Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007097 (carcinoma)
152,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This investigation studied the effect of topical application of apigenin on skin tumorigenesis initiated by 7,12-dimethylbenz(a)anthracene (DMBA) and promoted by 12-O-tetradecanoylphorbol-13-acetate (TPA) in SENCAR mice. Apigenin was a potent inhibitor of epidermal ornithine decarboxylase induction by TPA in a dose-dependent manner from 1 to 20 mumol. Two tumorigenesis studies were conducted. In the first study, 20 mumol of apigenin was applied topically and no effect on body weight was observed. By week 33 after DMBA initiation, 48% of DMBA/TPA-treated mice developed carcinomas, while none occurred in DMBA/apigenin/TPA-treated groups. In the second study, doses of 5 and 20 mumol of apigenin were used. The papilloma incidence for 0, 5, and 20 mumol apigenin at 26 weeks after DMBA was 93.3, 58, and 39.3%, and papilloma numbers per mouse were 7.5, 2.5, and 1.8, respectively. Apigenin prolonged by 3 weeks the latency period of tumor appearance. In addition, apigenin significantly inhibited the incidence of carcinoma and the numbers of carcinomas. The incidence of carcinomas per tumor-bearing animal and the ratio of carcinomas/papillomas in two apigenin-treated groups decreased although there were no significant differences between the three groups. These data indicate that apigenin inhibited skin papillomas and showed the tendency to decrease conversion of papillomas to carcinomas.
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PMID:Inhibitory effect of apigenin, a plant flavonoid, on epidermal ornithine decarboxylase and skin tumor promotion in mice. 210 57

In the present study 18 cases of malignant ovarian neoplasm were studied to determine the possible role of sex steroid hormones and gonadotropins on tumor development. Twelve cases of serous cystadenocarcinoma, 2 of mucinous cystadenocarcinoma, 2 of endometrioid carcinoma, one malignant Brenner tumor, and one yolk sac tumor were examined with respect to their response to estradiol (E2), [D-Ser(But)6]-LHRH (1-9) nonapeptide-etylamide (Buserelin), human menopausal gonadotropin (HMG), RU 38486 (RU), and pure FSH by subrenal capsule assay (SRCA). Also 125I-FSH binding assay and the protein kinase C (CK) activity were studied in vitro. The results showed; 1) Seventy-three% cases showed a significant increase (p less than 0.05) in size due to SRCA. 2) In the FSH, HMG, and Buserelin treated groups, the size of xenografts increased (p less than 0.05) and the highest response was obtained with FSH. 3) Ninety-one% of cases demonstrated in vitro FSH specific binding which was significantly higher (p less than 0.05) in the cases which responded to gonadotropins in SRCA (42,288 +/- 25,454 vs 6,980 +/- 1,952, mean +/- SD, cpm/mg tissue). 4) CK activity was increased significantly (p less than 0.05) by gonadotropin (204.5 +/- 2.4 vs 363.9 +/- 7.2, mean +/- SD, cpm/mg tissue). These results suggest that gonadotropins possibly play a role in prompting the tumorigenesis of the malignant ovarian neoplasms through specific receptors and this mechanism may modify the CK system in malignant ovarian neoplasms.
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PMID:[Effects of gonadotropin on the growth of malignant ovarian neoplasms assessed by subrenal capsule assay]. 211 9

Numerous epidemiological studies have made it possible to isolate groups of women at risk or developing an epidermoid carcinoma of the uterine cervix. Among the factors studied, age at the time of the first sexual intercourse and number of male partners were found to be statistically significant factors. No study has yet proved that smegma facilitates cancer and that circumcision may prevent its occurrence. However, the importance of the "male factor" has been enhanced by many studies suggesting the possibility of an oncogenic factor transmissible by sexual intercourse. Several data suggest that some types of human papillomavirus are the necessary, if not sufficient, factors of cervical oncogenesis. Some types of herpes virus, notably HPV 16, can be identified in the majority of invasive cancers and their direct precursors: intraepithelial neoplasias. The carcinogenic role of papillomaviruses in animals ans in laboratory experiments supports the theory that these sexually transmissible viruses are involved in the origin of epidermoid cervical carcinoma.
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PMID:[Cancer of the uterine cervix: epidemiology and virology]. 215 29

