The cytogenetic and in vitro growth characteristics of 3 cases of extraskeletal myxoid chondrosarcoma (EMC) are described. In cell culture, the tumor cells retained the immunocytochemical and ultrastructural characteristics of EMC. Cytogenetically, 2 of the cases showed an apparently identical t(9;22)(q22;q12). In one case, the t(9;22) was found together with a dup(I)(q12q44), and in the other case it was found together with several other aberrations. The third case had an inv(10)(p11.2q22) as the sole karyotypic abnormality. Of 4 cases of EMC previously analyzed, 2 showed a t(9;22)(q22;q11-12) and one case of a t(9;22;15)(q31;q12.2;q25). Thus, 5 out of 7 cases of EMC showed recombination between 9q22-31 and 22q11-12, indicating that this represents a tumor specific abnormality. The breakpoints on 22q were in all 5 cases cytogenetically indistinguishable from those seen in Ewing's sarcoma with t(11;22), clear-cell sarcoma with t(12;22), and desmoplastic small round cell tumors with t(11;22). Molecular cloning of these translocation breakpoints revealed involvement of the EWS gene (located at 22q12) in all 3 tumor types. These observations raise the intriguing question of whether the EWS gene might also be involved in the t(9;22) in EMC.

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Sulforaphane-induced activation of the transcription factor NF-E2 related factor 2 (Nrf2 or the gene Nfe2l2) and subsequent induction of the phase II antioxidant system has previously been shown to exert neuroprotective action in a transient model of focal cerebral ischemia. However, its ability to attenuate functional and cellular deficits after permanent focal cerebral ischemia is not clear. We assessed the neuroprotective effects of sulforaphane in the photothrombotic model of permanent focal cerebral ischemia. Sulforaphane was administered (5 or 50 mg/kg, i.p.) after ischemic onset either as a single dose or as daily doses for 3 days. Sulforaphane increased transcription of Nrf2, Hmox1, GCLC and GSTA4 mRNA in the brain confirming activation of the Nrf2 system. Single or repeated administration of sulforaphane had no effect on the infarct volume, nor did it reduce the number of activated glial cells or proliferating cells when analyzed 24 and 72 h after stroke. Motor-function as assessed by beam-walking, cylinder-test, and adhesive test, did not improve after sulforaphane treatment. The results show that sulforaphane treatment initiated after photothrombosis-induced permanent cerebral ischemia does not interfere with key cellular mechanisms underlying tissue damage.

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The present study demonstrates that two important components of reactive gliosis, cellular activation and proliferation, can be attenuated by octanol and carbenoxolone.