Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of dietary manipulations on fatal neoplasms in male Fischer 344 rats was assessed. Particular attention was paid to leukemia and pituitary adenoma because they are the most common potentially fatal neoplasms that occur in this rat strain. The only dietary manipulation which depressed the mortality rates due to neoplastic disease was that involving a reduction in energy intake. Reduction of mineral or protein or fat intake without a reduction of energy had, at most, marginal effects on fatal neoplastic disease.
 ...
PMID:Influence of diet on fatal neoplastic disease in male Fischer 344 rats. 183 25

A case of malignant astrocytoma following radiotherapy for pituitary adenoma is presented in detail with a review of the literature. A 38 year-old housewife had developed a growth-hormone secreting pituitary adenoma, and received a total of 50 Gy at the pituitary region. Four years and six months later, she began suffering headache and vomiting. Computed tomography showed an extensive low density with ring enhancement in the right temporal region, corresponding to the previously irradiated field. A right frontotemporoparietal craniotomy was carried out, and a soft and reddish tumor was partially removed. The histological diagnosis was that of malignant astrocytoma. The patient was submitted to postoperative radiochemotherapy, receiving a total of 60 Gy, nimustine hydrochloride (ACNU), and tegafur (FT). Subsequently, after three months of clinical relief, she developed tumor regrowth, and died four months later. The present case fulfills the criteria for radiation-induced tumor established by Cahan et al.: A tumor location within irradiated area, no evidence of tumor prior to radiotherapy, a long latency period between radiation and tumor occurrence, and histological verification of the tumor. Thirty-nine cases of radiation-induced gliomas including the present case have been reported in the literature. It is noteworthy that the majority occur in the younger age bracket. Male preponderance is noted as it is in primary cerebral gliomas. The primary lesions for radiation frequently include leukemia and lymphoma. Craniopharyngioma, pituitary adenoma, and medulloblastoma etc are also included.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Malignant astrocytoma following radiotherapy in pituitary adenoma: case report]. 268 39

The age-related incidence of spontaneously occurring neoplastic and non-neoplastic lesions in untreated F-344/Jcl rats, used as controls in carcinogenicity testing, were studied from the histological examination of tissues from 469 males and 354 females. The incidence of spontaneous tumors was 83.2% in the males and 71.2% in the females. The most common neoplasms were leukemia (males: 24.3%, females: 24.0%), pituitary adenoma (males: 16.0%, females: 45.2%), pheochromocytoma (males: 14.7%, females: 7.3%), testicular interstitial cell tumor (males: 79.1%), and uterine endometrial stromal polyp(females: 16.4%). The incidence of other tumors of almost all the organs and/or tissues was low. Non-neoplastic lesions generally increased with advancing age of the animals.
 ...
PMID:Spontaneous tumors in F-344/Jcl rats. 281 Apr

The types and incidences of spontaneous tumors in F344/DuCrj rats were examined in 960 males and 959 females served as the control groups of separate twelve 2-year chronic and oncogenicity studies carried out during a 1978-1983 period. The major tumors occurred at more than 5% incidence were leukemia (mononuclear cell), testicular interstitial cell tumor, preputial gland adenoma, pituitary anterior adenoma, thyroid C-cell adenoma, adrenal pheochromocytoma and subcutis fibroma for males, and leukemia, uterine endometrial polyp, pituitary anterior adenoma, thyroid C-cell adenoma and mammary gland adenoma/fibroadenoma in females. Analyses on age-related occurrence of tumors revealed that the incidences of most of the major tumors in males attained already to the plateau between 85 and 97 weeks of age while those in females showed a steep rise during the last interval of observation, 98 to 110 weeks of age. An intralaboratory heterogeneity in incidence was observed in the thyroid C-cell adenoma and the adrenal pheochromocytoma for males, and the anterior pituitary adenoma for females.
 ...
PMID:Spontaneous tumors in F344/DuCrj rats from 12 control groups of chronic and oncogenicity studies. 362 7

