In advanced GIST patients where a course of treatment of
In advanced GIST patients where a course of treatment of Imatinib is interrupted by disease progression, subsequent rechallenge with Imatinib restored tumor control in most patients. In the prospective BFR14 trial, 25 patients with disease progression after interruption of one year of treatment restarted Imatinib 400 mg/day, and 20 patients (80%) achieved treatment response. Among a group of 6 patients interrupting Imatinib after 5 years of treatment that showed disease progression, 5 patients (88.3%) had response when rechallenging Imatinib. In the current case, the patient had disease progression after interruption of 3 years drug treatment, and later reintroduction of Imatinib showed efficacy in disease control.
Conflict of interest
Introduction Male breast cancer is rare, accounting for approximately 1% of all breast cancers, and has an incidence of only 0.7 per 100,000 male population. A hormonal imbalance with elevated prostaglandin receptor and decreased testosterone levels may play an important role in the development of male breast cancer. Hepatocellular carcinoma (HCC) is a much more common cancer, and is associated with liver cirrhosis in 70%–80% of cases. Liver cirrhosis is shown to be associated with an increased level of estrogen, and is therefore related to breast cancer. An alteration in hormonal metabolism may contribute to the coexistence of HCC and breast cancer in male patients. Although a serum alpha-fetoprotein (AFP) level greater than 400 ng/mL has been shown to have high specificity (100%) for the diagnosis of HCC, it has low sensitivity (about 20%) and is present in <50% patients. However, the AFP levels are normal in up to 30% of HCC cases, and may be elevated in a number of metastatic liver diseases.
Case report An 80-year-old male patient suffered from nausea and abdominal pain after food intake. On physical examination, a large, protruding, lobulated, and hard mass with skin discoloration was observed at the left chest wall, in the area of the left breast (Fig. 1). A history of alcoholism for many years was noted. The body mass index (BMI) was 18.7 kg/m2 and therefore within the normal limit (body height, 150 cm; body weight, 42 kg). The blood analysis revealed a mildly elevated white blood cell count (11,800/μL; normal value, 4,500–11,000/μL), increased fasting glucose (116 mg/dL; normal value, 60–108 mg/dL), and decreased albumin level (3.3 g/dL; normal value, 3.5–5.5 g/dL). The other blood data were within the normal range including glutamic pyruvic transaminase (11 U/L; normal value, 4–44 U/L), glutamic oxaloacetic transaminase, (26 U/L; normal value, 8–38 U/L), HbA1C (5.6%; normal value, 4%–6%), alpha-fetoprotein (AFP, 1.3 ng/mL; normal value < 10 ng/mL), carcinoembryonic antigen (4.1 ng/mL; normal value < 5 ng/mL), hepatitis B surface antigen (HBsAg; 0.2 s/c; normal value < 1 s/c [s/c = signal per cutoff ratio]), and anti-hepatitis C virus antibody (0.1 s/c; normal value < 0.8 s/c). Ultrasonography (US) of the abdomen revealed a small hyperechoic nodule in the dependent site of the gallbladder, associated with gallbladder distension and wall thickening. The liver showed coarse parenchymal texture, small size, and undulated surface. Additionally, a 5.1 cm, lobulated mass of mixed echogenicity in S6 of the liver was observed; increased blood flow was found inside the mass on color Doppler imaging (images not shown). Cholelithiasis, acute cholecystitis, liver cirrhosis, and liver tumor, especially hepatocellular carcinoma, were suspected based on the US findings. Computed tomography (CT) of the chest and abdomen with and without intravenous contrast administration, including arterial and portal venous phases, was performed. Distension and minimal wall thickening of the gallbladder, and calcified nodules inside the gallbladder were noted, which were compatible with cholelithiasis and acute cholecystitis. On CT also, irregular liver surface and coarse liver parenchyma were identified; a 5.1 cm, lobulated, hypodense, and heterogeneously hypervascular mass was identified in S6 of the liver, showing an early washout pattern and delayed rim enhancement on the portal venous phase. These findings were consistent with liver cirrhosis and associated HCC (Fig. 2). The patient had Child-Pugh class A liver cirrhosis with a score of 6. The liver tumor was classified as stage B in accordance with the Barcelona Clinic Liver Cancer (BCLC) staging system.