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PubMedDate not supplied

Targeted therapy for cancer: the HER-2/neu and Herceptin story.

The HER-2/neu oncogene encodes a transmembrane tyrosine kinase receptor with extensive homology to the epidermal growth factor receptor. In this article, the association of HER-2/neu gene and protein abnormalities with prognosis and response to therapy with Herceptin and other therapies in breast cancer is presented. By considering a series of 80 published studies encompassing more than 25,000 patients, the relative advantages and disadvantages of Southern blotting, polymerase chain reaction amplification, and fluorescence in situ hybridization assays designed to detect HER-2/neu gene amplification are compared with HER-2/neu protein overexpression assays performed by immunohistochemical techniques applied to frozen and paraffin-embedded tissues and enzyme immunoassays performed on tumor cytosols. The significance of HER-2/neu overexpression in ductal carcinoma in situ and the HER-2/neu status in uncommon female breast conditions and male breast cancer also are considered. The role of HER-2/neu testing for the prediction of response to Herceptin therapy in breast cancer is presented as well as its potential impact on responses to standard and newer hormonal therapies, cytotoxic chemotherapy, and radiation. The review also will evaluate the status of serum-based testing for circulating HER-2/neu receptor protein and its ability to predict disease outcome and therapy response.

Antibodies, Monoclonal↗
PubMed2003

[Does targeted therapy of type 2 diabetes prevent cardiovascular incidents?].

An impaired glucose tolerance results in a significantly increased cardiovascular risk. In view of the dramatically increasing population with non-insulin-dependent diabetes mellitus, metabolic syndrome and impaired glucose tolerance, new therapeutic options are urgently required. In the past, studies of an intensified diabetes therapy generally did not reveal a relevant effect on the incidence of macrovascular complications. Consequently, the phrase of the "glucose paradoxon" was coined. The STOP-NIDDM study (study to prevent non-insulin-dependent diabetes mellitus) for the first time showed a reduction of cardiovascular events by 49% in patients with impaired glucose tolerance treated with acarbose compared with placebo. Furthermore, a retrospective metaanalysis of seven placebo-controlled long-term-studies of acarbose in patients with non-insulin-dependent diabetes mellitus showed a reduction of cardiovascular events by 41% (p = 0.0017). In summary, there is good evidence from placebo-controlled studies of a significant reduction of cardiovascular risk by acarbose in patients with impaired glucose tolerance or non-insulin-dependent diabetes mellitus.

Acarbose↗
PubMed2003

Microcirculation: target therapy in cardiovascular diseases - a clinical perspective.

Microcirculation conduit, distribution, exchange and reception vessels usually retain a demand-dependent vascular-tissue match as well as a nutrient friendly capillary-matrix tissue match. Various stimuli can initiate a vascular-capillary matrix-tissue mismatch. Counter-regulatory mechanisms result in hyperplasia or apoptosis. Microvascular disease (MVD) as a consequence or outcome of supply-demand mismatch has clinical therapeutic and prognostic implications in the hypertensive syndrome and coronary artery disease (CAD) cases. Recognition of the role of apoptosis and MVD may initiate a paradigm shift in clinical practice. Digitalis and other anti-hypertensive agents have anti-apoptotic action and MVD blunting effects that can control LVH development to reduce congestive heart failure (CHF) progression.

Animals↗
PubMed2002

GABAA-benzodiazepine-chloride receptor-targeted therapy for tinnitus control: preliminary report.

Our goal was to attempt to establish neuropharmacological tinnitus control (i.e., relief) with medication directed to restoration of a deficiency in the gamma-aminobutyric acid-benzodiazepine-chloride receptor in tinnitus patients with a diagnosis of a predominantly central type tinnitus. Thirty tinnitus patients completed a medical audiological tinnitus patient protocol and brain magnetic resonance imaging and single-photon emission computed tomography of brain. Treatment with GABAergic and benzodiazepine medication continued for 4-6 weeks. A maintenance dose was continued when tinnitus control was positive. Intake and outcome questionnaires were completed. Of 30 patients, 21 completed the trial (70%). Tinnitus control lasting from 4-6 weeks to 3 years was reported by 19 of the 21 (90%). The trial was not completed by 9 of the 30 (30%). No patient experienced an increase in tinnitus intensity or annoyance. Sequential brain single-photon emission computed tomography in 10 patients revealed objective evidence of increased brain perfusion. Patients with a predominantly central type tinnitus experience significant tinnitus control with medication directed to the gamma-aminobutyric acid-benzodiazepine-chloride receptor.

