demecolcine and Skin-Neoplasms

Topics: Alkaloids; Demecolcine; Dimethyl Sulfoxide; Drug Combinations; Drug Evaluation; Facial Neoplasms; Head and Neck Neoplasms; Humans; Ointments; Skin Neoplasms

Topics: Administration, Topical; Carcinoma, Basal Cell; Clinical Trials as Topic; Demecolcine; Drug Evaluation; Facial Neoplasms; Female; Humans; Male; Middle Aged; Neoplasm Recurrence, Local; Ointments; Radiotherapy Dosage; Skin Neoplasms

Analysis of the expression of a number of known genes in cultured human cells has revealed UVB-induced changes that may be specific for melanocytic cells. The response of c-fos, p53 and HIV-LTR reporter constructs to UVB and UVC was reduced in MM96L melanoma cells compared to HeLa. Cell cycle arrest produced by UVA, gamma radiation, cisplatin or the antimetabolite deoxyinosine differed from that of UVB. Cell cycle analysis after multiple doses of UVB raised the possibility that UVB-induced pRb depletion could result in increased mutation and thus enhanced tumourigenesis of irradiated melanocytes in skin subjected to a defined pattern of UVB exposure. To extend the analysis of gene expression in cultured melanocytic cells to uncharacterised genes, promoter trap cell clones containing unknown genes 'tagged' by a beta-galactosidase reporter construct were generated from MM96L cells. Altered gene expression in clones treated with a panel of DNA-damaging agents was quantitated by measurement of beta-galactosidase activity. Of the clones containing 'tagged' endogenous promoters induced by UVB, 52% were induced only by UVB and not by other DNA-damaging agents (cisplatin, N-methyl-N-nitro-nitrsoguanidine, fotemustine). One third of the clones were also activated by TPA suggesting that general DNA damage responses involving PKC are activated less frequently than unique pathways of gene activation. Overall, 60% of the 50 clones that responded to the panel of agents were induced by only one of the agents, indicating that a high proportion of genes are induced by agent-specific mechanisms. In the long term, promoter trapping may allow the full repertoire of UVB-inducible genes to be characterised.

Topics: Antineoplastic Agents; beta-Galactosidase; Cell Cycle; Cisplatin; Demecolcine; Genes, fos; Genes, p53; HeLa Cells; HIV Long Terminal Repeat; Humans; Hydroxyurea; Inosine; Melanocytes; Melanoma; Methylnitronitrosoguanidine; Neoplasms, Radiation-Induced; Nitrosourea Compounds; Organophosphorus Compounds; Proto-Oncogene Proteins c-fos; Recombinant Proteins; Skin Neoplasms; Tetradecanoylphorbol Acetate; Transfection; Tumor Cells, Cultured; Ultraviolet Rays

Cell kinetic variables in normal untreated hairless mice were studied in order to observe possible age-related changes. Generally, groups of 4 male and 4 female mice were subjected to study at various ages from one to 115 weeks. The number of basal and suprabasal cells per microscopic field was observed, and after injection of tritiated thymidine the mean labelling index, the average specific activity and the mean grain count were scored. After injection of Colcemid, the average number of Colcemid-arrested mitoses was counted. With flow cytometry the fraction of cells in S and in G2 + M was also observed. In general, both the number of suprabasal cells and the proliferative variables were significantly lower in the very young mice. They increased to slightly above normal values at about 20-22 weeks of age, and then fluctuated a little with two additional possible peaks at 40-50 and around 80 weeks, respectively, and two troughs some weeks after the peaks. However, this rhythmicity was slight and not significant. Thus the only significant age-related pattern was that very young mice have a thin epidermis and low proliferative variables. These values increase up to the age of 20 weeks, and from then on there are no obvious and significant alterations, only slight rhythmic undulations almost within normal limits. The importance of cell kinetic changes with age for epidermal carcinogenesis is discussed in relation to these observations.

