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Results for “MOUTH NEOPLASMS”

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At least 631 records · Page 35Linked to original sources
PubMed1951

An epulis.

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Giant Cell Tumors↗
PubMedDate not supplied

Tobacco and oral health.

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Carcinoma, Squamous Cell↗
PubMed2004

[An advanced case of squamous cell carcinoma in the left buccal mucosa, upper gingiva, and maxillary sinus (T4N0M0) showing a complete response to chemotherapy with TS-1].

We report a case of advanced squamous cell carcinoma in the left buccal mucosa, upper gingiva, and maxillary sinus (T4N0M0) showing a complete response to oral chemotherapy with TS-1. The patient was an 89-year-old female with severe dementia. We carried out chemotherapy with TS-1 50 mg/day, without surgical treatment. The tumor disappeared clinically at 4 months after 3 courses of the TS-1 administration. Adverse drug reactions, including vomiting, leukopenia and thrombopenia, forced a stop of the administration of TS-1. Although she finally died of in senescence 2 months from the cease of administration, there was no recurrence of the cancer at the time.

Aged↗
PubMedDate not supplied

Apoptosis-inducing activity of cisplatin (CDDP) against human hepatoma and oral squamous cell carcinoma cell lines.

The sensitivity of human hepatoma (HepG2) and oral squamous cell carcinoma (HSC-2) cell lines against various apoptosis-inducing agents was compared. HepG2 cells were generally more resistant to an oxidant (H2O2), antioxidants (sodium ascorbate, gallic acid, epigallocatechin gallate) and anticancer drugs (doxorubicin, methotrexate, cisplatin (CDDP), etoposide, 5-fluoro-2,4(1H,3H)-pyrimidinedione (5-FU), peplomycin sulfate) as compared to HSC-2 cells. Lower concentrations of CDDP, but not other anticancer drugs, induced comparable cytostatic effects on both HSC-2 and HepG2 cells. CDDP induced internucleosomal DNA fragmentation and activation of caspases 3, 8 and 9 in HepG2 cells. On the other hand, CDDP did not induce DNA fragmentation and activated caspase 3 only marginally in HSC-2 cells. Combination treatment with CDDP (10 microM) and 5-FU (100 microM) additively activated all three caspases in HepG2 cells, but not in HSC-2 cells. The present study demonstrated the chemotherapeutic potential of combined treatment of CDDP and 5-FU against hepatoma cells and the considerable variation of drug sensitivity between cancer cell lines.

Antineoplastic Agents↗
PubMed2002

Furin expression in squamous cell carcinomas of the oral cavity and other sites evaluated by tissue microarray technology.

Furin is a proprotein convertase that activates many cancer development-related substrates such as growth factors, growth factor-receptors, adhesion molecules, and matrix degrading enzymes. Furin expression was studied in sections from tissue microarrays (TMA) and conventional paraffin blocks in a collection of squamous cell carcinomas (SCC) from three different sites. A total of 118 SCCs from the oral cavity, lung and esophagus as well as 34 precursor lesions (intraepithelial neoplasia) from the oral and bronchial mucosae were studied by immunohistochemistry. Furin expression was notably higher in most precursor lesions than in normal epithelia. Tumors from either the TMAs or the conventional blocks showed significant differences when compared to the mostly negative normal epithelia. High levels of furin expression were observed in approximately 50% SCCs of three different sites as well as in precursor lesions of the oral and bronchial mucosae. In addition another 30% showed low furin expression that was localized in all tumor cells including those in a basaloid position. Normal epithelia sometimes showed low level expression but the normal basal cells were always negative. These results show that furin is up-regulated in SCCs from three different organs and validates its use as a tumor marker in both invasive and pre-invasive neoplasia.

Biomarkers, Tumor↗
PubMed1992

Alcohol and cancer.

Although ethanol has generally not been found to induce cancer in experimental animals, the consumption of alcoholic beverages has been linked to increased risks of several cancers in humans. Risks of oral, pharyngeal, laryngeal, esophageal, and liver cancer are elevated among drinkers, typically in proportion to the amount consumed. Evidence associating colorectal and breast cancer with alcohol drinking is suggestive but awaits confirmation. All types of alcoholic beverages seem to be implicated, pointing to an etiological role for ethanol or its metabolites. The mechanisms, however, by which alcohol induces cancer in humans are not clear. This review summarizes epidemiological studies of alcohol and cancer, focusing primarily on characteristics of the association that may provide clues to causal pathways.

Alcohol Drinking↗
PubMed2004

[Locoregional recurrence of ORL cancer: the place of surgery].

Surgery of locoregional failures is mainly represented by salvage surgery after radiotherapy. Due to progress of radiotherapy, especially modification of fractionation and association with chemotherapy, the problem of salvage surgery is nowadays emphasized. Despite the reduction of postoperative mortality and morbidity by the use of myocutaneous flaps the complications are still frequent and the rehabilitation long and difficult. Oncologic results are disappointing too, especially in salvage surgery for oropharyngeal and hypopharyngeal tumors with less than a half of patients being candidates for salvage surgery and 5 year survival rates inferior to 30% in these patients. Laryngeal tumors are more favorable for salvage surgery but in the majority of the cases recurrences after radiotherapy require a total laryngectomy. The poor postoperative, functional and oncologic results after salvage surgery, especially in pharyngeal tumors must be taken into account for the decision of primary treatment. Regarding the important locoregional aggressivity of squamous cell carcinomas of the upper aerodigestive tract, these results must be kept in mind when preservation protocols are in question.

Humans↗
PubMed2004

[Locoregional recurrences of HNSCC: place of re-irradiations].

Unresectable forms of HNSCC relapses occurring in a previously irradiated area are relatively common and may be difficult to manage from a therapeutic point of view. Full dose re-irradiation with concomitant chemotherapy constitutes an alternative to palliative chemotherapy. Indeed, the feasibility of this approach has been shown, and may be associated with a curative potential in a relatively low proportion of these relapses.

Clinical Trials, Phase II as Topic↗