Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been reported that twice-weekly i.p. injections of 4 mg phorbol for 10 weeks, after a single feeding of 6 mg dimethylbenz(a)anthracene (DMBA) in female Wistar rats, led to a significant augmentation of mammary adenocarcinoma incidence and of lymphatic leukemia incidence as compared to 6 mg DMBA alone. In an experiment reported here, in female Sprague-Dawley rats, using the same doses of DMBA and phorbol and the same injection schedule, phorbol given after DMBA did not augment mammary adenocarcinoma incidence or lymphatic leukemia incidence as compared to DMBA given alone. It thus appears that there is a strain-related sensitivity between Wistar and Sprague-Dawley rats with regard to the promoting activity of phorbol when phorbol treatment follows DMBA treatment, and mammary adenocarcinoma incidence and lymphatic leukemia incidence are studied. Further, in Sprague-Dawley rats, phorbol did not promote mammary fibroadenoma incidence in DMBA-treated rats, mammary adenocarcinoma incidence in procarbazine-treated rats, and mammary adenocarcinoma incidence or mammary fibroadenoma incidence in X-ray-treated rats. DMBA and procarbazine, with or without phorbol, tended to induce more mammary neoplasms in the anterior (thoracic) than in the posterior (abdominal) mammary glands. X-irradiation tended to induce mammary neoplasms in approximately equal numbers in the anterior and posterior mammary glands. It was suggested that regional differences in chemically induced mammary carcinogenesis were due to a difference in the transport and delivery of the chemical carcinogens to the regions rather than a difference in the amount of mammary gland tissue in the regions. An analysis of the numbers of Sprague-Dawley rats that developed either no mammary neoplasms, or only mammary adenocarcinomas, or only mammary fibroadenomas, or both mammary adenocarcinomas and mammary fibroadenomas in response to DMBA, procarbazine, and X-ray, suggested that the development of a mammary adenocarcinoma or the development of a mammary fibroadenoma are independent processes.
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PMID:Apparent rat strain-related sensitivity to phorbol promotion of mammary carcinogenesis. 11 89

An epidemiologic study of clear cell vaginal adenocarcinoma in young women (15-22 years old) showed an apparent association with maternal ingestion of diethylstilbestrol (DES) during 1st trimester pregnancy. In 1971, a Registry of Clear Cell Adenocarcinoma of the Genital Tract in Young Females was established, and shortly thereafter the Food and Drug Administration warned that DES and chemically related nonsteroidal estrogens were contraindicated during pregnancy. DES-exposed females have a 0.14 to 1.4/1000 risk of developing adenocarcinoma of the cervix/vagina by age 24. Diagnoses of these cancers usually are made in girls between the age of 14 and 23 years with peak incidence at age 19; data further shows that DES is an incomplete carcinogen and that additional factors contribute to its carcinogenesis. About 20% of DES-exposed women will have a deformity of the upper vagina/cervix, and approximately 95% will have abnormal columnar epithelium on the cervix/upper vagina. 75% of patients whose mothers were exposed to DES in utero during the 8th week of gestation or earlier will have vaginal adenosis; 7% will have this finding if the mother's exposure occurred after the 17th week. Recent reports also indicate a high incidence of abnormalities in the uterus/oviducts associated with gross changes in the upper vagina/cervix. Asymptomatic girls who had DES exposure in uteru should have a complete annual pelvic examination at menarche or by age 14 years. Younger girls who develop abnormal vaginal bleeding/discharge should also have a periodic thorough examination and Pap smear, as well as palpation of the entire length of the vagina/cervix. So far, cervical/vaginal adenocarcinoma has been diagnosed at initial examination, with the ratio of vaginal to cervical adenocarcinoma being almost 2:1. There is no standard therapy yet for adenocarcinoma of young women. Treatment is on a case to case basis, and prognosis depends on the stage of the disease when diagnosed.
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PMID:Congenital diethylstilbestrol-associated vaginal/cervical adenosis (DES babies). 15 73

