Tongue Carcinoma (tongue + carcinoma)

Distribution by Scientific Domains
Distribution within Medical Sciences

Kinds of Tongue Carcinoma

  • oral tongue carcinoma


  • Selected Abstracts


    Isolation of Differentiated Squamous and Undifferentiated Spindle Carcinoma Cell Lines with Differing Metastatic Potential from a 4-Nitroquinoline N-Oxide-induced Tongue Carcinoma in a F344 Rat

    CANCER SCIENCE, Issue 12 2000
    Shinichi Takeuchi
    One differentiated squamous cell carcinoma (SCC) cell line (RSC3-E2) and two undifferentiated tumor cell lines (RSC3-LM and RSC3-E2R) with different metastatic potential were established from a 4-nitroquinoline N-oxide (4NQO)-induced differentiated SCC in F344 rat tongue. The RSC3-E2 subline was isolated from a parental cell line (RSC3-P) by single cell cloning in vitro, whereas the RSC3-LM subline was isolated from a lung metastatic focus after subcutaneous (s.c.) injection of RSC3-P cells. The RSC3-E2R cell line was isolated from a lung metastatic focus following s.c. injection of RSC3-E2 cells after X-irradiation in vitro. The RSC3-E2 cell line is keratinpositive and grows as a keratinizing tumor in nude mice, whereas RSC3-LM and RSC3-E2R cells are keratin-negative, vimentin-positive and form undifferentiated tumors. When s.c. injected into nude mice, the RSC3-E2 cell line proved to be non-metastatic, while the RSC3-LM cell line was metastatic by both hematogenous and lymphogenous routes, and the RSC3-E2R cell line was metastatic only hematogenously. In vitro relative growth rates and in vitro invasion activity of these cell lines were in the order RSC3-LM>RSC3-E2R>RSC3-E2. Chromosome analysis revealed two peaks with modal chromosome numbers of 83 and 78 for RSC3-P cells and single peaks at 83, 78 and 56 for RSC3-LM, RSC3-E2 and RSC3-E2R cell lines, respectively. Common structural abnormalities on chromosome 11 were shared by all cell lines. Mutation analysis of the p53 gene using a yeast functional assay demonstrated RSC3-LM cell line to have a point mutation at codon 269, whereas RSC3-E2 and RSC3-E2R had double mutations at codons 106 and 170 on each allele. These results suggest that the two undifferentiated RSC3-LM and RSC3-E2R tumor cell lines with different metastatic potential were generated from differentiated SCC cells via different genetic pathways as a consequence of tumor progression in vivo and in vitro, respectively. These cell lines should provide a useful model for understanding mechanisms of hematogenous and lymphogenous metastasis, as well as tumor progression of oral SCCs. [source]


    Definitive radiotherapy with interstitial implant boost for squamous cell carcinoma of the tongue base

    HEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 5 2005
    Omur Karakoyun-Celik MD
    Abstract Background. The purpose of this study was to examine the long-term outcome of a cohort of patients with unresected base of tongue carcinoma who received interstitial brachytherapy after comprehensive external beam radiation therapy. Methods. Between 1983 and 2000, 122 patients with primary or recurrent squamous cell carcinoma of the oropharynx or oral cavity received interstitial brachytherapy as part of their overall management. Forty patients had primary, unresected carcinoma of the base of tongue and are the subjects of this analysis. The median age was 54 years. Fifty-four percent had T3 or T4 disease, and 70% had clinical or radiographic lymphadenopathy. Twenty-four (60%) received two to three cycles of neoadjuvant chemotherapy. The oropharynx, bilateral neck, and supraclavicular fossae were comprehensively irradiated, and the tongue base received a median external beam dose of 61.2 Gy (50,72 Gy). The primary site was then boosted with an interstitial 192Iridium implant by use of a gold-button single-strand technique and three-dimensional treatment planning. The dose rate was prescribed at 0.4 to 0.5 Gy/hr. The median implant dose was 17.4 Gy (9.6,24 Gy) and adjusted to reach a total dose to the primary tumor of 80 Gy. N2 to 3 disease was managed by a planned neck dissection performed at the time of the implant. Results. The median follow-up for all patients was 56 months, and the overall survival rates were 62% at 5 years and 27% at 10 years. The actuarial primary site control was 78% at 5 years and 70% at 10 years. The overall survival and primary site control were independent of T classification, N status, or overall stage. Systemic therapy was associated with an improvement in overall survival (p = .04) and a trend toward increased primary site control with greater clinical response. There were seven documented late effects, the most frequent being grade 3 osteonecrosis (n = 2), grade 2 swallowing dysfunction (n = 2), trismus (n = 2), and chronic throat pain (n = 1). Conclusions. In an era of greatly improved dose distributions made possible by three-dimensional treatment planning and intensity-modulated radiation therapy, brachytherapy allows a highly conformal dose to be delivered in sites such as the oropharynx. If done properly, the procedure is safe and delivers a dose that is higher than what can be achieved by external beam radiation alone with the expected biologic advantages. The long-term data presented here support an approach of treating advanced tongue base lesions that includes interstitial brachytherapy as part of the overall management plan. This approach has led to a 78% rate of organ preservation at 5 years, with a 5% incidence of significant late morbidity (osteonecrosis) that has required medical management. © 2005 Wiley Periodicals, Inc. Head Neck27: XXX,XXX, 2005 [source]


