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

Indications for radiotherapy of benign dermatoses have decreased markedly during the past decades. The remaining indications are reviewed. Side effects of ionizing radiation therapy are discussed in detail, with special emphasis on radiodermatitis and radiation cancer of the skin, mutagenic and genetic effects of x rays, and induction of carcinogenesis of interanl organs. Thyroid cancer is used as an example to discuss modern theories of radiocarcinogenesis and risk coefficients of various organ systems. Guide lines for radiotherapy of benign dermatoses are proposed.
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PMID:[Roentgen therapy of dermatoses: indications and hazards]. 14 96

Six hundred patients with primary differentiated thyroid carcinoma had follow-up studies for a minimum of 15 years and a maximum of 45 years. Recurrence rate and death rate were significantly different in defined high-risk and low-risk groups of patients. These basic risk groups were defined by age and sex alone; low risk consisted of men 40 years of age and younger and women 50 years of age and younger whereas the high-risk group were older patients. Recurrence and death rates in patients at high risk were 33% and 27% while respective figures for patients at low risk were 11% and 4%. In more recent years these results have shown significant improvement. Basic risk group definition outweighed the effect of pathologic type, local disease extension, type of treatment, and site of recurrence or metastasis. For instance, radioactive iodine cured 70% of patients at low risk with metastatic disease but only 10% of patients at high risk. Less aggressive biologic behavior of thyroid cancer before the age of menopause implies that an estrogen-rich milieu may alter the effects of initiating and promoting factors in carcinogenesis. It also suggests that therapeutic trials of estrogen be undertaken in progressive metastatic differentiated thyroid cancer.
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PMID:Risk factor analysis in differentiated thyroid cancer. 42 22

A population-based case-control study of the association of diet and other factors and thyroid cancer was conducted between 1980 and 1987 on Oahu, Hawaii. Study participants included 51 men and 140 women with thyroid cancer, and 113 male and 328 female controls matched on age (+/- 5 years) and sex. A significant, positive monotonic dose-response relation of weight in late adulthood (5 years prior to interview) and the risk for thyroid cancer was found for men and women. A greater than five-fold increase in the risk for thyroid cancer among men, and more than a two-fold increase in risk among women, was found for subjects in the highest compared with the lowest quartile of weight in late adulthood. Height was significantly related to the risk for thyroid cancer among men, but not women. Among men, there was a significant dose-response relation of weight in early adulthood (20-29 years of age) and the odds ratios (ORs) for thyroid cancer, although the trend was not significant after adjustment for height. Among women, there was also a positive relation of adult weight gain and thyroid cancer, with an OR of 2.6 associated with more than a 14% increase in weight. The effects of relative weight and weight gain on thyroid cancer risk were stronger in post-menopausal women than in premenopausal women. There was a significant positive interaction between fertility drug use and early adult weight and the risk for thyroid cancer in women. Odds ratios were also significantly elevated for women above the median weight in early adulthood who experienced a miscarriage or stillbirth at first pregnancy. In summary, these data show an association of weight, particularly in late adulthood, and the risk for thyroid cancer in men and women, and further suggest a positive interaction between weight in young adulthood and fertility drug use on thyroid carcinogenesis in women.
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PMID:The association of body size, reproductive factors and thyroid cancer. 145 62

We developed a new approach for detecting the gene amplification of cancer DNAs with restriction landmark genomic scanning (RLGS). In cancer research, much effort has been made to find the amplified loci of cancer DNAs, because many lines of evidence indicate association between oncogene amplification and carcinogenesis. Conventionally, such gene amplification has been detected by using Southern hybridization with DNA probes. However, only the information of one locus can be obtained by one hybridization procedure, and analysis of many loci throughout the genome is too laborious and time consuming, even if only several candidate genes are investigated. On the other hand, the "in-gel renaturation method" was reported as another alternative for detection of amplified regions. However, even though this method is much improved, it is difficult to detect less than 7-fold amplification, which is often higher than the amplification of many cancer cases. To overcome these limitations and, in addition, to locate the amplified DNA two dimensionally, we applied RLGS for analysis of DNA amplification in cancer tissues, such as breast cancer (infiltrative tubuloadenocarcinoma), neuroblastoma, meningioma (endotheliomatous meningioma), and thyroid cancer (papillary adenocarcinoma). In some cases of breast cancer, several amplified spots located on the same amplicon were detected. In thyroid cancer, in which no amplification has yet been reported, low-grade amplification was also detected. In this report, we demonstrated that RLGS allows us to screen 2000-3000 restriction landmarks distributed on the genome simultaneously, and even low-grade amplification could be detected effectively. Thus, RLGS has proven to be a very useful method in detecting DNA amplification.
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PMID:New approach for detection of amplification in cancer DNA using restriction landmark genomic scanning. 161 37