In the past few years there have been a number of reports correlating a high frequency of herpes simplex virus type 2(HSV-2) infection with lesions of the uterine cervix. These studies have used a clinical history of herpetic infection or the demonstration of herpetic antibodies in the cancer patients. The present study was performed to evaluate any possible carcinogenic activity of the formalin-inoculated herpes simplex virus type 2 in the reproductive tract of the female mouse. This approach to the study was selected because of previous experience with a model system of carcinogenesis of the cervix uteri using coal tar hydrocarbons. Cytologic and histologic preparations from experimental animals and controls are presented to demonstrate the mucosal alterations and tumors observed in the animals. Noninvasive lesions of the cervix were identified in 76.8% and invasive adenocarcinoma detected in 30.2% of the mice.
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PMID:Cervical carcinogenesis with herpes simplex virus, type 2. 16 21

We find that colonic adenocarcinoma, which is an extremely rare neoplasm of all animals except man and carcinogen-treated rodents, occurs spontaneously in some marmosets. The cotton-topped Saguinus oedipus oedipus is particularly prone to develop it, but we have found it also at necropsy in Callimico goeldii (Goeldi's marmoset). Numerous metastases to regional lymph nodes develop. The cancers arise de novo in the mucosa and early invade the submucosa and lymphatic apparatus and paracolonic lymph nodes. These findings and the continuing occurrence of this cancer in our colony suggests that the marmoset may be the long-sought primate model for experimental intestinal carcinogenesis.
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PMID:Spontaneous colonic adenocarcinoma in marmosets. 41 16

Carcinogenicity of phenacetin was tested using Sprague-Dawley rats. Two groups of animals containing 50 males and 50 females per group were fed respectively with 2.5% and 1.25% phenacetin diet for 18 months and fed thereafter with basal diet for 6 months. Control animals containing 65 males and 65 females were fed with basal diet for 24 months. Animals surviving more than 24 months were regarded as effective animals and killed. Rats that died of tumor development within 24 months were also regarded effective animals. Every organ from the killed and dead animals was fixed in 10% formaldehyde solution and examined histopathologically. Effective number of rats was 27 males and 27 females in 2.5% phenacetin feeding group, and 22 males and 25 females in 1.25% phenacetin feeding group. In control group, 19 males and 25 females were effective. Neoplasms including spontaneous tumors were detected in 26 out of 27 males (96.3%) and 21 out of 27 females (77.8%) of 2.5% phenacetin feeding group, and in 20 out of 22 males (90.9%) and 19 out of 25 females (76.0%) of 1.25% phenacetin feeding group. In control group, 1 out of 19 males (5.3%) and 6 out of 25 females (24.0%) showed spontaneous tumor development. Histopathologically, carcinomas of the nasal cavity, such as adenocarcinoma, squamous cell carcinoma, and transitional cell carcinoma, and the urinary passage, as renal cell carcinoma of the kidney pelvis, and transitional cell carcinoma of the urinary bladder, were most conspicuous, suggesting the target organs of phenacetin carcinogenesis. Males showed higher tumor incidence compared to females. The higher the concentration of phenacetin given, higher incidence of tumors was observed.
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PMID:Tumors of Sprague-Dawley rats induced by long-term feeding of phenacetin. 44 75

Characteristic red cell deformation, echinocytosis peculiar to mammary tumour susceptible C3H mice, were revealed by a comparative study of erythrocytes in animals with a different natural resistance to spontaneous carcinogenesis. 58.6% of spiny red cells was found at the early latent period (at the age of 3-4 months) and reached 91.1% at the late latent period (at the age of 11-12 months). In the blood of intact C57BL/6 mice resistant to mammary carcinogenesis, at the same ages the echinocyte count ranged from 16.0 to 18.7%. The tumour growth (spontaneous tumour in C3H mice and transplantable Ehrlich adenocarcinoma in C57BL/6 mice was accompanied by an increase in the echynocyte count and in the expression of echinocytosis (up to 96.6 and 65.3%, respectively). Possible pathogenetic mechanisms of echinocytosis in carcinogenesis are discussed.
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PMID:[State of the erythrocyte surface (echinocytosis) in experimental carcinogenesis]. 45 24

