[A case of cardiopulmonary arrest due to hypersensitivity reaction to oxaliplatin for multiple liver and lung metastases of colon cancer].

A 69-year-old man underwent right hemicolectomy and D3 lymphadenectomy for transverse colon cancer in 2009. Under the postoperative pathological diagnosis of Stage IIIb (pT3pN2cM0) cancer, he was given 8 courses of adjuvant chemotherapy with capecitabine. After the chemotherapy, in April 2013, we detected recurrence of the multiple liver and lung metastases; thus, we administered modified 5-fluorouracil, Leucovorin, oxaliplatin (mFOLFOX6) and bevacizumab. Six courses of oxaliplatin infusion were completed uneventfully. However, 3 min after starting the seventh infusion courses, the patient experienced cardiopulmonary arrest. We immediately performed cardiopulmonary resuscitation. The patient's anaphylaxis symptoms resolved after treatment with intravenous epinephrine. He was discharged 3 days after the event with no further complications. Clinicians should be aware that oxaliplatin-induced anaphylactic shock often occurs during the eighth infusion cycle and that this severe hypersensitivity reaction is difficult to predict and prevent.

Expression of receptor tyrosine kinases in esophageal carcinosarcoma.

Esophageal carcinosarcoma (ECS) is a rare malignant neoplasm associated with a poor patient prognosis. It is characterized by the presence of both malignant epithelial and mesenchymal components. Molecular-targeted therapy of several receptor tyrosine kinases (RTKs) has been reported to be effective in the treatment of various malignant tumors, including carcinosarcoma of several organs. This study aimed to assess the therapeutic potential of targeting RTKs in ECS. Overexpression of RTKs was assessed in 21 ECS cases by immunohistochemistry (IHC). Positively stained cases were further examined for RTK gene mutations and amplifications by direct sequencing analysis and fluorescence in situ hybridization. In epithelial components, KIT, platelet-derived growth factor receptor (PDGFR)A, PDGFRB, MET, epidermal growth factor receptor (EGFR) and HER-2 were overexpressed in 1 (4.8%), 1 (4.8%), 0 (0%), 11 (52.4%), 13 (61.9%) and 2 (9.5%) cases, respectively. In the mesenchymal components the corresponding numbers of cases were 2 (9.5%), 2 (9.5%), 0 (0%), 12 (57.1%), 11 (52.4%) and 0 (0%). No mutations in the c-kit, PDGFRA and c-met genes were found. Among 19 EGFR-positive tumors, 2 had EGFR missense mutations (T790A, exon 20) only in the mesenchymal component. Gene amplification or high polysomy of c-kit, PDGFRA, c-met and EGFR was observed in 1 (33.3%), 0 (0%), 3 (18.8%) and 10 (52.6%) cases, respectively. In conclusion, various RTKs, particularly MET and EGFR were overexpressed in ECSs suggesting that molecular-targeted therapies directed to MET, EGFR or other RTKs may be effective in inhibiting the growth or progression of the epithelial and/or mesenchymal component of ECS.

Urgent surgery for intraperitoneal bleeding from GIST during imatinib therapy.

The rupture or bleeding of a gastrointestinal stromal tumor (GIST) is a life-threatening adverse event that can happen during imatinib therapy, but few such cases have been reported in the medical literature. Here, we report a case of intraperitoneal bleeding from GIST during imatinib therapy. A 75-year-old man was diagnosed with a large GIST with liver metastasis and admitted to our hospital for abdominal pain on the 13th day of imatinib therapy. The pain disappeared after 7 days of hospitalization; however, the patient complained of diffuse abdominal pain 5 days after discharge. He presented with muscular guarding, and abdominal-pelvic CT demonstrated dense ascites. The tentative diagnosis was peritoneal hemorrhage from GIST, and urgent laparotomy was performed. During the laparotomy, we noted hemoperitoneum of approximately 500 ml; we resected a bulky metastatic tumor on the greater omentum and a primary tumor on the jejunum. The patient took imatinib (400 mg daily) from the ninth postoperative day and underwent monthly checkups for 9 months after the surgery. When GIST patients complain of sudden and severe abdominal pain during imatinib therapy, bleeding from GIST should be considered as a possible adverse effect of imatinib.

Clinicopathological and immunohistochemical characteristics of esophageal carcinosarcoma.

BACKGROUND: Esophageal carcinosarcoma is a very rare neoplasm and its clinicopathological characteristics and the prognostic factors that influence the clinical outcome of the patient remain a matter of controversy. PATIENTS AND METHODS: Twenty patients with esophageal carcinosarcoma were referred to our institutions. Tissue blocks were reviewed and sections containing both carcinomatous and sarcomatous components were stained for epithelial and mesenchymal markers and a proliferating cell marker. The prognosis of the esophageal carcinosarcoma patients was compared with 142 cases of esophageal squamous cell carcinoma. RESULTS: In the carcinomatous component, the expression of cytokeratin, epithelial membrane antigen, vimentin, smooth muscle actin, and S100 were detected in 20, 20, 1, 1, and 1 case, respectively, whereas in the sarcomatous component, expression of these were detected in 4, 2, 18, 15, and 3 cases, respectively. The Ki-67 labeling index of carcinomatous and sarcomatous components was 35.5% and 41.8%, respectively. The 5-year survival rate was not statistically different between squamous cell carcinoma and carcinosarcoma (p=0.219). However, for T1 cases only, carcinosarcoma patients had statistically poorer prognosis than did squamous cell carcinoma patients (p=0.008). CONCLUSION: The sarcomatous component shows various histological and immunohistochemical forms. In comparison with squamous cell carcinoma patients, carcinosarcoma patients had poorer prognosis amongst the T1 cases. For the treatment of esophageal carcinosarcoma, it is important to monitor lymph nodes and be watchful for hematogenous metastasis, as in cases of esophageal squamous cell carcinoma.