Indocyanine green perfusion assessment of the gastric conduit in minimally invasive Ivor Lewis esophagectomy.

BACKGROUND: Anastomotic leak is a serious complication following esophagectomy. The aim of the study was to report our experience with indocyanine green fluorescence angiography (ICG-FA)-PINPOINT® assisted minimally invasive Ivor Lewis esophagectomy (MILE) and assess factors associated with anastomotic leak. METHODS: We reviewed consecutive patients undergoing MILE from 2013 to 2018. Intraoperative real-time assessment of gastric conduit was performed using ICG-FA with PINPOINT®. Perfusion was categorized as good perfusion (brisk ICG visualization to conduit tip) or non-perfusion (any demarcation along the conduit). RESULTS: 100 patients (81 males, median age 68 [60-72]) underwent MILE for malignancy in 96 patients and benign disease in 4 patients. There were six anastomotic leaks all managed with endoscopic stent placement. There was no intraoperative mortality and no 30-day mortality in leak patients. Patients with a leak were more likely to be overweight with BMI > 25 (100% versus 53%, p = 0.03), have pre-existing diabetes (50% versus 13%, p = 0.04), and have higher intraoperative estimated blood loss (260 mL [95-463] versus 75 mL [48-150], p = 0.03). Anastomotic leaks occurred more frequently in the non-perfusion (67%) versus the good perfusion category (33%, p = 0.03). By multivariable analysis, diabetes (odds ratio [OR] 6.42; p = 0.04) and non-perfusion (OR 6.60; p = 0.04) were independently associated with leak. CONCLUSION: Intraoperative use of ICG-FA may be a useful adjunct to assess perfusion of the gastric conduit with non-perfusion being independently associated with a leak. While perfusion plays an important role in anastomotic integrity, development of a leak is multifactorial, and ICG-FA should be used in conjunction with the optimization of patient and procedural components to minimize leak rates. Prospective, randomized studies are required to validate the interpretation, efficacy, and application of this novel technology in minimally invasive esophagectomies.

Intrahepatic cholangiocarcinoma as a rare secondary malignancy after allogeneic hematopoietic stem cell transplantation for childhood acute lymphoblastic leukemia: A case report.

Secondary malignancies are a significant cause of non-relapse mortality in patients who undergo allogeneic HCT. However, secondary liver cancer is rare, and ICC following HCT has never been reported in the literature. Secondary solid cancers typically have a long latency period, and cholangiocarcinoma is classically a malignancy occurring in older individuals. Here, we report the first case of secondary ICC, which presented just 3 years after HCT in a young adult with a history of childhood ALL. A 26-year-old male with history of precursor B-cell ALL presented with asymptomatic elevated liver function tests 3 years after HCT. Laboratories were indicative of biliary obstruction. ERCP showed focal biliary stricturing of the common and left hepatic ducts. MRCP revealed left intrahepatic duct dilatation, suggestive of intrahepatic obstructing mass. Additional workup lead to a clinical diagnosis of ICC. The patient underwent left hepatectomy with extrahepatic bile duct resection and portal lymphadenectomy. Surgical pathology was consistent with moderately differentiated cholangiocarcinoma. Our case illustrates a rare SMN following HCT for ALL. It is the first case report of ICC occurring as a secondary cancer in this patient population. Although cholangiocarcinoma is characteristically diagnosed in the older population, it must remain on the differential for biliary obstruction in post-HCT patients.

T-Cell Transfer Therapy Targeting Mutant KRAS in Cancer.

We identified a polyclonal CD8+ T-cell response against mutant KRAS G12D in tumor-infiltrating lymphocytes obtained from a patient with metastatic colorectal cancer. We observed objective regression of all seven lung metastases after the infusion of approximately 1.11×1011 HLA-C*08:02-restricted tumor-infiltrating lymphocytes that were composed of four different T-cell clonotypes that specifically targeted KRAS G12D. However, one of these lesions had progressed on evaluation 9 months after therapy. The lesion was resected and found to have lost the chromosome 6 haplotype encoding the HLA-C*08:02 class I major histocompatibility complex (MHC) molecule. The loss of expression of this molecule provided a direct mechanism of tumor immune evasion. Thus, the infusion of CD8+ cells targeting mutant KRAS mediated effective antitumor immunotherapy against a cancer that expressed mutant KRAS G12D and HLA-C*08:02.