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T S Argyris

Publications and source records attributed to T S Argyris.

At least 19 recordsLinked to original sources
PubMed1985

Promotion of epidermal carcinogenesis by repeated damage to mouse skin.

Chemically induced epidermal carcinogenesis is usually divided into two stages: initiation, which involves the conversion of some epidermal cells into latent neoplastic cells; and promotion, which results in tumors. The hallmark of chemical promoters is epidermal hyperplasia. The hyperplasia caused by a strong promoter, such as 12-O-tetradecanoylphorbol-13-acetate (TPA), differs morphologically from that caused by weak promoters, such as acetic acid and mezerin. The epidermal regeneration that follows abrasion results in a hyperplastic epidermis that resembles the effects of strong promoters. Repeated mechanical injuries are capable of enhancing papillomas and carcinomas in mouse skin initiated with 7,12-dimethylbenzanthracene (DMBA). Thus, a regenerative epidermal hyperplasia appears to be a precondition for tumor promotion. It is highly probable that many epidermal cells are initiated during the lifetime of man. In the work place, repeated mechanical injury could predispose to epidermal neoplasms.

Age Factors↗
PubMed1985

Regeneration and the mechanism of epidermal tumor promotion.

Chemically induced epidermal carcinogenesis is often divided into two stages: initiation, which involves the conversion of some epidermal cells into latent neoplastic cells, and promotion, which allows the evolution of this neoplastic change into the formation of a neoplasm. The hallmark of epidermal tumor promotion is the transformation of the normal epidermis into a hyperplastic epidermis. A major unanswered question about epidermal tumor promotion is whether the epidermal hyperplasia that characterizes promoted skin is a regenerative epidermal hyperplasia resulting from damage produced by the promoter. The opinion currently held is that the epidermal hyperplasia produced by tumor promoters is not simply a regenerative epidermal hyperplasia and possesses characteristics which a regenerative hyperplasia does not have, enabling it to evolve into an epidermal neoplasm. The purpose of this review is to present recent evidence which strongly suggests that promoter-induced epidermal hyperplasia is a regenerative hyperplasia. Three principal lines of evidence are reviewed. The first demonstrates that an epidermal regenerative hyperplasia repeatedly produced by wounding or abrasion can promote epidermal carcinogenesis in the initiated skin of mice. The second line of evidence demonstrates that the epidermal hyperplasia produced by the application of 12-O-tetradecanoyl-phorbol-13-acetate (TPA), the most powerful and widely used promoter of skin carcinogenesis, is preceded by damage to the epidermis. This strongly suggests that the epidermal hyperplasia which ensues is a regenerative hyperplasia. Thirdly, evidence is presented which demonstrates that hyperplasia-producing agents which do not promote, produce an epidermal hyperplasia which is different from that produced by tumor promoters. Finally, the review discusses the evidence which suggests that the production of a hyperplasia may be the mechanism for tumor promotion in other organs, such as the liver, bladder, and intestine.

Acetates↗
PubMed1981

Ribosomal RNA synthesis throughout epidermal hyperplastic growth induced by abrasion or treatment with 12-0-tetradecanoyl-phorbol-13-acetate.

During the production of an epidermal hyperplasia following abrasion, or the application of 17 nmoles of 21-0-tetradecanoyl-phorbol-13-acetate (TPA) on the back skin of female CD-1 mice there is a marked increase in ribosomes. During the period of regression, when the epidermis returns to its normal size, the ribosome content also returns to normal. To determine the contribution of ribosome synthesis to the accumulation of ribosomes, mice at varying intervals after abrasion or treatment with 17 nmoles of TPA were injected with (5-3H) uridine (100 muCi, I.P.), 3 hr later the mice were sacrificed, the cytoplasmic ribosomes isolated, and the incorporation of (5-3H) uridine into the cytoplasmic ribosomes was determined. During the production of epidermal hyperplasia, following either abrasion or TPA treatment, there is a significant increase in the incorporation of (5-3H) uridine into the rRNA of the cytoplasmic ribosomes, suggesting that there is an increase in ribosome synthesis. During the period of epidermal regression, ribosome synthesis returns toward normal levels. There is a rough correlation between the amount of hyperplastic growth and the degree of ribosome synthesis. Abrasion induces about a 2-fold greater increase in epidermal mass, compared to TPA treatment. Accordingly, at its peak ribosome synthesis is about 2 times greater after abrasion than after TPA treatment.