Acetates↗
PubMed2004

Involvement of base excision repair in response to therapy targeted at thymidylate synthase.

Thymidylate synthase (TS) is an important target of several classes of chemotherapeutic agents. Although the precise mechanism of cytotoxicity in thymidylate deprivation remains obscure, uracil misincorporation and DNA strand breaks are recognized as important events during thymidylate deprivation. Base excision repair (BER) plays a primary role in removing damaged or modified bases from the genome, including uracil. Because of uracil misincorporation, BER is hypothesized to play a role in the cellular response to thymidylate deprivation. In this study, we used murine embryo fibroblasts wild-type or homozygous null for DNA polymerase beta (beta-pol), which plays a central role in BER. We found that, compared with wild-type, beta-pol null cells were resistant to the toxic effects of raltitrexed (Tomudex, ZD1694), a folate inhibitor of TS. There was little difference in TS levels or in TS-ligand complex formation between the cell lines. Furthermore, cells deficient in XRCC1, a scaffold protein for the final steps of BER, were also modestly resistant to raltitrexed compared with XRCC1-proficient cells. Cell cycle analysis revealed that the responses of the wild-type and beta-pol null cells were similar during drug exposure. However, following drug removal, the beta-pol null cells appeared to resume cell cycle progression more rapidly than the wild-type cells. The results suggest that BER plays a role in modulating the toxic effects of TS inhibitors, and that this role occurs during recovery from TS inhibition.

Animals↗
PubMed2004

Unraveling the complexities of targeted therapy treatment in cancer care.

This program discussed the rationale for treatment choices in non-Hodgkin lymphoma and HER-2 positive breast cancer. The mechanisms and management of infusion, cytokine-mediated, and allergic reactions related to monoclonal antibody (MOAB) therapy were covered, as well as a summary of the mechanisms of action and toxicities of MOAB therapy in breast cancer.

Antibodies, Monoclonal↗
PubMed2005

B cell-targeted therapy in diseases other than rheumatoid arthritis.

There are now numerous case reports and small series using rituximab in autoimmune diseases. While these data must be interpreted with caution, they suggest that rituximab (RTX) may be a promising addition to the therapeutic armamentarium. In patients with refractory chronic idiopathic thrombocytopenic purpura, treatment with RTX was effective in inducing complete responses in a significant proportion of patients, and these responses were usually durable. RTX has also been shown to be effective and well tolerated in children with refractory autoimmune hemolytic anemia. In patients with IgM antibody-associated polyneuropathy, RTX improved muscle strength, and repeated treatments over 2 years were well tolerated. In several case series of patients with systemic lupus erythematosus, depletion of B cells during RTX therapy was associated with improvement in global disease activity. Based on these reports, further controlled studies are warranted to optimize RTX as monotherapy and to develop combination therapies in patients with refractory autoimmune diseases.

Anemia, Hemolytic, Autoimmune↗
PubMed2005

[Experimental study of targeting therapy of breast cancer with 131I-labeled epidermal growth factor].

OBJECTIVE: To investigate the effectiveness of (131)I-epidermal growth factor (EGF) on the proliferation of a heterologous graft in nude mice bearing human breast infiltrating duct carcinoma. METHODS: EGF/HAS was labeled with (131)I by chloramines-T method. Human breast cancer xenografts with positive EGFR expression were established in nude mice. The nude mice were injected with normal saline, Epirubicin Hydrochloride, (131)I-EGF, (131)I-HAS, (131)I intravenously and (131)I-EGF intratumoral administration respectively. The tumor growth inhibition rate was determined by measurement of tumor volume. Different examinations were carried out. RESULTS: There was remarkable significant difference of tumor volumes at 26th day among (131)I-EGF trial groups, (131)I, (131)I-HAS, and the negative control group. The tumor growth inhibition rate of (131)I-EGF trial groups was 82.0%, 80.7% respectively. Compared with the negative control group, the (131)I-EGF trial groups remarkably suppressed the growth of tumor (P < 0.05). Irreversible destruction of tissues in (131)I-EGF groups was observed under light and electron microscope. There was no evidence of hepatotoxicity, renal toxicity and myelotoxicity in nude mice bearing human breast cancer given (131)I-EGF over a 4-wk observation period. CONCLUSION: (131)I-EGF has obvious antitumor effects on a heterologous graft in nude mice bearing human breast infiltrating duct carcinoma, with little obvious side effects.

Animals↗