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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to investigate papillomavirus (HPV)-DNA in precancer and cancer of the cervix, vulva, and endometrium by in situ/dot blot/Southern blot hybridization and polymerase chain reaction (PCR). Myc/erbB-2 expression was examined by Northern blot analysis. PCR was the most sensitive HPV detection method, demonstrating HPV-DNA in all pre-invasive and invasive cervical lesions (n = 21) and most (3 of 4) vulvar carcinomas in contrast to an overall rate of 60% with other techniques. Particular phenotypes (adenoid cystic/basal cell carcinoma of the vulva, cervical adenocarcinoma) were found to contain HPV. Endometrium harboured HPV not only in two cases of cervical cancer, but also in 3 of 8 primary endometrial carcinomas and 3 of 8 non-malignant conditions. Myc activation was confined to three squamous cell carcinomas, most markedly in one HPV-6-positive verrucous variant. ErbB-2 over-expression was only seen in one HPV-18 infected advanced endometrial tumour. Our findings point to a range of HPV-infected lesions broader than previously supposed and possible contributions of HPV-independent molecular events to carcinogenesis in this field.
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PMID:Human papillomavirus and c-myc/c-erbB2 in uterine and vulvar lesions. 166 Oct 47

The process of mouse skin tumor formation is subdivided into three operational stages. These stages include initiation, promotion and progression. Ionizing radiation has been found to be a weak initiating agent in the production of malignant squamous cell carcinomas, a complete carcinogen and an agent effective in causing tumor progression. Four skin tumor histologies have been seen with ionizing radiation: benign papillomas, squamous (SCC) and basal (BCC) cell carcinomas and fibrosarcomas. Distinct non-ras transforming genes have been detected in radiation initiated SCCs. A benign papilloma cell line (308) was used as a model system to study ionizing radiation induced progression. A variant 308 cell line (308 10 Gy 5) derived by irradiation of the parental 308 cell has been characterized. The 308 10 Gy 5 cells unlike the parental 308 cells form malignant tumors in athymic nude mice upon subcutaneous injection. The variant 308 10 Gy 5 cells unlike the parental cells also show by northern analysis high steady state levels of the following gene transcripts: stromelysin, metallothionein II A and the proto-oncogenes c-fos and c-jun. Transient transfection studies with a chimeric mouse stromelysin promoter sequence upstream of a chloramphenicol (CAT) reporter gene into 308 and 308 10 Gy 5 cells indicated that the stromelysin promoter was constitutively active in the 308 10 Gy 5 but not in the 308 cells. The ability to divide the process of carcinogenesis into multiple stages in the mouse skin mode has facilitated mechanistic studies that may elucidate the molecular pathways involved in radiation induced tumor development.
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PMID:Molecular events involved in ionizing radiation induced skin carcinogenesis. 182 59

Activation of the Ha-ras oncogene by point mutations has been suggested to play a role in animal skin carcinogenesis models. In this study, we investigated the significance of the Ha-ras mutations in human epidermal tumors. DNAs from paraffin-embedded tissues of benign and malignant human epidermal tumors (27 samples from 25 patients) were prepared and examined for point mutations of codons 12, 13 and 61 of Ha-ras gene by polymerase chain reaction and oligonucleotide hybridization. Only one sample of basal cell carcinoma and one sample of keratoacanthoma were found to carry an A to T transversion at the second position of codon 61. This low incidence of Ha-ras mutations suggests that the mutational activation of the gene may not be primarily involved in human epidermal tumorigenesis.
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PMID:Low incidence of Ha-ras oncogene mutations in human epidermal tumors. 191 19

