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Results for “Targeted Therapy”

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At least 757 records · Page 42Linked to original sources
PubMed2006

Role of epidermal growth factor receptor pathway-targeted therapy in patients with recurrent and/or metastatic squamous cell carcinoma of the head and neck.

The development of epidermal growth factor receptor (EGFR) inhibitors was greeted with tremendous enthusiasm in the therapy of squamous cell carcinoma of the head and neck (SCCHN) based on the nearly universal expression of this protein, the negative prognostic associations with expression, and robust preclinical data. Clinical trials to date have demonstrated modest activity of these drugs as single agents with reproducible major response rates of 5% to 15% in SCCHN depending on agent, dose, and schedule. The biology of responsiveness to these agents remains unclear, although an association of development of cutaneous toxicity with positive outcome has been reported repeatedly. Nevertheless, molecular markers of response or resistance have yet to be fully delineated. In the near future, phase III clinical trials will elucidate the role of these agents in second-line recurrent and/or metastatic (R/M) disease, the combination of EGFR inhibitors with other therapeutic strategies will be broadly advanced, and a set of molecular predictors of benefit will begin to emerge. This article will review the progress in utilization of EGFR inhibitors in R/M SCCHN.

Antibodies, Monoclonal↗
PubMed2005

Genomic and proteomic profiling of lung cancers: lung cancer classification in the age of targeted therapy.

Both proteomic and genomic methods offer promise for the classification of human lung carcinomas. This review summarizes the range of proteomic methods in development for lung cancer classification, and describes a number of recent analyses of messenger RNA expression in lung cancer. Multiple independent studies of mRNA expression profiles in lung adenocarcinoma have proven highly reproducible. Analyses of the relationship between expression profiles and tumor development and differentiation, the presence or absence of specific pathogenic mutations, patient prognosis and survival after surgical treatment, and specific histopathology all appear to be promising.

Gene Expression Profiling↗
PubMed1996

ALS therapy: targets for the future.

There are four main hypotheses about the cause of ALS: excitotoxicity linked to glutamate receptor overactivation; mutation of the superoxide dismutase gene; production of autoantibodies to calcium channels; neurofilament accumulation. The motoneuron degeneration characteristic of ALS could be caused by any one or a combination of these mechanisms. Future therapeutic approaches should be based on these mechanisms and given in combination so that different levels of the degenerative process are targeted. Protection against excitotoxicity could be achieved with a combination of pharmacologic agents having neuroprotective activity, such as antiglutamate agents (e.g., riluzole), N-methyl-D-aspartate (NMDA) and non-NMDA antagonists, free-radical scavengers, calcium-channel blockers, and neurotrophic factors. Gene transfer is a possible future approach when causative mutations are identified. Transfer of genes encoding neuroprotective agents or genetically modified cells stably expressing these agents is another possible strategy.

Amyotrophic Lateral Sclerosis↗
PubMed1995

Screening and production of arylsulfatases for target therapy with etoposide 4'-sulfate, an antitumor prodrug.

Two arylsulfatase-producing streptomycetes that desulfated etoposide 4'-sulfate were isolated from soil samples. Taxonomical study identified one soil isolate as Streptomyces griseorubiginosus S980-14 (Es-1 arylsulfatase producer), while the other was considered new and tentatively designated Streptomyces sp. T109-3 (Es-2 arylsulfatase producer). Both strains produced extracellular arylsulfatase activities, provided that cultivation media were prepared with distilled water. Unlike the two known types of arylsulfatases, which had significant activity on p-nitrophenyl sulfate but none on etoposide 4'-sulfate, the crude streptomycete arylsulfatases efficiently desulfated etoposide 4'-sulfate and p-nitrophenyl sulfate, which supports the establishment of a new type of arylsulfatases.

Antineoplastic Agents↗
PubMed2006

Haematopoietic stem and progenitor cell-targeted therapies for thrombocytopenia.

This review discusses the present outlook for new thrombocytopenia therapies that induce haematopoietic stem and progenitor cells to proliferate, differentiate and produce functional platelets. A brief overview of megakaryopoiesis and its regulation by thrombopoietin (TPO) is followed by a discussion of how early experience with recombinant TPO therapies stimulated the search for novel TPO receptor ligands. A summary is then provided of the results of Phase I clinical trials with the new small molecule and peptide TPO mimetics that are in development at present. Finally, recent developments in the ex vivo expansion of primitive haematopoietic cells and the potential enhancement of cell-based therapies by haematopoietic growth factors in vivo are briefly summarised as part of a look towards the future.

Animals↗
PubMed2006

Biology, clinical relevance, and molecularly targeted therapy in acute leukemia with FLT3 mutation.

Overexpression and activating mutations of receptor tyrosine kinases (RTKs) are known to be involved in the pathophysiology of several kinds of cancer cells. FMS-like receptor tyrosine kinase 3 (FLT3), together with KIT, FMS, and platelet-derived growth factor receptor, is a class III RTK. FLT3 mutations were first reported as internal tandem duplication (FLT3/ITD) of the juxtamembrane domain-coding sequence; subsequently, a missense point mutation at the D835 residue and point mutations, deletions, and insertions in the codons surrounding D835 within a FLT3 tyrosine kinase domain (FLT3/KDMs) have been found. FLT3 mutations are the most frequent genetic alterations so far reported in acute myeloid leukemia and are involved in the signaling pathway of autonomous proliferation and differentiation block in leukemia cells. Several large-scale studies have confirmed that FLT3/ITD is strongly associated with leukocytosis and a poor prognosis. Therefore, routine screening for FLT3 mutations is recommended to stratify patients into distinct risk groups. However, because high-dose chemotherapy and stem cell transplantation cannot overcome the adverse effects of FLT3 mutations, the development of FLT3 kinase inhibitors is expected to produce a more efficacious therapeutic strategy for leukemia therapy.

Acute Disease↗