Table 1

Demographic and baseline clinical characteristics of the study population

Number of patients37
Age in years, median (range)61 (39–92)
Gender, n (%)
 Male9 (24.3)
 Female28 (75.7)
Ethnic origin, n (%)
 Caucasian37 (100)
Eastern Cooperative Oncology Group performance status, n (%)
 024 (64.9)
 19 (24.3)
 24 (10.8)
Time from diagnosis in months, median (range)*26.1 (1–228)
Primary tumour site, n (%)
 Breast15 (40.5)
 Stomach5 (3.5)
 Colon/rectum4 (10.7)
 Ovary3 (8)
 Pancreas2 (5.4)
 Oesophagogastric junction2 (5.4)
 Lung2 (5.4)
 Distal oesophagus1 (2.7)
 Bladder1 (2.7)
 Parotid gland1 (2.7)
 Adenocarcinoma, primary site unknown1 (2.7)
HER2 expression, n (%)
 Immunohistochemistry†34 (91.9)
  1+13 (35.1)
  2+6 (16.2)
  3+15 (40.5)
 Fluorescence in situ hybridisation (FISH)‡25 (67.6)
  Negative18 (48,6)
  Amplified7 (18.9)
FcγRIIIa status, n (%)§36 (97.3)
 FF14 (37.8)
 FV16 (43.2)
 VV6 (16.2)
Prior chemotherapy regimens, n (%)¶35 (94.6)
 12 (5.4)
 20 (0)
 ≥333 (89.2)
Any prior antibody therapy, n (%)**20 (54.1)
 Trastuzumab12 (32.4)
 Bevacizumab11 (29.7)
 Cetuximab1 (2.7)
 Panitumumab2 (5.4)
  • *(Date of first dose of study drug − date of initial diagnosis of disease +1)/30.

  •   †IHC was performed locally, at each study centre. Three IHC results missing.

  •   ‡FISH (PathVysion Kit II, Abbott Molecular, Wiesbaden, Germany) was performed centrally (Department of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany). Adequate tumour samples were not available in 12 cases. 

  • ¶Two patients did not receive chemotherapy.

  • §One patient refused consent to FcγRIIIa genotyping. 

  • **Four patients received more than one antibody.

  • F, phenylalanine; HER2, human epidermal growth factor receptor 2; V, valine.