Background Adhesion to lymph nodes, rather than growth stimulation, ac
counted for preferential colonization of lymph nodes by a metastatic B
16 melanoma. We investigated these adhesive interactions. Methods. Fou
r classes of molecules were tested for inhibition of melanoma adhesion
to cryostat sections of lymph node. Results. Calcium chelators ethyle
nediaminetetraacetic acid and l-bis-(beta-aminoethylether)-N,N,N',N'-t
etraacetic acid completely inhibited adhesion (50% adhesion, half-maxi
mal inhibition, at 1 to 3 mmol/L). Cytochalasin B, which impairs contr
actile microfilaments, inhibited adhesion (60% adhesion at .001 mmol/L
, 28% at .01 mmol/L). Colchicine, which disaggregates microtubules, ha
d a similar effect (20% at .01 mmol/L, lowest dose tested). Trypsin sl
ightly increased adhesion (125% adhesion at 10 mug/ml). Neuraminidase,
which removed sialic acid residues, inhibited it (50% adhesion at 5 m
ug/ml). Gly-arg-gly-asp-ser, a peptide with a cell binding sequence of
fibronectin, did not consistently inhibit adhesion (69% adhesion at 0
.1 mg/ml, 83% adhesion at 1 mg/ml) or substantially differ from gly-ar
g-gly-glu-ser-pro (59% adhesion at 0.1 mg/ml, 90% adhesion at 1 mg/ml)
. In contrast, a peptide with a cell binding region of laminin (tyr-il
e-gly-ser-arg) inhibited adhesion (50% adhesion at .05 mg/ml). Conclus
ions. Tumor cell-lymph node adhesion is a calcium-dependent process, r
equiring a functional cytoskeleton, that is mediated by both sialic ac
id moieties and trypsin-resistant, laminin-related, adhesion molecules
.