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Growth factor receptor inhibitor

About: Growth factor receptor inhibitor is a research topic. Over the lifetime, 4730 publications have been published within this topic receiving 297500 citations.


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Journal ArticleDOI
TL;DR: The data indicate that the type II insulin-like growth factor receptor does not function as a transducer of insulin- like growth factor II's mitogenic effect in human fibroblasts.

98 citations

Journal ArticleDOI
TL;DR: The studies suggest that cell proliferation is controlled by a synergistic interaction among several growth factors and, perhaps, other hormones.
Abstract: A new class of polypeptide hormones known collectively as growth factors has been identified. These polypeptides are able to stimulate DNA synthesis and mitosis of cells cultured in vitro. Growth factors have been isolated from several sources, including platelets, submaxillary glands, pituitary, brain, and medium conditioned by cells grown in vitro. Growth factors appear to behave like classic polypeptide hormones. In the cases of epidermal growth factor and nerve growth factor, specific cell membrane receptors have been studied in detail and partially purified. Platelet-derived growth factor and somatomedin-C interact synergistically and apparently, sequentially to promote cell proliferation in vitro. These studies suggest that cell proliferation is controlled by a synergistic interaction among several growth factors and, perhaps, other hormones. Several in vivo roles for growth factors and a role for tumor-cell-derived growth factors in neoplasia have been suggested.

98 citations

Journal ArticleDOI
01 Feb 2011-Cancers
TL;DR: This review focuses on the growing literature which shows that neurotrophins contribute to pro-survival signaling in many different types of cancer, with a particular emphasis on nerve growth factor regulation of cell death and survival in cancer.
Abstract: One of the major challenges for cancer therapeutics is the resistance of many tumor cells to induction of cell death due to pro-survival signaling in the cancer cells. Here we review the growing literature which shows that neurotrophins contribute to pro-survival signaling in many different types of cancer. In particular, nerve growth factor, the archetypal neurotrophin, has been shown to play a role in tumorigenesis over the past decade. Nerve growth factor mediates its effects through its two cognate receptors, TrkA, a receptor tyrosine kinase and p75NTR, a member of the death receptor superfamily. Depending on the tumor origin, pro-survival signaling can be mediated by TrkA receptors or by p75NTR. For example, in breast cancer the aberrant expression of nerve growth factor stimulates proliferative signaling through TrkA and pro-survival signaling through p75NTR. This latter signaling through p75NTR promotes increased resistance to the induction of cell death by chemotherapeutic treatments. In contrast, in prostate cells the p75NTR mediates cell death and prevents metastasis. In prostate cancer, expression of this receptor is lost, which contributes to tumor progression by allowing cells to survive, proliferate and metastasize. This review focuses on our current knowledge of neurotrophin signaling in cancer, with a particular emphasis on nerve growth factor regulation of cell death and survival in cancer.

98 citations

Journal ArticleDOI
TL;DR: It is suggested that TNF-induced transactivation of EGFR may provide an early signal for the entry of hepatocytes into the cell cycle and may integrate proliferative and survival pathways at the start of liver regeneration.

98 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202352
20225
20211
20201
20191
201811