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  • PROGRESSION  (2)
  • 1
    Keywords: CANCER ; EXPRESSION ; Germany ; human ; PROSTATE ; THERAPY ; DIAGNOSIS ; GENE ; GENES ; PROTEIN ; PROTEINS ; validation ; BIOMARKERS ; IDENTIFICATION ; PROGRESSION ; prostate cancer ; PROSTATE-CANCER ; FUSION ; TARGETS ; SINGLE ; molecular biology ; THERAPIES ; TISSUE MICROARRAYS ; development ; HIGH-THROUGHPUT ; USA ; CANCERS ; TARGETED THERAPY ; ANNEXIN A3
    Abstract: Significant cellular alterations required for the development and progression of cancers are detectable at the molecular level and represent potential targets for gene-specific therapies. Modern chip techniques allow the parallel analysis of virtually all known human genes and proteins in a single experiment. Using modern high-throughput techniques, numerous potential new biomarkers for the diagnosis and prediction of prostate cancer have been identified. However, so far none of these markers has improved clinical practice. One of the most important challenges in the coming years is the extensive clinical validation of molecular data using clinically relevant end points. For this venture the pivotal prerequisite is the availability of large, comprehensively annotated and standardized high-quality bioresources
    Type of Publication: Journal article published
    PubMed ID: 19139898
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  • 2
    Keywords: RECEPTOR ; INHIBITOR ; tumor ; TUMORS ; PATIENT ; ACTIVATION ; PHOSPHORYLATION ; TYROSINE KINASE INHIBITOR ; PROGRESSION ; COMPARATIVE GENOMIC HYBRIDIZATION ; cytogenetics ; MUTATION ; TUMOR PROGRESSION ; MUTATIONS ; PROGNOSTIC-SIGNIFICANCE ; INTERSTITIAL-CELLS ; CHROMOSOMAL IMBALANCES ; COPY NUMBER CHANGES ; SMOOTH-MUSCLE TUMORS ; C-KIT ; CD117 (KIT) ; DIFFERENTIAL-DIAGNOSIS ; gastrointestinal stromal tumor ; imatinib (STI571/Glivec (R)) ; KIT mutation ; NERVE SHEATH TUMORS
    Abstract: Recent morphological and molecular genetic findings have greatly expanded our understanding of gastrointestinal stromal tumors (GISTs). GISTs are now defined by their overexpression of CD117 (KIT), the receptor for the stem cell factor, and can thus be discriminated from smooth muscle tumors. Cytogenetically, GISTs are characterized even in early lesions by frequent entire or partial loss of the chromosomes 14 and 22 and terminal deletions of the chromosomal arm 1p. During tumor progression further chromosomal imbalances accumulate. Following the first report on activating KIT mutations in GISTs, several studies have addressed the role of wild-type and mutant KIT in GISTs and demonstrated activating KIT mutations in the majority of cases. Moreover, KIT tyrosine phosphorylation is even present in KIT mutation-negative GISTs, implicating KIT activation as a central event in the pathogenesis of GISTs. Imatinib (ST1571/Glivec((R))) is a selective inhibitor of BCR/ABL, PDGFR and KIT receptor-tyrosine kinases. First therapeutic applications of imatinib in patients with progressive GISTs have yielded promising results. This review focusses on the morphological and molecular findings in GISTs which have opened up a new therapeutic perspective
    Type of Publication: Journal article published
    PubMed ID: 12739051
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