p53 expression in concurrent chemoradiotherapy with docetaxel for head and neck squamous cell carcinoma.

Background: The current study aimed to evaluate the significance of an immunohistochemical assessment of tumor suppressor p53 as a prognostic marker in head and neck squamous cell carcinoma (HNSCC) patients treated with docetaxel and radiotherapy.

Methods: The expression of tumor suppressor p53 and its phosphorylated form at the Ser392 residue was retrospectively evaluated by immunohistochemistry in 51 Stage T1-3N0-2M0 (except T1N0 glottis) HNSCC patients who were treated with 10mg/m(2)/week docetaxel four to six times and received concurrent chemoradiotherapy.

Results: Kaplan-Meier univariate analysis revealed that no difference in rates for overall and disease-free survival (DFS) between patients with p53-positive and -negative tumors (p=0.

Prognostic significance of cyclin D1 and p16 in patients with intermediate-risk head and neck squamous cell carcinoma treated with docetaxel and concurrent radiotherapy.

Background: The current study aimed to evaluate the significance of the cell-cycle-control proteins cyclin D1 and p16 as prognostic markers in head and neck squamous cell carcinoma (HNSCC) patients treated with docetaxel and radiotherapy.

Methods: Cyclin D1 and/or p16 protein expression was retrospectively evaluated by immunohistochemistry in 53 patients with stage T1-3N0-2M0 (except T1N0 glottis) HNSCC who were treated with 10 mg/m(2)/week docetaxel 4 to 6 times and received concurrent chemoradiotherapy.

Results: Kaplan-Meier univariate analysis revealed that patients with cyclin D1-positive tumors or p16-negative tumors had a worse prognosis compared with those with cyclin D1-negative tumors or p16-positive tumors (p = .

"Watch-and-see" policy for the clinically positive neck in head and neck cancer treated with chemoradiotherapy.

Background: Chemoradiotherapy (CRT) is becoming more widely used for head and neck cancer. However, there are conflicting theories regarding the best management options for patients with advanced nodal disease.

Methods: From 1990 to 1999, we treated 96 patients with N1-N2 neck disease by concomitant CRT for organ preservation, using weekly carboplatin or a low daily dose of cisplatin, followed by a "watch-and-see" policy for the neck.

[Olfactory neuroblastoma: the Hokkaido University experience].

Olfactory neuroblastoma is such a rare malignancy that no consensus has been reached on its management. We analyzed 17 patients with olfactory neuroblastoma treated between April 1980 and March 2004--9 men and 8 women, aged 16 to 76 years old(mean: 50.4 years).

Hypermethylation and silencing of the putative tumor suppressor Tazarotene-induced gene 1 in human cancers.

A variety of tumor suppressor genes are down-regulated by hypermethylation during carcinogenesis. Using methylated CpG amplification-representation difference analysis, we identified a DNA fragment corresponding to the Tazarotene-induced gene 1 (TIG1) promoter-associated CpG island as one of the genes hypermethylated in the leukemia cell line K562. Because TIG1 has been proposed to act as a tumor suppressor, we tested the hypothesis that cytosine methylation of the TIG1 promoter suppresses its expression and causes a loss of responsiveness to retinoic acid in some neoplastic cells.

Induction of TIG3, a putative class II tumor suppressor gene, by retinoic acid in head and neck and lung carcinoma cells and its association with suppression of the transformed phenotype.

Retinoids can regulate the proliferation and differentiation of various tumor cells. It is thought that nuclear retinoid receptors mediate these effects by regulating gene transcription. The identity of specific retinoid target genes is only beginning to be unraveled.

Differentially expressed genes associated with CIS-diamminedichloroplatinum (II) resistance in head and neck cancer using differential display and CDNA microarray.

Background: The mechanism by which cancer cells become resistant to cis-Diamminedichloroplatinum (II) (cDDP) is not completely understood. To investigate the molecular markers involved in the cDDP resistance, we compared the gene expression profiles between a head and neck squamous cell carcinoma (HNSCC) line sensitive to cDDP and its cDDP-resistant variant.

Methods: Both a fluorescent differential display and a cDNA microarray analysis were applied to distinguish the gene profiles between KB, a human HNSCC line, and its cDDP-resistant variant (KB/cDDP).