Background Over a century ago, Virchow proposed that cancer represents a chronically inflamed, poorly healing wound. Normal wound healing is represented by a transitory phase of inflammation, followed by a pro-resolution phase, with prostaglandin (PGE2/PGD2)-induced ‘lipid class switching’ producing inflammation-quenching lipoxins (LXA4, LXB4). Objective We explored if lipid dysregulation in colorectal cancers (CRCs) is driven by a failure to resolve inflammation. Design We performed liquid chromatography and tandem mass spectrometry (LC–MS/MS) untargeted analysis of 40 human CRC and normal paired samples and targeted, quantitative analysis of 81 human CRC and normal paired samples. We integrated analysis of lipidomics, quantitative reverse transcription-PCR, large scale gene expression, and spatial transcriptomics with public scRNASEQ data to characterize pattern, expression and cellular localisation of genes that produce and modify lipid mediators. Results Targeted, quantitative LC–MS/MS demonstrated a marked imbalance of pro-inflammatory mediators, with a dearth of resolving lipid mediators. In tumours, we observed prominent over-expression of arachidonic acid derivatives, the genes encoding their synthetic enzymes and receptors, but poor expression of genes producing pro-resolving synthetic enzymes and resultant lipoxins (LXA4, LXB4) and associated receptors. These results indicate that CRC is the product of defective lipid class switching likely related to inadequate or ineffective levels of PGE2/PGD2. Conclusion We show that the lipidomic profile of CRC tumours exhibits a distinct pro-inflammatory bias with a deficiency of endogenous resolving mediators secondary to defective lipid class switching. These observations pave the way for ‘resolution medicine’, a novel therapeutic approach for inducing or providing resolvins to mitigate the chronic inflammation driving cancer growth and progression.

Background/Objectives: Nonoperative management (NOM) of patients with locally advanced rectal cancer (LARC) who achieve a complete clinical response (cCR) to total neoadjuvant therapy (TNT) has been shown to be oncologically safe and is an attractive treatment option for patients. However, identifying responders to TNT that may benefit from nonoperative management is clinically challenging. Circulating tumor DNA (ctDNA) testing has shown promise in detecting minimal residual disease but has not yet been studied extensively within this clinical context. Methods: This is a single-institution retrospective case series study of LARC patients treated with TNT from 2019 to 2023 who underwent ctDNA testing as an adjunct to standard clinical response assessments. Results: A total of 28 patients had ctDNA testing as part of their response assessments after TNT. In total, 9 patients had positive ctDNA, and 19 patients had negative ctDNA during surveillance. Baseline characteristics of these two groups were not different. In this study, 6/9 (67%) patients who had positive ctDNA required surgery for residual rectal cancer, whereas only 4/19 (21%) patients who had negative ctDNA required surgery (p = 0.035). Conclusions: ctDNA testing has the potential to detect MRD in LARC patients treated with TNT.

William N. Doyle Jr, Ashley J. Alden, Jetsen A. Rodriguez-Silva, Jin Kim, Sharan Poonja, Melissa A. Kendall, Kaylee Smith, Carolina Martinez, Allen Chudzinski, Lisa Moudgill, Paul Cavallaro, Jorge E. Marcet, Robert D. Bennett. Journal of Minimally Invasive Surgery 2026;29:22-30. https://doi.org/10.7602/jmis.2026.29.1.22

The modified Graham patch repair is a well-established technique for management of perforating foregut injuries, often learned by surgeons during general surgery training. There is, however, little to no data regarding the utilization of this technique for perforation of the distal midgut or in the re-operative field. We present two cases of midgut anastomotic complications successfully managed with modified graham patch repair at our institution. The first case is a 79-year-old female who underwent an emergent right hemicolectomy at an outside institution for management of an iatrogenic perforation during endoscopic polypectomy. Over the course of two years she underwent numerous abdominal operations, due to various complications, ultimately resulting in multiple resections and end ileostomy creation. She then had her ileostomy reversed by laparoscopic single incision (SILS) technique at our institution. This was also complicated by anastomotic leak. Intraoperatively, adequate mobilization of the anastomosis for resection was deemed not safe due to dense fibrosis and adhesions in the re-operative field; therefore, she underwent a SILS modified Graham patch repair of an ileocolic anastomotic defect with diverting loop ileostomy. Post-operatively, she had no radiographic evidence of leak from the repaired anastomosis, which facilitated successful loop ileostomy reversal five months later. Our second case is a 64-year-old male referred to our institution for management of his stage IV colon cancer. He underwent an open right hemicolectomy and hepatic metastectomy, which was complicated by anastomotic leak. The small defect was repaired via a SILS modified Graham patch technique. Five months postoperatively, he had neither radiographic nor endoscopic evidence of a leak; therefore, he successfully underwent ileostomy reversal without complication. We encourage further investigation and reporting of the role of the modified graham patch repair in management of midgut anastomotic complications, particularly when resection and re-anastomosis is unsafe due to a hostile re-operative field.