Corticosteroids and Lymphoid Cells

Claman, Henry N.

doi:10.1056/nejm197208242870806

Cited by 956 publications

(261 citation statements)

References 97 publications

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“…Glucocorticoids also inhibited the growth of mammary tumors (Brunschweiger and Schiffer 1981) and other murine experimental tumors (Grasso and Johnson 1977). The therapeutic effects of glucocorticoids may involve specific glucocorticoid receptors found in lymphoid cells (Claman 1972;Schmidt and Tompson 1978). Holbrook et al (1984) suggested that the lability of cytosolic glucocorticoid-receptor complexes may in part be related to the state or the tendency of differentiation of the leukemic cells.…”

Section: Discussionmentioning

confidence: 99%

Metastatic enhancement and growth inhibition by glucocorticoid and its receptors in mouse teratocarcinoma OTT6050 in vivo.

Kubota

Kubota²,

Matsuzawa³

et al. 1987

Tohoku J. Exp. Med.

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To elucidate the mechanism of glucocorticoid-induced metastases and growth inhibition of mouse teratocarcinoma OTT6050, syngeneic 129/Sv-CP+SP mice were subcutaneously (s.c.) injected with the tumor and treated with daily intraperitoneal (i.p.) injections of hydrocortisone in doses of 1.5 to 12.5 mg per mouse. The number of lymphnode and visceral metastases was greatly increased by the treatment with hydrocortisone unrelated to the doses and sexes. Tumor growth (the products of three principal diameters) of lymphnode metastases was dosedependently inhibited by the treatment. Histologically, lymphnode metastatic tumors contained large masses of well-differentiated tissues compared with the s.c. transplanted tumor of the same size. The glucocorticoid receptors were measured using dextran-coated charcoal adsorption techniques with [3H] hydrocortisone. Glucocorticoid receptor contents were higher in lymphnode metastatic tumor (100 fmole/mg cytoplasmic protein, mean) than in s.c. transplanted tumors (74.5 fmole/ mg, mean) respectively treated with 12.5 mg of hydrocortisone. The metastatic growth inhibition by hydrocortisone might be closely related to the receptormediated mechanisms and histological differentiation, teratocarcinoma OTT6050 ; glucocorticoid ; metastases Teratocarcinomas are malignant tumors which are characterized by the presence of a distinctive cell type known as embryonal carcinoma, and of a variety of differentiated cell types (Stevens and Pierce 1975). Mouse teratocarcinoma 0TT6050 originated from a six-day-old 129/Sv strain mouse embryo that was grafted into the testis of a F1 hybrid mouse (Stevens 1970). The solid tumors, produced by s.c. injections of ascitic embryoid bodies into mice, can differentiate into a wide range of tissue types (Pierce et al. 1960). Another characteristic of teratocarcinoma is its sensitivity to its host environment (Pierce 1967). Various

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Section: Discussionmentioning

confidence: 99%

Metastatic enhancement and growth inhibition by glucocorticoid and its receptors in mouse teratocarcinoma OTT6050 in vivo.

Kubota

Kubota²,

Matsuzawa³

et al. 1987

Tohoku J. Exp. Med.

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“…3 (Table III). (Pearsall and Weiser, 1968;Levy and Wheelock, 1975 (Claman, 1972). TB inhibits lysosomal enzymes of macrott received phages (Beck, Lloyd and Griffiths, 1967) metastatic and abrogates non-specific resistance to of meta-growth of ascitic tumour in mice treated 29) was with BCG or toxoplasma (Hibbs, 1975).…”

Section: Macrophage Impairmentmentioning

confidence: 99%

Immunological mechanisms in metastatic spread and the antimetastatic effects of C. parvum

Jones¹,

Castro²

1977

Br J Cancer

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Summary. The effects of the host's immune response on metastatic spread was investigated by observing the numbers of pulmonary metastases that developed from an s.c. implant of the Lewis lung carcinoma in C57BL mice in which different cell populations had been suppressed. Macrophage function was impaired by treatment with silica (Si), cortisone acetate (CA), or trypan blue (TB). T-cell function was depressed by adult thymectomy and sublethal irradiation, or by treatment with antilymphocyte serum (ALS).Metastasis was significantly increased and phagocytic activity decreased by Si and CA, but were unaffected by TB. Thymectomy and irradiation had no effect on metastases, whereas ALS when given before, but not after tumour growth, reduced their number.The antimetastatic action of the immunopotentiating agent C. parvum was investigated in these immunologically impaired mice. It was unaffected by Si, CA or TB. However, the inhibiting effect of these agents on phagocytic activity was overcome by treatment with C. parvum. Its antimetastatic action was unaffected in mice which had been thymectomized and irradiated, but could be abrogated by ALS. However, ALS was only able to prevent this activity if given before tumour growth; it was ineffective if given after tumour growth.This study showed that metastatic spread was inversely related to phagocytic activity. The antimetastatic effect of C. parvum appears to be mediated through macrophages in concert with a subpopulation of T lymphocytes, which were considered to be necessary in the sensitization arm of the response as opposed to the effector arm of this response.

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“…During an operation, adrenal corticoid production quadruples (Cosgrove and Jenkins, 1974) and corticosteroids are known to have powerful suppressive effects on T-cells and macrophage activity (Conning and Heppleston, 1966;Claman, 1972). It is possible that during amputation the increase in steroid production depressed the macrophage system, resulting in increased pulmonary metastases.…”

Section: Discussionmentioning

confidence: 99%

“…Corticosteroids are released during operative stress, and their reported effects on metabolism and immunological competence (Claman, 1972;Conning and Heppleston, 1966) may be responsible for enhanced tumour growth.…”

mentioning

confidence: 99%

Effects of amputation and Corynebacterium parvum on tumour metastases in mice

Mosley¹,

Sadler²,

Castro³

1978

Br J Cancer

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Summary. The effects of operation (lower-limb amputation) on the growth of the Lewis lung tumour and its metastases were studied. The role of C. parvum in counteracting these effects was investigated.Anaesthesia alone or with amputation did not affect primary tumour growth. C. parvum depressed this growth.Anaesthesia did not affect the number of pulmonary metastases, but amputation caused a significant increase. C. parvum inhibited metastases and completely counteracted the effects of operation on them. Large doses of cortisone acetate significantly increased metastases but small doses had no effect. Experiments with adrenalectomized mice suggested the effects of operation were due to non-specific stress.

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Corticosteroids and Lymphoid Cells

Cited by 956 publications

References 97 publications

Metastatic enhancement and growth inhibition by glucocorticoid and its receptors in mouse teratocarcinoma OTT6050 in vivo.

Metastatic enhancement and growth inhibition by glucocorticoid and its receptors in mouse teratocarcinoma OTT6050 in vivo.

Immunological mechanisms in metastatic spread and the antimetastatic effects of C. parvum

Effects of amputation and Corynebacterium parvum on tumour metastases in mice

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