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. 2000 Jul 11;97(15):8658–8663. doi: 10.1073/pnas.140210697

Table 1.

Loss of drug resistance, aFGF, and bFGF upon disaggregation of metastatic tumors and upon passaging in monolayer cultures

Culture conditions Concentration producing 50% inhibition
Amount in CM, pg/ml
Pac, nM Dox, nM 5-FU, μM aFGF bFGF
Histocultures*
 Primary >14 18 33 62 130
 Lymph node >227 165 NM 195 660
 Lung >1,804 NM 122 269 845
Monolayers
 (passage 0)
  Primary 10.7 8.0 0.79 62 93
  Lymph node 32.9 31.0 1.90 100 243
  Lung 92.4 77.0 2.84 118 302
Monolayers
 (passage 1)
  Primary 10.5 8.6 0.85 NM NM
  Lymph node 21.8 17.9 1.29 NM NM
  Lung 28.1 31.7 1.52 NM NM
Monolayers
 (passage 2)
  Primary 10.3 8.0 0.79 NM NM
  Lymph node 15.0 11.0 1.09 NM NM
  Lung 21.5 16.6 1.20 NM NM
Monolayers
 (passage 3)
  Primary 10.0 8.0 0.78 54 95
  Lymph node 11.7 7.8 0.83 51 89
  Lung 11.4 8.0 0.81 58 103

Paired rat primary and metastatic tumors were cultured as histocultures or monolayers. For histocultures, tumors were treated with paclitaxel (Pac) for 24 h (12 pairs of primary and lymph node tumors and 2 pairs of primary and lung tumors), and with doxorubicin (Dox) (3 pairs of primary and lymph node tumors) and 5-fluorouracil (5-FU) (2 pairs of primary and lung tumors) for 96 h. For monolayers, cells were treated with drugs for 96 h, and drug effect was measured by the BrdUrd incorporation method. Mean values. NM, not measured. 

*

In histocultures, Pac at 10,000 nM produced <50% inhibition; data shown are the concentrations that produced 30% inhibition. 

P < 0.05 for differences between primary and metastatic tumors (unpaired Student's t test).