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Progression toward metastatic phenotype with loss of growth‐inhibiting tumor‐cell/cell interactions in vivo
Author(s) -
Takeda Yasutaka,
Sayama Kazutoshi,
Saegusa Yoshiyuki,
Matsuzawa Akio
Publication year - 1995
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910620515
Subject(s) - cell culture , biology , in vivo , endocrinology , phenotype , cell growth , medicine , mammary tumor , cell , tumor progression , hormone , cancer research , pathology , cancer , biochemistry , genetics , breast cancer , gene
Five autonomous sub lines, T4‐O1320, T4‐O1320CY, T4‐O1165, T4‐O1145 and T4‐O196, were established from the transplantable hormone‐dependent mouse mammary tumor, TPDMT‐4, by pass aging under different conditions. These autonomous tumors were characterized by rapid growth in DDD virgin mice and the parental TPDMT‐4 by no growth in these mice. Thus, 10 5 T4‐O1320, 2 × 10 4 T4‐O1320CY, 2 × 10 3 T4‐O1165, 2 × 10 3 T4‐O1145 and 10 3 T4‐O196 cells were co‐injected with 5 × 10 2 TPDMT‐4 cells into virgin mice to determine whether or not hormone‐dependent tumor cells influence the growth of autonomous tumor cells. TPDMT‐4 cells retarded the growth of T4‐O1320 and T4‐O1320CY tumors but accelerated that of T4‐O1165, T4‐O1145 and T4‐O196. Irradiated TPDMT‐4 cells stimulated the growth of all the sub lines except T4‐O1320. In 3‐dimensional collagen‐gel culture, T4‐O1320 and T4‐O1320CY cells formed branched or stellate structures similar to normal mammary glands, as did TPDMT‐4, but T4‐O1165, T4‐O1145 and T4‐O196 cells grew as rounded masses with knobs and showed a completely different morphology. T4‐O1165, T4‐ O1145 and T4‐O196 cells, but not the others, had lung‐colonizing ability. Chromosomal aberration was found in T4‐O1320CY and T4‐O196 but not in the others. Thus, the susceptibility of autonomous sub line tumor cells to growth‐inhibitory regulation from the parental hormone‐dependent tumor cells correlated well with growth morphology within collagen gels and meta‐static ability, but not with chromosomal aberration. The results suggest that meta‐statically‐competent tumor‐cell variants, once they appear, may have a growth advantage in hormone‐ dependent mammary tumors. © 1995 Wiley‐Liss, Inc.