Autocrine loops, signal transduction, and cell cycle abnormalities in the molecular biology of lung cancer.
Lung cancers produce a variety of mitogenic neuropeptides and growth factors and express receptors for these signaling peptides leading to autocrine and paracrine loops that stimulate tumor cell proliferation and migration and promote neovascularization. The effects of these autocrine and paracrine factors are mediated by a variety of intracellular signal transduction pathways that ultimately converge on the regulation of cell cycle proteins whose expression and activity are abnormal in lung cancer cells. During the past year, further advances have been made in unraveling autocrine loops, signal transduction pathways, and cell cycle abnormalities in both small cell lung carcinoma (SCLC) and in non-SCLC. In addition, the hunt for novel tumor suppressor genes has continued. As our understanding of the fundamental cell and molecular biology of lung cancer increases, novel possibilities for translational research are emerging for improving the diagnosis, prognosis, and treatment of the disease.
Rozengurt
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Department of Medicine, University of California, Los Angeles 90095-1786, USA.
D019898:Autocrine Communication / Q000502:physiology*; D002453:Cell Cycle / Q000502:physiology*; D016147:Genes, Tumor Suppressor; D006801:Humans; D008175:Lung Neoplasms / Q000378:metabolism*; D019899:Paracrine Communication / Q000502:physiology; D015398:Signal Transduction