Treatment strategies for hepatic metastasis from colorectal cancer

Abstract

Hepatic micrometastases of the parenchyma adjacent to a macroscopic lesion were detected in 17 of 31 resected liver metastases. Fifty-nine micrometastatic lesions were detected in total; 26 lesions were situated in the portal vein (PV), 22 in the central vein (CV), 5 in the bile duct (BD), and 6 in the sinusoid (SS). A histological study confirmed the direct invasion of the macrometastatic cancer cells into the adjacent PV, CV, BD, and SS. According to the tumor doubling time, the mean diameter of the macrometastases in 19 remnant livers was calculated to have been 0.57 _+ 0.87cm at the time of the primary resection. The 9 calculated diameter of 3 of these 19 macrometastases was found to be less than 0.01cm, the minimum implantable size, indicating that the cancer recurrence in these specimens may have developed from macroscopic metastatic lesions as a satellite, and not from the primary tumor. In 13 patients who received doses of 5250mg or more of 5 fluorouracil (FU) via the hepatic artery, the cumulative disease-free rate 2 years postoperatively was 100%; this value was 47.6% in 11 patients who received less than 5250mg of 5 FU via the hepatic artery, and 0% in 39 patients who received no chemotherapy (P < 0.005). These results suggest that anatomical hepatic resection for satellite lesions, combined with prophylactic hepatic arterial chemotherapy for micrometastases, decreases the recurrence rate of hepatic metastases in the remnant liver.

Pre-hepatectomy prognostic staging to determine treatment strategy for colorectal cancer metastases to the liver

“…Most recurrences after hepatectomy are likely to arise from occult tumors that are present at the time of resection [36]. Microscopic satellite lesions have been detected in vessels and bile ducts surrounding macroscopic lesions [14]. Most patients in stage III, whose macroscopic tumors have been completely resected, still harbor microscopic disease and, therefore, have much higher recurrence rates and a poorer prognosis.…”

“…T-DT was calculated by the expression: log 2/3[(T 2 T 1 )/(log D 2 log D 1 )], where T 1 and T 2 are time and D 1 and D 2 are tumor diameter at any two time points in the clinical course prior to hepatectomy. CEA-DT was calculated by the expression, log 2[(T 2 T 1 )/(log C 2 log C 1 )], where T is time and C is CEA concentration, as previously reported [10][11][12][13][14]. We have shown that T-DT of the hepatic metastasis is highly correlated with the CEA-DT in patients with no extrahepatic metastases [14]; T-DT does not correlate with CEA-DT when extrahepatic metastases are present [13].…”

“…CEA-DT was calculated by the expression, log 2[(T 2 T 1 )/(log C 2 log C 1 )], where T is time and C is CEA concentration, as previously reported [10][11][12][13][14]. We have shown that T-DT of the hepatic metastasis is highly correlated with the CEA-DT in patients with no extrahepatic metastases [14]; T-DT does not correlate with CEA-DT when extrahepatic metastases are present [13]. Therefore, patients with concomitant extrahepatic metastases were excluded from the CEA-DT analysis; in those cases only T-DT was measurable.…”

Investigation into the Appropriate Post-neoadjuvant Chemotherapy Hepatectomy Margin to Include Both Macro- and Micrometastasis from Colorectal Carcinoma

“…Takenami et al 3) and Shimada et al 23) also reported that the number of MiMs increased with increases in the size of the macrometastases.…”

Tumor doubling time and local immune response to hepatic metastases from colorectal cancer

“…Here, T1 and T2 represent two time points, and C1 and C2 are serum carcinoembryonic antigen (CEA) concentrations at the respective times before hepatectomy [15][16][17][18][19]. When CEA-DT was not measurable, we used tumor size DT (T-DT), which was calculated using the following equation:…”