K-ras gene mutation in colorectal tumors from patients with familial polyposis coli were investigated using oligonucleotide probes specific for a mutation at codon 12, 13, or 61 of the K-ras gene. The authors examined 22 colorectal carcinomas and 51 colorectal adenomas from 41 familial polyposis coli patients and observed mutations at codons 12 and 13 in eight of 22 colorectal carcinomas (36%) and six of 51 colorectal adenomas (12%). Thus, the frequency and sites of K-ras gene mutation in colorectal carcinoma from familial polyposis coli patients are similar to those in cases of sporadic colorectal carcinoma and may not be the first genetic event linked to the tumorigenesis.
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PMID:K-ras activation in colorectal tumors from patients with familial polyposis coli. 215 40

Epidemiologic studies suggest that certain psychosocial factors increase the risk of cancer. Yet, animal studies suggest that psychosocial stress inhibits the development of chemically induced tumorigenesis. The purpose of this study was to examine the effect of three different chronic mild stressors on the development of dimethylhydrazine (DMH)-induced colorectal carcinoma in rats. Results of this study show that the development of DMH-induced colorectal carcinoma was not significantly inhibited or altered by each individual stress treatment. Additionally, results indicate that mild stressors can induce neurochemical changes commonly associated with stress, without the confounding effects of more aversive stressors that are likely to compromise the nutritional and physiological status of the animal and thereby alter tumor formation.
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PMID:The effect of mild stress on DMH-induced colorectal cancer. 222 23

Abnormalities in oncogenes, which are broadly classified into viral and cellular oncogenes, and suppressor genes appear critical for the development of colon cancer. Cellular oncogenes contribute to malignant transformation when they become activated by point mutation, translocation, amplification, or loss of regulator sequences. The properties of the oncoproteins, the proteins encoded by oncogenes which are essential for carcinogenesis, are unclear. Suppressor genes normally suppress the tumorigenic phenotype by keeping the growth of cells in check; it is their inactivation that contributes to malignant transformation. Development of colon cancer appears to take place by stepwise accumulation of multiple genetic alterations during the progression from normal colon to adenoma and carcinoma. Activation of ras, an early event in this sequence, is found in 50% of colon cancers; overexpression of c-myc is found in approximately 80%. Inactivation of suppressor genes, which occurs during later stages, is noted in greater than 70% of tumors. A current model of colonic tumorigenesis is presented.
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PMID:Oncogenes and suppressor genes: their involvement in colon cancer. 222 91

The occurrence of thyroid tumors induced by N-methyl-N-nitrosourea (MNU) and low iodine diet in Long-Evans (LE) rats was studied with special reference to sex difference, effect of gonadectomy, and estradiol administration. Rats of experimental groups 1-6 were given i.v. injections of 40 mg of MNU/kg of body weight at 50 days of age and fed on low iodine diet from 28 days of age to the end of the experiment (30 weeks after MNU administration). They consisted of male, female, castrated male, ovariectomized female, and gonadectomized male and female rats given 2.5 mg estradiol pellets s.c. Rats of groups 7-10 served as the respective controls without MNU or low iodine diet. Levels of serum thyroid stimulating hormone and estrogen receptor of the thyroid lesions were also examined. It was noted that the incidence of thyroid carcinoma was higher in females than in males (P less than 0.01) and did not change by castration in males but decreased in ovariectomized rats (P less than 0.01). Administration of estradiol after gonadectomy significantly increased the incidence of thyroid carcinomas in castrated and ovariectomized rats. Increase of mean serum thyroid stimulating hormone levels and thyroid and pituitary weights was also predominant in females. Mean thyroid stimulating hormone levels of both sexes were decreased by gonadectomy. Mean thyroid and pituitary weights were inhibited from increasing not by castration but by ovariectomy. Estradiol supplemented after gonadectomy significantly increased all of these factors. Estrogen receptors were detected in transplanted thyroid tumors but not in euthyroid tissues. The results suggest that estradiol promoted the thyroid tumorigenesis through activation of thyrotrophs in pituitary or direct interaction of estradiol and estrogen receptors in the thyroid.
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PMID:Effects of sex difference, gonadectomy, and estrogen on N-methyl-N-nitrosourea induced rat thyroid tumors. 225 11

