tumor promoter

tumor promoter

Cocarcinogen A substance, often lipid-soluble, that has no intrinsic carcinogenic potential, but which, when applied repeatedly, amplifies cancer-inducing effects of other (initiator) substances. See Antipromoter. Cf Tumor initiator.
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.
References in periodicals archive ?
specific genes such as ND5 were evaluated for tumor promoter and promoter effects.
It has been shown that TET1 functions as a tumor suppressor and tumor promoter in a cancer type-dependent manner.
In addition, controversies still exist whether PGC-1[alpha] acts as a tumor promoter or a tumor suppressor in cancer.
Kapila, "SIRT3 and cancer: tumor promoter or suppressor?," Biochimica et Biophysica Acta, vol.
However, whether the role of ACS5 is being a tumor suppressor or a tumor promoter remains controversial, and its underlying mechanisms have not been clarified.
All eight substances also exhibited moderate inhibitory effects on Epstein-Barr virus early antigen (EBV-EA) in Raji cells as a primary screening test for tumor promoter inhibitors.
Notch signaling is one of the most studied pathways involved in tumorigenesis, and increasing evidence indicates that the Notch pathway can function as a tumor promoter or suppressor, depending on the cell type and context (7).
As already mentioned, TGF-[beta] can act either as a tumor suppressor or as a tumor promoter. Suppression of tumor cell growth by TGF-[beta] depends on its ability to upregulate the cyclin kinase inhibitors which inhibit cell proliferation.
Treatment with carcinogen (7,12-dimethylbenz[[alpha]]anthracene, DMBA) followed by tumor promoter (12-O-tetradecanoylphorbol-13-acetate, TPA) is known to cause tumor formation [113].
decreased lysophosphatidic acid (a tumor promoter that accelerates plaque build-up in arteries in animal models) and less atherosclerotic plaque.
This particular experiment suggests that vemurafenib is acting as a tumor promoter in cell lines with this pre-existing HRAS Q61L mutation via the paradoxical activation of the MAPK pathway in non-melanomatous cells with wild type BRAF, as evidenced by increased ERK phosphorylation and increased expression of ERK-related genes.

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