Anaplastic transformation of thyroid cancer in mesentery metastases presenting as intestinal perforation: a case report.

BACKGROUND: Anaplastic thyroid carcinoma is a highly aggressive form of thyroid cancer associated with a very poor prognosis. Anaplastic transformation most commonly occurs in the thyroid itself or within regional lymph nodes. Here we report the case of a patient with papillary thyroid cancer, presenting with colon perforation as a result of anaplastic transformation of metastases in the mesentery tissue. There have been no previous reports of this form of anaplastic transformation. CASE PRESENTATION: A 74-year-old man was admitted to our hospital, presenting with abdominal pain that he had been experiencing for 1 week prior to admission. The patient had a history of papillary thyroid carcinoma, for which he underwent a total thyroidectomy and mediastinal lymph node dissection 6 years earlier, and subsequently received radioactive iodine therapy for postoperative recurrence in the lung 2 years later. During the present reported admission, a computed tomography scan revealed a large intra-abdominal mass infiltrating into the colon and retroperitoneum and also highlighted the pneumoperitoneum. The patient was diagnosed with generalized peritonitis as a result of colon perforation, as such, we conducted an emergency laparotomy. Intraoperative findings showed a mass affecting the ascending colon and kidney, following which, an ileostomy and biopsy were completed. Poorly differentiated spindle cells were identified in the biopsy specimens, and histopathological and immunohistochemical findings revealed the absence of thyroid carcinoma cells. The tumor was therefore believed to be a primary sarcoma. Following surgery, the patient recovered from sepsis that had arisen as a result of colon perforation, however, rapidly developed systemic metastases and died 1 month post-operation. An autopsy was performed, and the patient was diagnosed with anaplastic papillary thyroid cancer at the mesentery site of metastasis. This conclusion was reached owing to the presence of the squamous differentiation of lymph node cells, and because tumor cells were positive results for paired-box gene 8 expressions. CONCLUSIONS: Anaplastic transformation of papillary thyroid carcinoma should be considered in the diagnosis of a large mesentery mass in patients with a history of papillary carcinoma. An appropriate biopsy and paired-box gene 8 immunostaining can be useful in confirming such a diagnosis.

Pathological complete response by advanced hepatocellular carcinoma with massive macrovascular invasion to hepatic arterial infusion chemotherapy: a case report.

BACKGROUND: Advanced hepatocellular carcinoma (HCC) with macrovascular invasion has an extremely dismal prognosis. We report a rare case of multiple HCC with tumor thrombosis in the portal vein and inferior vena cava that was initially treated with hepatic arterial infusion chemotherapy (HAIC); later resection revealed pathological complete response. CASE PRESENTATION: A 75-year-old man presented with HCC in his right liver, with tumor thrombosis growing to the right portal vein and the inferior vena cava, and bilateral intrahepatic liver metastases. He underwent HAIC (5-fluorouracil [170 mg/m2] + cisplatin [7 mg/m2]) via an indwelling port. Although the tumor shrank and tumor marker levels decreased rapidly, we abandoned HAIC after one cycle because of cytopenia. We resumed HAIC 18 months later because of tumor progression, using biweekly 5-fluorouracil only [1000 mg] due to renal dysfunction. However, after 54 months, the HAIC indwelling port was occluded. The patient therefore underwent a right hepatectomy to resect the residual lesion. Histopathological findings showed complete necrosis with no viable tumor cells. The patient has been doing well without postoperative adjuvant therapy for more than 10 years after initially introducing HAIC and 6 years after the resection, without evidence of tumor recurrence. CONCLUSIONS: HAIC can be an effective alternative treatment for advanced HCC with macrovascular invasion.

Significance of macrophage chemoattractant protein-1 expression and macrophage infiltration in squamous cell carcinoma of the esophagus.