To evaluate the role of human papillomaviruses (HPV) in the development of premalignant lesions and cancers of the skin in the general population, 314 biopsies obtained from 227 patients with benign neoplasms, premalignant lesions, and cancers of the skin and from 25 patients with squamous cell carcinoma of the lip were analyzed by Southern blot hybridization. DNA probes specific for various cutaneous and genital HPV types were used in hybridizations conducted under nonstringent or stringent conditions. HPV DNA sequences were only detected in eight specimens obtained from six patients: HPV 34 in one case of periungual Bowen's disease, HPV 36 and an as yet uncharacterized HPV in two cases of actinic keratosis, HPV 20 in one case of basal cell carcinoma, an as yet unrecognized HPV in one case of squamous cell carcinoma, and HPV 16 in one case of squamous cell carcinoma of the lip. None of the specimens of cutaneous horn and keratoacanthoma contained detectable HPV DNA. In contrast, HPV DNA sequences, mostly HPV 16, were detected in 13 of 23 cases of anogenital Bowen's disease and invasive Bowen's carcinoma. HPV DNA sequences were not detected in 90 cutaneous samples further analyzed by the polymerase chain-reaction technique, using amplification primers that contain conserved sequences among the genomes of HPV. These results strongly suggest that the known HPV types play only a minor role, if any, in skin carcinogenesis in the general population.
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PMID:Premalignant lesions and cancers of the skin in the general population: evaluation of the role of human papillomaviruses. 217 90

This review relates concepts derived from the study of chemically induced skin cancer in animal models to the pathogenesis of malignant melanoma in humans. Most chemically induced experimental cancers in animals, including melanomas in rodents, arise within a benign precursor lesion. The initiation-promotion-progression sequence is a central concept in animal models for carcinogenesis. Many human melanomas appear to arise from epidermal melanocytes, with no associated precursor lesion. This article considers why there is no apparent precursor in many human melanomas and the consequences of this absence. Melanocyte physiology and factors that govern escape from defenses such as DNA repair, local tissue environment, and immunity presumably influence melanocyte conversion to melanoma. These factors may determine the absence of a precursor lesion in primary melanomas. In addition, it is possible that some human melanomas arise by cellular mechanisms different from those causing cancer in rodent models. Both molecular and prospective clinical studies will be required to explain this apparent paradox in the pathogenesis of melanoma. A similar approach may help to explain the origin of basal cell carcinoma and perhaps other human cancers that appear to arise directly from normal cells. From a clinical point of view, the absence of an identifiable, benign precursor lesion requires even greater emphasis on melanoma prevention. Research on mechanisms of ultraviolet carcinogenesis indicates that appropriate postexposure treatments may be useful in preventing long-term consequences of sunburn, including melanoma.
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PMID:Apparent absence of a benign precursor lesion: implications for the pathogenesis of malignant melanoma. 267 14

Malignant melanomas were found in 15.8% of xeroderma pigmentosum (XP) patients with skin cancer in Japan. When multiple cancers were scored separately depending on the histopathologic types, 12.1% of the skin cancers in XP patients was malignant malignant melanoma. The relative incidence of malignant melanoma in skin cancer in XP patients is similar to that in skin cancer in general (12.6%), reported previously. Most of the malignant melanoma in XP patients developed in skin exposed to sunlight, in contrast to the high incidence of malignant melanoma in general in the unexposed skin of Japanese people. A DNA repair defect of UV damage is strongly suggested to be responsible for the high incidence of skin cancer in XP patients. The onset of malignant melanoma in XP patients was about ten years old, and was as early as those of basal cell carcinoma and squamous cell carcinoma in the patients with very low DNA repair capacities. Among nine genetic complementation groups and a variant type, group A XP cells were found to be extremely hypermutable by ultraviolet light, while group C XP cells were also hypermutable, but at the same level as normal cells when adjusted for survival. Mutagenesis as a possible mechanism of carcinogenesis in XP is supported by these results, but evidence in other cancer-prone hereditary diseases is yet to be obtained.
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PMID:Melanoma and other skin cancers in xeroderma pigmentosum patients and mutation in their cells. 271 57

