A self-expanding esophageal nitinol stent was implanted under fluoroscopic guidance in 40 patients with malignant esophageal strictures and clinically significant dysphagia. The strictures were caused by squamous cell carcinoma (n = 14), adenocarcinoma (n = 12), recurrent anastomotic carcinoma (n = 8), and mediastinal tumors (n = 6). Eight stents were balloon dilated to maximum diameter immediately after insertion. Sixteen stents self-expanded to maximum diameter within 24 hours, and the other stents expanded to maximum diameter during further observation. There were no serious stent-related complications, and the dysphagia was reduced considerably in all patients immediately after stent insertion. Persistent tumor bleeding occurred in two patients, and ingrowth of tumor into the stent was seen in eight patients. Two stents occluded due to tumor ingrowth but were successfully recanalized with endoscopic laser coagulation. At the end of the study, 28 patients were dead with a mean survival of 2.9 months (range, 0.1-7.0 months), and 12 patients were alive with a mean follow-up of 8.8 months (range, 4.0-15.0 months).

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Summary Cytogenetic analysis of short-term cultures from seven pulmonary hamartomas revealed an abnormal karyotype in six of them. The most characteristic aberration was an exchange of material between 6p21 and 14q24, found in three tumours. Abnormalities of either 6p or 14q were seen in another two hamartomas. Other regions that were rearranged more than once were 12q (three times) and 17p (twice), sometimes in exchange with 6p or 14q and giving rise to complex derivative chromosomes. Only one tumour had aberrations that did not involve 6p, 12q, 14q, or 17p. These results -together with the data on three previously reported pulmonary hamartomas, two of which also had t(6;14) -show that recombinations between 6p2l and 14q24 are common, and hence probably pathogenetically important. The data support the view that these tumours are genuine neoplasms rather than developmental anomalies. The coexistence of a common 14q24 breakpoint in uterine leiomyomas and pulmonary hamartomas indicates that a gene important in the genesis of both tumours exists in this band.

Two adenoid cystic carcinomas, one of the nasal cavity, the other a bronchial tumor, were cytogenetically analyzed. The former had a t(6;9)(q21-22;p 13-21) as the sole karyotypic abnormality. The latter had two related abnormal clones, resulting in the mosaic karyotype 46,XY,t(9;17)(p13;p13)/46,Y,t(X;6)(p22;q23),t(9;17)(p13;p13). The karyotypic profiles of the two cases, the only respiratory tract adenoid cystic carcinomas that have been cytogenetically characterized, differ little from those of previously reported adenoid cystic carcinomas of the major salivary glands, underscoring the fundamental biologic similarity among these tumors even when they develop from different structures and in different anatomical sites and organs. Because in the second case the t(9;17) obviously must have preceded the t(X;6), we conclude that both tumors had rearrangement of 9p13 as the primary cytogenetic change. The data thus add to the evidence that 6q changes are frequent, albeit at least sometimes secondary, aberrations in malignant salivary gland tumors. A subset of adenoid cystic carcinomas instead have rearrangement of 9p as the primary, and presumably pathogenetically essential, abnormality.

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