Hemorrhage from brain tumor was confirmed clinically, surgically, or on autopsy in 94 of 1861 cases (5.1%) treated during the past 18 years: 49 of 311 pituitary adenomas (15.8%) and 45 of 1550 other brain tumors (2.9%). The higher incidence of hemorrhage from pituitary adenoma was statistically significant (p less than 0.001). In brain tumors other than pituitary adenoma, the incidence of hemorrhage was significantly higher in the patients under 14 years old (17 of the 322 cases, 5.3%) than in the patients over 15 years old (28 of the 1228 cases; 2.3%) (p less than 0.001). Nineteen patients showed no evidence of clinical symptoms related to bleeding. Twenty-six patients had a definite history of an acute episode that suggested sudden bleeding. In 11 of these, the apoplectic syndrome was the initial presenting symptoms. The incidence of hemorrhage was not statistically correlated with sex. The hemorrhage was intratumoral in 30 cases, intracerebral in 7, subarachnoid in 7, and subdural in 1. The tumors were supratentorial in 36 cases, pineal in 1, and infratentorial in 8. Primary and metastatic choriocarcinoma and primary embryonal carcinoma seemed to cause hemorrhage most frequently. The following precipitating factors were found in 7 of the 17 patients aged under 14: ventricular drainage in 2, ventriculoperitoneal shunt in 2, carotid angiography in 1, head injury in 1, and leukemia in 1. Seven of the 17 patients under 14 years old died of massive bleeding from the tumor. Unless there is evidence of vascular disease such as cerebral aneurysm, vascular malformation, or hypertensive cerebrovascular disease, intracranial hemorrhage should be suspected of being due to a brain tumor.
 ...
PMID:Spontaneous intracranial hemorrhage caused by brain tumor: its incidence and clinical significance. 709 93

CT and MR imaging findings of 57 sphenoidal masses were retrospectively reviewed to assess the possibility of differential diagnosis between them. Various kinds of masses such as pituitary adenoma, epipharyngeal cancer, mucocele, chordoma, chondroma, chondrosarcoma, distant metastasis, multiple myeloma, fibrous dysplasia, craniopharyngioma, hemangiopericytoma, giant cell tumor, primary sphenoidal cancer, malignant melanoma, leukemia, histiocytosis X, and giant cell tumor were included in this series. CT scanning was performed in all cases, while MR images were obtained in 48 cases using a spin-echo pulse sequence. The relative density of the masses, bony changes and calcification were evaluated on CT, and on MR images, signal intensity of the masses relative to the normal gray matter, contrast enhancement and extension/contour were evaluated. Although no single feature appeared to be specific to the masses, detection of calcification on CT, identification of the normal pituitary gland as deformed or displaced on T1-weighted images, signal intensity on T2-weighted images, and extension of the masses seemed to be useful and should be examined in terms of their ability to assist in differential diagnosis. Finally, accommodative classification of sphenoidal masses primarily based on presumed origin or mode of extension was attempted.
 ...
PMID:[CT and MR imaging findings of sphenoidal masses]. 807 65

The influence of dietary components on the occurrence of, and mortality from spontaneous neoplasms in male F344 rats was investigated. The dietary regimens studied included restriction of specific dietary components (energy, fat, protein and mineral), as well as different sources of dietary protein (casein, soy protein and lactalbumin). A statistical approach based on contributing causes of death was used to obtain the mortality due to all neoplasms, and the relative onset rate of frequently observed neoplasms, e.g., leukemia, pituitary adenoma, testicular interstitial cell tumor, etc. Only the regimen involving energy restriction reduced the mortality due to all neoplasms. Neither reduction of individual components without energy restriction, nor replacement of casein with soy protein or lactalbumin as the protein source affected mortality. Analyses of the relative onset rate of selected neoplasms also indicated that only a reduction of energy intake suppressed the occurrence of most of these neoplasms. Other dietary regimens, at most, suppressed a few types of neoplasm. It is concluded that a reduction in energy intake is a key dietary factor for the prevention of neoplastic diseases in rats.
 ...
PMID:Influence of dietary components on occurrence of and mortality due to neoplasms in male F344 rats. 890 55

