Home  About us  Contact
 

Oral Tongue Carcinoma (oral + tongue_carcinoma)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Prognostic factors of clinically stage I and II oral tongue carcinoma,A comparative study of stage, thickness, shape, growth pattern, invasive front malignancy grading, martinez-gimeno score, and pathologic features

HEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 6 2002
Anthony Po Wing Yuen FHKAM(ORL)
Abstract Purpose This study aims at evaluation of the different prognostic models, including stage, tumor thickness, shape, malignancy grading of tumor invasive front, Martinez-Gimeno score, and pathologic features in the prediction of subclinical nodal metastasis, local recurrence, and survival of early T1 and T2 oral tongue squamous cell carcinoma. The results will have important implication for the management of patients. Patients and Methods Seventy-two clinically T1 and T2 glossectomy specimens of oral tongue carcinoma were serially sectioned in 3-mm thickness for the evaluation of various pathologic features. The prognostic value in the prediction of subclinical nodal metastasis, local recurrence, and survival of different models were compared. Results Among all the tumor parameters and predictive models being evaluated, tumor thickness was the only significant factor that had significant predictive value for subclinical nodal metastasis, local recurrence, and survival. With the use of 3-mm and 9-mm division, tumor of up to 3-mm thickness has 8% subclinical nodal metastasis, 0% local recurrence, and 100% 5-year actuarial disease-free survival; tumor thickness of more than 3 mm and up to 9 mm had 44% subclinical nodal metastasis, 7% local recurrence, and 76% 5-year actuarial disease-free survival; tumor of more than 9 mm had 53% subclinical nodal metastasis, 24% local recurrence, and 66% 5-year actuarial disease-free survival. Conclusions Tumor thickness should be considered in the management planning of patients with early oral tongue carcinoma. © 2002 Wiley Periodicals, Inc. Head Neck 24: 513,520, 2002 [source]

Loss of E-cadherin expression resulting from promoter hypermethylation in oral tongue carcinoma and its prognostic significance

CANCER, Issue 2 2002
Hsiao Wen Chang Ph.D.
Abstract BACKGROUND E-cadherin is expressed on the surface of normal epithelial cells. Loss of E-cadherin expression has been found in cancers and is postulated to facilitate tumor cell dissociation and metastasis. This study evaluated the role of promoter dense methylation in the downregulation of E-cadherin expression in oral tongue carcinoma. METHODS E-cadherin expression of 109 oral tongue carcinomas (93 primary tumors, 7 locally recurrent tumors, and 9 metastatic lymph nodes) was evaluated by immunohistochemical staining of tumor tissues. The methylation status of the CpG islands at the promoter region of E-cadherin which flanked five HpaII (methylation sensitive restriction enzyme) digestion sites were evaluated by methylation sensitive polymerase chain reaction in 86 tumors (70 primary tumors, 7 locally recurrent tumors, and 9 metastatic lymph nodes). RESULTS Underexpression of E-cadherin was found in 83% of primary tumors, 86% of recurrent tumors, and 89% of nodal metastases. Hypermethylated E-cadherin promoter was found in 64% of primary tumors, 71% of recurrent tumors, and 67% of nodal metastases. Downregulation of E-cadherin expression was found to be related to promoter hypermethylation. Consistently weak expression of E-cadherin by promoter hypermethylation was observed in primary tumors, their corresponding metastatic lymph nodes, and recurrent tumors. Downregulation of E-cadherin expression was a significant poor prognostic factor for survival. CONCLUSIONS Methylation of CpG sites at the promoter region played a key role in the inhibition of E-cadherin expression in both primary oral tongue carcinomas and their corresponding recurrences and nodal metastases. The resulting downregulation of E-cadherin expression had adverse effects on the prognosis of patients who were treated by primary surgery. Cancer 2002;94:386,92. © 2002 American Cancer Society. [source]