BACKGROUNDCyclin D1 (CCND1) and p16 alterations have been detected in oral squamous cell carcinomas (SCCs), suggesting that abnormalities of these genes may play an important role in the genesis or progression of oral SCCs and serve as independent prognostic indicators. The detection of CCND1 and p16 aberrations using a simple and sensitive method would be valuable for the development of effective treatment modalities for oral cancer. The objective of the current study was to determine whether CCND1 numerical aberrations and p16 deletions in oral SCCs detected by fluorescence in situ hybridization (FISH) have any impact on clinical outcome.METHODSUsing genomic DNA probes for CCND1 and p16, FISH was performed on specimens that were obtained by fine‐needle aspiration (FNA) from 57 primary oral SCCs.RESULTSThe CCND1 numerical aberration was observed in 28 of 57 patients (49%) with oral SCCs and was associated significantly with reduced disease‐free survival (P = .0004) and overall survival (P = .0179). Conversely, p16 deletion was detected in 22 of 57 patients (39%). The disease‐free and overall survival rates for patients with p16 deletion were lower than those among patients without the p16 deletion, although the difference just failed to reach statistical significance (P = .0516 and P = .1878, respectively). The p16 deletion in the presence of the CCND1 numerical aberration conferred significantly worse disease‐free survival (P = .0002) and overall survival (P = .0153).CONCLUSIONSAlthough the CCND1 numerical aberration was a good predictor of aggressive tumors, recurrence, and poor prognosis in patients with oral SCCs, the authors were able to identify subgroups of patients that had early disease recurrence and a poor prognosis more efficiently by assessment of p16 deletion in addition to CCND1 genetic status using FISH on FNA biopsy samples compared with the analysis of either alteration alone. Cancer 2007. © 2007 American Cancer Society.
BackgroundAlthough chromosomal instability (CIN) has been detected in many kinds of human malignancies by means of various methods, there is no practical assessment for small clinical specimens. In this study, we evaluated CIN in fine-needle aspiration (FNA) biopsied oral squamous cell carcinomas (SCCs) using fluorescence in situ hybridization (FISH) analysis, and investigated its prognostic significance.MethodsTo evaluate CIN status of tumors, FISH with genomic probes for the centromeres of chromosomes 7, 9, and 11 was performed on specimens obtained by FNA from 77 patients with primary oral SCCs.ResultsHigh-grade CIN (CIN3) was observed in 11.7% (9/77) of patients with oral SCCs and was associated significantly with reduced disease-free survival (p = .008) and overall survival (p = .003). Multivariate Cox proportional hazards analysis showed that CIN status was significantly correlated with disease-free survival (p = .035) and overall survival (p = .041).ConclusionAnalysis of CIN status using FISH on FNA biopsy specimens may be useful in predicting of recurrence and poor prognosis in patients with oral SCCs.
Cyclin D1 gene (CCND1) numerical aberrations are independent prognostic indicators of head and neck squamous cell carcinomas (HNSCCs). High epidermal growth factor receptor gene (EGFR) copy number is associated with poor prognosis in lung cancer, but such findings are controversial in oral SCCs (OSCCs). We analyzed copy number status in CCND1 and EGFR in OSCC patients and its association with clinical outcome. EGFR and CCND1 statuses were analyzed in 85 OSCC patients by fluorescence in situ hybridization (FISH) of specimens obtained by fine‐needle aspiration biopsy. CCND1 numerical aberration was found in 35 of 85 tumors (41%), and aberrant EGFR copy number was observed in 36 (42%). Gene amplification (GA) was dominant among CCND1 copy number changes (14/35:40%). Balanced trisomy (BT) was the most frequently observed EGFR aberration (17/36:47%). In a multivariate Cox’s proportional hazards analysis, CCND1 GA was correlated with disease‐free survival (P < 0.001), whereas EGFR BT was significantly correlated with overall survival (P = 0.001). Patients with a combination of CCND1 GA and/or EGFR BT had significantly poorer clinical outcome. CCND1 and EGFR copy number changes were frequent in OSCC and had differing aberration patterns. CCND1 GA and EGFR BT statuses by dual‐color FISH were the predominant predictors of clinical outcome. Further investigation is needed to determine the implications for EGFR inhibitor therapy in OSCC.
Between 2011 and 2018, 518 respiratory adenovirus infections were diagnosed in a pediatric clinic in Shizuoka, Japan. Detection and typing were performed by partial sequencing of both hexon- and fiber-coding regions which identified: adenovirus type 1 (Ad-1, n = 85), Ad-2 (n = 160), Ad-3 (n = 193), Ad-4 (n = 18), Ad-5 (n = 27), Ad-11 (n = 2), Ad-54 (n = 3), and Ad-56 (n = 1). Considering previous reports of the circulation of an endemic recombinant Ad-2, e.g., Ad-89, 100 samples typed as Ad-2 were randomly selected for further molecular typing by sequencing the penton base-coding region. Despite the high nucleotide sequence conservation in the penton base- coding region, 27 samples showed 98% identity to Ad-2. Furthermore, 14 samples showed 97.7% identity to Ad-2 and 99.8% identity to Ad-89, while the remaining 13 samples showed an average 98% pairwise identity to other Ad-C types and clustered with Ad-5. The samples typed as Ad-89 (n = 14) and as a recombinant Ad type (P5H2F2) (n = 13) represented 27% of cases originally diagnosed as Ad-2, and were detected sporadically. Therefore, two previously uncharacterized types in Japan, Ad-89 and a recombinant Ad-C, were shown to circulate in children. This study creates a precedent to evaluate the epidemiology and divergence among Ad-C types by comprehensively considering the type classification of adenoviruses.
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