We have shown previously that the risk of tumor initiation, promotion, and progression in animals initiated with alkylating agents can be drastically altered by hyperthermia treatments. We show here that ionizing radiation can also alter the risk of tumor initiation by alkylating agents. Using a two-step skin tumorigenesis protocol in female SENCAR mice (initiation by MNNG, promotion with TPA), we exposed the dorsal skin of the mice to various doses of 90Sr/90Y beta radiation near the time of initiation. The radiation produced a dose-dependent reduction in the number of papillomas which appeared after TPA promotion, with about a 20% reduction in animals receiving 0.5 Gy surface dose just before initiation, about 50% reduction after 2.5 Gy, and greater than 80% at doses above 5 Gy. A dose of 2.5 Gy in animals initiated with DMBA produced no significant reduction. One skin hyperthermia treatment (44 degrees C, 30 min) along with radiation in MNNG-initiated animals partially blocked the protective effect of radiation and increased the papilloma frequency. Radiation (2.5 Gy) given either 6 days before or after MNNG initiation was less effective but still reduced papilloma frequency about 20%. In sharp contrast to the marked reduction in papilloma formation, these same animals showed no change in carcinoma frequency with any of the doses or schedules of beta radiation. MNNG initiation alone produced three types of initiated cells. One type, produced in low yield, was promotion-independent with a high probability of progression to a carcinoma and appeared unaffected by the radiation. A second type, produced in intermediate yield, was promotion-dependent and also had a high progression probability, but was likewise unaffected by the radiation. The third and most abundant type was promotion-dependent with a very low progression probability. Radiation exposure resulted in a decrease in the risk of an MNNG initiation event which led only to the third type of cell. The data therefore indicate that the risk of some, but not all, tumor-initiating events caused by alkylating agents can be reduced by an exposure to ionizing radiation.
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PMID:Beta-radiation-induced resistance to MNNG initiation of papilloma but not carcinoma formation in mouse skin. 230 36

The role of epidermal growth factor (EGF) in oncogenesis and progression of malignant tumors is a subject of vast interest. In this study, radioimmunoassay and radioreceptor assay of EGF were established. EGF contents in malignant and benign pancreatic tumors, in normal pancreas tissue, and in culture media of a human pancreatic carcinoma cell line were determined. EGF receptor binding studies were performed. It was shown that EGF contents in pancreatic carcinomas were significantly higher than those in normal pancreas or benign pancreatic tumors. EGF was also detected in the culture medium of a pancreatic carcinoma cell line. The binding of 125I-EGF to the pancreatic carcinoma cells was time and temperature dependent, reversible, competitive, and specific. Scatchard analysis showed that the dissociation constant of EGF receptor was 2.1 X 10(-9) M, number of binding sites was 1.3 X 10(5) cell. These results indicate that there is an over-expression of EGF/EGF receptors in pancreatic carcinomas, and that an autocrine regulatory mechanism may exist in the growth-promoting effect of EGF on tumor cells.
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PMID:Epidermal growth factor and its receptors in human pancreatic carcinoma. 234 41

Fish oil has been shown to have a protective effect in some cancer models. To determine whether fish oil alters skin tumorigenesis, a study was designed using the initiation-promotion mouse skin carcinogenesis model, feeding mice during the promotion stage a constant overall amount of dietary fat (10%) in which the levels of menhaden oil (MO) varied from 0 to 8.5% or corn oil (CO) at 10%. SENCAR mice were initiated with 10 nmol dimethylbenz[a]anthracene. Two weeks later mice were divided into five groups and maintained on one of the following AIN-76 based diets consisting of: 8.5% coconut oil (CT)/1.5% CO (diet A); 1% MO/7.5% CT/1.5% CO (diet B); 4% MO/4.5% CT/1.5% CO (diet C); 8.5% MO/1.5% CO (diet D); or 10% CO (diet E). Two weeks later, promotion with twice weekly applications of 1 micrograms 12-O-tetradecanoylphorbol-13-acetate (TPA) was begun and continued for 24 weeks. No statistically significant differences in kcal food consumed or body wts were observed between diet groups during the study. The final papilloma and carcinoma incidence was not different among the diet groups. However, differences were seen in the rate of papilloma appearance with the group fed diet E (10% CO) being the slowest and diet B being the most rapid. In a parallel study, ornithine decarboxylase activity, a suggested marker of promotion, was greatly elevated in the epidermis of all TPA-treated mice and the effect of diet tended to reflect the different rates of tumor formation observed among the groups. These data indicate that the diets containing fish oil were not protective in the final incidence of tumor formation and suggest that a better understanding of the complex interactions is warranted before recommendations are made to alter the human diet for cancer prevention.
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PMID:Lack of a protective effect of menhaden oil on skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate. 240 Oct 54


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