Epidermal growth factor receptor (EGFR) in oral squamous cell carcinomas: overexpression, localization and therapeutic implications.

Dysregulation of oncogenes, overproduction of growth factor receptors and their ligands, and loss of function of tumor suppressor genes are thought to contribute to multi-step process of carcinogenesis. It is suggested that proliferation markers like epidermal growth factor receptor (EGFR) actively participate in oral carcinogenesis, during initiation or promotion stage of the process. Potent mitogens such as epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-a) mediate their growth responses through the common transmembrane glycoprotein receptor, EGFR.

High prevalence of expression of p53 oncoprotein in oral carcinomas from India associated with betel and tobacco chewing.

A recent study reported a low prevalence of p53 expression (11%) in oral squamous cell carcinomas (SCCs) from South Asia, in contrast to a high prevalence (averaging 52%) in other studies. It was proposed that the different aetiologies for oral SCCs in the South Asia population, i.e.

The value of epidermal growth-factor receptor (egfr) as a tumor-marker for human oral premalignant and malignant lesions.

A previous study demonstrated increased epidermal growth factor receptor (EGFR) in oral dysplasia while another showed decreased EGFR in oral dysplasia. The present study examined immunohistochemical expression of EGFR in 33 dysplastic oral lesions as well as in 9 normal oral mucosa specimens, 12 hyperplastic oral lesions and 10 oral squamous cell carcinomas (SCCs). There were no significant differences in EGFR staining either in intensity or in the epithelial layers stained among the normal oral epithelium, hyperplastic and dysplastic lesions.

Effect of dietary supplementation of vitamin E on serum lipids and lipoproteins in rabbits fed a cholesterolemic diet.

The effect of dietary supplementation of vitamin E on serum cholsterol, triglycerides, lipoproteins and lipoprotein composition was studied in rabbits fed a one per cent cholesterol diet for a period of twelve weeks. Vitamin E supplemented animals were found to maintain significantly lower concentrations of serum cholesterol, triglycerides and very low density lipoproteins (d less than 1.006).

Deranged diurnal feeding pattern and altered brain serotonin turnover in heroin-dependent rats.

Rats rendered tolerant to and dependent on heroin by administering escalating dosages of heroin from 5 mg/kg-1 to 30 mg/kg-1 s,c, twice daily for 10 days exhibited disrupted diurnal feeding patterns. Daylight food intake was significantly increased, whereas night-time feeding was significantly decreased, as compared with the saline-control group. Growth rate evaluated on the basis of changes in daily body weights was considerably attenuated.

Experimental acetaminophen-induced hepatic necrosis: biochemical and electron microscopic study of cysteamine protection.

In an attempt to elucidate the biochemical mechanism of acetaminophen-induced hepatic necrosis, the present study in hamsters was undertaken to evaluate the possible changes in lipid peroxidation and microsomal enzyme activities. The protective action of cysteamine was likewise assessed in the light of these biochemical variables and the fine structural features of the liver were seen by electron microscopy. One group of golden Syrian hamsters was administered a toxic dosage of acetaminophen (600 mg .

Lithium protection against oxygen toxicity in rats: ammonia and amino acid metabolism.

1. The use of Li pre-treatment in rats before high pressure oxygen exposure has been reported effective in controlling convulsions. This is an effect which is better demonstrated if exposure to oxygen follows shortly after Li injection than exposure following several hours later.

Radiation-induced enzyme efflux from rat heart: sedentary animals.

Serum levels of lactate dehydrogenase, creatine kinase, and glutamate oxaloacetate transaminase show initial elevations within 12 hr of exposure to 2,000 rads of gamma-radiation to the thoracic region of rats. Significant decreases in heart muscle homogenate levels of these enzymes parallel initial elevations in the serum and may suggest that enhanced leakage of enzymes is a consequence of radiation injury to heart muscle. Insignificant alterations in mitochondrial glutamate oxaloacetate transaminase levels after exposure indicate that in vivo injury to the mitochondria from therapeutic levels of gamma-radiation is questionable.