Linguistic validation of the N-QOL (ICIQ), OAB-q (ICIQ), PPBC, OAB-S and ICIQ-MLUTSsex questionnaires in 16 languages.

OBJECTIVE: Overactive bladder (OAB) is a highly prevalent condition with a negative impact on both health-related quality of life and sexual functioning. We aimed to create and validate conceptually equivalent tools to assess OAB for use in diverse cultural and linguistic settings. RESEARCH DESIGN AND METHODS: To evaluate the linguistic validity of harmonised translations of the Nocturia Quality of Life (N-QOL) questionnaire, Overactive Bladder Questionnaire (OAB-q) family, Patient Perception of Bladder Condition (PPBC) questionnaire, Overactive Bladder Satisfaction Questionnaire (OAB-S) and International Consultation on Incontinence Questionnaire (ICIQ) Male Sexual Matters associated with Lower Urinary Tract Symptoms Questionnaire (ICIQ-MLUTSsex), bilingual (target language and English) interviewers cognitively debriefed subjects to assess their ability to paraphrase and understand the instructions, questions and responses within each questionnaire. RESULTS: Overall item comprehension rates were 96% for the N-QOL, 98.9% for the OAB-q, 92% for the PPBC, 98.5% for the OAB-S and 94.3% for the ICIQ-MLUTSsex. DISCUSSION: We found that the translations were well-understood by subjects, although a number of minor changes were made to the N-QOL, OAB-q, OAB-S and ICIQ-MLUTSsex translations in an effort to improve clarity and cultural appropriateness. In a few instances, the majority of subjects in a language were unable to paraphrase a specific term or phrase prior to the revisions. In several cases, problems arose from the wording of the question in the source language. CONCLUSIONS: The translated instruments in this study demonstrated a high level of overall linguistic validity.

Re-expression of procollagen type IIA in oral squamous cell carcinoma.

There are two forms of procollagen type II (IIA and IIB), both of which are expressed during chondrogenesis. Procollagen type IIA also is present at sites of developmental epithelial-mesenchymal interaction. Malignant transformation is associated with disturbed epithelial-mesenchymal interaction and the reappearance of fetal characteristics. This study aims to determine whether or not procollagen type IIA is re-expressed in oral squamous cell carcinoma (OSCC). Immunoperoxidase techniques were applied to frozen and paraffin sections of OSCC (n = 30) and normal oral mucosa (n = 5). In the carcinoma group, strong cytoplasmic staining for collagen type II was present (25/30). Staining was weak or absent in the stroma, and absent from the normal oral mucosa. Frozen sections from 10 of the carcinoma cases which showed positive staining were incubated with antibodies specific for procollagen type IIA and visualised using immunofluorescence. Staining was evident in each case and was particularly strong in the region of the basement membrane. Slot-blot analysis of collagen extracts from OSCC supported the immunohistochemical findings. We conclude, therefore, that procollagen type IIA is re-expressed in OSCC.

DNA studies underestimate the major role of CDKN2A inactivation in oral and oropharyngeal squamous cell carcinomas.

Loss of CDKN2A expression was demonstrated by immunohistochemistry in 87% of oral and oropharyngeal squamous cell carcinoma (OSCC) primary tumor samples. By contrast, DNA studies showed a much lower frequency of loss of the CDKN2A gene. Point mutations and promoter methylation of CDKN2A were seen in 7% and 23%, respectively, of primary tumors. Loss of heterozygosity analysis using a dense set of 9p markers showed allelic imbalance that included CDKN2A in only 31% of samples, but a further 47% showed loss at loci near CDKN2A with apparent retention of CDKN2A. No tumor with any allelic imbalance expressed CDKN2A, whether or not the imbalance appeared to involve the CDKN2A locus. We interpret these data as showing partially overlapping deletions on the two 9p homologues, with homozygous deletion of CDKN2A masked by amplification of contaminating stromal material. Our data show that inactivation of the CDKN2A gene products is a near-universal step in the development of oral and oropharyngeal squamous cell carcinomas, and we suggest that homozygous deletion is the most common mechanism of inactivation. The CDKN2A locus may be particularly prone to deletion because it encodes two unrelated tumor suppressor proteins, CDKN2A (p16INK4a) and p19ARF, and deletion, but not point mutation or methylation, would inactivate both gene products. However, our results also suggest that complex patterns of allelic imbalance in primary squamous carcinomas in general may not provide reliable evidence for the existence of multiple tumor suppressor genes within a single chromosomal region.