Topics: Aging; Animals; Cell Count; Demecolcine; Epidermal Cells; Female; Humans; Interphase; Kinetics; Male; Mice; Mice, Hairless; Mitosis; Skin Neoplasms

Fifteen malignant melanomas were subjected to chromosomal analysis, in order to determine whether the number of chromosomes in a tumor cell could be correlated to a clinical prognosis. The protocol involved a direct technique which utilized a Colcemid blockade of spindle formation in mitosis to allow study of metaphase chromosomes. The direct method was chosen to reveal chromosome changes in the tumor cell in situ rather than changes in the cultured cell. Two tumors yielded chromosome spreads which could be counted and correlated with a clinical prognosis. Failure to obtain other adequate chromosome spreads were accounted for by the presence of tissue necrosis and the absence of viable tumor cells.

Topics: Adult; Aged; Chromosome Aberrations; Demecolcine; Female; Humans; Karyotyping; Male; Melanoma; Metaphase; Middle Aged; Prognosis; Skin Neoplasms

Topics: Administration, Topical; Demecolcine; Humans; Ointments; Radiation-Sensitizing Agents; Skin Neoplasms

The literature concerning the use of metaphase inducing agents as clinical sensitisers to radiation is briefly reviewed, and five cases are reported, which suggest that under ordinary clinical conditions, these agents are not likely to be of value. These results accord with animal experiments and a possible reason is suggested.

Topics: Adenocarcinoma; Adult; Aged; Anus Neoplasms; Carcinoma, Squamous Cell; Demecolcine; Female; Humans; Lip Neoplasms; Male; Middle Aged; Mitotic Index; Neoplasms; Radiation-Sensitizing Agents; Skin Neoplasms; Stomach Neoplasms

Topics: Bronchial Neoplasms; Carcinoma; Carcinoma, Squamous Cell; Cell Division; Colchicine; Demecolcine; Drug Therapy; Female; Humans; Mediastinum; Neoplasm Metastasis; Neoplasms; Prognosis; Skin Neoplasms; Thoracic Diseases; Uterine Cervical Neoplasms

The topical application of demecolcine (Colcemid, N-desacetyl methyl colchicine), N-desacetyl thiocolchicine (Thio-Colciran), and methotrexate preferably in combination, exerts a selectively destructive action on rodent (basal cell) carcinomas, solar keratoses, Bowen's disease, and keratoacanthomas, while sparing surrounding normal tissues. The former two exert their action by inhibiting mitosis in the metaphase, and the latter inhibits the commencement of mitosis by interference with the synthesis of desoxyribonucleic acid. The cosmetic results are particularly good when the ears or nose are affected, and the cure rate compares favorably with that resulting from other treatments. Although ineffective against squamous carcinomas, the fact that this form of therapy is effective for keratoacanthomas could prove a valuable additional diagnostic point between the two in doubtful cases.

Topics: Administration, Topical; Antimetabolites, Antineoplastic; Antineoplastic Agents; Antineoplastic Agents, Alkylating; Antineoplastic Agents, Phytogenic; Antineoplastic Combined Chemotherapy Protocols; Bowen's Disease; Carcinoma, Basal Cell; Colchicine; Demecolcine; Humans; Keratoacanthoma; Methotrexate; Precancerous Conditions; Skin Neoplasms; Triaziquone

Topics: Anus Neoplasms; Bowen's Disease; Carcinoma; Carcinoma, Squamous Cell; Colchicine; Demecolcine; Humans; Male; Penile Neoplasms; Penis; Skin Neoplasms

Topics: Animals; Colchicine; Cowpox; Demecolcine; Humans; Immunotherapy, Active; Melanoma; Skin Neoplasms; Smallpox; Vaccines; Variola virus

Topics: Carcinoma; Carcinoma, Basal Cell; Colchicine; Demecolcine; Humans; Skin Neoplasms

Topics: Colchicine; Demecolcine; Skin Neoplasms

Topics: Carcinoma, Basal Cell; Carcinoma, Squamous Cell; Colchicine; Demecolcine; Dermatology; Humans; Skin Diseases; Skin Neoplasms

Topics: Carcinoma; Carcinoma, Basal Cell; Cell- and Tissue-Based Therapy; Colchicine; Demecolcine; Humans; Neoplasms, Glandular and Epithelial; Skin Neoplasms