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MINIMALLY INVASIVE COLORECTAL RESECTION (MICR) IS ASSOCIATED WITH SIGNIFICANTLY ELEVATED PLASMA LEVELS OF PRO ANGIOGENIC ENDOTHELIN -1 FOR THREE WEEKS AFTER COLORECTAL RESECTION
Hmc Shantha Kumara
*1, Yi-Ru Chen
1, Neil Mitra
1, Elizabeth Nilsson Sjolander
1, Xiaohong Yan
2, Vesna Cekic
1, Richard L. Whelan
11Department of Surgery, Lenox Hill Hospital , Northwell Health, Ney York, NY; 2Department of Pathology and Cell Biology, Columbia University Medical Center, Vanderbilt Clinic, 635 West 168th Street,, Ney York, NY
Introduction: Endothelin-1 (ET-1) is a widely expressed member of the endothelin family and is synthesized in vascular endothelial cells (EC), macrophages, leukocytes, and fibroblasts. ET-I is involved in various biological functions mediated by two receptor subtypes, ETAR and ETBR. ET-1 via ETBR modulates EC proliferation, migration, and invasion. ET-1 also activates mast cells and the release of TNF-? and IL-6. ET-1 modulates tumor angiogenesis indirectly via the induction of VEGF. ET-1 can induce EMT, a process that contributes to cancer progression and metastasis. ET-1 also functions as an anti-apoptotic factor that affects cellular survival mechanisms via activation of PI3K-dependent AKT/NF-?B signaling which play a role in tumor progression. ET-1 is overexpressed in many cancers including colorectal cancer (CRC). Plasma ET-1 levels after Minimally invasive colorectal resection (MICR) has been poorly studied. The aim of this research was to assess plasma ET-1 levels prior to, and during the first month following MICR for CRC.
Method: Patients who underwent MICR for CRC in an IRB approved data/plasma bank for whom adequate plasma samples were available were eligible. Clinical and pathological data were reviewed. Blood specimens were collected/processed preoperatively (PreOp), on Postoperative Day (POD) 1, POD 3, and at least one late postop time point (POD 7-41). Late samples were bundled into 7-20 day blocks and treated as single time points (POD 7-13, POD14-20, POD 21-27, POD21-41). ET-1 concentration was measured in duplicate via ELISA. The Wilcoxon paired t-test was used for analysis (significance p<0.05).
Results: 102 CRC patients who had a MICR met inclusion criteria (66% colon and 34% rectal lesions). The mean incision length was 7.83± 3.51cm and mean length of stay was 6.38± 3.12 days. The cancer stage (STG) breakdown was; STG I, 37%, STG II, 24%, STG III, 34% and STG IV, 5%. The mean PreOp ET-1 level was 1.51±1.01pg/ml. Significantly elevated mean plasma levels were found on POD1 (2.83±1.50 pg/ml, n= 102,p=< 0.0001), POD3 (2.41±1.32 pg/ml, n= 79,p=< 0.0001), POD7-13 (1.86±1.10 pg/ml,n=68,p=< 0.001) and POD14-20 (1.82±1.29 pg/ml, n=41,p=< 0.001) when compared to PreOp levels. The plasma ET-1 level differences for POD 21-27 and POD 21-41 were not significant.
Discussion: Plasma levels of ET-1 are significantly increased for three weeks following MICR for CRC. The etiology of the initial rise in ET-1 levels may be attributed to the surgery-related acute inflammatory response while the subsequent elevations could be associated with tissue remodeling processes linked to wound healing. The elevated plasma ET-1 concentrations, along with other previously noted plasma protein changes, may facilitate tumor angiogenesis, potentially leading to enhanced residual tumor growth. Further studies are warranted.
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