Recently, we found that prediagnostic serum selenium concentration was significantly lower for cases developing thyroid cancer (n = 43) than for controls. We assumed that redistribution of serum selenium into the affected tissue took place in the prediagnostic period. The present study was carried out to determine the physiological concentration of selenium in the thyroid, since very few data are available in the literature. The concentrations of selenium in the thyroid (n = 45) and liver samples from Norwegians who had died because of acute illness or accidents were determined by hydride generation atomic absorption spectrometry. The mean selenium concentration was found to be 0.72 +/- 0.44 microgram/g in the thyroid and 0.45 +/- 0.11 microgram/g in the liver tissue. The surprisingly high concentration of selenium in apparently normal thyroids indicates that selenium has important functions in this organ. The remarkably broad range, together with the observation that no significant correlation exists between thyroid and liver concentrations, suggest that factors other than the selenium status are important determinants for the selenium concentration in the thyroid gland. This observation is consistent with our hypothesis that in carcinogenesis, prediagnostic processes influence the serum-/thyroid-ratio of selenium.
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PMID:Selenium concentrations in the human thyroid gland. 170 66

Women have a greater incidence of autoimmune thyroiditis, thyroid cancer and radiation-induced carcinogenesis than men. Over the past several years we have examined for the presence of steroid receptors in both humans and non-human primates. In this study we examined the nuclear uptake and retention of 3H-testosterone, the main circulating androgen in mammals, in different cells of the thyroid gland of baboons, our non-human primate model. Castrated-adrenalectomized male baboons were injected with 3H-testosterone (1 microgram/kg bw) and killed 1 1/2 h later. The thyroid glands and other tissues were removed and processed for autoradiography. Nuclear localization of 3H-testosterone or one of its metabolites was found in a small fraction of the follicular cells (approximately 10-20%). The discrepancy between these findings and those previously obtained with 3H-dihydrotestosterone (virtually 100% of the follicular cells concentrated the 3H-steroid) are discussed. The results from this study and those of the past strongly support a direct action of androgen on the thyroid. Whether a direct action of androgen on the thyroid is related to smaller incidence in autoimmune thyroiditis, thyroid cancer and radiation-induced carcinogenesis in men than women remains an unanswered question at the present time.
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PMID:A differential nuclear uptake and retention of 3H-androgens in the thyroids of baboons. 324 65

Iodine is an essential nutrient for the normal growth and development of humans and animals and is necessary for normal metabolism and regulation of thyroid hormones. Iodine excess can produce thyrotoxicosis but not cancer. However, radioiodine is carcinogenic for the thyroid gland. Dietary iodine deficiency is associated with goiter in humans and animals. The goiter develops because of a feedback system between thyroid hormones, the pituitary gland, and the hypothalamus, and it regulates the synthesis and release of thyroid-stimulating hormone. Chronic hypersecretion of thyroid-stimulating hormone causes profound goiter (diffuse thyroid hyperplasia), which appears to be related to carcinogenesis. Chronic dietary iodine deficiency in rats leads to thyroid follicular adenomas by 12 months and follicular carcinomas by 18 months. An increased risk of thyroid cancer has been reported in humans with goiter and those living in some iodine-deficient areas of the world. In very recent animal studies, iodine deficiency, chemical goitrogens, and thyroid toxins have been shown to have potent tumor-promoting effects. In rats, iodine deficiency is a much more effective tumor promoter than it is a carcinogen, suggesting that a similar relationship may exist in human populations. These studies suggest that a major role of iodine is to prevent the formation of thyroid tumors in humans and animals.
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PMID:The role of iodine in carcinogenesis. 359 38

