ABSTRACT
BACKGROUND & OBJECTIVE: Colorectal cancer is the third most common cause of cancer death worldwide. Stanniocalcin 2 (STC2) is a glycoprotein hormone over-expressed in many human cancers where it regulates tumor progression and invasion. Evaluating its expression in colorectal cancer and its relation with different clinicopathological parameters can provide valuable information about its role in colorectal cancer progression and behavior. METHODS: This retrospective study was conducted on tissue samples of colorectal cancer. The STC2 immunohistochemical expression was detected and evaluated in 60 cases of colorectal cancer tissue samples of formalin-fixed and paraffin-embedded blocks. Then statistical analysis was performed to assess the relationship between its expression level and several clinicopathological parameters in the studied cases. RESULTS: Statistically significant associations were found between the high level of STC2 immunohistochemical expression and histological tumor grade (P<0.001), tumor depth of invasion (T stage) (P=0.004), lymph node metastasis (N stage) (P=0.001), tumor Dukes' stage (P<0.001), the presence of lymphovascular invasion (P<0.001), and perineural invasion (P<0.001). CONCLUSION: STC2 over-expression in colorectal cancer may be associated with more aggressive tumor behavior including increased tumor invasion, higher histological grade, higher rate of nodal metastasis and increased incidence of lymphovascular and perineural invasions. These data suggest a potential role for STC2 as a predictive biomarker for tumor behavior in colorectal cancer patients.
ABSTRACT
Mercury is a highly toxic metal. It induces its toxicity via production of reactive oxygen species. Brain tissues are more susceptible to oxidative damage. Melatonin and its metabolites are free radical scavengers. The aim of this work is to elucidate the neuroprotective effect of melatonin on mercuric chloride-induced neurotoxicity in rats. Fifty male albino rats were used and divided into five groups. Group I acts as normal control. Group II (LD HgCl2) received mercuric chloride at a dose of 2 mg/kg. Group III (HD HgCl2) received HgCl2 at a dose of 4 mg/kg. Rats in group IV (LD HgCl2 +MLT) received HgCl2 2 mg/kg + Melatonin 5 mg/kg. Rats in group V (HD HgCl2+MLT) received HgCl2 4 mg/kg + Melatonin5 mg/kg. This study revealed that mercuric chloride decreased the activity of superoxide dismutase, catalase and glutathione peroxidase enzymes and increased malondialdehyde levels. Toxicity of mercuric chloride lead to upregulation of the gene expression level vascular endothelial growth factor. HgCl2 induced fragmentation of rough endoplasmic reticulum, ballooning of Golgi apparatus, nuclear and cytoplasmic degeneration of pyramidal neurones of rat cerebral cortex. This neuronal damage caused by HgCl2 was significantly improved by melatonin.
ABSTRACT
Peeling skin syndrome is a relatively rare clinical case with pathology of apparently normal skin that needs clinical details to reach accurate diagnoses. Hence, this case was used as examples to declare how it is important for both the pathologist and the dermatologist to cooperate to reach an accurate diagnosis.
