Interactions between initiating chemical carcinogens, tumor promoters, and adenovirus in cell transformation

Fisher, Paul B.; Dorsch-Häsler, Karoline; Weinstein, I. Bernard; Ginsberg, Harold S.

doi:10.1002/tcm.1770010302

Cited by 8 publications

(3 citation statements)

References 35 publications

(15 reference statements)

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“…The rat embryo cells (CREF) used are a subelone ofthe Fischer cell line, isolated by Paul Fisher in this laboratory (8). Cell culture media were from GIBCO.…”

Section: Methodsmentioning

confidence: 99%

Identification of receptors for phorbol ester tumor promoters in intact mammalian cells and of an inhibitor of receptor binding in biologic fluids.

Horowitz¹,

Greenebaum²,

Weinstein³

1981

Proc. Natl. Acad. Sci. U.S.A.

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human serum led to a 135-fold purification of an inhibitory factor with a molecular weight in the range 40,000 to 80,000.In contrast to chemicals that initiate the carcinogenic process apparently by binding covalently to cellular DNA, the primary site of action of the phorbol ester tumor promoters appears to be the cell surface membrane (for review, see refs. 1 and 2). In previous papers (3, 4) from this laboratory, it was postulated that the potent tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA) actually binds to and usurps the function of a membrane-associated receptor that is normally utilized by an endogenous polypeptide growth factor. Indirect evidence for this hypothesis includes the facts that: (a) TPA and related compounds act in a concentration range similar to that of several hormones and growth factors (i.e., 0

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“…The rat embryo cells (CREF) used are a subelone ofthe Fischer cell line, isolated by Paul Fisher in this laboratory (8). Cell culture media were from GIBCO.…”

Section: Methodsmentioning

confidence: 99%

Identification of receptors for phorbol ester tumor promoters in intact mammalian cells and of an inhibitor of receptor binding in biologic fluids.

Horowitz¹,

Greenebaum²,

Weinstein³

1981

Proc. Natl. Acad. Sci. U.S.A.

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“…Historically, exposure to these metals has been associated with the onset many cancers, including lung cancer – a highly lethal form of cancer 4 . Our studies analyze the effects of three known carcinogens (As, Cr, and Ni) and one possible carcinogen (V) on gene expression in human bronchial epithelial cells via an accepted experimental method 5 .…”

Section: Introductionmentioning

confidence: 99%

Gene expression changes in human lung cells exposed to arsenic, chromium, nickel or vanadium indicate the first steps in cancer

et al. 2012

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The complex process of carcinogenesis begins with transformation of a single cell to favor aberrant traits such as loss of contact inhibition and unregulated proliferation – features found in every cancer. Despite cancer’s widespread prevalence, the early events that initiate cancer remain elusive, and without knowledge of these events cancer prevention is difficult. Here we show that exposure to As, Cr, Ni, or Vanadium (V) promotes changes in gene expression that occur in conjunction with aberrant growth. We exposed immortalized human bronchial epithelial cells to one of four metals/metalloid for four to eight weeks and selected transformed clonal populations based upon anchorage independent growth of single cells in soft agar. We detected a metal-specific footprint of cancer-related gene expression that was consistent across multiple transformed clones. These gene expression changes persisted in the absence of the progenitor metal for numerous cell divisions. Our results show that even a brief exposure to a carcinogenic metal may cause many changes in gene expression in the exposed cells, and that from these many changes, the specific change(s) that each metal causes that initiate cancer likely arise.

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“…are subclones of a Fischer rat embryo cell line which were isolated by Paul Fisher in this laboratory (7). CREF N cells display normal growth control and a normal fibroblast morphology.…”

mentioning

confidence: 99%

Inhibition of phorbol ester-receptor binding by a factor from human serum.

Horowitz¹,

Greenebaum²,

Nicolaides³

et al. 1982

Mol. Cell. Biol.

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It has recently been found that mammalian cells of diverse types contain high-affinity receptors for the tumor-promoting phorbol esters (3-5, 8, 10, 20-22). Binding of the tumor promoter[3H]phorbol-12,13-dibutyrate (PDBu) to these "phorboid receptors" is saturable and specific, occurs in the range of physiological activity of PDBu, and is inhibited by other phorbol esters (4,8,20) and by the related compound teleocidin (24) with potencies that correlate with biological activity. In most of these studies, [3H]PDBu rather than the stronger tumor promoter 12-0-tetradecanoylphorbol-

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Interactions between initiating chemical carcinogens, tumor promoters, and adenovirus in cell transformation

Cited by 8 publications

References 35 publications

Identification of receptors for phorbol ester tumor promoters in intact mammalian cells and of an inhibitor of receptor binding in biologic fluids.

Identification of receptors for phorbol ester tumor promoters in intact mammalian cells and of an inhibitor of receptor binding in biologic fluids.

Gene expression changes in human lung cells exposed to arsenic, chromium, nickel or vanadium indicate the first steps in cancer

Inhibition of phorbol ester-receptor binding by a factor from human serum.

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