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Results for “Targeted Therapy”

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At least 811 records · Page 45Linked to original sources
PubMed1999

Refined testing and targeted therapy lead new fight against prostate cancer. Interview by Wayne Kuznar.

Prostate cancer screening and intervention remain controversial, despite significant strides in the detection and treatment of this common malignancy. False-positive results from the test for prostate specific antigen (PSA) lead to unnecessary workups and biopsies, as well as psychological stress for patients. Radial prostatectomy remains the most effective treatment for organ-confined cancer, yet many patients opt for the opt for the organ-sparing advantage of radiation therapy. Others may opt for unproven interventions such as cryoablation. Recently-developed tools designed for use with PSA testing are helping to improve screening accuracy in the lower tier of serum total PSA (2.5 to 10.0 ng/mL).

Adult↗
PubMed1999

Antiangiogenic therapy targeting the tyrosine kinase receptor for vascular endothelial growth factor receptor inhibits the growth of colon cancer liver metastasis and induces tumor and endothelial cell apoptosis.

Increased vascular endothelial growth factor (VEGF) expression is associated with colon cancer metastases. We hypothesized that inhibition of VEGF receptor activity could inhibit colon cancer liver metastases. BALB/c mice underwent splenic injection with CT-26 colon cancer cells to generate metastases. Mice received daily i.p. injections of vehicle, tyrosine kinase inhibitor for Flk-1/KDR (SU5416) or tyrosine kinase inhibitor for VEGF, basic fibroblast growth factor, and platelet-derived growth factor receptors (SU6668). SU5416 and SU6668 respectively inhibited metastases (48.1% and 55.3%), microvessel formation (42.0% and 36.2%), and cell proliferation (24.4% and 27.3%) and increased tumor cell (by 2.6- and 4.3-fold) and endothelial cell (by 18.6- and 81.4-fold) apoptosis (P<0.001). VEGF receptor inhibitors increased endothelial cell apoptosis, suggesting that VEGF may serve as an endothelial survival factor.

Animals↗
PubMed1998

Targeting Therapy in Unstable Angina.

Patients presenting to hospital with unstable angina should be risk profiled on admission and categorized as low, intermediate or high risk based on demographics, the presence and duration of ischemia, electrocardiographic changes and biochemical markers such as troponins T and I. Patients categorized as low risk can be assessed as outpatients for confirmation of the diagnosis, institution of therapy, non-invasiveive testing for inducible ischemia, and modification of risk factors. Patients categorized as intermediate risk should be admitted and treated with antithrombotic therapy and glycoprotein IIb/IIIa receptor antagonists while undergoing careful monitoring for ischemia. If any high-risk features occur during this period, the patient should be recategorized as high risk. Alternatively, if the symptoms and signs of ischemia settle, they can be recategorized as low risk and undergo noninvasiveive testing before discharge. Patients categorized as high risk should be treated with antithrombotic therapy and IIb/IIIa receptor antagonists with a plan to perform expeditious angiography and revascularization (if appropriate) before early discharge. Further studies are required comparing this approach in high-risk patients with one of IIb/IIIa receptor antagonist therapy without revascularization. The increased risk of cardiac events continues beyond the acute phase, and long-term strategies, including administration of either low molecular weight heparin or oral IIb/IIIa receptor antagonists, are being tested in ongoing clinical trials.

Journal Article↗
PubMed2000

A novel approach for nasopharyngeal carcinoma treatment uses phenylbutyrate as a protein kinase C modulator: implications for radiosensitization and EBV-targeted therapy.

Sodium phenylbutyrate (NaPB) represent a new non-toxic class of compounds with antiproliferative activities to different tumors and has been shown to modulate many gene expressions by inhibiting histone deacetylation and DNA methylation as the major mechanism. Butyrate and other protein kinase C (PKC) activators have been reported to be able to activate virus enzymes. The present work investigates whether NaPB has an antiproliferative effect or modulatory effects on EBV-associated nasopharyngeal carcinoma (NPC) and whether EBV thymidine kinase gene can be activated to make cells susceptible to ganciclovir (GCV) therapy. NaPB treatment displayed a dose- and time-dependent antiproliferative effect on the NPC cell line CNE2. Cell cycle analysis revealed an inhibitory effect of NaPB on G1-S-phase progression. Shortly after NaPB treatment, we found that PKC activity was activated rapidly but also decreased rapidly. Down-regulation of PKC-alpha and translocation of PKC-alpha from the cytosol to membrane were seen by Western blot. The decrease in PKC activity by NaPB corresponds to an enhanced response to radiation on CEN2 cells. Moreover, NaPB up-regulated EBV thymidine kinase activity to render EBV-associated Daudi cells susceptible to killing by GCV. Based on the observations of NaPB as a PKC modulator, the combination of NaPB, GCV, and radiation may provide a potential novel approach for treatment of EBV-associated NPC.