    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]


    , -secretase inhibitors exerts antitumor activity via down-regulation of Notch and Nuclear factor kappa B in human tongue carcinoma cells

    ORAL DISEASES, Issue 6 2007
    J Yao
    Objective:, To investigate the effect of the , -secretase inhibitors (GSIs) on the growth of human tongue carcinoma cells and to provide the molecular mechanism for potential application of GSIs in the treatment of tongue carcinoma. Materials and methods:, Human tongue carcinoma Tca8113 cells were cultured with the GSI L-685 458. Cell growth was determined by the methylthiazole tetrazolium method. Cell cycle and apoptosis were analyzed by flow cytometry and/or confocal microscopy. RT-PCR and Western blot were employed to determine the intracellular expression levels. Nuclear factor kappa B (NF- ,B) activation was examined by electrophoretic mobility shift assay. Results:, L-685,458 dose-dependently inhibited the growth of human tongue carcinoma Tca8113 cells by inducing G0,G1 cell cycle arrest and apoptosis. The mRNA and protein levels of Hairy/Enhancer of Split-1, a target of Notch activation, were decreased dose-dependently by L-685,458. Furthermore, L-685,458 down-regulated cyclin D1, B-cell lymphocytic-leukemia proto-oncogene 2 and c-Myc expressions, which are regulated by the transcription factor NF- ,B. Coincident with this observation, L-685,458 induced a dose-dependent reduction of constitutive NF- ,B activation in Tca8113 cells. Conclusions:, The GSI L-685,458 may have a therapeutic value for the treatment of human tongue carcinoma. Moreover, the effects of L-685,458 in tumor inhibition may act partially via the modulation of Notch and NF- ,B. [source]


    Racial Differences in Stage and Survival in Head and Neck Squamous Cell Carcinoma,

    THE LARYNGOSCOPE, Issue 5 2007
    Anthony C. Nichols MD
    Abstract Objectives: The goal of this study was to characterize differences in survival between black patients and white patients with squamous cell carcinoma of the head and neck (HNSCCA). Design: Cases of oral tongue and glottic SCCA in black patients or white patients were extracted from the Surveillance, Epidemiology, and End Results (SEER) database (years 1988,2002). For each primary site, TNM staging was imputed, and staging distributions were compared between races. For each black patient, a randomly selected white control was matched for age at diagnosis, sex, stage, surgical treatment, and radiation. Kaplan-Meier survival comparisons for both overall and disease-specific survival were then conducted for the matched pairs. Results: From 1,919 cases of carcinoma of the oral tongue, those of 151 black and 1,768 white patients were extracted. Black patients had a significantly elevated T stage (P = .001) and N stage (P = .002) at primary presentation. Of glottic carcinoma, 4,578 cases (625 black and 3,953 white patients) were extracted. Black patients again presented with significantly elevated T stage (P < .001) and N stage (P < .001) compared with white patients. For 43 matched pairs with tongue carcinoma, mean overall survival for black patients was 66.1 months versus 74.8 months for matched white controls (P = .502, log-rank test). Disease-specific survival was 91.1 months for black patients versus 109.6 months for white patients (P = .168). For 401 matched pairs with glottic carcinoma, mean overall survival for black patients was 96.6 months versus 114.5 months for white controls (P < .001). Similarly, the mean disease-specific survival was 149.4 months for black patients versus 167.1 months for white patients (P < .001) Conclusion: Controlling for stage and treatment, black patients demonstrate poorer overall and disease-specific survival with SCCA, implying other intrinsic or extrinsic factors influencing survival. [source]