OBJECTIVES: Macrophage chemoattractant protein-1 (MCP-1) is a chemokine-inducing infiltration of macrophages, which can play several roles in tumor growth and metastasis. We have attempted to clarify the relationship between MCP-1 expression and macrophage infiltration in esophageal squamous cell carcinoma (SCC). METHODS: Paraffin-embedded sections of tissue samples taken from 56 patients with esophageal SCC after curative surgery were immunohistochemically stained for MCP-1, CC chemokine receptor 2 (CCR-2), and thymidine phosphorylase (TP). Macrophage recruitment in SCC was evaluated by monocytic count based on CD68 immunostaining. Microvessels immunostained for Factor VIII-related antigen were counted in SCC, and microvessel density (MVD) was determined. Ki-67 labeling index was calculated based on Ki-67 immunostaining, and an apoptotic index was calculated based on the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate biotin nick end labeling. RESULTS: MCP-1 was expressed in cancer cells of 31 SCC (55.4%) and in stromal cells mainly identified as macrophages of 16 SCC (28.6%). CCR-2 was expressed in stromal cells of all SCC and in vascular endothelial cells of 15 SCC (26.8%). There was a significant correlation between the expression of MCP-1 in cancer cells and of CCR-2 in stromal cells. TP was expressed in stromal cells in 76.7% of the SCC. Monocytic count, MVD, and Ki-67 LI in SCC with MCP-1 expression in cancer cells were higher than that without, and apoptotic index in SCC with MCP-1 expression in cancer cells were lower than that without. Furthermore, the monocytic count was positively correlated with MVD, while it was inversely correlated with apoptotic index. Clinicopathologically, MCP-1 expression in cancer cells was correlated with venous invasion, distant metastasis, and lymph node metastasis. Monocytic count in SCC with venous invasion, distant metastasis, or lymph node metastasis was higher than that without them. Five-year survival rate in the patients with high monocytic count or MCP-1 expression was worse than that with a low monocytic count or without MCP-1 expression. CONCLUSIONS: These results suggest that MCP-1 expression and macrophage infiltration is associated with angiogenic promotion in esophageal SCC. MCP-1 expression may be interactively associated with macrophage infiltration in esophageal SCC; MCP-1 may play an important role in tumor angiogenesis through production of angiogenic factors, such as TP, by recruited macrophages in esophageal SCC. Furthermore, CCR-2 expression in vascular endothelial cells may participate partially in angiogenesis. Clinicopathologically, esophageal SCC patients with MCP-1 expression have no favorable prognosis.

Cell proliferation, apoptosis and angiogenesis in gastric cancer and its hepatic metastases.

BACKGROUND/AIMS: The levels of cell proliferation, apoptosis and angiogenesis were compared histochemically in gastric cancer and its hepatic metastases. METHODOLOGY: Tissue samples were taken from 7 patients with gastric cancer associated with synchronous and/or metachronous hepatic metastases. In the 7 gastric cancers and in 4 synchronous and 4 metachronous hepatic metastases, Ki-67 immunostaining was performed to measure the labeling index (Ki-67 LI). Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling was performed to measure the apoptotic index, and immunostaining for factor VIII-related antigen was performed to measure the microvessel density. RESULTS: The Ki-67 LI was higher in the gastric cancer and the metachronous hepatic metastasis than in the synchronous hepatic metastasis (primary lesions vs. synchronous foci vs. metachronous foci: 47.1% vs. 39.3% vs. 48.0%; P < 0.05). The apoptotic index was lower in the gastric cancer and the metachronous hepatic metastasis than in the synchronous hepatic metastasis (3.50% vs. 5.01% vs. 2.64%; P < 0.05). The microvessel density was higher in the gastric cancer and the metachronous hepatic metastasis than in the synchronous hepatic metastasis (36.0 vs. 22.2 vs. 34.2; P < 0.05). CONCLUSIONS: The present results suggest that tumor growth as indicated by cell proliferation, apoptosis and angiogenesis is less vigorous in synchronous hepatic metastasis than in primary lesion and/or metachronous hepatic metastasis.