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  • GENE COPY NUMBER  (1)
  • Keywords: Brain metastasis; stereotactic radiosurgery; surgery.  (1)
  • 1
    Keywords: SURVIVAL ; carcinoma ; ACTIVATION ; protein expression ; EGFR ; C-MET ; GENE COPY NUMBER ; ALK ; TUMOR REGISTRY
    Abstract: BACKGROUND: CMET represents an emerging therapy target for monoclonal antibodies and tyrosine kinase inhibitors in non-small cell lung cancer (NSCLC). METHODS: We investigated CMET gene amplification status by fluorescence in-situ hybridization (FISH) and CMET protein expression by immunohistochemistry in a large series of 209 NSCLC brain metastases (BM; 165 adenocarcinoma, 20 squamous cell carcinoma, 11 adenosquamous carcinomas, 11 large cell carcinomas and two large cell neuroendocrine carcinomas) and correlated our results to clinic-pathological parameters and molecular data from previous studies. RESULTS: We found CMET gene amplification in 36/167 (21.6%) and CMET protein expression in 87/196 (44.4%) of evaluable BM. There was a strong correlation between the presence of CMET gene amplification and CMET protein expression (P 〈 0.001, chi-square test). Furthermore, presence of CMET amplification correlated positively with presence of ALK amplifications (P = 0.039, chi-square test) and high HIF1 alpha index (P = 0.013, Mann-Whitney U-test). Neither CMET expression nor CMET gene amplification status correlated with patient outcome parameters or known prognostic factors. CONCLUSIONS: CMET overexpression and CMET amplification are commonly found in NSCLC BM and may represent a promising therapeutic target.
    Type of Publication: Journal article published
    PubMed ID: 25039982
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  • 2
    ISSN: 0942-0940
    Keywords: Keywords: Brain metastasis; stereotactic radiosurgery; surgery.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary  Stereotactic radiosurgery (RS) and surgery have proved to be effective treatment modalities for brain metastasis. We followed 133 patients whose treatment for intracranial disease was either RS or a single surgical resection at the University of Vienna from August 1992 through October 1996. All patients who received additional Whole Brain Radiotherapy were included. This was a retrospective, case-control study comparing these treatment modalities.  Sixty-seven patients were treated by RS and 66 patients were treated by microsurgery. The median size of the treated lesions for RS patients was 7800 mm3, and 12500 mm3 for microsurgery patients, respectively. The median dose delivered to the tumour margin for RS patients was 17 gray.  The median survival for patients after RS was 12 months, and 9 months for patients after microsurgery. This difference was not statistically significant (p=0.19). Comparison of local tumour control, defined as absence of regrowth of a treated lesion, showed that tumours following RS had a preferred local control rate (p〈0.05). Univariate and multivariate analysis showed that this fact was due to a greater response rate of “radioresistant” metastasis to RS (p〈0.005). Postradiosurgical complications included the onset of peritumoural oedema (n=5) and radiation necrosis (n=1). Two patients after microsurgery experienced local wound infection. One postoperative death occurred due to pulmonary embolism in this group.  On the basis of our data we conclude that RS and microsurgery combined with Whole Brain Radiotherapy are comparable modalities in treating single brain metastasis. Concerning morbidity and local tumour control, in particular in cases of “radioresistant” primary tumours, RS is superior. Therefore we advocate RS except for cases of large tumours (〉3 cm in maximum diameter) and for those with mass effect.
    Type of Medium: Electronic Resource
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