BACKGROUND Little is known about the genetic alterations that occur in sinonasal adenocarcinomas. The goal of the current study was to detect recurrent chromosomal gains and losses in a series of 21 primary sinonasal adenocarcinomas using comparative genomic hybridization (CGH). METHODS The authors examined ethmoid sinus adenocarcinoma samples from 21 patients. All 21 adenocarcinomas were associated with work‐related exposure to wood dust. CGH was used to detect chromosomal abnormalities, and the results of CGH analysis were evaluated for correlations with clinicopathologic characteristics. RESULTS Chromosomal gains and losses were detected in all 21 adenocarcinomas. Gains were detected at high frequencies at 7q11–21 (n = 15 [71%]), 18p11 (n = 14 [66%]), 8q11–22 (n = 13 [62%]), 5p11–13 (n = 12 [57%]), 12q11–13 and 19p (n = 11 [52%]), 20q (n = 10 [47%]), X and 5p (n = 9 [43%]), and 3q26–27 (n = 8 [38%]); and losses were detected at 8p22–23 (n = 18 [86%]), 18q22–23 (n = 17 [80%]), 17p13 (n = 12 [57%]), and 5q31–qter (n = 11 [52%]). Aside from low‐level gains, 43 high‐level amplifications were observed in the current series of 21 tumors, most commonly at Xq13 (n = 7 [33%]). CONCLUSIONS CGH revealed that ethmoid sinus adenocarcinomas carry a large number of chromosomal losses and gains, including high‐level amplifications. To the authors' knowledge, the current study represents the first attempt to investigate sinonasal adenocarcinomas on a genetic level by using CGH. The pattern of chromosomal abnormalities in these tumors was different from the pattern in other tumors within the same anatomic region (e.g., squamous cell carcinomas and salivary gland tumors); this finding may be explained by differences in etiology. Nonetheless, sinonasal adenocarcinomas appear to be genetically similar to adenocarcinomas of the stomach and colon, which also have an etiology that differs from that of sinonasal adenocarcinomas. Further study is necessary to better understand the molecular genetic basis underlying the development of sinonasal adenocarcinomas. In the near future, this type of understanding may present new possibilities for prevention and treatment of malignant disease. Cancer 2004;100:335–41. © 2003 American Cancer Society.

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The aim of this study was to assess by flow cytometry the cell cycle of brown bear fibroblast cells cultured under different growth conditions. Skin biopsies were taken in Cantabria (Spain) from a live, anaesthetized brown bear. DNA analysis was performed by flow cytometry following cell DNA staining with propidium iodide. Serum starvation increased (P < 0.01) the percentage of G0/G1 phase cells (92.7 AE 0.86) as compared to cycling cells (39.7 AE 0.86) or cells cultured to confluency (87.3 AE 0.86). DMSO included for 48 h in the culture significantly increased (P < 0.01) the percentage of G0/G1 phase of the cell cycle at all concentrations used and decreased percentages of S phase in a dose-dependent fashion. Roscovitine increased the G0/G1 phase of the cell cycle (P < 0.01) at 15 mM concentration. Interestingly, the G2/M stage significantly increased at 30 and 50 mM compared to the control and 15 mM (P < 0.02). The cell cycle of brown bear adult fibroblast cells can be successfully synchronized under a variety of culture conditions. Ó