No abstract

Background and Objectives: Lymph node metastasis is known as a significant predictor of prognosis in colorectal cancer patients. Recently, reverse transcriptase polymerase chain reaction (RT‐PCR) has been applied to detecting micrometastasis. To assess the risk of recurrence and accurately determine the spread of tumor cells, we examined lymph node micrometastases in a series of colorectal cancer patients. Methods We examined 202 lymph nodes obtained from 13 colorectal cancer patients who underwent curative operation and were histologically diagnosed to be node‐negative, using RT‐PCR to amplify mRNAs for two epithelial markers, carcinoembryonic antigen (CEA) and cytokeratin 20 (CK‐20). Results All the cases, including early stage patients, had micrometastases. A total of 102 among 202 lymph nodes (50.5%) were positive for either CEA or CK‐20, or both (47.0, 40.1, and 36.6% respectively). Positive lymph nodes were spread along the courses of vascular trunks as well as being located in more distant regions. Conclusions Even in histologically negative lymph nodes, there is a considerable possibility that micrometastases may exist. Their detection by RT‐PCR may improve clinical staging and indications for cancer therapy. We should also take care in the choice of surgical approach. J. Surg. Oncol. 1998;68:34–40. © 1998 Wiley‐Liss, Inc.

Summary The SMAD-2 gene, which is located at 1 8q21, has been identified as a candidate tumour-suppressor gene from work on colorectal cancers. The aim of the present study was to determine the clinical alterations and the significance of its mutations in a series of colorectal cancers previously examined for SMAD-4/DPC-4 gene. Mutation analyses of the SMAD-2 gene were carried out on cDNA samples from 36 primary colorectal cancer specimens using a combination of the polymerase chain reaction (PCR), single-strand conformation polymorphism (SSCP) and DNA sequencing. Only one missense mutation (2.8%), producing an amino acid substitution in the highly conserved 1996). is somatically mutated in a proportion of colorectal cancers in vivo (Takagi et al. 1996). However. the observed frequency of SMAD-4 mutations was significantly lower than expected from the numbers of 18q21 deletions in colorectal cancers. indicating that another tumour-suppressor gene might be present in this chromosome region. For instance. the DCC was the first candidate tumour suppressor in the region. although data on DCC mutations in the same set of tumour samples presented here are not available at present because of its length and complexity.More recently. a novel gene. termed SMAD-2. has been isolated and revealed to be closely related to the SMAD-4 gene (Riggins et al. 1996: Eppert et al. 1996. Of interest. it w-as mapped to the 18q21 region within a short distance. 3 Mb. from the SMAD4 gene. These observations led us to examine whether the SMAD-2 gene might also be mutated in the same set of colorectal cancers already examined for SMAD-4 gene changes. We herein report our results for SMAD-2 mutations from 36 colorectal cancer specimens. taken at surgery from Japanese patients. together with comparatis e data for the molecular status of the SMAD4 gene. Somatic in vivo SMAD-2 mutations were found. although at very low frequency. providing further evidence that alterations of MAD-related genes at 1 8q2 1 are indeed involved in the pathogenesis of colon cancers.

A patient with small-cell carcinoma of the stomach with long survival after percutaneous microwave coagulating therapy (PMCT) for liver metastasis Abstract A 66-year-old man was admitted to our hospital with epigastralgia. Preoperative examinations revealed an 8.0 ϫ 8.0-cm, Borrmann type 2 tumor in the posterior wall of the cardia, without distant metastases. Total gastrectomy with pancreato-splenectomy and regional lymph node dissection was performed curatively. Histologically, the tumor was composed mainly of small cells with hyperchromatic nuclei and scant cytoplasm, which showed positive staining for Grimelius, γ-neuron-specific enolase (γ-NSE), chromogranin A, and serotonin. About 10 months after the operation, a solitary tumor was revealed in S8 of the liver by abdominal computed tomography (CT), and it was histologically confirmed by needle biopsy to be a metastasis of the small-cell carcinoma from the stomach. Instead of hepatectomy, percutaneous microwave coagulating therapy (PMCT) was indicated, because of the patients' liver dysfunction (ICG R15, 39.9%); CT showed complete necrosis of the metastatic focus in the liver after the PMCT. Now, 33 months after the first detection of the liver metastasis (43 months after the gastrectomy), the patient is still alive without any growth of the liver metastasis. The 67 previously reported cases of small-cell carcinoma of the stomach in Japan, including ours, are also reviewed.

Influences of operative stress on nonspecific cell-mediated immunity and on liability to tumor metastasis and preventive effects thereon of a nonspecific immunopotentiator OK-432 were examined. Syngeneic female SD rats were inoculated SC with 200 mg of a transplantable mammary carcinoma MRMT-1 at the dorsal flank. After 2 weeks the tumor was surgically excised simply or combined with 30-min laparotomy. It was revealed by follow-up examination that the laparotomy stress significantly increased incidence of postoperative lung metastasis. It was found that PHA-induced blastogenesis of peripheral lymphocytes was markedly reduced in the early period following laparotomy. Preoperative or post-operative (especially the former) administration of OK-432 was effective for preventing both the postlaparotomy facilitation of lung metastasis and the postlaparotomy reduction in PHA lymphoblastogenesis.