However, we did not find a significant increase in laryngeal cancer risk for the homozygous Pro/Pro TP53 genotype OR=2.093 (95% CI=1.046-4.192, P=0.0530).
p53 expression seems to negatively influence survival in non-smoking non-alcoholic patients with squamous cell laryngeal carcinoma. p53 might be implicated in the oncogenic pathways leading to neoplastic transformation in this population of patients.
While p53 does not seem to be involved in 5-FU induced apoptosis and cell cycle arrest in laryngeal carcinoma, further studies are needed to examine the roles of retinoblastoma protein and p21WAF1/CIP1 in laryngeal carcinoma receiving chemotherapy.
In papillomatosis, pRb and p53 levels were higher than in normal larynxes, whereas laryngeal cancer presented the lowest levels. c-Myc oncogene expression was very low in normal and cancer tissues but highly increased in papillomatosis.
Flow cytometric Annexin V assay demonstrated that HEp-2 cells (human laryngeal cancer) were persistently resistant to CDDP as compared to HeLa cells (human uterine cervical cancer), despite the same histological type and wild-type p53 status.
We analyzed ionizing radiation (IR)- or ultraviolet (UV)-induced apoptosis in human laryngeal carcinoma (HEp-2) and uterine cervical carcinoma (HeLa) cells, and found that HeLa cells were significantly more sensitive to both IR- and UV-induced apoptosis compared to HEp-2 cells, in spite of the same histological type and p53 status.
We screened exons 5-8 of TP53 for mutations in DNA from tumor biopsies (n = 44) and blood samples (n = 42) from the same LC patients, and blood samples from a healthy, matched control group (n = 40), using polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) analysis and direct sequencing.
However, ADH1B or ADH1C genotypes did not markedly modify the risk observed after stratification by alcohol consumption, and stratification by cumulative smoking exposure (in packyears) did not show an association of GSTM1 or GSTT1 genotype with laryngeal carcinoma either.
Paraffin sections of laryngeal carcinoma were studied using immunohistochemical staining with mouse and rabbit monoclonal antibodies, respectively, for p53 and c-erbB-2 proteins.
We showed that the risk of developing laryngeal cancer was increased by 2.6-fold [95% CI 1.6--6.1] in patients with the GSTM1 null genotype and by 2.8-fold [95% CI 0.9--8.1] in patients with the homozygous GSTP1 val105 genotype.
The results suggest that the co-transfer of human wild-type p53 and GM-CSF genes into tumor cells via recombinant adenovirus may be further developed into an effective and practical combination gene therapy strategy for laryngeal cancer.
Firstly, these results confirm the p53 mutational status of laryngeal cancer without any clinical correlation and secondly may suggest an oncogenic potential for the proline/proline genotype of codon 72 for laryngeal cancer as has already been assumed for lung cancer.
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).
Clinical application of proliferating cell nuclear antigen, oncoprotein p53 and tumor front grading analysis in patients operated on for laryngeal cancer.
On the basis of the results obtained, the techniques suggested for the morphological and biological evaluation of neoplastic cells in cancer of the larynx should include TNM classification + G + DNA + p53 + Ki67.
The effects of the GSTM1 and GSTT1 null genotypes on laryngeal cancer risk were evaluated using peripheral blood DNA from 129 larynx cancer patients and 172 noncancer controls, all of whom were regular smokers.