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)

The spectrum of progestin therapy has changed and expanded during the last few years. 1. The drug-therapy of choice in endometriosis is the medication of progestins for at least six months, for instance ethinyl-testosterone. If a patient wants additional children the "more gentle" dydrogesterone should be considered. 2. In the treatment of dysmenorrhea combination pills should be given, sequentials should be avoided. In the case of incompatibility of estrogens or in danger of oversuppression syndrome dydrogesterone should be applicated. 3. Dysfunctional bleedings should lead to an intense search for their cause. The treatment consists in an estrogen-progestin combination for 9 days and in cyclic continuation of this therapy for at least a further three months. In the case of hemorrhagic diathesis progestin treatment should be continued. 4. Cyclic adequate progestins have proofed to be successful in handling of hirsutism. The choice of the preparation depends on the patient's wish for children. 5. The progestin test is still the first step in diagnosis of amenorrhea. 6. Progestin therapy is indicated in progressive endometrial carcinoma. Some medical centres treat carcinoma of the mamma successfully with progestins. 7. Nowadays fast and early hormonal pregnancy tests are available. The progestin-pregnancy-test is limited to cases of premenopause. 8. The so-called short luteum phase has received considerable attention as a possible cause of infertility. In these cases a substitutional therapy of progestins should follow. Clomiphene or HCG-therapy is advisable. In short luteum phase and premenstrual spottings potent progestins should be given. 9. High dosage of progestins are in common use in the treatment of abortus imminens. 10. Combination pills and sequentials are widely used, the possible methods of a pure progestin contraception are: minipills, three-month-injections, implanted silastic capsules with progestional compounds, progestin impregnated intrauterine devices, vaginal silastic rings impregnated with progestional compounds. 11. Carcinogenesis of progestins was not detectable. 12. Some progestins are teratogenic.
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PMID:[Current status of gestagen administration. 2. Gestagen therapy in the area of reproduction]. 55 11

Ganciclovir (9-(1,3-dihydroxy-2-propoxymethyl) guanine, DHPG) is an acyclovir analog with excellent antiviral activity against human cytomegalovirus (CMV). Clinically, CMV infection occurs in from 60 to 90% of all renal transplant recipients and it is responsible for significant patient morbidity and graft loss. The likelihood of infection is closely related to the CMV status of both donor and recipient, with the greatest risk arising in the combination of a seronegative patient receiving a seropositive organ. Intracellularly, DHPG is converted to DHPG-triphosphate, which competitively inhibits DNA polymerase. This conversion is accelerated up to 10-fold in virally infected cells, providing some selectivity of action. Uncontrolled studies demonstrated DHPG efficacy in CMV disease, but experience in children remains limited. Although bone marrow suppression is a major immediate toxicity, long-term concerns about carcinogenesis and infertility mandate careful patient selection. Recently at the University of Minnesota, 93 solid organ recipients (45 renal transplants) including some children have been treated for tissue-invasive CMV with DHPG. All had a characteristic clinical picture and either a positive CMV culture or a biopsy with CMV inclusions. The patients received i.v. DHPG (10 mg/kg/day) with appropriate adjustments for renal function. In renal allograft recipients, 89% recovered within 30 days, although 21% had to be retreated with DHPG. Although no patient died, allograft survival was significantly reduced (P = 0.02). An additional subgroup of patients (N = 18) who had both biopsy-proven rejection and invasive CMV disease were simultaneously treated for both processes. All of these patients recovered from their CMV infection, but two grafts were lost to rejection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use of ganciclovir for cytomegalovirus infection. 132 40

Forty-four patients with relapsed or resistant Hodgkin's disease were treated with adriamycin 40 mg m-2 i.v. on day 1, vincristine 1.4 mg m-2 i.v. on days 1 and 8, prednisolone 40 mg m-2 orally daily for 8 days, etoposide 200 mg m-2 orally daily for 4 days according to the nadir white cell count, and bleomycin 10 mg m-2 i.v. days 1 and 8 (HOPE-Bleo). Median age was 27 (range 12-71). When stage was considered according to all sites currently or previously involved by Hodgkin's disease (cumulative stage) 26 patients (59%) had stage IV, 13 (29%) stage III and five (11%) stage II disease; 33 (75%) had B symptoms. All patients had received previous chemotherapy and 18 (41%) had received two or more regimens. Twenty-six patients (59%) achieved CR and 10 (23%) PR; the median duration of CR was 22 months and median survival for all patients was 48 months. Eight patients remain in continuous CR; none of these had received extensive previous chemotherapy. Among the 19 patients who had relapsed from CR achieved by a single previous chemotherapy regimen, six (32%) achieved long CR on HOPE-Bleo. The regimen was generally well tolerated but the principal toxicity was myelosuppression. There were two toxic deaths, one due to neutropenic sepsis and the other due to acute peritonitis. The HOPE-Bleo regimen is an effective treatment for relapsed or resistant Hodgkin's disease, with a low probability of carcinogenesis and infertility. These factors suggest that HOPE-Bleo deserves further evaluation as primary treatment for Hodgkin's disease and very careful selection of relapsed patients for high dose salvage chemotherapy with bone marrow transplants must be exercised.
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PMID:Etoposide and adriamycin containing combination chemotherapy (HOPE-Bleo) for relapsed Hodgkin's disease. 169 23