A 70-year-old woman developed a glioblastoma in the irradiated field 7 years after stereotactic radiosurgery for meningioma. Glioma induction has been previously reported after external beam radiation for leukaemia, pituitary adenoma, tinea capitus, and meningioma. This radiosurgery-induced malignancy may portend further reports of tumour induction. The theoretical risk of tumour induction by low doses of radiation to normal neural tissue after radiosurgery is now confirmed. Reports of additional cases of radiosurgery-induced tumours might temper the use of this increasingly used technique for benign surgically accessible lesions.
 ...
PMID:Glioblastoma induction after radiosurgery for meningioma. 1126 87

Diethylphthalate and dimethylphthalate are used as phthalate plasticizers, in an extensive array of products. The chronic dermal toxicity of diethylphthalate was evaluated in male and female F344/N rats and B6C3F1 mice in 2-year studies. In a series of special studies, the tumor initiation or promotion potential of diethylphthalate or dimethylphthalate was evaluated in male Swiss (CD-1(R)) mice by an initiation/promotion model of skin carcinogenesis. The genetic toxicity of diethylphthalate and dimethylphthalate in Salmonella typhimurium and cultured Chinese hamster ovary cells was also evaluated. 4-WEEK STUDY IN F344/N RATS: Groups of 10 male and 10 female rats were dermally administered diethylphthalate at volumes of 0, 37.5, 75, 150, or 300 &mgr;L (0, 46, 92, 184, or 369 &mgr;g) applied neat, 5 days per week for 4 weeks. All male and female rats survived to the end of the study. No evidence of dermatotoxicity was observed, with no adverse clinical signs observed and no effects on weight gain or feed consumption. Relative liver weights of 300 &mgr;L males and females and 150 &mgr;L females were greater than those of controls. Relative kidney weights of 150 and 300 &mgr;L males and 150 &mgr;L females were greater than those of controls. No other adverse effects were observed in this study. 4-WEEK STUDY IN B6C3F1 MICE: Groups of 10 male and 10 female mice were dermally administered diethylphthalate at volumes of 0, 12.5, 25, 50, or 100 &mgr;L (0, 15, 31, 62, or 123 &mgr;) applied neat, five days per week for 4 weeks. One control female died before the end of the study; all other mice survived. No evidence of dermatotoxicity or other adverse clinical signs were observed, and no clear adverse effects on weight gain or feed consumption were seen. Absolute and relative liver weights of 25 and 100 &mgr;L females were greater than those of the controls. Based on these 4-week study results, doses of 0, 35, and 100 &mgr;L diethylphthalate were recommended for the 2-year mouse studies. A chronic study in male and female B6C3F1 mice at 0, 35, and 100 &mgr;L (applied neat, once per day, 5 days per week) was started and subsequently stopped after 32 weeks when significant body weight reductions were noted in treated animals (males and females, 100 &mgr;L groups: 19% lower; males, 35 &mgr;L group: 12% lower; females, 35 &mgr;L group: 10% lower than controls). Based on these body weight reductions, doses of 0, 7.5, 15, and 30 &mgr;L in 100 &mgr;L acetone were recommended for the restart of the 2-year mouse study. 2-YEAR STUDY IN F344/N RATS: Based upon the results of the 4-week study, doses of 0, 100, or 300 &mgr;L diethylphthalate (0, 123, or 369 &mgr;) were chosen for the 2-year rat study. Groups of 60 male and 60 female rats received the doses applied neat 5 days per week for 103 weeks and up to 10 animals per group were evaluated after 15 months. Survival, Body Weights, and Clinical Findings: Survival of dosed rats during the first 15 months was similar to that of controls. However, 2-year survival was significantly reduced in all groups of male rats (survival probabilities, males: 0 &mgr;L, 8%; 100 &mgr;L, 12%; and 300 &mgr;L, 12%). The mean body weights of 300 &mgr;L males were slightly less than those of the controls throughout the study. No adverse clinical signs were observed, including no evidence of dermatotoxicity. Pathology Findings: No morphological evidence of dermal or systemic toxicity was observed in male or female rats. Skin neoplasms were not observed in female rats and were only rarely observed in male rats. A high incidence of anterior pituitary adenoma occurred in all groups of male and female rats. The incidence of anterior pituitary adenomas in the 0, 100, and 300 &mgr;L groups were: males, 39/44, 41/49, 41/49; females, 38/50, 33/49, 33/48. The incidence of this benign tumor in control males (84%) exceeded the historical control mean incidence [feed controls, (28.7%)] and range (12% to 60%). Anterior pituitary adenomas were considered a primary contributing factor in the increased mortality observed in all grtor in the increased mortality observed in all groups, regardless of treatment. A dose-related decreasing trend in the incidence of mammary gland fibroadenomas was observed in female rats (21/50, 12/48, 7/50). The incidence of mononuclear cell leukemia in male rats in this study was lower than the historical incidence and may be attributable to the shortened life span of male rats. Similarly, the incidence of interstitial cell tumors of the testes was markedly decreased in all groups of males (4/50, 3/50, 8/50), relative to historical control rates (90.1%; range 74%-98%). The incidence of fatty liver degeneration was notably lower in dosed rats than in controls (males: 26/50, 8/50, 4/51; females: 23/50, 11/50, 3/50). 