Experimental tumorigenesis in the hamster cheek pouch.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to I Wodinsky.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The mechanism(s) of cellular resistance to vincristine (VCR) are poorly understood. Four murine tumor cell lines with varying degrees of VCR resistance, as measured by prolonged survival of tumor-bearing mice following VCR treatment, were selected for study. These lines were P1534, P388, P388/VCR and L1210. Steady-state cellular VCR levels, bound intracellular VCR, displaceable intracellular VCR, influx velocities and efflux velocities following VCR preloading were all measured in vitro and correlated with augmentation of survival. Neither the influx velocity, efflux velocity nor the steady-state VCR level showed any apparent correlation with in vivo sensitivity. Moreover, the ratio of influx velocity to efflux velocity was highest in the most sensitive cell line (i.e. P1534) and lowest in the most resistant cell line (i.e. P388/VCR). Bound intracellular VCR correlated best with VCR sensitivity suggesting that high-affinity intracellular binding, presumably to tubulin (Ka congruent to 1 X 10(-7) M), is a critical determinant of VCR sensitivity.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Experiments are described in which four transplantable rodent tumors (L1210 lymphoid leukemia, P388 lymphocytic leukemia, B16 melanoma, and Walker 256 carcinosarcoma) were used to investigate the antitumor activity of amygdalin MF. Amygdalin MF was given alone and in combination with beta-glucosidase which was administered 1/2 hour prior to amygdalin MF, starting 24 hours after tumor implantation. No antitumor activity was observed in any of the four tumor systems tested with the drug alone or in combined therapy. The combined therapy showed potentiation of toxicity with doses of amygdalin MF greater than or equal to 100 mg/kg.