RESUMO
Colorectal cancer is a prevalent malignancy worldwide, and investigations are required to elucidate the underlying carcinogenic mechanisms. Amongst these mechanisms, de novo carcinogenesis and the adenoma to carcinoma sequence, are the most understood. Metastasis of colorectal cancer to the liver often results in fatality, therefore, it is important for any associated risk factors to be identified. Regarding the treatment of the disease, it is important to manage not only the primary colorectal tumor, but also the liver metastases. Previously, through gene variation analysis, chromosomal loss has been indicated to serve an important role in liver metastasis. Such analysis may aid in the prediction of liver metastasis risk, alongside individual responses to treatment, thus improving the management of colorectal cancer. In the present study, we aimed to clarify a cause of the liver metastasis of colorectal cancer using comparative genomic hybridization analysis. A total of 116 frozen samples were analyzed from patients with advanced colorectal cancer that underwent surgery from 2004 to 2011. The present study analyzed mutations within tumor suppressor genes non-metastatic gene 23 (NM23), deleted in colorectal carcinoma (DCC) and deleted in pancreatic carcinoma, locus 4 (DPC4), which are located on chromosomes 17 and 18 and have all been reported to affect liver metastasis of colorectal cancer. The association between chromosomal abnormalities (duplication and deletion) and liver metastasis of colorectal cancer was evaluated using comparative genomic hybridization. Cluster analysis indicated that the group of patients lacking the long arm of chromosome 17 demonstrated the highest rate of liver metastasis. No significant association was observed between the frequency of liver metastases for synchronous and heterochronous colorectal cancer cases and gene variation (P=0.206). However, when these liver metastasis cases were divided into the synchronous and heterochronous types, the ratio of each was significantly different between gene variation groups, classified by the existence of the 17q deletion (P=0.023). These results indicate that the deletion of 17q may act as a predictive marker of liver metastasis in postoperative states.
RESUMO
A 65-year-old woman with a history of constipation presented at our hospital and was subsequently diagnosed with advanced cecum cancer. We performed laparoscopic right hemicolectomy in January 2009, with pathological findings reveal- ing the presence of Stage III b (pT3, pN3, cM0, Cur A) disease. The patient was treated with a uracil/tegafur plus Leucovorin (UFT/LV) adjuvant chemotherapy regimen for six months. In June 2010, bold examination indicated an elevated level of tumor marker CA19-9. Computed tomography (CT) and positron emission tomography (PET)/CT revealed Virchow's and para-aortic lymph node metastasis. Therapy with XELOX and bevacizumab (Bmab) was administered and continued for 10 cycles. Capecitabine+Bmab treatment was also administered for 11 courses due to an adverse event of peripheral neuropathy. Follow-up revealed both the Virchow's and para-aortic lymph node metastasis had disappeared upon completion of treatment. In November, 2011 the patient was considered to have achieved a clinical complete response (CR) and continues to be followed with no further disease progression.