2-YEAR STUDY IN B6C3F1 MICE: Groups of 60 male and 60 female mice received doses of 0, 7.5, 15, or 30 μL diethylphthalate (0, 9, 18, or 37 μ) in 100 μL acetone 5 days per week for 103 weeks with a 1 week recovery period, and up to 10 animals per group were evaluated after 15 months. Survival, Body Weights, and Clinical Findings: Two-year survival of dosed mice was similar to that of controls: 43/50, 41/48, 46/50, and 43/50 (males), and 41/50, 38/51, 37/49, and 36/49 (females). Mean body weights of dosed male and female mice were similar to those of the controls throughout the study. No adverse clinical signs were observed in mice, including no gross evidence of dermatotoxicity. Feed consumption by male and female mice was similar to or up to 13% greater than that by controls. Pathology Findings: No morphological evidence of dermal toxicity was observed in male or female mice. No skin neoplasms were observed in dosed male mice. In female mice receiving 30 μL, one squamous cell carcinoma and one basal cell carcinoma were seen at the site of application. An increased incidence of liver neoplasms was observed in dosed male and female mice. The incidence of hepatocellular adenoma or carcinoma (combined) in B6C3F1 mice in the 0, 7.5, 15, and 30 μL groups were: (males) 9/50, 14/50, 14/50, and 18/50; (females) 7/50, 16/51, 19/50, and 12/50. The incidence of adenoma or carcinoma (combined) was increased in 30 μL male mice and the incidences of adenoma and of adenoma or carcinoma (combined) were increased in 7.5 and 15 μL females. A positive dose-related trend in the incidence of adenoma or carcinoma (combined) was also observed in male mice. The incidence of basophilic hepatic foci was increased in 15 μL male mice (0/50, 1/50, 9/50, 3/50). The increased incidence of liver neoplasms in this study was considered equivocal because the incidence of hepatocellular neoplasms in control and dosed males was within the historical range and because there was no clear dose-response relationship in females. No other treatment-related findings were observed in this study. 1-YEAR INITIATION/PROMOTION STUDY IN MALE SWISS (CD-1®) MICE: Groups of 50 male mice were dosed dermally with diethylphthalate or dimethylphthalate to study their effect as initiators and promoters. Diethylphthalate and dimethylphthalate were tested as initiators with and without the known skin tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Diethyl phthalate and dimethylphthalate were tested as promoters with and without the known skin tumor initiator 7,12-dimethylbenzanthrancene (DMBA). Comparative control groups used during the study of diethylphthalate and dimethylphthalate included: vehicle control (acetone/acetone); initiation/promotion control (DMBA/TPA); initiator control (DMBA/acetone); and promoter control (acetone/TPA). Based on the incidence of skin neoplasms diagnosed histologically and the multiplicity of skin neoplasms, there was no suggestion that either diethylphthalate or dimethylphthalate was able to initiate skin carcinogenesis when chronically promoted by TPA. Further, there was no evidence that either diethylphthalate or dimethylphthalate was able to promote skin carcinogenesis in skin previously initiated with DMBA. High incidences of both squamous cell papillomas and squamous cell carcinomas occurred among the initiation/promotion control animals initiated with DMBA and promoted with TPA. All TPA-dosed groups had significantly greater incidences of dermal acanthosis, ulceration, exudation, and hyperkeratosis than controls. GENETIC TOXICOLOGY: Neither diethylphthalate (10-10,000 μ/plate) nor dimethylphthalate (33-6,666 μ/plate) induced gene mutations in Salmonella typhimurium strains TA98, TA100, TA1535, or TA1537, with or without rat and hamster liver S9. In cultured Chinese hamster ovary cells, both diethylphthalate and dimethylphthalate induced sister chromatid exchanges in the presence of S9. Neither induced sister chromatid exchanges in the absence of S9. Neither chemical induced chromosomal aberrations, with or without S9, in cultured Chinese hamster ovary cells. CONCLUSIONS: Under the conditions of these 2-year dermal studies, there was no evidence of carcinogenic activity of diethylphthalate in male or female F344/N rats receiving 100 or 300 μL. The sensitivity of the male rat study was reduced due to low survival in all groups. There was equivocal evidence of carcinogenic activity of diethylphthalate in male and female B6C3F1 mice based on increased incidences of hepatocellular neoplasms, primarily adenomas. In an initiation/promotion model of skin carcinogenesis, there was no evidence of initiating activity of diethylphthalate or dimethylphthalate in male Swiss (CD-1®) mice. Further, there was no evidence of promotion activity of diethylphthalate or dimethylphthalate in male Swiss (CD-1®) mice. The promoting activity of TPA following DMBA initiation was confirmed in these studies. Minor dermal acanthosis was observed following dermal application of diethylphthalate in male and female F344/N rats dosed for 2 years and in male Swiss (CD-1®) mice dosed for 1 year. Synonyms: Diethylphthalate (CAS No. 84-66-2): 1,2-benzenedicarboxylic acid, diethyl ester; DEP; diethyl 1,2-benzenedicarboxylate; diethyl o-phthalate; diethyl phthalate; ethyl phthalate; o-benzenedicarboxylic acid diethyl ester; phthalic acid, diethyl ester; RCRA U088 Dimethylphthalate (CAS No. 131-11-3): 1,2-benzenedicarboxylic acid, dimethyl ester; dimethyl 1,2-benzenedicarboxylate; dimethyl benzene-o-dicarboxylate; dimethyl benzeneorthodicarboxylate; dimethyl o-phthalate; dimethyl phthalate; DMP; FIFRA 028002; methyl phthalate; go-dimethyl phthalate; phthalic acid, dimethyl ester; phthalic acid methyl ester; RCRA U102
 ...
PMID:NTP Toxicology and Carcinogenesis Studies of Diethylphthalate (CAS No. 84-66-2) in F344/N Rats and B6C3F1 Mice (Dermal Studies) with Dermal Initiation/ Promotion Study of Diethylphthalate and Dimethylphthalate (CAS No. 131-11-3) in Male Swiss (CD-1(R)) Mice. 1261 2

