[Detection of numerical chromosome aberrations in leukoplakia and squamous epithelial carcinomas of the head-neck area using fluorescence in situ hybridization].

The tumorigenesis of head and neck squamous cell carcinoma (HNSCC) has been proposed to represent a multistep process characterized by an accumulation of genetic alterations. To study numerical chromosomal aberrations and chromosomal imbalances, biopsies of 11 malignant tumours and biopsies of 16 oral premalignant lesions (leukoplakias) were analyzed by fluorescence in situ hybridization (FISH) using centromeric probes for chromosomes, 1, 7, 9, 10 and 17. The comparison of the alterations observed in simple leukoplakias (group 1, n = 8), dysplastic leukoplakias (group 2, n = 8) and malignant tumours (group 3, n = 11) by the Cochran-Armitage Trend Test revealed an increasing number of numerical chromosomal abberations.

Oral leukoplakias show numerical chromosomal aberrations detected by fluorescence in situ hybridization.

To examine at which stage in the multistep process of head and neck tumorigenesis numerical chromosomal alterations can be detected by fluorescence in situ hybridization (FISH), biopsies and cell smear preparations of clinically healthy oral tissue, premalignant lesions (leukoplakias), and tumors were analyzed by FISH using chromosome-specific centromeric probes. Aberrations found in tumor biopsies and in tumor cell smears consisted of trisomy of chromosomes 1, 7, 10, and 17 and monosomy of chromosomes 1, 7, 9, 10, and 17. In five of eight dysplastic oral leukoplakia biopsies, aberrations were seen consisting of trisomy of chromosome 1, 7, and 17, and monosomy of chromosome 9.

Etiological involvement of oncogenic human papillomavirus in tonsillar squamous cell carcinomas lacking retinoblastoma cell cycle control.

Two hundred eight primary squamous cell carcinomas of the head and neck have been analyzed with respect to the presence of the retinoblastoma tumor suppressor protein, pRb. Of these, 23 tumors (11%) that preferentially localized to the tonsils revealed complete absence or dramatic reduction in the amount of pRb. Other cell cycle components, cyclin D1 and p16INK4A, which are intimately related to pRb through an autoregulatory loop, were also dramatically decreased or overexpressed, respectively, in these pRb-defective tumors.

Erythropoietin production by fetal mouse liver cells in response to hypoxia and adenylate cyclase stimulation.

This study was done to investigate aspects of control of extrarenal erythropoietin (Ep) production. To this end we studied the effects of three stimuli of renal Ep production in the adult, i.e.