The present study investigated the problem of whether or not the intake of an Western-style diet will induce within the host a specified hormonal change that increases the risk for breast cancer (BC). The key observations obtained are as follows: 1) The risk for BC in Japan has been increasing for the last 20 years in parallel with the Westernization of dietary habits (increase of fat and animal protein in the diet). 2) A Japanese BC patient is distinguishable from a corresponding normal control by (a) an increase of waist/hip ratio (more specifically, an increase of abdominal fat) and (b) a decrease in the number of live births (relative infertility). Height, weight and height-adjusted weight all cannot distinguish the former from the latter. 3) The former is also distinguishable from the latter by dual steroidal disorders of ovarian dysfunction (progesterone depression) and hypercorticoidism, as revealed by a case control comparison of urinary steroid excretions. 4) The long-term maintenance of an experimental mouse on a fat-rich diet increased abdominal fat weight at an adult age, but not at a young age. 5) In the same experiment, the fat-rich diet produced a reduction of plasma progesterone at an early stage, and also produced dual changes of progesterone depression and corticosterone stimulation at a late stage of experiment. Plasma estradiol was little affected by an excess of dietary fat. 6) In an adult mouse, the weight of abdominal fat was increased by corticosterone treatment and was decreased by estradiol treatment. The suppressive effect of estradiol on abdominal fat weight was dose-dependent. In conclusion, our findings seem to suggest the possibility that a fat rich diet may produce dual steroidal disorders of ovarian dysfunction and hypercorticoidism which in turn will open the way to breast carcinogenesis by activating 2 proto-oncogens at the initiation and promotion steps.
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PMID:Nutrition and breast cancer risk in Japan. 206 29

The present study investigated the relation between the reproductive activity and the risk for cervical and endometrial cancers using both domestic and international materials. An association of increased risk for cervical cancer (C) with fertility at the levels of both an individual and a population was contrasted to another association of increased risk for endometrial cancer (E) with infertility at the same two levels. Both C and E patients experienced a delay of menstrual cycle (over 30 days) at high incidences (35-49%), whereas healthy controls and breast cancer patients were essentially free from such menstrual delay. The possible impact of the above hormonal characteristics of C and E patients on uterine carcinogenesis is discussed in the light of comparative endocrinology.
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PMID:Reproductive activity is a magic spell to connect the genesis of cancers of the uterine cervix and endometrium. 262 38

The mechanisms of carcinogenesis are not known in detail, but there is strong evidence that cancer usually arises from a single transformed cell. Hence, although the process of carcinogenesis appears to require a multiplicity of changes in the affected cancer-forming cell, such as may be associated with successive stages of tumour initiation, tumour promotion, and tumour progression, only one such change induced by radiation in an appropriate cell may be conceived to increase the probability of neoplasia in a suitably susceptible individual. For this reason, carcinogenic effects of radiation, like mutagenic effects of radiation, are considered for purposes of radiological protection to have no threshold and to behave as stochastic phenomena. In contrast, certain other effects of radiation, such as cataract of the lens, infertility, and depression of the bone marrow, require the killing of many cells in the affected organs. Thus, they vary in severity with the extent of cell loss and have thresholds of detectability which depend on the sensitivity with which the consequences of cell loss can be measured.
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PMID:Cancer induction and non-stochastic effects. 354 59

