Tumor Promotion by Abrasion Induced Epidermal Hyperplasia in the Skin of Mice

Argyris, Thomas S.

doi:10.1111/1523-1747.ep12531153

Cited by 73 publications

(37 citation statements)

References 8 publications

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“…In line with this, whilst the above changes brought about by TPA are also brought about by certain kinds of epidermal injury such as wounding and full thickness abrasion which are also promoting stimuli (Hennings & Boutwell, 1970;Clark-Lewis & Murray, 1978;Argyris, 1980a) they are also produced by non-promoting stimuli such as mild abrasion by sandpaper rubbing (Marks et al, 1979) and treatment of the skin with the calcium ionophore, A23187 (Marks et al, 1981;KleinSzanto et al, 1982). Similarly, with the exception of dark cell induction (Klein-Szanto et al, 1980 all the TPA-induced effects cited above are produced with at least equal potency by the second stage promoters mezerein (Mufson et al, 1979) and RPA (Furstenberger et al, 1981).…”

Section: Two-stage Epidermal Tumourigenesismentioning

confidence: 84%

“…Why for example, does wounding (Hennings & Boutwell, 1970;Clark-Lewis & Murray, 1978) or deep abrasion (Argyris, 1980a) promote tumours whereas milder forms of epidermal manipulation (Clark-Lewis & Murray, 1978;Marks et al, 1979) do not. Marks et al (1982) have introduced the concept that a 'woundspecific' response is crucial to tumour promotion by injury and by TPA and have suggested that the release of a 'wound-hormone' may be critical in the former instance.…”

Section: Two-stage Epidermal Tumourigenesismentioning

confidence: 99%

“…The reports that the effect of TGF-# is synergistic with EGF to promote wound repair , and that it is found in platelets (Childs et al, 1982;Assoian et al, 1983) and clotted blood serum (Childs et al, 1982) but not plasma (Childs et al, 1982), suggest that the release of TGF-f may occur as part of the natural process of wound healing following damage to blood vessels. Blood vessel damage and the release of TGF-,B would accompany the promoting stimuli of skin wounding (Hennings & Boutwell, 1980;ClarkLewis & Murray, 1978;Marks et al, 1979) and to a lesser extent deep abrasion (Argyris, 1980a), but not the non-promoting stimuli of superficial abrasion (Marks et al, 1979) or skin massage (Clark-Lewis & Murray, 1978;Marks et al, 1979).…”

Section: Two-stage Epidermal Tumourigenesismentioning

confidence: 99%

“…How TPA and other manipulations of the skin such as wounding (Hennings & Boutwell 1970;Clark-Lewis & Murray, 1978) or deep epidermal abrasion (Argyris 1980a) promote the growth of an initiated cell into a tumour has until recently remained obscure. The purpose of this review is to evaluate evidence supporting the suggestion that TPA stimulates the development of tumours by selecting for keratinocytes which have acquired a reduced response to terminal differentiation signals as a result of initiation (Yuspa & Morgan, 1981).…”

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confidence: 99%

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Defective responses of transformed keratinocytes to terminal differentiation stimuli. Their role in epidermal tumour promotion by phorbol esters and by deep skin wounding

Parkinson¹

1985

Br J Cancer

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Summary Epidermal tumourigenesis can be achieved in rodents by the application of a single subthreshold dose of a carcinogen (initiation) followed by repeated applications of a tumour promoter such as 12-0-tetradecanoyl phorbol, 13-acetate (TPA). TPA induces terminal differentiation in the majority of epidermal keratinocytes in vitro. However, transformed keratinocytes respond weakly to this terminal differentiation signal, and it is suggested that this property allows initiated cells and their progeny to obtain a selective advantage over their normal counterparts during promotion of papilloma formation by TPA.New data are reviewed which suggest that a putative wound hormone TGF-P has similar differential effects on normal and transformed epithelial cells to those of TPA. It is proposed that the release of TGF-,B from platelets following deep skin wounding may be an explanation as to why wounding is a promoting stimulus but milder forms of epidermal injury are not. Weakly promoting hyperplasiogenic agents are also discussed within the context of a selection theory of tumour promotion.

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Section: Two-stage Epidermal Tumourigenesismentioning

confidence: 84%

Section: Two-stage Epidermal Tumourigenesismentioning

confidence: 99%

Section: Two-stage Epidermal Tumourigenesismentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Defective responses of transformed keratinocytes to terminal differentiation stimuli. Their role in epidermal tumour promotion by phorbol esters and by deep skin wounding

Parkinson¹

1985

Br J Cancer

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“…Sci. USA 90 (1993) ogen-treated mice but not in untreated mice (21)(22)(23). Of special interest is the fact that those tumors developed close to the wound edge.…”

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confidence: 99%

Transgenic mouse model of malignant skin melanoma.

