ABSTRACT
The present study reports a case of eosinophilia-associated rectal cancer that was successfully stabilized using chemotherapy, and reviews the mechanisms of eosinophilia and the importance of chemotherapy. A 65-year-old man, who had previously been diagnosed with suspected rectal cancer, presented with the chief complaint of melena. Eosinophilia, abnormal blood coagulation, and elevated carcinoembryonic antigen and carbohydrate antigen 19-9 tumor marker levels were observed, and the patient was subsequently diagnosed with advanced rectal cancer accompanied by multiple lymph node metastases that extended from the para-aortic lymph nodes to the left axillary lymph nodes. The complication of deep vein thrombosis was also observed. Tumor hemorrhage was exacerbated, and thus, Hartmann's procedure was performed. Pathological findings included poorly- to moderately-differentiated adenocarcinoma; however, no eosinophil infiltration was observed within the tumor. Following surgery, the eosinophilia and lymph node metastasis were exacerbated, and an oxaliplatin plus capecitabine chemotherapy regimen was initiated. The patient's eosinophil count and tumor marker levels normalized, and the lymph nodes decreased in size; however, re-enlargement of the lymph nodes was observed 6 months after surgery. The patient was then administered a chemotherapeutic regimen of irinotecan/fluorouracil/folinic acid + bevacizumab, and stable disease was maintained until pleural and peritoneal dissemination were observed at 22 months post-surgery. Following a rapid deterioration in condition, the patient succumbed to the disease at 23 months post-surgery. The present case indicates that although eosinophilia-associated colon cancer exhibits a poor prognosis, early chemotherapeutic intervention may improve this.
ABSTRACT
A number of previous studies have reported that 30-50% of patients with colorectal cancer (CRC) harbor Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations, which is a major predictive biomarker of resistance to epidermal growth factor (EGFR)-targeted therapy. Treatment with an anti-EGFR inhibitor is recommended for patients with KRAS wild-type metastatic colorectal cancer (mCRC). A recent retrospective study of cetuximab reported that patients with KRAS p.G13D mutations had better outcomes compared with those with other mutations. The aim of this retrospective study was to assess the prevalence of KRAS p.G13D mutations and evaluate the effectiveness of cetuximab in mCRC patients with KRAS p.G13D or other KRAS mutations. We reviewed the clinical records of 98 mCRC patients with KRAS mutations who were treated between August, 2004 and January, 2011 in four hospitals located in Tokyo and Kyushu Island. We also investigated KRAS mutation subtypes and patient characteristics. In the patients who received cetuximab, univariate and multivariate analyses were performed to assess the effect of KRAS p.G13D mutations on progression-free survival (PFS) and overall survival (OS). Of the 98 patients, 23 (23.5%) had KRAS p.G13D-mutated tumors, whereas 75 (76.5%) had tumors harboring other mutations. Of the 31 patients who received cetuximab, 9 (29.0%) had KRAS p.G13D mutations and 22 (71.0%) had other mutations. There were no significant differences in age, gender, primary site, pathological type, history of chemotherapy, or the combined use of irinotecan between either of the patient subgroups. The univariate analysis revealed no significant difference in PFS or OS between the patients with KRAS p.G13D mutations and those with other mutations (median PFS, 4.5 vs. 2.8 months, respectively; P=0.65; and median OS, 15.3 vs. 8.9 months, respectively; P=0.51). However, the multivariate analysis revealed a trend toward better PFS among patients harboring p.G13D mutations (PFS: HR=0.29; 95% CI: 0.08-1.10; P=0.07; OS: HR=0.23; 95% CI: 0.04-1.54; P=0.13). In conclusion, treatment with cetuximab may be more clinically beneficial in mCRC patients with a KRAS p.G13D mutation, compared with those harboring other mutations. However, further investigation is required to clearly determine the benefits of cetuximab treatment in patients with KRAS p.G13D mutation-positive mCRC.