Reliable data on familial risks are important for clinical counseling and cancer genetics. We wanted to study incidence trends and familial risks for pituitary adenomas and associated tumors through parental and sibling probands, using the nation-wide Swedish Family-Cancer Database on 10.5 million individuals, containing families with parents and offspring. Cancer data were retrieved from the Swedish Cancer Registry from years 1958 to 2002, including 3239 pituitary tumor patients. Familial risk for offspring was defined through standardized incidence ratio (SIR), adjusted for many variables. The incidence of pituitary adenoma has increased moderately from 1958 to the 1990s and declined thereafter. There were only three offspring-parent pairs with a concordant pituitary tumor, the SIR was not significant. Parental skin cancer (SIR 1.60) and leukemia (1.90, chronic lymphatic leukemia 2.59) were associated with offspring pituitary adenoma diagnosed at any age up to 70 years. There was a strong association of pituitary adenomas with nervous system hemangiopericytomas, SIR 182. The only significant association among siblings was between pituitary tumors and breast cancer (1.46). The risk of pituitary adenoma was marginally increased in individuals whose siblings were diagnosed with colorectal cancer. The results suggest an association of pituitary adenomas with nervous system hemangiopericytomas and breast and colorectal cancers, in addition to some other tumor types. Whether these associations can be explained by the recently identified pituitary adenoma predisposing gene, AIP, remains to be established.
 ...
PMID:Incidence and familial risks in pituitary adenoma and associated tumors. 1739 79


1 2 Next >>