In view of the current interest in the use of lymphoid cells in adoptive immunotherapy of patients with advanced cancer, we have studied the homing patterns of various lymphoid effector cells in mammary-tumor-bearing mice. Single-cell suspensions of total splenocytes, natural killer (NK) cells, and lymphokine-activated killer (LAK) cells were prepared from the spleens of C3H/OuJ mice. Tumor-infiltrating lymphocytes (TIL) were isolated from mammary adenocarcinomas excised from retired breeder females of the same substrain. Effector cells were labeled with indium-111 and injected via a tail vein into female C3H/OuJ mice bearing one or more mammary tumors. Twenty-four hours after administration, total splenocytes, NK cells, and LAK cells distributed themselves evenly between normal mammary tissue and mammary adenocarcinomas. Only TIL had a higher concentration in tumors than in corresponding normal mammary tissue. The ability of the different lymphocyte preparations to lyse YAC-1 cells was determined by means of a 4-h 51Cr-release cytotoxicity assay. Cells harvested from LAK cell cultures and further enriched by centrifugation through a discontinuous Percoll gradient and interleukin-2 (IL-2)-stimulated TIL demonstrated the highest levels of cytotoxicity, while total splenocytes and fresh TIL were characterized by the lowest levels. Since IL-2-stimulated TIL were highly cytotoxic and exhibited better tumor localization than both NK cells and LAK cells in this system, they may be the lymphoid effectors of choice for adoptive immunotherapy of advanced cancer.
The chemical composition of a membrane‐bound plastid inclusion observed in genetic tumor cells of the amphiploid Nicotiana suaveolens X N. langsdorffii was studied by means of electron microscope cytochemistry. Treatment with the following enzymes had no effect on the ultrastructure of the inclusion: α‐amylase, DNase, lipase, papain, pronase, protease, RNase, and trypsin. The only enzyme to alter the fine structure of the inclusion was pepsin, which decreased the electron density of the granular component of the structure. These results indicate that protein is the major chemical constituent of this membrane‐bound plastid inclusion. This finding is discussed in relation to the possible role of the inclusion in plastid ontogeny.
Young seedlings of the tumor-prone amphiploid Nicotiana suaveolens X N. langsdorjjii were grown aseptically on nutrient medium in a controlled environment chamber. At regular intervals after the seeds had been sown, the incidence of tumor formation was scored and plants were harvested. Indole-3-acetic acid was extracted, purified, and assayed spectrofluorometrically. A close correlation in time between onset of tumor formation and decline in endogenous level of indole-3-acetic acid was demonstrated.It has been suggested that the trigger for tumor induction in certain Nicotiana hybrids is a reduction in the endogenous level of auxin (5). There is considerable evidence in support of this hypothesis, and it is beginning to look as though the mechanism of tumor induction in this system is similar to that by which axillary buds are released from the dominance of the apical meristem. First, it has been demonstrated that correlative inhibition of axillary buds diminishes as a plant gets older (18). Tumors appear most frequently on mature Nicotiana hybrids during and after the flowering period when growth of the shoot apex is reduced (15). Second, growth of inhibited axillary buds can be stimulated by decapitation of the apical bud, and this loss of apical dominance can be prevented by applying IAA to the cut surface of decapitated plants (27). Decapitation of primary and secondary shoots accelerates tumor formation in Nicotiana, and the appearance of internodal tumors can be suppressed with exogenous IAA (5). Third, triiodobenzoic acid has been shown to break apical dominance in a variety of plants (6,13,20,25,28) While the available evidence supports the suggestion that auxin is involved in the trigger for tumor induction in genetically tumor-conditioned Nicotiana hybrids, a reduction in auxin at potential centers of growth prior to tumor initiation has not been reported. The aim of the present investigation was to study the rate of tumor formation and fluctuations in the endogenous level of IAA with time in young tumor-prone Nicotiana seedlings. MATERIALS AND METHODSSeeds of the amphiploid Nicotiana suaveolens X N. lanigsdorffii were surface-sterilized in a Clorox-Kromet solution for 12 min, and then sown in 125-ml Erlenmeyer flasks on 30 ml of a modified Hildebrandt-Riker nutrient medium (pH 5.3-5.4) which was solidified with 1.0% (w/v) agar (14). Seedlings were grown in a controlled environment chamber at 22 ± 1 C and 60 to 65% relative humidity under 18 hr illumination (1900 -4-150 ft-c). Beginning 11 days after the seeds had been sown, the plants were examined at regular intervals in order to score the incidence of tumor formation as evidenced by visible outgrowth of undifferentiated tissue.In order to determine the endogenous level of IAA, plants were harvested, the roots were removed, and the tops were immediately frozen in liquid nitrogen. The seedlings (3-5 g fresh weight) were ground to a fine powder in a prechilled mortar and pestle. The powdered material was extracted, the extract was purified, ...
Young seedlings of two tumorous Nicotiana amphiploids and the parental species, grown aseptically on nutrient medium, were treated with 2,3,5-triiodobenzoic acid. The incidence of tumor formation was scored for 18 days subsequent to exposure. Triiodobenzoic acid markedly accelerated the rate of tumorigenesis in both amphiploids, but it did not induce tumors in the parental species. The compound also induced tumor formation in a small percentage of seedlings of a non-tumorous mutant of the N. glauca × N. langsdorffii amphiploid. These results are discussed in relation to the problem of the trigger mechanism for tumor induction in Nicotiana species hybrids.<
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