Expression of cell cycle regulators and growth factor/receptor systems in gastric carcinoma in young adults: association with Helicobacter pylori infection.

2000 ◽  
Author(s):  
K Haruma ◽  
M Ito ◽  
K Kohmoto ◽  
T Kamada ◽  
Y Kitada ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Helicobacter Pylori ◽  
Young Adults ◽  
Growth Factor ◽  
Gastric Carcinoma ◽  
Growth Factor Receptor ◽  
Helicobacter Pylori Infection ◽  
Cell Cycle Regulators

Human Epidermal Growth Factor Receptor-2 in Sri Lankan Gastric Carcinoma Patients with Clinicopathological Association and Survival

2017 ◽  
Vol 62 (9) ◽  
pp. 2498-2510
Author(s):  
Duminda Subasinghe ◽  
Sivasuriya Sivaganesh ◽  
Ananthi Samarsekera ◽  
Mariyan Priyanthi Kumarasinghe ◽  
Dharmabandhu Nandadeva Samarasekera ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Gastric Carcinoma ◽  
Growth Factor Receptor ◽  
Sri Lankan ◽  
Human Epidermal Growth Factor ◽  
Epidermal Growth

Androgen receptors in prostate cancer.

2002 ◽  
pp. 155-170 ◽  
Author(s):  
Z Culig ◽  
H Klocker ◽  
G Bartsch ◽  
A Hobisch
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Point Mutations ◽  
Growth Factor Receptor ◽  
Clinical Situation ◽  
Activation Function ◽  
Flufenamic Acid ◽  
Cell Cycle Regulators ◽  
Industrialized Countries ◽  
Chemopreventive Agents

The androgen receptor (AR), a transcription factor that mediates the action of androgens in target tissues, is expressed in nearly all prostate cancers. Carcinoma of the prostate is the most frequently diagnosed neoplasm in men in industrialized countries. Palliative treatment for non-organ-confined prostate cancer aims to down-regulate the concentration of circulating androgen or to block the transcription activation function of the AR. AR function during endocrine therapy was studied in tumor cells LNCaP subjected to long-term steroid depletion; newly generated sublines could be stimulated by lower concentrations of androgen than parental cells and showed up-regulation of AR expression and activity as well as resistance to apoptosis. Androgenic hormones regulate the expression of key cell cycle regulators, cyclin-dependent kinase 2 and 4, and that of the cell cycle inhibitor p27. Inhibition of AR expression could be achieved by potential chemopreventive agents flufenamic acid, resveratrol, quercetin, polyunsaturated fatty acids and interleukin-1beta, and by the application of AR antisense oligonucleotides. In the clinical situation, AR gene amplification and point mutations were reported in patients with metastatic disease. These mutations generate receptors which could be activated by other steroid hormones and non-steroidal antiandrogens. In the absence of androgen, the AR could be activated by various growth-promoting (growth factors, epidermal growth factor receptor-related oncogene HER-2/neu) and pleiotropic (protein kinase A activators, interleukin-6) compounds as well as by inducers of differentiation (phenylbutyrate). AR function is modulated by a number of coactivators and corepressors. The three coactivators, TIF-2, SRC-1 and RAC3, are up-regulated in relapsed prostate cancer. New experimental therapies for prostate cancer are aimed to down-regulate AR expression and to overcome difficulties which occur because of the acquisition of agonistic properties of commonly used antiandrogens.

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