Abstract: The present invention relates to the field of cancer, and in particular hormone dependent cancers including, but not limited to prostate, breast, endometrial, ovarian, thyroid, bone, and testis. The present invention also relates to the use of steroid analogues, and in particular analogues of ?5-androstene-3-?, 17?-diol, and its epimer ?5-androstene-3-?, 17?-diol for the treatment and prevention of cancer.

Abstract: The instant application provides means of accelerating cell aging and programed cell death in tumor cells by administration of 3?,17? androstenediol (?AED) or its ethers or esters.

Abstract: The present invention provides a means to regulate nuclear transcription and/or gene expression. The present invention also provides a means to regulate the levels of PPAR-&ggr;, COX-2 and/or NF&kgr;B in a patient. The method of the present invention involves administering &agr;AED (or an analogue thereof) or &bgr;AED (or an analogue thereof) or both to a patient in need of regulation of nuclear transcription and/or gene expression and/or levels of PPAR-&ggr;, COX-2, and/or NF&kgr;B. The methods of the present invention can be used to control adipogenesis (i.e. to treat obesity), angiogenesis, atherosclerosis, mesenteric fat hypertrophy, inflammatory bowel disease, colitis, Alzheimer's disease, and inflammatory glial responses in the brain. The methods of the present invention can also be used for treating diabetes, for regulating the immune response, and for regulating inflammation in a patient.

Abstract: The present invention relates to the field of cancer, and in particular hormone dependent cancers including, but not limited to prostate, breast, endometrial, ovarian, thyroid, bone, and testis. The present invention also relates to the use of steroid analogues, and in particular analogues of &Dgr;5-androstene-3-&bgr;, 17&agr;-diol, and its epimer &Dgr;5-androstene-3-&bgr;, 17&bgr;-diol for the treatment and prevention of cancer.

Abstract: The instant application provides means of accelerating cell aging and programed cell death in tumor cells by administration of 3&bgr;, 17&agr; androstenediol (&agr;AED) or its ethers or esters.

Abstract: This invention relates to the field of pharmaceuticals for tumor-inhibitory effects. The 5-androstene 3.beta., 17.alpha. diol (.alpha.AED), its esters and ethers, are taught herein to achieve tumor-inhibiting effect.

Abstract: Androsta-5,7-diene-3.beta., 17.beta.-diol, its esters and ethers and related compounds wherein ring opening of the steroid ring system between carbons 9 and 10 has occurred are active as regulators of immune response and cell proliferation and differentiation.

Abstract: The present invention provides a composition comprising a dosage from containing 0.2 to 30 mg of 5-androstene 3 .beta.,17.beta. diol in a pharmaceutical carrier, and a method of preventing cells from adhering to one another by exposing the cells to an adhering-inhibiting amount of 5-androstene 3.beta.,17.beta. diol or 5-androstene 3.beta.,7.beta.,17.beta. triol.

Abstract: Androsta-5,7-diene-3.beta.,17.beta.-diol, its esters and ethers and related compounds wherein ring opening of the steroid ring system between carbons 9 and 10 has occurred are active as regulators of immune response and cell proliferation and differentiation.

Abstract: 3.beta.,7.beta.,17.beta.-androstenetriol (".beta.AET") may be used to increase production of IL-2 in cell culture and in the intact animal. Increase in IL-2 under stimulating effect of .beta.AET provides benefits associated with IL-2 administration without the untoward effects such as increased cortisol production.

Abstract: The present invention provides an improved compositions and methods for regulating the immune response, for ameliorating effects of stress, and for avoiding untoward effects of chemotherapy or exposure to irradiation by administration of androstenediol (AED) and androstenetriol (AET). The improved means of regulating immune response can be utilized in treating infectious diseases and immune diseases such as diabetes and chronic fatigue syndrome, both diseases now considered to be immune response related syndromes.

Abstract: Dehydroepiandrosterone (DHEA) has an immune response regulating effect in vertebrates to protect from morbid effect of infection and immune suppressive therapies. DHEA is also effective for use in treatment of alopecia. Protection results from a generalized host response.

Abstract: 3.beta.,17.beta.-androstenediol (".beta.AED") and 3.beta.,7.beta.,17.beta.-androstenetriol (".beta.AET") may be used to counteract the antiproliferative and immunosuppressive effects of hydrocortisone and other corticosteroids (i.e., to act as buffers to counteract the lymphosuppressive response to such steroids). .beta.AED and .beta.AET are steroids which mediate immune response to provide the body protection against immune down-regulation. A method for testing analogues of .beta.AED and .beta.AET to compare the effectiveness of such analogues as buffers of certain effects of hydrocortisone and other corticosteroids, including immune response and proliferative effects is described. Cytokines, including most particularly IL-3, are produced by addition of .beta.AET and .beta.AED and their analogues to the growth media of cell cultures of lymphatic cells.

Abstract: The addition of 5-androstene 3.beta.,17.beta.diol and/or 5-androstene 3.beta.,7.beta.,17.beta. triol to growth media increases proliferation of lymphocytes in culture. By methods of the invention it is possible to increase production of autogenous lymphocytes for administration to the patient.

Abstract: The steroid hormone dehydroepiandrosterone (DHEA), when administered by feeding or by subcutaneous injection, significantly improves the host response to viral infection. Experimental animal data shows that, with infection (100,000 plaque forming units/animal) of a human coxsackievirus B4 strain, which causes mortality in about 90% of infected animals, mortality was reduced to 37% when animals were treated with DHEA. Moreover, DHEA induced an 80% elevation in the number of antibody forming cells, particularly in cells forming gamma globulin M (early antibodies), and gamma globulin G (secondary antibodies). This elevation in the number of antibody forming cells was evident only in DHEA treated and virus infected animals, but not in uninfected animals treated with DHEA or in infected animals not treated with DHEA. In virus infected and DHEA treated animals there was also an elevation in the number of monocyte cells, the particular white blood cell associated with a resistance to this infection.