    SIGNIFICANCE OF TUMOUR VOLUME MEASUREMENTS IN TONGUE CANCER: A NOVEL ROLE IN STAGING

    ANZ JOURNAL OF SURGERY, Issue 8 2007
    Min H. Chew
    Background: Tongue cancers are staged by the American Joint Committee on Cancer and the Union Internationale Contre le Cancer TNM staging systems. Cancer, however, evolves in a 3-D plane. Hence, using the largest tumour diameter will not reflect total cancer volume. We aim to evaluate the use of tongue cancer tumour volume (Tv) as a prognostic predictor of disease recurrence and survival. Methods: The study is a retrospective analysis of patients in Singapore General Hospital who underwent complete resection for histologically proven tongue carcinoma from 2000 to 2002. The Tv was measured on staging T2 -weighted magnetic resonance imaging datasets by semiautomated methods. Results: Seventeen patients with a median follow-up duration of 57.9 months were studied. A wide range of volumes was noted in each T stage. The median time to relapse was 8.6 months for those with Tv , 13 cc but was not achieved for those with Tv < 13 cc. The hazard ratio comparing Tv ,13 cc versus <13 cc is 9.02 (95% confidence interval (CI) 1.70,47.94, P = 0.014). Of the seven deaths reported, five patients had Tv , 13 cc. The median overall survival was 15.8 months for those with Tv , 13 cc but was not achieved for those with Tv < 13 cc. The hazards of death for Tv , 13 cc was 3.91 times that of Tv < 13 cc (95%CI 0.86,17.86, P = 0.078). Conclusion: Tongue cancer Tv measurement allows a more refined and accurate assessment of tumour status. This can be a possible prognostic indicator and be used in a novel staging method for the future. [source]


    A case of tongue carcinoma associated with chronic graft-versus-host disease after allogeneic haematopoietic stem cell transplantation

    AUSTRALIAN DENTAL JOURNAL, Issue 2 2010
    K Noguchi
    Abstract Graft-versus-host disease (GVHD) can occur at various sites, including the oral mucosa, where it is associated with a high risk of head and neck cancer. We report the case of a 46-year-old woman with tongue cancer that developed following Hodgkin's lymphoma and chronic GVHD, and we discuss the possible causes of cancer development. [source]


    Secondary or concomitant neoplasms among adults diagnosed with acute lymphoblastic leukemia and treated according to the LALA-87 and LALA-94 trials

    CANCER, Issue 12 2007
    Emmanuelle Tavernier MD
    Abstract BACKGROUND. Second malignant neoplasms are a serious complication after successful treatment of childhood acute lymphoblastic leukemia (ALL). Although treatment intensity and outcome were not comparable, with improvements in survival it is important to evaluate the rate and the type of second neoplasms in adults with ALL. METHODS. The data from the GET-LALA group were analyzed. A cohort of 1494 patients, aged 15 to 60 years and enrolled in 2 successive multicenter protocols between 1987 and 2002, was observed to determine the incidence of second neoplasms and associated risk factors. The median follow-up from diagnosis was 6 years. RESULTS. By February 2005 secondary or concomitant neoplasms were documented in 23 patients, including 9 acute myeloid leukemias (AML) or myelodysplasias (MDS), 4 non-Hodgkin lymphomas (NHL), 5 skin tumors, and 5 other solid tumors (1 lung cancer, 1 tongue carcinoma, 1 thymoma, 1 condrosarcoma, 1 histiocytosis). Neoplasms developed 0.5 to 13.8 years (median, 4.5 years) after the diagnosis of ALL. There were 22 patients in first remission and 1 was in second remission. The overall cumulative risk of secondary neoplasms was 2.1% at 5 years, 4.9% at 10 years, and 9.4% at 15 years. The cumulative risk of developing a second hematologic malignancy was 1.8% at 5 years, 2.2% at 10 years, 3.3% at 18 years; that of developing a solid tumor was 0.2% at 5 years, 2.8% at 10 years, 6.2% at 15 years. The development of secondary neoplasm was not associated with the use of any specific cytotoxic agent. However, the risk of skin tumor increased with radiation dose and transplantation (P = .01). Overall survival (OS) after the diagnosis of a second malignant neoplasm was 55% at 10 years. However, the median OS in patients developing AML/MDS was 5.7 months. CONCLUSIONS. The data document that adult ALL survivors are at an increased risk of later malignancy. The risk of secondary or concomitant neoplasm appeared higher than that of childhood ALL previously reported in the literature. Considering the low survival rate of this large unselected adult ALL cohort (32% at 10 years) as compared with that observed in childhood ALL, the risk of second malignancy remains underestimated. Larger series with long-term follow-up are necessary, as well as methods of screening and identification of patients at increased risk. Cancer 2007. © 2007 American Cancer Society. [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]