p53 GENE ALTERATIONS AND p53 PROTEIN IN ORAL EPITHELIAL DYSPLASIA AND SQUAMOUS CELL CARCINOMA

Kusama, Kaoru; Okutsu, Seijiro; Takeda, Akio; Himiya, Takao; Kojima, Akira; Kidokoro, Yoshihiro; Chu, Ling; Iwanari, Shinkichi; Kudo, Itsuro; Moro, Itaru

doi:10.1002/(sici)1096-9896(199604)178:4<415::aid-path548>3.0.co;2-1

Cited by 39 publications

(5 citation statements)

References 27 publications

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“…In a preliminary sequencing analysis of 17 nondysplastic leuoplakia biopsies with p53 overexpression we failed to detect any p53 mutations (data not shown). In contrast to nondysplastic lesions (22), mutations can be detected in dysplastic lesions (23,24), and in the malignant lesions p53 overexpression is associated with missense mutations in 75% of cases (15). Furthermore, it was noted that p53 mutations can persist in oral premalignant lesions for several years without progression to malignancy to occur (25).…”

Section: Discussionmentioning

confidence: 99%

Aberrant expression of p53, p16INK4a and Ki-67 as basic biomarker for malignant progression of oral leukoplakias

Nasser

Flechtenmacher

Holzinger

et al. 2011

Journal of Oral Pathology &Amp; Medicine

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Section: Discussionmentioning

confidence: 99%

Aberrant expression of p53, p16INK4a and Ki-67 as basic biomarker for malignant progression of oral leukoplakias

Nasser

Flechtenmacher

Holzinger

et al. 2011

Journal of Oral Pathology &Amp; Medicine

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“…The timing and significance of p53 mutation in oral cancer progression could vary in different ethnic populations and geographic areas (84). Mutations of p53 have also been observed in a variety of dysplastic epithelial lesions from various aerodigestive tissues, including oral cavity (85,86), esophagus (87,88), and lung (89), suggesting this to be a common genetic event in tobacco associated carcinogenesis (90). Furthermore, some studies in the literature support wild-type (WT) p53 to be over expressed without gene mutations (91,92).…”

Section: P53mentioning

confidence: 99%

Molecular markers in oral epithelial dysplasia: review

Pitiyage

Tilakaratne

Tavassoli

et al. 2009

J Oral Pathology Medicine

168

126

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The clinical and histologic features alone cannot accurately predict whether potentially malignant disorders of the oral mucosa remain stable, regress or progress to malignancy. Some of them, with or without epithelial dysplasia, may transform to invasive oral squamous cell carcinomas (OSCC). Identification of molecular markers which can predict disease progression is necessary to improve the management of these disorders. Many genes and signaling pathways have been shown to be involved in the development of OSCC. This review summarizes some molecular markers researched in the detection of pre-cancer. We highlight selected markers that are reported to be significantly associated with progression of potentially malignant disorders to OSCC. These include alterations in genes/pathways which control cellular signaling, cell cycle, apoptosis, genomic stability, cytoskeleton, angiogenesis, etc. However, these genetic tumor markers have so far not gained any use in routine diagnosis and their utility in the prediction of risk of malignant transformation remains unknown. It is, however, clear from the large number of studies, some described in this review, that multiple genes/pathways are involved in the progression from normal to metaplastic/dysplastic, and subsequently to cancer. It is therefore necessary to study those significant alterations in multiple genes simultaneously in biopsy samples from large cohorts of subjects.

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“…There is the view that in an individual lesion, the more severe the dysplasia, the greater the likelihood is of progression to malignancy [3,4]. However, nondysplastic lesions may also show transformation.…”

Section: Introductionmentioning

confidence: 99%

Podoplanin expression during dysplasia–carcinoma sequence in the oral cavity

et al. 2011

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Human podoplanin, a type-1 transmembrane sialomucin-like glycoprotein, is involved in cell migration, tumor cell invasion, and metastasis. However, the role of the protein in squamous cell carcinoma (SCC) has been unclear and immunohistochemical reactivity for podoplanin differs from organ-to-organ. In the present study, immunohistochemical and molecular biological analyses were performed to examine the importance of podoplanin expression in oral precancerous and cancerous lesions and metastases. We immunohistochemically investigated the expression of podoplanin in 103 precancerous lesions, 69 primary oral squamous cell carcinomas (OSCCs), and 32 metastases, and that of E-cadherin and vimentin in primary OSCCs with metastasis. Furthermore, human OSCC-derived cell lines preincubated with fibrous growth factor-basic, epidermal growth factor (EGF), and tumor growth factor-β1 were subjected to real-time reverse transcription polymerase chain reaction. Immunoreactivity for podoplanin was detected in 89 (86.4%) of the precancerous lesions and the intensity was correlated with the degree of epithelial dysplasia (P = 0.016). Enhanced podoplanin expression was observed in 66 (95.7%) of the OSCCs and was significantly associated with a poor pathologic grade of differentiation (P = 0.020). Epithelial-mesenchymal transition was observed in 18 (58.1%) of the primary OSCCs with metastasis to regional lymph nodes. Messenger RNA for podoplanin was markedly increased after treatment with EGF in three OSCC cell lines. The present findings suggest that podoplanin is associated with tumor development via the oral dysplasia-carcinoma sequence and could be involved in a signaling pathway governing tumor growth and invasion in OSCC.

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p53 GENE ALTERATIONS AND p53 PROTEIN IN ORAL EPITHELIAL DYSPLASIA AND SQUAMOUS CELL CARCINOMA

Cited by 39 publications

References 27 publications

Aberrant expression of p53, p16INK4a and Ki-67 as basic biomarker for malignant progression of oral leukoplakias

Aberrant expression of p53, p16INK4a and Ki-67 as basic biomarker for malignant progression of oral leukoplakias

Molecular markers in oral epithelial dysplasia: review

Podoplanin expression during dysplasia–carcinoma sequence in the oral cavity

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