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Oral Dysplasia (oral + dysplasia)

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Medical Sciences100%

Selected Abstracts

Multiple pathways in the FGF signaling network are frequently deregulated by gene amplification in oral dysplasias

INTERNATIONAL JOURNAL OF CANCER, Issue 9 2009
Ivy F.L. Tsui
Abstract Genetic alteration in oral premalignant lesions (OPLs), the precursors of oral squamous cell carcinomas (OSCCs), may represent key changes in disease initiation and development. We ask if DNA amplification occurs at this early stage of cancer development and which oncogenic pathways are disrupted in OPLs. Here, we evaluated 50 high-grade dysplasias and low-grade dysplasias that later progressed to cancer for gene dosage aberrations using tiling-path DNA microarrays. Early occurrences of DNA amplification and homozygous deletion were frequently detected, with 40% (20/50) of these early lesions exhibiting such features. Expression for 88 genes in 7 recurrent amplicons were evaluated in 5 independent head and neck cancer datasets, with 40 candidates found to be overexpressed relative to normal tissues. These genes were significantly enriched in the canonical ERK/MAPK, FGF, p53, PTEN and PI3K/AKT signaling pathways (p = 8.95 × 10,3 to 3.18 × 10,2). These identified pathways share interactions in one signaling network, and amplification-mediated deregulation of this network was found in 30.0% of these preinvasive lesions. No such alterations were found in 14 low-grade dysplasias that did not progress, whereas 43.5% (10/23) of OSCCs were found to have altered genes within the pathways with DNA amplification. Multitarget FISH showed that amplification of EGFR and CCND1 can coexist in single cells of an oral dysplasia, suggesting the dependence on multiple oncogenes for OPL progression. Taken together, these findings identify a critical biological network that is frequently disrupted in high-risk OPLs, with different specific genes disrupted in different individuals. © 2009 UICC [source]

Systematic review of the follow-up of oral dysplasia

CLINICAL OTOLARYNGOLOGY, Issue 3 2006
T. Rattay
Objectives.,To assess effectiveness, safety, and acceptability of follow-up regimens for oral dysplasia with regards to malignant transformation rate and duration to transformation. Method.,Study design,Systematic literature review with criteria for identifying studies, assessing quality and data extraction. Selection criteria,Cohort studies, case-control studies, or randomised-controlled trials (RCTs). Interventions,Clinical follow-up and surveillance, surgical and non-surgical treatment, modification of aetiological factors. Outcome measures,Malignant transformation rate, predictive value of clinical prognostic indicators. Data collection and analysis,Using selection criteria, we identified published data by electronic searching. The validity of studies and extracted data was independently assessed by two authors. Quantitative data is compared and summarized in a table. Qualitative data is also discussed. Results. There are no RCTs assessing follow-up strategies. Nineteen cohort studies (level II and III evidence) reported follow-up, of which 12 were included in the meta-analysis. The malignant transformation rate varies widely between studies (6.6,36.0%). Surgical treatment appears to be more effective than non-surgical modalities, but recurrence is high. Tobacco and alcohol use, site and histological grade of the lesion are associated with progression to cancer. Conclusions. There is currently no evidence-based or consensus strategy for malignant risk quantification and follow-up of patients with oral dysplasia. We present a follow-up protocol based on best evidence. Large randomised-controlled trials are needed to assess these new strategies, including the use of molecular markers to quantify risk and follow-up these lesions. [source]

Multiple pathways in the FGF signaling network are frequently deregulated by gene amplification in oral dysplasias

INTERNATIONAL JOURNAL OF CANCER, Issue 9 2009
Ivy F.L. Tsui
Abstract Genetic alteration in oral premalignant lesions (OPLs), the precursors of oral squamous cell carcinomas (OSCCs), may represent key changes in disease initiation and development. We ask if DNA amplification occurs at this early stage of cancer development and which oncogenic pathways are disrupted in OPLs. Here, we evaluated 50 high-grade dysplasias and low-grade dysplasias that later progressed to cancer for gene dosage aberrations using tiling-path DNA microarrays. Early occurrences of DNA amplification and homozygous deletion were frequently detected, with 40% (20/50) of these early lesions exhibiting such features. Expression for 88 genes in 7 recurrent amplicons were evaluated in 5 independent head and neck cancer datasets, with 40 candidates found to be overexpressed relative to normal tissues. These genes were significantly enriched in the canonical ERK/MAPK, FGF, p53, PTEN and PI3K/AKT signaling pathways (p = 8.95 × 10,3 to 3.18 × 10,2). These identified pathways share interactions in one signaling network, and amplification-mediated deregulation of this network was found in 30.0% of these preinvasive lesions. No such alterations were found in 14 low-grade dysplasias that did not progress, whereas 43.5% (10/23) of OSCCs were found to have altered genes within the pathways with DNA amplification. Multitarget FISH showed that amplification of EGFR and CCND1 can coexist in single cells of an oral dysplasia, suggesting the dependence on multiple oncogenes for OPL progression. Taken together, these findings identify a critical biological network that is frequently disrupted in high-risk OPLs, with different specific genes disrupted in different individuals. © 2009 UICC [source]

Presence of human papilloma virus, herpes simplex virus and Epstein,Barr virus DNA in oral biopsies from Sudanese patients with regard to toombak use

JOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 8 2010
Jamshid Jalouli
J Oral Pathol Med (2010) 39: 599,604 Using PCR/DNA sequencing, we investigated the prevalence of human papillomavirus (HPV), herpes simplex virus (HSV) and Epstein,Barr virus (EBV) DNA in brush biopsies obtained from 150 users of Sudanese snuff (toombak) and 25 non-users of toombak in formalin-fixed paraffin-embedded tissue samples obtained from 31 patients with oral dysplasias (25 toombak users and 6 non-users), and from 217 patients with oral cancers (145 toombak users and 72 non-users). In the brush tissue samples from toombak users, HPV was detected in 60 (40%), HSV in 44 (29%) and EBV in 97 (65%) of the samples. The corresponding figures for the 25 samples from non-users were 17 (68%) positive for HPV, 6 (24%) positive for HSV and 21 (84%) for EBV. The formalin-fixed samples with oral dysplasias were all negative for HPV. In the 145 oral cancer samples from toombak users, HPV was detected in 39 (27%), HSV in 15 (10%) and EBV in 53 (37%) of the samples. The corresponding figures for the samples from non-users were 15 (21%) positive for HPV, 5 (7%) for HSV and 16 (22%) for EBV. These findings illustrate that prevalence of HSV, HPV and EBV infections are common and may influence oral health and cancer development. It is not obvious that cancer risk is increased in infected toombak users. These observations warrant further studies involving toombak-associated oral lesions, to uncover the possible mechanisms of these viral infections in the development of oral cancer, and the influence of toombak on these viruses. [source]