Epidemiologic, clinical and pathologic data on all cases of clear cell adenocarcinoma of the genital tract in women born in 1940 and later are collected by the Registry for Research on Hormonal Transplacental Carcinogenesis. Other cases of genital cancer are also recorded if there is a history of prenatal hormone exposure. Evidence strongly suggest a mullerian nature for clear cell adenocarcinomas. Of the 333 cases accessioned between 1970 and 1976, about 2/3 of the completely investigated cases had histories of prenatal exposure to stilbestrol (DES) or similar compounds. Estimated risk of clear cell adenocarcinoma ranges from 0.14 to 1.4 per 1000 DES-exposed, with age-incidence peaking at age 19. Cytology and a thorough pelvic examination are important tools for accurate diagnosis. Surgery and radiation are used to treat these tumors, but follow up in most cases has been limited to 5 years. Several cases of small or superficial tumors have been observed to spread to regional pelvic nodes, with recurrences in the lungs or supraclavicular areas. For inquiries, contact the Registry for Research on Hormonal Transplacental Carcinogenesis, 5841 S. Maryland Ave., Chicago, Ill 60637. Analysis of pathologic specimens should be directed to Robert E. Scully, MD, Dept of Pathology, Massachusetts General Hospital, Boston, Mass 02114.
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PMID:DES-associated clear cell adenocarcinoma of the vagina and cervix. 52 31

The association between mammary carcinogenesis induced by 7,12-dimethylbenz(alpha)anthracene (DMBA) in the rat, the influence by manipulations of its hepatic metabolism and the secretion of prolactin has been investigated. Various test compounds: coumarin, 4-methylcoumarin, phenobarbital and CCl4 all elevated serum prolactin level, but only coumarin and 4-methylcoumarin reduced tumor incidence. These observations do not support the assumption that the suppression of DMBA-induced breast adenocarcinoma by coumarin and 4-methylcoumarin is mediated via prolactin.
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PMID:Is there any association between elevated serum prolactin level and mammary adenocarcinoma induced by 7,12-dimethylbenz(alpha)anthracene. 80 60

Weaning male and female C3HAvyfB mice were fed a low-fat (4.5%) diet until they were 60-70 days of age when they were fed high-fat (18.6%) diets containing either sunflower-seed oil (polyunsaturated fat diet) or tallow (saturated fat diet). After receiving either of the high-fat diets for 4 weeks, each mouse received an inoculum of approximately 1,700 single cells from a transplantable mammary adenocarcinoma. The cumulative incidence of tumor-bearing mice was significantly greater among both males and females fed the polyunsaturated fat diet than among males and females fed the saturated fat diet. The mean times elapsed before palpable tumors developed were less when mice were fed the polyunsaturated fat diet than when mice were fed the saturated fat diet, but these differences were not statistically significant. The cumulative incidence of tumor-bearing mice was also significantly greater among females than males. The results supported the suggestion from previous work in this laboratory that the polyunsaturated fat diet exerts its effect on the promotional stage of carcinogenesis rather than on the initial event of neoplastic transformation.
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PMID:Effect of dietary polyunsaturated fat on the growth of a transplantable adenocarcinoma in C3HAvyfB mice. 83 68

Invasive adenocarcinoma of the glandular stomach was induced in 3 BIO 87.20 inbred Syrian hamsters by the administration of 1 ppm N-nitrosodiethylamine or N-nitrosodimethylamine in the drinking water, and in 2 BIO 15.16 and 5 BIO 72.29 inbred Syrian hamsters by gavage of 3-methylcholanthrene. In contrast, many other similarly treated inbred Syrian hamster lines did not develop carcinoma of the glandular stomach. The glandular stomachs of rats and mice are resistant to polycyclic hydrocarcon carcinogenesis; however, the glandular stomachs of certain inbred Syrian hamsters develop adenocarcinoma after polycyclic hydrocarbon gavage. This work demonstrated the importance of genetic factors.
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PMID:Adenocarcinoma of the glandular stomach following 3-methylcholanthrene, N-nitrosodiethylamine, or N-nitrosodimethylamine feeding in carcinogen-susceptible inbred Syrian. 100 97


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