Antiviral Agents↗
PubMed2001

Triplet combination chemotherapy and targeted therapy regimens.

Current agents for the treatment of non-small-cell lung cancer include gemcitabine (Gemzar), paclitaxel (Taxol), docetaxel (Taxotere), vinorelbine (Navelbine), and irinotecan (CPT-11, Camptosar). Experimental agents include pemetrexed (LY231514, Alimta) and tirapazamine. Molecular and biological therapies include angiogenesis inhibitors, epidermal growth factor receptor inhibitors, HER2/neu inhibitors, and inhibitors of ras activation and function. Doublet chemotherapy is currently the standard treatment for advanced non-small-cell lung cancer. In the past 2 years, randomized trials have shown that many of the new two-drug combinations used to treat non-small-cell lung cancer have equivalent efficacy. These combinations produce 1-year survival rates of about 35% and 2-year survival rates of about 15%. Toxicity rates vary but are sufficiently low as to make the development of three-drug combinations feasible. Preliminary studies from several phase I and II trials suggest that triplet therapy can improve survival beyond that of double therapy regimens.

Carcinoma, Non-Small-Cell Lung↗
PubMed2002

Prostate stem cell antigen as therapy target: tissue expression and in vivo efficacy of an immunoconjugate.

We conducted an expression analysis of prostate stem cell antigen (PSCA)in normal urogenital tissues, benign prostatic hyperplasia (n = 21), prostatic intraepithelial neoplasia (n = 33), and primary (n = 137) and metastatic (n = 42) prostate adenocarcinoma, using isotopic in situ hybridization on tissue microarrays. In normal prostate, we observe PSCA expression in the terminally differentiated, secretory epithelium; strong expression was also seen in normal urothelium. Forty-eight percent of primary and 64% of metastatic prostatic adenocarcinomas expressed PSCA RNA. Our studies did not confirm a positive correlation between level of PSCA RNA expression and high Gleason grade. We characterized monoclonal anti-PSCA antibodies that recognize PSCA expressed on the surface of live cells, are efficiently internalized after antigen recognition, and kill tumor cells in vitro in an antigen-specific fashion upon conjugation with maytansinoid. Unconjugated anti-PSCA antibodies demonstrated efficacy against PSCA-positive tumors by delaying progressive tumor growth in vivo. Maytansinoid-conjugated antibodies caused complete regression of established tumors in a large proportion of animals. Our results strongly suggest that maytansinoid-conjugated anti-PSCA monoclonal antibodies should be evaluated as a therapeutic modality for patients with advanced prostate cancer.

Adenocarcinoma↗
PubMed2002

Targeted therapies for patients with rheumatoid arthritis.

Rheumatoid arthritis is characterised by an auto-immune response that eventually leads to the destruction of affected joints. This has major implications for patients' lives, with many becoming debilitated within three years of diagnosis. This paper describes the body's auto-immune mechanism and outlines new therapies that seek to block the body's destructive response to itself.

Anti-Inflammatory Agents↗
PubMed2002

Molecular evidence-based use of bone resorption-targeted therapy in prostate cancer patients at high risk for bone involvement.

BACKGROUND: To improve median survival of patients with prostate cancer that has metastasized to bone, we need to better understand the early events of the metastatic process in skeleton and develop molecular tools capable of detecting the early tumor cell dissemination into bones (micrometastasis stage). However, the initial phase of tumor cell dissemination into the bone marrow is promptly followed by the migration of tumor cells into bone matrix, which is a crucial step that signals the transformation of micrometastasis to macrometastasis stage and clinically evident metastasis. The migration of cancer cells into bone matrix requires the activation of local bone resorption. Such an event contributes to tumor cell hiding/ escaping from high immunologic surveillance of bone marrow cells. Within bone matrix, tumor cells are establishing plethoric cell-cell interactions with bone marrow-residing cells, ensuring their survival and growth. Recently, RT-PCR detections of tumor marker transcripts, such as PSA and PSMA mRNA performed in RNA extracts of peripheral blood nucleated cells and bone marrow biopsy, have enabled the stratification of patients with clinically localized prostate cancer being of high risk for extraprostatic disease and bone involvement. Therefore, it is conceivable that bisphosphonate blockade of bone resorption can inhibit the migration of tumor cells into bone matrix during the early phase of disease dissemination into bone marrow (micrometastasis stage). Consequently, assessment of the efficacy and efficiency of bisphosphonates to arrest the evolution of bone lesions in this particular clinical setting of patients with clinically localized prostate cancer and positive molecular staging status (high risk for bone involvement) is warranted.

Antineoplastic Agents↗