Disease relevance of Laryngeal Neoplasms

• Our data finally suggest that the MPO -463A variant is a protective factor in the etiology of lung and larynx cancer, but possibly not of pharyngeal cancer [1].
• Our results suggest an importance of the direct cell-cell interaction involving EMMPRIN rather than humoral factors such as cytokines for pro-MMP-2 production and activation followed by tumor progression, invasion, and metastasis in laryngeal cancer [2].
• The mean AHH inducibility in patients who had lung cancer was 3.20 +/- 0.20; in patients who had laryngeal cancer 2.96 +/- 0.18, and for all controls 3.29 +/- 0.04 (no significant difference at p = 0 05) [3].
• In addition, common mutations/variants in the 3 genes BRCA1, NOD2 and CYP1B1, known to be associated with early-onset breast cancer, were assessed to determine their frequency in 348 unselected laryngeal cancers [4].
• There is no evidence that the risk of laryngeal cancer or of stomach cancer are adversely affected by exposure to chrysotile [5].

Psychiatry related information on Laryngeal Neoplasms

• The safe administration of electroconvulsive therapy (ECT) in a man with steroid-induced depression and a history of craniotomy and gamma knife surgery for two separate foci of metastatic laryngeal cancer is reported [6].
• PURPOSE OF REVIEW: To review recent literature on the possible mechanisms and role of gastroesophageal reflux in the etiology of laryngeal cancer, in patients with and without the accepted risk factors of smoking and alcohol consumption [7].

High impact information on Laryngeal Neoplasms

• SAHSU analysed the incidence of cancers of the larynx and lung near the incinerator of waste solvents and oils at Charnock Richard, Coppull, Lancashire (which operated between 1972 and 1980) and nine other similar incinerators in Great Britain, after reports of a cluster of cases of cancer of the larynx near the Charnock Richard site [8].
• Moreover, a positive interaction was found between mEH activity and GSTM3 genotype for laryngeal cancer [9].
• Correlation of p53 and the proto-oncogene eIF4E in larynx cancers: prognostic implications [10].
• The tumor marker eIF4E is overexpressed in 100% of larynx cancers, and overexpression of eIF4E in histologically "tumor-free" margins predicts a significantly higher recurrence [10].
• METHODS: Patients with advanced laryngeal cancer received two cycles of cisplatin 100 mg/m2 and fluorouracil (5-Fu) 1,000 mg/m2/d for 5 days [11].

Chemical compound and disease context of Laryngeal Neoplasms

• Cholesterol intake showed significant correlations with lung and laryngeal cancers [12].
• In conclusion, our data indicate that quercetin and tamoxifen could be potentially useful in laryngeal cancer treatment [13].
• Association of arylamine N-acetyltransferases NAT1 and NAT2 genotypes to laryngeal cancer risk [14].
• A significant inverse association (odds ratio (OR) = 2.1) was found between low carotene intake and the risk of laryngeal cancer, but no association was found with total vitamin A or retinol intake [15].
• A significantly increased risk of laryngeal cancer was observed for animal protein (continuous OR = 1.21, 95% CI 1.03-1.41), polyunsaturated fats other than linoleic and linolenic fatty acids (OR = 1.43, 95% CI 1.19-1.70), and cholesterol intake (OR = 1.43, 95% CI 1.19-1.71) [16].

Biological context of Laryngeal Neoplasms

• Only 6/22 (27%) of the laryngeal cancers we examined demonstrated LOH of the BRCA2-containing region [17].
• The objective of this work was an analysis of mutations in the p53 gene detected from fresh tumor samples of larynx cancer patients using single-strand conformation polymorphism (SSCP) and direct DNA sequencing of exons 5-8 [18].
• However, there was a significant overrepresentation of 20 (7.8%) homozygous NAT2 genotypes coding for rapid acetylation (NAT2*4/*4 and NAT2*4/*12A) amongst laryngeal cancer patients versus 19 (3.7%) such individuals in the control group (odds ratio 2.18, 95% confidence limits 1.13, 4.22; P = 0.018) [14].
• CONCLUSIONS: Laryngeal cancer cases have a higher energy intake than control subjects, and report a higher intake of animal protein and cholesterol [16].
• Our findings suggest that overexpression of p21 protein is associated with a malignant phenotype in laryngeal cancer [19].

