ABSTRACT
Purpose To investigate the pathological characteristics of loco-regional recurrent nasopharyngeal carcinoma ( rNPC ) . Methods Nasopharyngeal biopsy specimens of 46 rNPCs and 63 primary NPCs were collected. HE staining, immunohistochemistry and EBV small RNAs ( EBERs) in-situ hybridization were performed. Results The over-expression rates of both p63 and CK5/6 in rNPC were significantly higher than those of primary NPCs (P=0. 005, P=0. 026), while no statistical significance of Ki-67 over-ex-pression existed between the two groups ( P=0. 387 ) . More necrotic tissues, inflammatory exudates, giant bizarre carcinoma cells, desmoplastic stroma, giant bizarre tumor cells and higher degree of squamous differentiation were found in rNPCs. The carcinoma cells of 5 rNPCs were negative for both EBERs in-situ hybridization and LMP-1 immunohistochemical staining. Conclusion The loco-re-gional rNPC has two peaks of latency interval:2~5 and 9~11 years. The loco-regional rNPC cells have higher degree of squamous differentiation with higher expression of p63 and CK5/6, as well as more invasive ability. In addition, both EBERs in-situ hybridization and LMP-1 immunostaining are negative in 10. 87% (5/46) of loco-regional rNPC.
ABSTRACT
<p><b>OBJECTIVE</b>To effectively screen p16 protein expression of different clinical stage nasopharyngeal carcinoma (NPC) by constructing and applying high-throughput tissue microarray/tissue chip.</p><p><b>METHODS</b>A series of tissue chips were prepared by using tissue arrayer with samples from different clinical stage NPC tumors and noncancerous nasopharynx tissue. Specimens from 259 cases of nasopharyngeal lesions were detected immunohistochemically on a tissue chip for p16 protein expression and the correlation of p16 protein expression to clinical stage of NPC was analyzed statistically.</p><p><b>RESULTS</b>p16 protein expression was detected in all 18 histologically normal nasopharyngeal epithelia. No p16 protein was detected in 3 of 3 (100%) stage I NPC, 38 of 44 (86.3%) stage II NPC, 59 of 68 (86.8%) stage III NPC, 23 of 28 (82.1%) stage IV NPC, 87 of 98 (88.8%) unclear stage NPC. The efficiency of p16 protein expression in NPC tissues was significantly lower than that in normal nasopharyngeal epithelia (chi(2) = 82.58, P < 0.001), and there was no apparent relationship between p16 protein expression and clinical stages (chi(2) = 0.09, P = 0.769).</p><p><b>CONCLUSIONS</b>The frequent deletion of p16 protein in NPC suggests that p16 gene has an important role in the development and progression of NPC. The consistency of p16 protein deletion in different stages of NPC suggests that the deletion of p16 protein is an early event in the development of NPC, and it is feasible to utilize tissue microarray for a rapid, economic and accurate screening of clinical tissue specimens on a large scale.</p>
Subject(s)
Humans , Cyclin-Dependent Kinase Inhibitor p16 , Immunohistochemistry , Nasopharyngeal Neoplasms , Metabolism , Pathology , Neoplasm StagingABSTRACT
<p><b>OBJECTIVE</b>To investigate the loss of heterozygosity (LOH) on chromosomal arms 13q and 14q in nasopharyngeal carcinoma (NPC) using 21 microsatellite polymorphic markers and to study whether there is a correlation between LOH and clinicopathologic parameters and/or Epstein-Barr virus (EBV) infection in NPC.</p><p><b>METHODS</b>Sixty cases of NPC were studied using polymerase chain reaction based microsatellite analysis with genescan and genotyping techniques.</p><p><b>RESULTS</b>LOH was detected on 13q in 78% of NPC tumors, high frequency LOH loci (more than 30%) clustered to 13q12.3-q14.3 and 13q32. On chromosome 14q, LOH was detected in 80% of NPC tumors; high frequency LOH loci clustered to 14q11-q13, 14q21-q24 and 14q32. High frequency LOH at 13q31-q32 correlated with a lower level of EBV infection; LOH on chromosome 14q was closely associated with poor differentiation of NPC tumor cells.</p><p><b>CONCLUSION</b>Our results suggest that in NPC, LOH on chromosome 13q and 14q are common genetic events, and putative tumor suppressor genes (TSG) residing in these regions may be involved in tumorigenesis.</p>