n = 10 animals/group, Kruskal Wallis Test/Dunn’s Multiple Comparison Test, observation time: 21d, mean ±95% CI.</p

Wound-promoted tumor growth and SDF-1α levels in wound fluid are dependent on the host background.

<p><b>A,B.</b> The host background influenced wound-promoted tumor growth. <b>A.</b> Wound-promoted tumor growth was assessed in female animals of the F1 generation derived from BALB/c mice bred with BALB/c (control), FVB/nJ, AKR/J, C57Bl/6JNcr, DBA/2J animals. <b>B</b>. Cumulative tumor volumes. Unpaired t-test. Mean ±95% CI. Representative of 2 independent experiments is shown. <b>C,D.</b> The host background influences SDF-1α levels in wound fluid. <b>C.</b> SDF-1α levels were analyzed by ELISA in healthy hosts 2 d or 9d after subcutaneous implantation of PVA sponges. <b>D.</b> SDF-1α levels in wound fluid (ELISA). Mann-Whitney test. N.A. : sample number not sufficient to perform statistical analysis. Bar: mean.</p

Wound-induced SDF-1α/CXCR4 signaling in tumor cells alters tumor cell proliferation, stromal composition and vascularization of tumors.

<p><b>A, C</b>. BALB/c mice were inoculated with 4T1 cells that were pre-treated for 5d with wound fluid or mouse plasma. <b>B, D.</b> BALB/c mice were inoculated with 4T1 cells and underwent wounding or sham surgery 9 days later. CXCR4 signaling was systemically inhibited by AMD3100. <b>A, B.</b> Mitotic figures in tumor sections. <b>A.</b> Unpaired t-test, p<0.0001, n = 10 specimens/group, observation time: 18 days. <b>B</b>. Bonferroni’s Multiple Comparison test, p<0.0001, n = 8–12 specimens/group, observation time: 28, mean ±95% CI. <b>C, D</b>. Top: Collagen staining with Picrosirius red. Bottom: CD34-positive blood vessels in tumors. Numbers in the lower left corner of images represent the density of CD34-positive structures/mm³. <b>C.</b> p = 0.0173, Mann-Whitney test. <b>D.</b> p = 0.0155, ANOVA, mean ±95% CI).</p

SDF-1α increases tumor growth by directly acting on tumor cells.

<p><b>A.</b> Experimental design. <b>B.</b> Pretreatment of 4T1 cells with wound fluid derived from WT animals but not wound fluid derived from BALB/c nu/nu animals increased tumor growth <i>in vivo</i> as compared to pretreatment of 4T1 cells with plasma. mean ±95% CI, p<0.0001, n = 15 animals/group, ANOVA/Bonferroni’s Multiple Comparison Test, observation time: 18d. <b>C.</b> Pre-treatment of 4T1 cells with SDF-1α and plasma <i>in vitro</i> resulted in increased tumor growth <i>in vivo</i> as compared to pretreatment of 4T1 cells with plasma only. p = 0.0015, n = 15 animals/group, unpaired t-test, observation time: 22d, mean ±95% CI. <b>D.</b> Inhibition of SDF-1α/CXCR4 signaling with AMD3100 (AMD) during pre-treatment of 4T1 cells with wound fluid abolished increased tumor growth observed after pretreatment of 4T1 cells with wound fluid. p = 0.0016, n = 15 animals/group, ANOVA/Bonferroni’s Multiple Comparison Test, observation time: 22d, mean ±95% CI.</p