Anatomical context of Laryngeal Neoplasms

• Altogether, our data allow us to speculate that the increased insulin effectiveness we observed in the larynx carcinoma cell line HEp-2 after androgen treatment might be involved in the regulation of larynx cancer cells growth [20].
• CONCLUSIONS: The present study helps to establish EMMPRIN as a widely expressed protein in dysplastic mucosa and supraglottic laryngeal cancer, but not in normal epithelial counterparts [21].
• A standard immunoradiometric technique was used to investigate the distribution of the intracellular aspartic proteinase cathepsin D in 33 malignant and in the corresponding histologically-proven non-malignant fragments obtained from lymph node negative patients suffering from larynx cancer [22].
• Heavy drinkers, i.e. males who drank 90 g ethanol daily had an approximately 15-fold risk of cancer of the oral cavity, an 11-fold risk of pharyngeal cancer and an 11-fold risk of laryngeal cancer compared with non-drinkers [23].
• Laryngeal cancer cells and mast cells may control the angiogenic response by releasing VEGF [24].

Gene context of Laryngeal Neoplasms

• RESULTS: Neither the putative risk genotypes ADH1B*2/*1 (OR 0.86, 95% confidence interval (CI): 0.41-1.82) or ADH1C*1/*1 (OR 1.06, CI 0.7-1.62) nor GSTM1 null (OR 0.94, CI 0.62-1.42) or GSTT1 null (OR 1.34, CI 0.74-2.42) were associated with an overall increased risk for laryngeal cancer [25].
• Individuals with concurrent lack of GSTM1 and GSTT1 genes had a doubled, although not significant, risk for larynx cancer when compared with those having at least one of these genes (OR = 2.0, 95% CI = 0.8-5.2) and had almost a 3-fold risk (OR = 2.7, 95% CI = 1.0-7.4) when compared with those with both genes [26].
• Impairment of MLH1 and CDKN2A in oncogenesis of laryngeal cancer [27].
• PURPOSE: To evaluate EGFR and HER2 copy number changes and to assess their significance to tumor progression in a large group of patients with larynx cancer through the construction of a tissue microarray (TMA) consisting of 1,385 biopsies [28].
• CONCLUSION: Our results suggest that shRNA directed against hTERT inhibits telomerase activity through suppression of the hTERT expression in laryngeal cancer cells and that RNA interfering technology may be a promising strategy for the treatment of laryngeal cancers [29].

Analytical, diagnostic and therapeutic context of Laryngeal Neoplasms

• PURPOSE: To evaluate the effectiveness of 2-[fluorine 18]fluoro-2-deoxy-D-glucose (FDG) positron emission tomography (PET) in the identification of early stage (T1-T2) primary and recurrent laryngeal cancer [30].
• PURPOSE: To study the role of two possible prognostic factors, p53 and tumor bulk, and their interaction with other tumor and treatment variables in early-stage laryngeal cancer patients treated with curative radiotherapy [31].
• SUBJECTS: A total of 97 patients with advanced laryngeal cancer (46 Stage III, 51 Stage IV) were given a single course of induction chemotherapy (cisplatin 100 mg/m2 on Day 1 and 5-FU 1,000 mg/m2/day x 5 days), followed by assessment of response [32].
• METHODS AND MATERIALS: Paraffin-embedded tumor samples from 90 laryngeal cancer patients were stained for cyclin A and the Ki-67 antigen by immunohistochemistry [33].
• PURPOSE: To visualize directly a sequence of genetic changes underlying the entire spectrum of epithelial hyperplastic laryngeal lesions (EHLL) and laryngeal cancer by the use of non-isotopic in situ hybridization (ISH) for chromosomes 7 and 17 in correlation with overexpression of p53 protein and epidermal growth factor receptor (EGFR) [34].

References