Clinicopathologic findings on small thyroid carcinomas measuring 10 mm or less in diameter were analyzed in 78 thyroidectomied cases. The authors divided small thyroid tumors into two subgroups according to diameter: 0 less than or equal to 5 mm (classified as minute carcinoma) and 5 less than 0 less than or equal to 10 mm (classified as tiny carcinomas). Characteristics including sex, age, histologic type, extrathyroid invasion, and lymph node metastasis were examined in each subgroup. In patients with minute carcinoma, very few incidences of extrathyroid invasion and lymph node metastasis were found. However, these involvements, especially lymph node metastasis, were found more frequently in patients with tiny carcinoma. The incidence of cervical lymph node metastasis was 13% in minute carcinoma and 59% in tiny carcinoma. (P less than 0.01). These findings suggest the need for more careful observation and treatment of tiny carcinomas, especially with respect to lymph node metastasis. In accordance with World Health Organization (WHO) classification, the histologic types of thyroid carcinoma were classified into papillary and follicular carcinomas. The papillary carcinoma and follicular carcinoma ratios were compared between the two subgroups. The discovery rate of follicular carcinoma was significantly higher in minute carcinoma than in tiny carcinoma (P less than 0.005). This suggests that the papillary carcinoma/follicular carcinoma ratio (p/f) increases as the size of the carcinoma increases, and that follicular carcinoma is the "seed," or initial form, of thyroid cancer. The female-male ratio in small thyroid cancer suggests that there is no sex difference in carcinogenesis but that there is more probability for cancer development in the thyroid in women.
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PMID:New subgrouping of small thyroid carcinomas. 365 5

Among 15 human tumor cell strains from Japanese patients, one strain derived from a patient with thyroid cancer showed inability to support the growth of adenovirus 5 treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). When plated on this Mer- strain, adenovirus 5 showed 3-4 times higher sensitivity to MNNG-induced killing than when plated on any of the other 14 Mer+ tumor cell strains. Biochemical analysis showed that the Mer- strain was defective in demethylation repair of O6-methylguanine produced by MNNG treatment. The sensitivities of 12 of the 15 human tumor strains, including the Mer- strain, to MNNG were compared by measuring their colony-forming abilities. All the strains tested showed the Rem- phenotype (having higher sensitivity to MNNG-produced cell killing than normal fibroblasts). The differential killing effects of MNNG on Mer- and Mer+ tumor cells under in vivo conditions were tested using the Mer+ HeLa S3 strain and its Mer- variant. Mer+ cells and Mer- cells were implanted subcutaneously into the left and right flanks, respectively, of 10 nude mice and the next day, MNNG solution (0.25 ml at 1 mg/ml) was injected into the implantation sites of eight mice. Mer- tumor cells in six of eight treated mice showed no growth and those in the other two mice did grow, but regressed after approximately 3 weeks. In contrast, Mer+ tumor cells continued to grow in all the eight mice treated, indicating that Mer- tumor cells may be selectively inactivated by suitable therapeutic regimens with appropriate methylating drugs.
Carcinogenesis 1985 Apr
PMID:Analysis of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced DNA damage in tumor cell strains from Japanese patients and demonstration of MNNG hypersensitivity of Mer xenografts in athymic nude mice. 398 62

Hormone-related cancers account for almost 30% of all cancer cases in the United States. Data from animal experiments and from epidemiological and endocrinological studies in humans support the hypothesis that the individual hormones which control normal growth of target organs can also create the proper conditions for neoplastic transformation. The concept that hormones can cause, i.e., increase the incidence of, human cancer is most developed for the four hormone-related cancers which are numerically the most important, namely, breast, prostate, endometrium, and ovary. Even for these sites, large gaps remain in our knowledge of the responsible hormones and the conditions which create the optimal opportunity for carcinogenesis. Although scanty, the available epidemiological evidence also suggests a hormonal role in the pathogenesis of testis cancer, thyroid cancer, and osteosarcoma. We believe that the primary prevention of all these cancers will probably depend on modification of the factors which affect the secretion and metabolism of the responsible hormones rather than on control of exposure to classical exogenous initiators.
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PMID:Endogenous hormones as a major factor in human cancer. 704 21


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