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M Salzer-Kuntschik

Publications and source records attributed to M Salzer-Kuntschik.

74 records · Page 5Linked to original sources

[Results following spongiosa transplantation in giant cell tumor of bone].

Between 1952-1988 47 giant cell tumors of the bone were treated at the Orthopedic University Clinic of Vienna with different surgical margins: In 9 cases a radical or wide, in 3 cases a marginal and in 35 cases an intralesional resection was performed. In the cases with intralesional resections the tumors were diligently curatted and the resulting bone cavity was shaved with a rase. In addition in eleven cases a chemical cauterization was done with phenol. Afterwards the lesion was filled up with autogenous or homogeneous bone chips with or without fibrin tissucol. In the cases where phenol was used no local recurrence was observed over a mean period of 39 months (max. 91, min. 6) of follow up. Because of the subchondral joint location of the giant cell tumors of the extremities a radical or wide resection usually causes the loss of a part of the joint which is followed by poor functional results. Intralesional resections in combination with phenol cauterization not only achieved good functional results, but also succeeded in reducing the rate of local recurrencies from 25-44% in 0 as described by other authors.

Adolescent↗

[The EWS gene rearrangement in Ewing tumors: key to the disease].

The family of Ewing tumors (ET) is characterised by a unique gene rearrangement which is represented by a translocation t(11;22) (q24;q12) or a deletion del 22q12 in most cytogenetically analysable cases. The recent cloning of the underlying gene fusion provides the basis for the diagnostic detection of minimal amounts of residual tumor cells at resection margins, in blood and bone marrow. In addition, the very first steps in ET tumorigenesis can be studied on a functional basis. In this study, a variety of fusion products were identified with a sensitivity of 10(-6) by means of RT-PCR. In 20 of 22 ET, a gene rearrangement was identified which resulted in the substitution of the effector domain of one of the closely related DNA-binding oncogenes, FLI-1 or ERG, by the transactivating domain of a new gene, EWS. Presumably, the oncogene and consequently its target genes are activated by this type of translocation. If the EWS domain was replaced with a transcriptionally irrelevant domain by transfection of a recombinant gene into ET cells, competition with the endogenous chimeric oncogene-product for DNA-binding was observed resulting in a partial growth inhibition. Activation of FLI-1 has been previously shown to occur as a primary event in Friend virus induced mouse erythroleukemia. During progression of this disease, inactivating p53 mutations have been observed frequently. In contrast, such aberrations were found to be extremely rare in ET.

Adolescent↗