A novel hypothesis: Specific oncogenes and tumor suppression genes are involved in the expression of the proopiomelanocortin gene by small cell lung cancer

The endogenous opioid β-endorphin, a derivative of proopiomelanocortin, stimulates the growth of cloned human small cell lung carcinoma. The present hypothesis states that mutations of the retinoblastoma gene (a tumor suppressor gene) associated to the malignant transformation of bronchial cells wou...

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Veröffentlicht in:	Medical hypotheses 1994-06, Vol.42 (6), p.397-399
Hauptverfasser:	Amsler, U.J., Pasi, A., Qu, B.X.
Format:	Artikel
Sprache:	eng
Schlagworte:	ACTH Syndrome, Ectopic - etiology beta-Endorphin - metabolism Biological and medical sciences Carcinoma, Small Cell - genetics Carcinoma, Small Cell - metabolism Cushing Syndrome - etiology Cushing Syndrome - genetics Female Gene Expression Regulation, Neoplastic Genes, fos Genes, Retinoblastoma Hormones, Ectopic - biosynthesis Hormones, Ectopic - genetics Humans Lung Neoplasms - genetics Lung Neoplasms - metabolism Medical sciences Models, Biological Neoplasm Proteins - biosynthesis Neoplasm Proteins - genetics Pneumology Pro-Opiomelanocortin - biosynthesis Pro-Opiomelanocortin - genetics Protein Processing, Post-Translational Proto-Oncogene Proteins c-fos - physiology Retinoblastoma Protein - deficiency Retinoblastoma Protein - physiology Tumors of the respiratory system and mediastinum
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Zusammenfassung:	The endogenous opioid β-endorphin, a derivative of proopiomelanocortin, stimulates the growth of cloned human small cell lung carcinoma. The present hypothesis states that mutations of the retinoblastoma gene (a tumor suppressor gene) associated to the malignant transformation of bronchial cells would trigger a cascade of biomolecular events leading to ‘de novo’ proopiomelanocortin expression in small cell lung carcinoma.
ISSN:	0306-9877 1532-2777
DOI:	10.1016/0306-9877(94)90162-7