[A case of sigmoid colon cancer with liver and ovarian metastases effectively treated by panitumumab after acquiring resistance to prior chemotherapy regimens].

A 44-year-old female was referred to our hospital with a complaint of abdominal fullness. Computed tomography(CT) showed multiple liver masses and a huge ovarian tumor. Colonoscopy revealed a type 4 advanced cancer in the sigmoid colon. She was diagnosed with unresectable liver and ovarian metastases from advanced sigmoid colon cancer, for which we were obliged to select chemotherapy. As the first line, FOLFOX was applied and performed for 6 cycles, followed by FOLFOX plus bevacizumab(BV)for 5 cycles. While no deterioration of liver and ovarian metastases was observed during the course of those chemotherapy regimens, the patient developed a considerable level of acute sensorimotor neuropathic symptoms associated with oxaliplatin-induced peripheral neurotoxicity, forcing us to replace FOLFOX plus BV with FOLFIRI plus BV. Three cycles of FOLFIRI plus BV, however, turned out to be progressive disease with deterioration of liver and ovarian metastases. Since her oxaliplatin-induced neurotoxicity was improved, a regimen of FOLFOX plus BV was once again applied to her for 3 cycles, which failed to prevent her from having a progressive disease. The sequencing of K-RAS genes from the biopsy specimens of sigmoid colon cancer revealed an expression of a wild-type K-RAS. Thus, an addition of panitumumab to FOLFOX was made. Surprisingly, after 3 cycles of the chemotherapy regimen over 3 months, a significant reduction in the size of liver and ovarian metastases was observed. Her sense of abdominal fullness was apparently reduced and was even lower than what it was at admission. Panitumumab has great potential for effective treatment of patients with unresectable stage IV colorectal cancer, even after having acquired resistance to prior chemotherapy regimens.

[A case of mesenteric desmoid tumor].

A 53-year-old man was admitted hospital because of frequent vomiting and poor digestion. Abdominal computed tomography showed a tumor, about 5 cm in diameter at the duodeno-jejunal junction. A barium contrast duodeno-small bowel series revealed stenosis in the therd portion, where push enteroscopy could not pass with normal mucosa. The preoperative diagnosis was submucosal or mesenteric tumor. Open surgery was performed. The tumor derived from the mesenterium and involved the anal side of the small intestine. The tumor was removed with partial excision of the upper jejunum. The diagnosis of mesenteric desmoid tumor was confirmed, histologically.

[A case of gastric carcinoma with metachronous liver metastases that responded to percutaneous ethanol injection therapy (PEIT) and TS-1].

A 57-year-old male underwent a total gastrectomy with D1 lymph node dissection for gastric carcinoma. The main tumor was located in area UM, measuring 15 x 6 cm and was classified as type 5. Histopathologically, the cancer cells invaded the subserosal layer with a moderately differentiated tubular pattern. Lymph node metastases (No. 1, 3, 7 and 9) were detected. Lymphatic involvement was revealed (ly 2). Three years after the first surgery, a liver metastasis (area S4) with a diameter of 30 mm was detected by abdominal ultrasonography. Percutaneous ethanol injection therapies (PEIT) were performed twice for the lesion. After PEIT, a TS-1 intake program (80 mg/day, for 4 weeks) was started for the metastatic lesion. Both treatments were effective. The patient has survived without recurrence for over 5 years after the total gastrectomy.

[Clinical study of individual TS-1 therapy for inoperable gastric cancer].

TS-1 is a novel oral anticancer drug that is a formation of 5-FU. It consists of tegafur, CDHP (which inhibits 5-FU degradation enzyme), and Oxo (which reduces gastrointestinal toxicities) for an increased anticancer effect. We applied individual TS-1 therapy in 22 cases (cs) of inoperable gastric cancer and studied the clinical and adverse effects. Patients were treated with daily oral administration of 80-100 mg TS-1 for 4 weeks, followed by a rest for 1 or 2 weeks. The response rate was found to be 27.3% (6/22) (PR: 6 cs, NC: 4 cs, PD: 10 cs, NE: 2 cs). Overall, the median survival time was 8.2 months and the one-year survival rate was 23.6%. By location, the response rate of the primary lesion was 27.3% (6/22), abdominal lymph node metastasis 18.8% (3/16), and liver metastasis 33.3% (4/12). There was no significant difference in the response rate by tissue type. A comparison by whether or not patients had undergone previous chemotherapy revealed a response rate of 37.5% (6/16) in patients who had undergone previous chemotherapy, and 0% (0/6) in those who had not. The prevalence of adverse effects was 68.2% (15/22), with the main adverse effects being myelosuppression, pigmentation and appetite loss. However, adverse effects with a grade of more than 3 occurred in only one case of neutropenia. We could observe the course of all patients on an outpatient basis.

Allelic imbalance of 14q32 in esophageal carcinoma.

It has been demonstrated that the accumulation of alterations in several oncogenes and tumor suppressor genes plays a role in the initiation and progression of esophageal carcinoma. However, to our knowledge, very few studies have described the molecular genetic changes of chromosome arm 14q in esophageal carcinoma. In this study, we examined 35 primary esophageal carcinomas for allelic imbalance on 14q32. Analysis of four polymorphic microsatellite markers identified 13 (37%) tumors exhibiting allelic imbalance on 14q32 in at least one locus. In particular, the allelic imbalance of the D14S267 marker that has been reported in various tumors as having a high frequency of deletion was observed in 10 of 26 informative cases (38.5%). The commonly deleted regions were delineated by markers D14S65 and D14S250 on 14q32. In regard to the macroscopic features of tumor, the 14q allelic imbalance rate of protruding type tumors was higher than that of the ulcerative type. These data suggest that potential suppressor loci on 14q32 are related to the development and progression of esophageal carcinoma.