Between January 1980 and March 1983, data were collected to evaluate risk factors for breast cancer in a case-control study based on 368 women with breast cancer admitted to the General Hospital of Pordenone (a district in North Eastern Italy with a particularly high breast cancer mortality rate), and 373 age-matched controls. Nulliparity or low parity, late age at first birth and later menopause were associated with an increased risk of breast cancer. The elevated risk associated with nulliparity could be almost completely explained by marital status, thus pointing to a specific protection given by parity, rather than some putative influence of infertility or subfertility in breast cancer cases. Likewise, risk did not vary materially according to history of abortions when marital status was controlled for. Increased risk associated with later age at first birth, on the other hand, was not accounted for by marital status or parity. The population studied, though frequently multiparous, showed late average at first birth: this might, at least partly, explain its high mortality rate from breast cancer. The risk estimate was higher if menarche occurred below age 15; however, there was no evidence of a trend for the relative risk to rise with lower age at menarche. The use of oral contraceptives or other female hormones (such as oestrogen replacement therapy) did not appear to be related to the risk of breast cancer. The role of the major menstrual and reproductive variables considered (age at menarche, parity, age at first birth) was apparently stronger in pre-menopausal women, thus suggesting an influence of these factors (and possibly, their hormonal correlates) on one of the latter stages of the process of carcinogenesis.
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PMID:Reproductive and hormonal factors and breast cancer in a Northern Italian population. 398 43

To clarify the role of marital status in human carcinogenesis, a 1968 Cancer Institute study analyzed the cancer mortality experience of 31,658 white Catholic nuns from 41 religious orders in the U.S. from 1900-1954. The national white female population was used for cause-specific comparison and both groups were assigned cohorts depending upon the year of birth. When examined by 10-year age groups, rates for cancer at all sites was generally lower for nuns than for controls aged 59 or 69 but were substantially higher at older ages. Postmenopausal nuns (aged 69 and over) displayed a higher rate (38.6%) of cancer of the large intestine than did controls (22.6%) but had a lower proportion of deaths from cancer of the biliary passages and liver (13.0% vs. 22.6%). Nuns displayed a striking excess in breast cancer mortality over the age span of 40-74 years and had consistently higher rates than controls for each age group above 39 years. Lower cervical cancer rates for nuns (10.8%) than for controls (56.6%) seemed related to coital factors. Cancer of the uterus accounted for 63% of the genital cancer deaths among sisters. Overall, the genital cancer mortality rates for nuns were consistent with high mortality rates for the single, white female population of the U.S. The increased risk of breast cancer and cancers of the corpus uteri and ovary would seem to reflect an established link with infertility. Combination of these factors with the excess incidence of cancer of the large intestine among postmenopausal nuns suggests a common pathogenic mechanism of a hormonal nature operating in some women.
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PMID:Cancer mortality among nuns: role of marital status in etiology of neoplastic disease in women. 577 91

Advances in the treatment of Hodgkin's disease in the last 20 years have led to a marked improvement in survival but also to a significant increase in treatment-related complications. Infertility, growth disturbance and carcinogenesis have attracted well deserved attention. This paper reviews the thyroid complications of treatment since these are important to patient and clinician and if missed may result in unnecessary morbidity.
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PMID:Thyroid damage--after treatment for Hodgkin's disease. 634 93

Dietary phytoestrogens have been implicated in infertility among ruminants and may relate to human breast cancer risk. Formononetin is an isoflavonoid phytoestrogen found in animal fodder and in certain human foodstuffs. To investigate a possible mechanism by which phytoestrogens might influence mammary carcinogenesis, this study examined the capacity of formononetin to stimulate mammary gland proliferation. Formononetin was administered to castrated female BALB/c mice by daily subcutaneous injection; then mammary gland proliferation and estrogen receptor expression were quantified, and plasma prolactin levels were measured. A preliminary dose-finding study demonstrated an estrogenic effect on vaginal cytology when formononetin was injected at 40 mg/kg sc. Peak plasma concentrations of 2.5 +/- 0.8 (SD) micrograms/ml at two hours and peak mammary tissue concentrations of 2.0 +/- 0.2 ng/mg tissue at four hours were noted after a single injection at this minimally bioactive dose. Among animals treated with formononetin at 40 mg/kg/day for five days, mammary gland proliferation was enhanced 3.3-fold over saline-treated controls and was comparable to that of animals treated with estradiol-17 beta at 1 microgram/kg/day for five days. Mammary tissue estrogen receptor expression was 2-fold higher among the formononetin-treated animals (P < 0.01 vs. saline-treated controls), and plasma prolactin concentrations were increased 1.7-fold (P < 0.001 vs. saline-treated controls). In subsequent in vitro binding studies, formononetin competitively bound murine mammary estrogen receptors, but with a relative binding affinity 15,000 times less potent than that of estradiol-17 beta. The results demonstrate an ability of formononetin to support mammary gland proliferation. However, the estrogenic potency of formononetin appears extremely weak compared with that of estradiol-17 beta and is roughly proportional to estrogen receptor-binding capacity.
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PMID:Proliferative response of mammary glandular tissue to formononetin. 764 82


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