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E B Walthall

Publications and source records attributed to E B Walthall.

5 recordsLinked to original sources
PubMed1989

Glucocorticoids stimulate the release of a viral tumor marker (MMTV gp52) while inhibiting tumor cell growth.

The influence of glucocorticoid treatments on the release of mouse mammary tumor virus (MMTV) envelope antigen (gp52) has been studied in C3H mammary tumor cell cultures and compared to treatment-mediated effects on tumor cell growth. Simultaneous assessment of extracellular viral antigen levels and tumor cell growth has indicated that both are coordinately affected by glucocorticoid treatment. While gp52 release is stimulated by treatment, this effect is accompanied by an inhibition of tumor cell growth. These stimulatory and inhibitory effects are mediated by dexamethasone (DEX) in a dose-dependent fashion, and both effects are more pronounced with the synthetic glucocorticoids DEX or triamcinolone acetonide (TA). Quantitation of media gp52 levels by RIA revealed the following hierarchy of glucocorticoid enhancement: TA greater than DEX greater than prednisolone greater than hydrocortisone greater than triamcinolone. A similar order of activity was observed in terms of inhibition of cell growth. The ability of TA to enhance gp52 release was 2.4-2.7 times greater than DEX, a previously proven stimulator of MMTV expression. Cell density of B9 mammary tumor cells was reduced 73% following 72 h of 10(-8) MTA treatment while C3H Mm5mt/cl mammary tumor cells were reduced by 53%. Hormone-mediated changes in in vitro gp52 release suggest that hormones might also influence plasma levels of MMTV gp52 as a systemic marker for the presence and status of murine mammary tumors. Coordinate stimulatory and inhibitory effects suggest that glucocorticoids may play a complex role in murine mammary tumorigenesis and subsequent mammary disease.

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PubMed1989

Shedding of virus-free MMTV gp52 by nonproducer mammary tumor cells: a source of tumor marker in the presence and absence of dexamethasone.

The envelope glycoprotein of the mouse mammary tumor virus (MMTV gp52), a useful plasma marker for mammary tumors in mice, was measured in extracellular medium by radioimmunoassay to quantitatively compare gp52 levels released by a C3H MMTV producer and its subcloned B9 nonproducer cell line. Experiments analyzed levels of viral gp52 released from nonproducer cells both in the presence and absence of dexamethasone (DXS) to compare levels with those of producer cells and to assess quantitative changes in nonproducer release of both soluble and virion-associated gp52. Basal gp52 levels of producer cells were 2.4- to 7.0-fold higher than nonproducer cells. Very little virion-associated gp52 was detected in nonproducer cultures, whereas soluble gp52 was abundant and easily detectable in both cultures. DXS stimulated virus production in B9 cultures, converting nonproducer cells into producers. However, under identical conditions of DXS stimulation, B9 cells never reached the same elevated levels of gp52 as producer cells (90 ng/10(6) cells versus 216 ng/10(6) cells). Significant soluble gp52 release by B9 cells in the absence of DXS and enhancement in the presence of DXS argues that nonproducer cells can influence extracellular levels of viral antigen. By analogy to in vivo studies, results suggest that nonproducer cells in a tumor might also contribute to the pool of gp52 which serves as a systemic plasma marker for tumor.

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PubMed1989

Positive and negative modification of dexamethasone-mediated MMTV gp52 release by progesterone pretreatment of tumor cells.

Murine mammary tumor cells (C3H Mm5mt/cl) were grown in charcoal-stripped serum to examine the effects of hormonal treatments on the expression and release of the mouse mammary tumor virus (MMTV) envelope glycoprotein (gp52). The ability of progesterone to modify extracellular levels of soluble and virion-associated MMTV gp52 was tested singly and as a pretreatment prior to dexamethasone (DXS) stimulation. Single treatments with DXS or progesterone demonstrated that DXS was substantially more effective at elevating gp52 than progesterone; however, a small but significant increase in gp52 levels was noted after 72 h of progesterone treatment. Progesterone pretreatments at 10- to 100-fold excess of DXS altered subsequent DXS-stimulated gp52 levels. Progesterone effectively antagonized DXS and reduced gp52 levels to those of controls but this reduction was accomplished only at the lowest concentrations of DXS (10(-8) M) and shortest treatment interval (24h). While some pretreatment protocols of varied dose slightly reduced gp52 levels at a point in time after treatment, the majority of progesterone pretreatments at 10(-7), 10(-6), and 10(-5) M resulted in MMTV gp52 levels which were equal to and in many cases significantly greater than those obtained with DXS alone. The ability to augment DXS-stimulated gp52 levels with progesterone pretreatment suggests that, under certain hormonal conditions, gp52 expression and release from mouse cells may be progesterone-dependent as well as glucocorticoid-dependent.

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PubMed1988

Elevation of mouse mammary tumor virus envelope glycoprotein (Gp52) by growth factors.

Murine mammary tumor cells (C3H Mm5mt/cl and B9) were grown in serum-free culture to examine the effects of different polypeptide growth factors on viral glycoprotein (gp52) release into extracellular culture fluids. Epidermal growth factor (EGF) elevated extracellular virion-associated and soluble gp52 levels of mouse mammary tumor virus producer and nonproducer cells. While EGF effectively and consistently elevated gp52 levels at 20 ng/ml, fibroblast growth factor was less effective, and platelet-derived growth factor failed to elevate gp52 levels. Growth factors, EGF and fibroblast growth factor, stimulated cell growth to a greater degree than platelet-derived growth factor and were also more consistently mitogenic. The EGF-mediated elevation in gp52 was statistically significant as compared to controls; however, increases were smaller in magnitude than those obtained with the classical glucocorticoid stimulator, dexamethasone. The results demonstrate that EGF can quantitatively influence extracellular levels of gp52 detected in viral particle and virus-free soluble antigen fractions. These in vitro findings suggest that growth factors such as EGF may play a role in determining tumor cell levels of mouse mammary tumor virus production and levels of gp52 shed as a soluble marker for tumor.

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