Mintz

Silvers

1993

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

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Tyr-SV40E transgenlc mice are spedflcay susceptbl to meanma due to expresion of the oncogene in pigment ceDs. Mice of the more nes die young of early-onset eye meanmas, when skin menas are stfll infrequent and benig. To surmount this oa, in from donors oftwo high-cepiblitlines was grafted to hosts of a low-septibi line of the same inbred strain, thereby enabling the skin to outlive the donors and continue to grow in hmmunocompetent but tolerant hosts. Unexpectedly, donor pIgment cells in all the grafts soon seectivdy proliferated dose to areas of greatest wound healing, formig a dense black tracer, e at the outer rim of the grfts. These transcriptional control of the tyrosinase promoter expressed in pigment cells. Melanocytes in the hair follicles of the mice are hypomelanotic and the hairs, to which these cells contribute pigment granules, are lighter than normal as a result (5, 6). With increasing age, the skin itself becomes slightly darker due to melanocytic hyperplasia in the dermis. Localized foci appear as small flat black macules, some of which enlarge and thicken to become moles or nevi.Three classes of neoplasms have occurred: eye melanomas (4, 7), various other nonskin tumors associated with widespread distribution and hyperplasia of neurl crest-derived pigment cells (5), and skin melanomas (4). Different inbred lines of the mice, descended from separate founders, all express the T antigen to a degree specific for each line, as seen in the coat color reduction characteristic of each. They differ correspondingly in onset and progression of eye melanomas and were expected to differ in susceptibility to skin melanomas. At the extremes, early and rapidly growing eye tumors arise in mice oflines with lighter grey coats, while eye tumors are late and slow-growing in mice ofvery dark grey lines. Early eye tumors are fatal at a young age, due to invasion and metastasis; skin melanomas are then still infrequent and usually benign (4). The ultimate capacity ofthe transgenic skin melanocytes for malignancy was nevertheless demonstrated by establishing the cells in culture soon after birth and obtaining tumors after subcutaneous injection into immunodeficient nude (nu/nu) hosts (8,9). However, cell culture and injection do not reflect the genesis and biology of a melanoma in the skin. Some experimental intervention was therefore needed.The strategy we have devised is to circumvent the lethality of eye melanomas in the more susceptible transgenics by grafting skin from them to low-susceptibility young adult transgenic hosts. The skin can thus outlive the donor and grow for a long period in a histocompatible C57BL/6 host tolerant of the SV40 T antigen, which is known to be immunogenic (10). Such hosts have the further advantage that their skin (unlike that ofnude mice) is structurally similar to the donor skin; moreover, they would be capable (unlike any immunodeficient hosts) of responding to tumorassociated antigens.While the expectation of obtaining malignant skin melanomas was indeed fulfilled, the g...

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Relationship between the recurrence of hepatocellular carcinoma (HCC) and serum alanine aminotransferase levels in hepatectomized patients with hepatitis C virus-associated cirrhosis and HCC

Tarao

Takemiya

Tamai

et al. 1997

Cancer

130

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BACKGROUND The relationship between the recurrence of hepatocellular carcinoma (HCC) and the serum alanine aminotransferase (ALT) level was studied in hepatectomized patients with hepatitis C virus (HCV)‐associated cirrhosis and HCC. METHODS Twenty‐six hepatectomized patients with HCV‐associated cirrhosis and HCC whose resected specimens showed neither portal vein nor hepatic vein invasion by HCC histologically were divided into 2 groups: 15 patients who had no recurrence 3 years after surgery (Group A) and 11 patients whose disease recurred 1‐3 years after surgery (Group B). The patients' serum ALT levels during this period were examined. RESULTS In Group A, serum ALT generally showed sustained low levels < 80 international units (INU) in 12 patients (80%). In contrast, ALT levels in Group B showed several peaks or plateaus > 80 INU in all patients except 2. The recurrence rate of HCC in the hepatectomized patients with sustained low levels of ALT was 14.3% (2 of 14 patients) at 3 years, and was significantly lower (P < 0.01) than that in those patients whose ALT levels showed several peaks or plateaus > 80 INU (9 of 12 patients; 75.0%). The average level of mode of ALT in Group A (48.8 ± 26.0 INU) was significantly smaller than that in Group B (101.1 ± 47.3 INU) (P < 0.005). CONCLUSIONS The importance of hepatocytic necrosis in the recurrence of HCC in hepatectomized patients with cirrhosis and HCC of HCV origin was demonstrated and the significance of subsiding hepatic necroinflammatory process in the prevention of HCC recurrence suggested. Cancer 1997; 79:688‐94. © 1997 American Cancer Society.

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Tumor Promotion by Abrasion Induced Epidermal Hyperplasia in the Skin of Mice

Cited by 73 publications

References 8 publications

Defective responses of transformed keratinocytes to terminal differentiation stimuli. Their role in epidermal tumour promotion by phorbol esters and by deep skin wounding

Defective responses of transformed keratinocytes to terminal differentiation stimuli. Their role in epidermal tumour promotion by phorbol esters and by deep skin wounding

Transgenic mouse model of malignant skin melanoma.

Relationship between the recurrence of hepatocellular carcinoma (HCC) and serum alanine aminotransferase levels in hepatectomized patients with hepatitis C virus-associated cirrhosis and HCC

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