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  • MUTATIONS  (2)
  • BINDING  (1)
  • CD117 (KIT)  (1)
Keywords
  • 1
    Keywords: tumor ; Germany ; DIAGNOSIS ; imaging ; GENE ; TUMORS ; MARKER ; treatment ; MUTATION ; MARKERS ; MUTATIONS ; tomography ; adenocarcinoma ; sensitivity ; pathology ; COMPLICATIONS ; INITIATION ; COLONY-STIMULATING FACTOR ; GENE-MUTATIONS ; pancreas ; DUCTAL ADENOCARCINOMA ; methods ; pancreatic ; complication ; PHASE-I TRIAL ; FINE-NEEDLE-ASPIRATION ; K-RAS MUTATIONS ; technique ; CYSTIC LESIONS ; DEGUM INQUIRY ; ENDOSCOPIC ULTRASOUND ; endosonographically guided biopsy ; EUS-GUIDED FNA ; fine needle biopsy ; HIGH-SENSITIVITY ; indications ; MUCINOUS TUMORS ; NEEDLE BIOPSIES ; pancreas biopsy ; Sensitivity and Specificity
    Abstract: Pancreatic biopsy is an invasive diagnostic method that is only performed when all other diagnostic measures for establishing the diagnosis of a tumorous lesion of the pancreas have failed. Because of the advances in modern imaging techniques, fine needle biopsy of the pancreas guided by ultrasonography, computer tomography or endosonography has become a reliable method that allows the diagnosis of ductal adenocarcinoma or any of the other, rarer pancreatic tumors with high sensitivity and specificity. Complications are rare, particularly with the endosonographically guided biopsy. A new biopsy indication is the demonstration of certain markers or gene mutations that are needed for the initiation of special treatments, e.g. EGFR-Cetuximab
    Type of Publication: Journal article published
    PubMed ID: 15630570
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  • 2
    Keywords: PATHWAY ; HYBRIDIZATION ; DNA ; INFECTION ; CARCINOGENESIS ; BINDING ; CERVICAL-CANCER ; HUMAN KERATINOCYTES ; HUMAN-PAPILLOMAVIRUS ; E2 PROTEIN
    Abstract: Infections with human papillomaviruses (HPV) are a common occurrence in both men and women. In contrast HPV-associated neoplasias are relatively rare and occur only in certain areas of the body. The virus has obviously developed efficient mechanisms for its persistence without inducing too much damage to the host. The formation of neoplasia seems to be more an exception. Epigenetic mechanisms play an important role in the regulation of viral gene expression. Investigations have indicated that exactly the transition from the permissive infection stage to a transformation stage, where neoplastic alterations can occur due to expression of the viral oncogenes, is associated with certain methylation patterns of the viral genome which promote the expression of the oncogenes E6 and E7. The transforming stage is seen as the actual carcinogenic event and can be immunohistochemically detected by the biomarker p16(INK4a).
    Type of Publication: Journal article published
    PubMed ID: 22038132
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  • 3
    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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