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Biomedical subjects

R S Wells

Publications and source records attributed to R S Wells.

At least 55 records · Page 3Linked to original sources
PubMed1986

Widespread inhibition of neuroblastoma cells in the 13- to 17-day-old mouse embryo.

Previous experiments have demonstrated specific inhibition of tumor formation after neuroblastoma cells were injected into fragments of 8.5- to 9.5-day embryonic tissue (A.H. Podesta et al. Proc. Natl. Acad. Sci. USA, 81:7608-7611, 1984). The effect was localized to the somite and appeared specific for neuroblastoma as opposed to a variety of other tumor types. This regulation of neuroblastoma cells was believed to reflect an underlying event in the development of migrating embryonic neuroblasts. The current experiments were done to determine the effect on regulation with further embryonic development. The results indicated that later embryos (13 to 17 days of gestation) have a widespread inhibitory effect in all tissues tested, including the adrenal gland, testis, kidney, liver, limb bud, and heart. In contrast a leukemia cell line was not affected by any of these tissues. In organ culture demonstrable colony formation by neuroblastoma was likewise inhibited, and conditioned media from one of these embryonic sources (limb bud) slowed but did not abrogate growth of neuroblastoma cells.

Animals↗
PubMed1985

Metastatic cutaneous carcinoid.

A case of malignant bronchial carcinoid with multiple cutaneous metastases is reported. Despite the extremely aggressive behavior of the disease and the presence of multiple hepatic metastases, the patient did not exhibit the usual clinical features of the carcinoid syndrome. The relevance of the finding of elevated 24-hour urinary vanillylmandelic acid levels in patients with carcinoid tumors is discussed.

Aged↗
PubMed1984

The neurula stage mouse embryo in control of neuroblastoma.

The purpose of this study was to determine whether the neurula stage mouse embryo can regulate tumor formation of C-1300-3 neuroblastoma cells. Five neuroblastoma cells were injected into the second somite of neurula stage embryos, and their ability to form tumors was tested, 24 hr later, by transplanting the portion of the embryo containing the cancer cells into the testes of adult mice. Only one-third the number of tumors was obtained in comparison with controls in which (i) five neuroblastoma cells were injected into blocks of liver tissue that were then transplanted into the testes of adult animals or (ii) five C-1300-3 neuroblastoma cells were injected directly into the testes. When five C-1300-3 cells were injected into somites, which had been dissected from embryos, and the injected somites were placed in animals, significantly fewer tumors were obtained in relationship with controls. Although it is not known whether the neuroblastoma cells are induced to differentiate or are killed by the embryonic tissue, the effect appeared to be specific because the tumor-forming ability of L1210 leukemia, B-16 melanoma, embryonal carcinoma 247, and a parietal yolk sac carcinoma was unaffected by somites.

Animals↗
PubMed1984

Centrifugal lipodystrophy.

We describe a case of centrifugal lipodystrophy occurring in a young English girl, and compare the clinical and histopathological features with previous reports from Japan.

Child, Preschool↗
PubMed1984

Trophectoderm in control of murine embryonal carcinoma.

It has been shown previously that the intact blastocyst of the mouse can regulate tumor formation and colony formation of murine embryonal carcinoma. This effect is consistent with the close histogenetic correspondence between embryonal carcinoma and the inner cell mass of the blastocyst. The ability of inner cell mass, blastocele fluid, and inner and outer surfaces of trophectoderm to abrogate colony formation of a variety of malignant tumors has now been tested. Direct contact of the embryonal carcinoma cells with the blastocele surface of trophectoderm proved to be necessary for abrogation of colony formation of embryonal carcinoma. This effect was not seen with any of the other tumors tested. Some tumors, which lack a normal cellular counterpart in the blastocyst, grew poorly in the blastocele unless a fistula was made in the wall of the blastocyst. Colony formation of the embryonal carcinoma was regulated in blastocysts with fistulas, but the other tumors were not regulated under these conditions. It is concluded that colony formation of embryonal carcinoma cells is regulated by direct contact with the trophectoderm of its corresponding embryonic field in an unknown but specific manner.

Animals↗
PubMed1983

Razoxane: a review of 6 years' therapy in psoriasis.

