Tumor marker protein for cancer risk assessment

This invention relates to the isolation, identification and sequencing of a cancer associated protein, preparation of hybridization probes therefrom, preparation of antibodies thereto, and methods of cancer risk assessment and diagnosis.Board of Regents, University of Texas Syste

Avicin D: A Protein Reactive Plant Isoprenoid Dephosphorylates Stat 3 by Regulating Both Kinase and Phosphatase Activities

Avicins, a class of electrophilic triterpenoids with pro-apoptotic, anti-inflammatory and antioxidant properties, have been shown to induce redox-dependant post-translational modification of cysteine residues to regulate protein function. Based on (a) the cross-talk that occurs between redox and phosphorylation processes, and (b) the role of Stat3 in the process of apoptosis and carcinogenesis, we chose to study the effects of avicins on the processes of phosphorylation/dephosphorylation in Stat3. Avicins dephosphorylate Stat3 in a variety of human tumor cell lines, leading to a decrease in the transcriptional activity of Stat3. The expression of Stat3-regulated proteins such as c-myc, cyclin D1, Bcl2, survivin and VEGF were reduced in response to avicin treatment. Underlying avicin-induced dephosphorylation of Stat3 was dephosphorylation of JAKs, as well as activation of protein phosphatase-1. Downregulation of both Stat3 activity and expression of Stat 3-controlled pro-survival proteins, contributes to the induction of apoptosis in avicin treated tumor cells. Based on the role of Stat3 in inflammation and wounding, and the in vivo inhibition of VEGF by avicins in a mouse skin carcinogenesis model, it is likely that avicin-induced inhibition of Stat3 activity results in the suppression of the pro-inflammatory and pro-oxidant stromal environment of tumors. Activation of PP-1, which also acts as a cellular economizer, combined with the redox regulation by avicins, can aid in redirecting metabolism from growth promoting anabolic to energy sparing pathways

Tumor marker protein and antibodies thereto for cancer risk assessment or diagnosis

A tumor-associated marker protein was purified and antibodies thereto developed for cancer diagnosis and assessment of cancer risk associated with the long-term use of synthetic steroid hormones, both contraceptive and non-contraceptive, and other drugs that exhibit tumor promotional properties. The marker protein and antibodies thereto provided are interspecies immunologically cross-reactive. In summary, the marker p65 tumor-associated factor of the present invention has the following characteristics: PA1 (a) binds substantially completely to a phenyl hydrophobic interaction column in a buffer containing 20% ammonium sulfate and eluted at ca. 16% ammonium sulfate; PA1 (b) localized primarily in the nuclear envelopes with only small amounts present in the cytoplasm from where is released to the blood circulation in vivo or cell culture medium in vitro; PA1 (c) induced in normal, adult tissues by chemical carcinogens (initiators) but not by tumor promoters, the carcinogen-induced production being enhanced by the latter. Also disclosed herein are processes for purifying the 65 kDa tumor marker from plasma, tumor cytosol or ascitic fluid of carcinoma bearing animals; processes for producing antisera and purified antibody preparations to the 65 kDa tumor marker; and methods using antibody to the 65 kDa to diagnose or assess the likelihood of cancer.Board of Regents, University of Texas Syste

Tumor marker protein for cancer risk assessment

This invention relates to the isolation, identification and sequencing of a cancer associated protein, preparation of hybridization probes therefrom, preparation of antibodies thereto, and methods of cancer risk assessment and diagnosis.Board of Regents, University of Texas Syste

Formula and method for the prevention and treatment of hypercholesterolemia and cellular hyperproliferative disorders

The present invention provides a formula and method for the prevention and treatment of hypercholesterolemia and cellular hyperproliferation. More specifically, the present invention provides a method for administering a formula including glucaric acid or a pharmaceutically acceptable salt thereof for the prevention and treatment of hypercholesterolemia and cellular hyperproliferation in humans and animals. It has been determined that glucaric acid and pharmaceutically acceptable salts thereof significantly lower the total and LDL level of serum cholesterol and inhibit cellular hyperproliferation when administered in therapeutic amounts. It is intended that glucaric acid or a pharmaceutically acceptable salt thereof is employed alone or in combination with other medicinal agents for the prevention and treatment of hypercholesterolemia and cellular hyperproliferation.Board of Regents, University of Texas Syste

Nucleocytoplasmic Release of Repetitive DNA Transcripts in Carcinogenesis Correlates With a 60 Kilodalton Cytoplasmic Protein

Treatment of rats with the hepatocarcinogen 3′-methyl-4-dimethylaminoazobenzene (3′-MeDAB) causes the appearance in the liver cytosol of a 60 kilodalton oncofetal protein. The appearance of this factor occurs within 40 h of treatment and coincides with the increase in the amount of rapidly labeled RNA released from nuclei in a reconstituted cell-free system. Cross-over experiments show that this increase is due to an enhanced transport capacity of the cytosol. The 60 kilodalton RNA transport factor is also present in the cytosol of tumor cells. Addition of the 60 kilodalton factor to normal liver cytosol causes the transport of repetitive RNA sequences similar to those transported from liver nuclei to tumor cell cytosol and those transported to the tumor cell cytoplasm in vivo. This factor modifies nuclear RNA restriction, at least in part, by eliciting the transport of repetitive RNA normally retained within the nucleus of the normal cell