Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0262471 (ENT)
 5,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kinetics (growth fraction of tumour cell populations), death process of cancer cells (apoptosis and necrosis) and neovascularisation in tumour (angiogenesis) have influence on the growth of cancer. Sixty patients with laryngeal cancer treated in ENT Department of Medical Academy of Lodz were analysed. Proliferation activity of cancer cells was examined by means of selection appropriate antigen (Ki-67) characteristic for cell cycle utilising immunohistochemical techniques carried out on laryngeal cancer paraffin samples. Expression of selected protein connected with apoptosis (p-53) and intensity of angiogenesis were examine using selected antibody (anti-CD34) aimed against epithelial antigens. Above-mentioned markers were correlated with: stage of cancer progression, recurrences and metastasis of laryngeal cancer and follow-up of the patients. The morphological properties were examined as well. The researches on apoptosis, angiogenesis and proliferation of cancer cells can be used as prognostic factors for the patients with laryngeal cancer.
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PMID:[Assessment of cell proliferation antigen Ki-67, protein p53 related to apoptosis and angiogenesis in laryngeal cancer]. 1097 82

Apoptosis--the programmed sell death is the process of characteristic events on morphological, biochemical and molecular level which lead consequently to cell death. This process require activation of some genes i.e. p-53, mdm2 and inhibiting others i.e. bcl-2. Sixty patients with laryngeal cancer treated in ENT Department of Medical Academy of Lodz were analysed. Expression of the p-53 and bcl-2 genes' products was examined by means immunohistochemical techniques carried out on laryngeal cancer paraffin samples. Above-mentioned markers were correlated with: stage of cancer progression, recurrences and metastasis of laryngeal cancer and follow-up of the patients. Initial results indicate the possible utilisation of apoptosis as prognostic factors for the patients with laryngeal cancer.
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PMID:[Programmed cell death research in laryngeal cancer]. 1097 88

In this study, we investigated the time course gene expression profile of preneoplastic nodules and hepatocellular carcinomas (HCC) to define the genes implicated in cancer progression in a resistant hepatocyte model. Tissues that included early nodules (1 month, ENT-1), persistent nodules (5 months, ENT-5), dissected HCC (12 months), and normal livers (NL) from adult rats were analyzed by cDNA arrays including 1185 rat genes. Differential genes were derived in each type of sample (n = 3) by statistical analysis. The relationship between samples was described in a Venn diagram for 290 genes. From these, 72 genes were shared between tissues with nodules and HCC. In addition, 35 genes with statistical significance only in HCC and with extreme ratios were identified. Differential expression of 11 genes was confirmed by comparative reverse transcription-polymerase chain reaction, whereas that of 2 genes was confirmed by immunohistochemistry. Members involved in cytochrome P450 and second-phase metabolism were downregulated, whereas genes involved in glutathione metabolism were upregulated, implicating a possible role of glutathione and oxidative regulation. We provide a gene expression profile related to the progression of nodules into HCC, which contributes to the understanding of liver cancer development and offers the prospect for chemoprevention strategies or early treatment of HCC.
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PMID:Gene expression profile related to the progression of preneoplastic nodules toward hepatocellular carcinoma in rats. 1679 86

Malignant melanoma is the most deadly type of skin cancer. The lack of effective pharmacological approaches for this tumour can be related to the incomplete understanding of the pathophysiological mechanisms involved in melanoma cell proliferation. Adenosine has growth-promoting and growth inhibitory effects on tumour cells. We aimed to investigate effects of adenosine and its metabolic product, inosine, on human C32 melanoma cells and the signalling pathways involved. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) reduction and bromodeoxyuridine (BrdU) proliferation assays were used to evaluate adenosine, adenosine deaminase and inosine effects, in the absence or presence of adenosine receptor (AR), A3 AR and P2Y1 R antagonists and PLC, PKC, MEK1/2 and PI3K inhibitors. ERK1/2 levels were determined using an ELISA kit. Adenosine and inosine levels were quantified using an enzyme-coupled assay. Adenosine caused cell proliferation through AR activation. Adenosine deaminase increased inosine levels (nanomolar concentrations) on the extracellular space, in a time-dependent manner, inducing proliferation through A3 AR activation. Micromolar concentrations of inosine enhanced proliferation through A3 AR activation, causing an increase in ERK1/2 levels, and P2Y1 R activation via ENT-dependent mechanisms. We propose the simultaneous activation of PLC-PKC-MEK1/2-ERK1/2 and PI3K pathways as the main mechanism responsible for the proliferative effect elicited by inosine and its significant role in melanoma cancer progression.
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PMID:Inosine strongly enhances proliferation of human C32 melanoma cells through PLC-PKC-MEK1/2-ERK1/2 and PI3K pathways. 2490 96