Razoxane is an effective drug in the systemic treatment of psoriasis, with an initial response rate of 97%. After continuous therapy for up to 6 years we found that 72% of patients remained on the drug with a good therapeutic benefit. We found it to be useful in all forms of cutaneous psoriasis and psoriatic arthropathy. It does not appear to produce hepatic damage and is therefore particularly useful in patients intolerant of methotrexate. We use it as our drug of first choice in the systemic treatment of psoriasis, but it does have several well-recognized side-effects which make careful follow-up necessary. Eighteen per cent of patients stopped razoxane because of these side-effects. However, we feel that razoxane has a valuable place in the systemic treatment of severe psoriasis.

Adult↗
PubMed1982

Specificity of the control of tumor formation by the blastocyst.

An assay to determine the mechanism of regulation of embryonal carcinoma cells by the blastocyst, which is based on a comparison of tumors produced when the cancer cells are cloned alone or after incorporation into blastocysts, was refined by labeling embryonal carcinoma cells with fluorescent microspheres and by following their fate after injection into the blastocysts. Through the use of the new techniques, it was observed that cells of one line of nullipotent embryonal carcinoma were controlled at the 50% level, those from another were not controlled, and those from a multipotent but undifferentiated line were controlled in almost absolute fashion. Single Sarcoma 180 of L1210 leukemia cells were not controlled when injected into the blastocele, but C1300 neuroblastoma cells were partially controlled. None of these tumors have a normal cellular counterpart in the blastocyst, as does embryonal carcinoma, but neurulation follows blastulation by only a few days, so that the neuroblastoma cells may be regulated at that time. Parietal yolk sac carcinoma cells, which have a counterpart in the late blastocyst, were not controlled. On the basis of these data, it is postulated that, if one embryonic field can regulate its closely related cancer, then there may be an embryonic field capable of regulating each carcinoma.

Animals↗
PubMed1982

Role of anchorage in the expression of tumorigenicity of untransformed mouse cell lines.

Cultured mouse cells were tested for tumorigenicity in nude mice with both a conventional assay (injection of cell suspensions) and a new test involving implantation of cells grown on gelatin sponges. Sublines of Balb/3T3 cells, obtained from different sources, varied in their tumorigenic potential with either assay. One subline (A) formed distinctive precancerous nodules only in the sponge assay; these nodules often became progressive after a latent period of 3-4 months. However, suspensions of cells of this subline also caused tumors after a similar latent period, but no nodular phase preceded tumor formation. Another subline of Balb/3T3 (M) has failed to form tumors in either assay. The Balb/3T3 sublines did not differ in vitro properties, such as low saturation density, failure to grow in methylcellulose, and monolayer morphology. A second experimental approach involved tests on nude BALB/c mouse-embryo fibroblasts at various passage levels. The cells were passaged from primary culture, through crisis, to heteroploid, established cell lines. Tumorigenicity was demonstrable earlier in the sponge assay, at which time in vitro parameters putatively associated with malignant behavior were unchanged. Possible relationships with the in vivo phenomenon of solid-surface sarcomagenesis are discussed.

Animals↗
PubMed1982

An in vitro assay for growth regulation of embryonal carcinoma by the blastocyst.

An in vitro assay has been developed in order to examine the mechanism whereby the mouse blastocyst regulates embryonal carcinoma (EC). The assay measures the suppression of EC cell colony formation caused by exposure to the cavity of the blastocyst (i.e., blastocele), and the results are comparable to the previous results with blastocyst-mediated suppression of tumor formation for this same cell line. The assay has been used to determine the time necessary for the blastocyst to regulate the EC cell. In these experiments, immunosurgery is done to disrupt the interaction between the EC cell and the blastocyst, and the EC cell is then recovered and identified by its ability to form a colony. As compared to control cells, 84% of the EC cells are recovered after 2 hr of exposure to the blastocyst, 57% are recovered after 14 hr of exposure, and 27% are recovered after 24 hr of exposure. This long time course is similar to the prolonged doubling time of labeled EC cells within the blastocyst suggesting that the response of the EC cell may be related to the cell cycle within the blastocyst. Data presented show that synchronization of the EC cell cycle (using a mitotic selection procedure) produces synchronization of the response to the blastocyst. The response appears to be closely linked to the G1 phase of the EC cell cycle.

Animals↗