Abstract: A method of determining whether one or more forms of a nucleic acid analyte are present in a sample. The method includes dissolving an amplification reagent with a first solvent, where the amplification reagent contains oligonucleotides sufficient to amplify and detect a first region of a first form of the analyte, where the first solvent contains one or more oligonucleotides which, in combination with the oligonucleotides of the amplification reagent, are sufficient to amplify and detect a second region of a second form of the analyte, where the one or more oligonucleotides of the first solvent are insufficient to amplify and detect the first or second form of the analyte, and where the first and second regions each comprise a different nucleotide base sequence.

Abstract: An automated system for performing nucleic acid amplification assays on samples provided to the system, where the system includes data input components configured to enable input specifying one or more user-defined assay parameters; data storage media storing a first set of assay parameters, the first set of assay parameters consisting of system-defined parameters, and a second set of assay parameters, the second set of assay parameters including the one or more user-defined parameters; and command input components configured to enable input specifying (i) that a first nucleic acid amplification assay be performed on a first sample in accordance with the first set of assay parameters, and (ii) that a second nucleic acid amplification assay be performed on a second sample in accordance with the second set of assay parameters.

Abstract: A set of small molecules ER? biomodulators that kill therapy-resistant ER? positive breast, ovarian, and endometrial cancer cells. These small molecules have increased therapeutic potential because of an increased ability to kill therapy-resistant breast cancer cells compared to BHPI and other conventional therapies (endocrine therapies, tamoxifen and fulvestrant/ICI). The new compounds do not only inhibit proliferation of the cancer cells but actually kills them, which prevents reactivation of tumors years later.

Abstract: A set of small molecules ER? biomodulators that kill therapy-resistant ER? positive breast, ovarian, and endometrial cancer cells. These small molecules have increased therapeutic potential because of an increased ability to kill therapy-resistant breast cancer cells compared to BHPI and other conventional therapies (endocrine therapies, tamoxifen and fulvestrant/ICI). The new compounds do not only inhibit proliferation of the cancer cells but actually kills them, which prevents reactivation of tumors years later.

Abstract: A set of small molecules ER? biomodulators that kill therapy-resistant ER? positive breast, ovarian, and endometrial cancer cells. These small molecules have increased therapeutic potential because of an increased ability to kill therapy-resistant breast cancer cells compared to BHPI and other conventional therapies (endocrine therapies, tamoxifen and fulvestrant/ICI). The new compounds do not only inhibit proliferation of the cancer cells but actually kills them, which prevents reactivation of tumors years later.

Abstract: A set of small molecules ER? biomodulators that kill therapy-resistant ER? positive breast, ovarian, and endometrial cancer cells. These small molecules have increased therapeutic potential because of an increased ability to kill therapy-resistant breast cancer cells compared to BHPI and other conventional therapies (endocrine therapies, tamoxifen and fulvestrant/ICI). The new compounds do not only inhibit proliferation of the cancer cells but actually kills them, which prevents reactivation of tumors years later.

Abstract: A set of small molecules ER? biomodulators that kill therapy-resistant ER? positive breast, ovarian, and endometrial cancer cells. These small molecules have increased therapeutic potential because of an increased ability to kill therapy-resistant breast cancer cells compared to BHPI and other conventional therapies (endocrine therapies, tamoxifen and fulvestrant/ICI). The new compounds do not only inhibit proliferation of the cancer cells but actually kills them, which prevents reactivation of tumors years later.

Abstract: The disclosure herein relates to nuclear hormone receptors including steroid hormone receptors, for example in connection with estrogen, progesterone, and androgen. Embodiments of compositions and methods are disclosed including such relating to compounds, including substituted theophyllines, capable of functioning as inhibitors of estrogen receptor alpha-mediated gene expression and having the ability to modify cancer cells and treat cancer, including breast cancers and resistant breast cancers, particularly those that are resistant to tamoxifen. In embodiments, methods of inhibiting breast cancer cells and resistant breast cancer cells are provided. In embodiments, a useful inhibitor compound includes TPSF/NSC 97998 and other compounds.

Abstract: The disclosure herein relates to nuclear hormone receptors including steroid hormone receptors, for example in connection with estrogen, progesterone, and androgen. Embodiments of compositions and methods are disclosed including such relating to compounds, including substituted theophyllines, capable of functioning as inhibitors of estrogen receptor alpha-mediated gene expression and having the ability to modify cancer cells and treat cancer, including breast cancers and resistant breast cancers, particularly those that are resistant to tamoxifen. In embodiments, methods of inhibiting breast cancer cells and resistant breast cancer cells are provided. In embodiments, a useful inhibitor compound includes TPSF/NSC 97998 and other compounds.

Abstract: Novel tamoxifen inducible and ICI 182,780 repressible expression systems comprising mutant estrogen receptors and mutant estrogen response element are disclosed. Such systems have a wide variety of applications, including gene therapy and in vivo and in vitro expression, as well as their use in transgenic animals.

Abstract: Novel tamoxifen inducible and ICI 182,780 repressible expression systems comprising mutant estrogen receptors and mutant estrogen response element are disclosed. Such systems have a wide variety of applications, including gene therapy and in vivo and in vitro expression, as well as their use in transgenic animals.