The Melanesians of the North Solomons are exposed to intense equatorial sunlight and yet have a very low incidence of skin cancer. This study reveals no proven cases of basal cell carcinoma in these people, and demonstrates the rarity of squamous cell carcinoma and melanoma arising in normal pigmented skin. Most, if not all squamous cell carcinomas, arise in skin damaged by tropical ulceration, burns or osteomyelitis. Melanoma arises from the unpigmented skin of the sole of the foot. North Solomon Islanders are very deeply pigmented. Presumably, dense cutaneous melanin in normal undamaged skin provides the highly effective protection against solar carcinogenesis which these people enjoy. Chronic or recurrent skin ulceration with subsequent repair, scarring and loss of pigment is the precursor to almost all non-melanoma skin cancer in these people. Most of these cancers could be prevented by split thickness skin grafting of chronic ulcers, and protection of ulcerated, depigmented and scarred skin from solar radiation.
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PMID:Skin cancer in the North Solomons. 317 95

The lymphocyte response to u.v. radiation (254 nm) was investigated by two different methods in 29 unselected patients with multiple epidermal cancer. The u.v.-induced DNA synthesis was determined as the increase in incorporation of [3H]thymidine in irradiated cells compared with nonirradiated cells after incubation for 2 h. The u.v. tolerance was measured as the u.v. dose necessary for 50% reduction in phytohemagglutinin-stimulated lymphocyte proliferation. Patients with both squamous cell differentiated tumors and basal cell carcinomas had very high u.v.-induced DNA synthesis values (p less than 0.01, when compared with patients with basal cell carcinoma only and p less than 0.005, when compared with controls). The u.v. tolerance in patient lymphocytes was considerably lower than in control lymphocytes (p less than 0.001), with the lowest values occurring in patients with clinical sun intolerance (p = 0.05, when compared with the remaining patients). These investigations may be of predictive value in skin carcinogenesis.
Carcinogenesis 1985 Jun
PMID:Abnormal lymphocyte response to u.v. radiation in multiple skin cancer. 400 70

Nevoid basal cell carcinomas (NBCCs) are a prototype of a genetic form of basal cell carcinoma. These basal cell cancers, rather than being caused by genetic factors alone, are most likely the product of genetic and environmental factors. The NBCC syndrome provides a model for studying tumors induced by ionizing radiation and for viewing carcinogenesis as a multistage process explainable by a minimum of two steps. The interaction of genetic and environmental factors in producing tumors to which an individual is predisposed can be studied in patients with the NBCC syndrome and childhood medulloblastoma that was treated by radiation therapy. Individuals with the NBCC syndrome represent a special subgroup with a hereditary predisposition to basal cell carcinoma in whom ionizing radiation may supply the subsequent mutation necessary for tumor development. The genetically altered epidermis underlying the palm and sole pits found in patients with the syndrome represents basal cell carcinoma in situ from which basal cell carcinomas develop, albeit infrequently. The restrained biologic behavior of most of these tumors contrasts with the usual destructive behavior of the NBCCs of the head and neck in the same patient.
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PMID:Nevoid basal cell carcinoma syndrome. Profile of genetic and environmental factors in oncogenesis. 673 55

Skin cancer, the most common malignancy in white patients, is rare in black populations. Seventeen black patients have been diagnosed and treated for basal cell carcinoma in the past 20 years at the University of Mississippi Medical Center. Ten of them have died, six of various types of cancer. Of the seven living patients, one had two cancers at the time of study: a new basal cell carcinoma and generalized lymphoma. The majority of patients had some degree of mixed racial ancestry, with medium to light brown skin, a history of heavy sun exposure, and lesions appearing on the head or neck. Highly significant depression of cellular immunity was demonstrated in these patients by T-cell assay. Altered tumor surveillance is implied as an etiological factor in basal cell carcinogenesis in black patients.
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PMID:Cellular immune deficiency in black patients with basal cell carcinoma. 696 44


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