Tetsuro Kawagoe et.al. present a case of a 63-year-old woman was admitted to our institution for severe pain in her right lower abdomen caused by the perforation of cecal cancer. She underwent emergency surgery, from which she was diagnosed with cecal carcinoma with liver, lung, and lymph node metastases. She was a case of metastatic colorectal cancer who benefitted from the reintroduction of S-1, an oral prodrug of 5-FU, and anti-epidermal growth factor receptor antibodies after receiving standard 1st-, 2nd-, and 3rd-line chemotherapies.
A 63-year-old woman with a medical history of hypertension and cerebral infarction was admitted to our hospital with severe abdominal pain in October 2012.
Computed tomography (CT) scan of the abdomen and pelvis showed inflammation spread, abscess formation, lymphadenopathy around the cecum, and a huge mass with multiple nodules in the liver (Figures 1(a) and 1(b)). A chest CT also revealed multiple pulmonary nodules.
She was clinically diagnosed with intestinal perforation owing to cecal cancer and underwent emergency surgery. She was intraoperatively diagnosed with obstruction of the appendicular root owing to cecal cancer, perforation of the vermiform appendix, intraperitoneal abscess, and lymphadenopathy around the cecum and received an ileocecal resection, D1 lymph node dissection, and a peritoneal wash.
After surgery, she was finally diagnosed with moderately differentiated wild-type KRAS adenocarcinoma of the cecum (stage: T3N1M1b, per the Union for International Cancer Control criteria). A microsatellite instability (MSI) test was not performed. RAS and BRAF status were also not investigated. We initiated therapy using cetuximab (500 mg/m2; 14-day cycle) and the mFOLFOX6 regimen (5-FU 400 mg/m2 bolus injection; leucovorin (LV) 200 mg/m2, 46 h continuous infusion with 5-FU 2400 mg/m2; and oxaliplatin 85 mg/m2; 14-day cycle) in October 2012.
This treatment resulted in 7.75 months of partial response (PR), followed by a stable disease (SD) period of 6.25 months and progressive disease (PD) for a total progression-free survival (PFS) period of 14 months. As a 2nd-line treatment, we started the FOLFIRI regimen (5-FU 400 mg/m2 bolus injection, LV 200 mg/m2, 46 h continuous infusion with 5-FU 2400 mg/m2, and irinotecan 150 mg/m2; 14-day cycle), but she developed PD after 2.7 months.
We started trifluridine/tipiracil (35 mg/m2 administered twice daily on Days 1–5 and Days 8–12 of a 28-day cycle) as a 3rd-line treatment, but this led to PD after 1 month. As this patient had a history of cerebral infarction and used antiplatelet drugs, anti-VEGF (R) antibody and regorafenib therapies were contraindicated. Hence, at this stage, no new standard cancer drugs could be tried. However, the patient's general condition was still good, and she requested further chemotherapy. Therefore, we readministered the 5-FU oral preparation S-1 (80 mg/m2, Days 1–28, 42-day cycle), which provided a 7-month SD period.
When PD was again confirmed, we administered panitumumab (6 mg/kg once every 2 weeks) as an anti-EGFR antibody rechallenge. The patient achieved SD on this regimen for 7.5 months.
Finally, 39 months after her diagnosis, the patient died because of rapid disease progression. While receiving readministered drugs, her PS was well maintained; she suffered no grade ≥ 3 adverse events.