Animals↗
PubMed1981

Promotion of carcinomas by repeated abrasion in initiated skin of mice.

Repeated abrasion of the skin of Sencar mice initiated with 100 nmol of dimethylbenzanthracene resulted in the appearance of carcinomas in addition to papillomas. These results strongly support the argument that repeated epidermal regeneration is a sufficient stimulus for the promotion of both benign and malignant neoplasms in the skin of mice.

Animals↗
PubMed1980

The effect of short term incubation in vitro on the RNA content of regenerating mouse epidermis.

The effect of short term incubation in vitro on RNA content in regenerating and normal epidermis has been investigated. Regenerating mouse epidermis was incubated for three hours, either attached to its underlying dermis or by itself, in either buffered sucrose or Roswell Park Memorial Institute culture medium at 26 degrees C or at 37 degrees C. There is a significant loss of RNA when regenerating epidermis is incubated without being attached to its underlying dermis, at either 26 degrees C or 37 degrees C, although there was little loss of DNA, good incorporation of (3H) orotic acid into RNA, as well as good preservation of epidermal histological details. In contrast, when regenerating epidermis was incubated attached to its dermis, little loss of RNA occurred. Similarly, incubating normal epidermis attached to its dermis results in no loss of RNA. These conditions also result in no significant loss of DNA, good incorporation of (3H) orotic acid into RNA, and preservation of epidermal histological details.

Animals↗
PubMed1980

Modification of polypeptide composition in keratinocyte fibrous protein.

The thick paw epidermis of the rat and the guinea pig showed a relatively increased amount of the heaviest fibrous polypeptide compared to the thinner epidermis of back and ear. The hyperplastic epidermis of mouse and rat induced by abrasion or painting with 12-0-tetra-decanoyl-phorbal-13-acetate (TPA) also revealed an increase in the heaviest polypeptide. The fibrous polypeptides of epidermis from scarred skin lacked components present in normal epidermis. Cultured epidermal cells showed a different fibrous polypeptide composition than the parent tissue which was altered when the cells were transplanted to an animal or grown on a dermal substrate in culture. Thus multiple factors such as hyperplasia, the dermis and cellular environment may modify the polypeptides synthesized by the keratinocyte.

Animals↗
PubMed1980

Tumor promotion by abrasion induced epidermal hyperplasia in the skin of mice.

Regenerative epidermal hyperplasia produced by repeated abrasion every 21 days of the skin of female mice after initiation with 7, 12-dimethylbenz(a)anthracene results in the appearance of epidermal tumors. Full thickness wounds, approximately 2 cm in length, made every 14 days in mouse skin initiated with 7, 12-dimethylbenz(a)anthracene also results in the appearance of epidermal tumors adjacent to the wound edge. Repeated abrasion or wounding of normal female mouse skin does not result in the appearance of epidermal tumors. Repeated plucking of initiated mouse skin, which produces a milder epidermal hyperplasia than abrasion, does not result in the appearance of tumors. The data demonstrate that regenerative epidermal hyperplasia, of a sufficient intensity, can act as a tumor promoter.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1980

Epidermal growth following a single application of 12-O-tetradecanoyl-phorbol-13-acetate in mice.

A single application of 17 nm of 12-O-tetradecanoyl-phorbol-13-acetate (TPA) onto the backs of CD-1 female mice results in a significant increase in epidermal wet weight and protein, which reaches its peak by 2 days, remains high for the next two days, and then begins to decrease, reaching normal levels by 10 days. This increase in epidermal mass is brought about largely by an increase in cell number, as evidenced by increases in the total amount of DNA, the number of nucleated cell layers, and the total number of epidermal nuclei/mm of interfollicular epidermis (IFE). The increase in the total number of epidermal nuclei/mm IFE is due entirely to an increase in the number of suprabasal nuclei/mm IFE. The number of basal nuclei/mm IFE actually is reduced by 50% by Day 1, remains low for the next 2 days, and then slowly increases back to normal levels by Day 10. Histologic examination indicates that at Days 1 and 2, when there is a significant decrease in the number of basal cells, there is marked epidermal cell damage. During this time, mitotic activity of the basal epidermal cells increases significantly, reaching a peak of 19 X that above normal by Day 2, and then slowly returns toward normal levels by Day 10. Our results suggest that the epidermal hyperplasia produced by 17 nm of TPA is probably a regenerative epidermal hyperplasia.

Administration, Topical↗