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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

160 chickens hormonally bursectomized before hatching, and 160 controls were twice given a dose of 10 mg 3,4-benzo(a)pyrene 2 weeks and 6 weeks after hatching. After 24 weeks the controls had developed muscle sarcomas at a significantly higher rate than the bursectomized animals (49.6--32.1%). The tumors were identified as malignant polymorphocellular rhabdomyosarcomas in light and electron microscopy. When the experiment was stopped after 27 weeks, the controls showed more tumors than the bursectomized chickens (65.1% versus 58.9%). The effect of bursectomy lies in a prolongation fo tumor latency. The frequency of metastases is equally decreased to a significant degree (41.7% versus 21.7%). These results are interpreted as an illustration of the disturbed equilibrium between the T and B cell responses.
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PMID:The influence of embryonal bursectomy on benzpyrene-induced sarcoma of the chicken. 15 98

The metastatic capabilities of well-defined nodular hepatic lesions induced by benzo(a)pyrene, ethylnitrosourea, benzidine.2HCl, and diethylnitrosamine were evaluated. Coded liver and lung tissues from 1264 treated C57BL/6J x C3HeB/FeJ F1 mice were assessed independently for the presence of primary nodular lesions and metastases, respectively. Primary lesions were classified according to their size, cell morphology, and growth patterns into hyperplastic, adenomatous, and trabecular nodules. None of the 126 mice bearing hyperplastic nodules had pulmonary metastases. Four of 291 (1.4%) mice with adenomatous nodular lesions showed metastases. In contrast, of the 733 mice bearing the trabecular type of nodular lesions alone or in combination with other lesions 266 (36%) showed pulmonary metastases. The pulmonary metastases were first detected in mice dying between 51 and 60 weeks of age (5%). This rate increased as a function of age at death, reaching an incidence of 51% in mice surviving more than 81 weeks. It was concluded that nodules showing trabecular and the more anaplastic solid sheet type of growths represented bona fide hepatocellular carcinomas in the mouse.
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PMID:Morphology and metastatic nature of induced hepatic nodular lesions in C57BL x C3H F1 mice. 20 19

The report describes the antineoplastic activity of violamycin BI on three rodent tumour systems. The test systems are two syngeneic mouse tumours: a benzo(a)pyrene induced sarcoma and a spontaneously originated mammary carcinoma of the inbred strain XVII/Berlin. Both tumours grow in ascitic form and were weekly passaged by i.p. administrations. A third system is a dimethylhydrazine induced rectum carcinoma of the Wistar rat. This rat tumour represents a slowly growing system transplanted by s.c. administrations of tumour fragments. The principle of the screening consists of the evaluation of metastatic parameters, e.g. weight, number and growth rate of metastases, experimentally induced by i.v. administrations of tumour cell suspensions. Under the given experimental conditions violamycin BI represents an antineoplastic antibiotikum with a good effectivity which is superior to the effectivity of the reference antibiotic daunorubicin.
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PMID:[Antineoplastic activity of the anthracycline antibiotic violamycin BI in mice and rats using experimental metastases models (author's transl)]. 51 48

A clone of BALB/c 3T3 cells (A-31), which is highly resistant to spontaneous in vitro transformation, was treated with the carcinogen benzo(a)pyrene [B(a)P]. This agent was capable of inducing in vitro transformation in the presence of S9 activating system and 6 weeks after treatment large foci were detected. Transformation frequency in solvent control groups was very low. Three foci from a single plate of two different experiments were pooled and the cells tested for their in vitro invasive properties and in vivo tumorigenic and metastatic potential. B(a)P-transformed 3T3 cells grew in soft agar and were highly tumorigenic when injected s.c. in nude mice (75% incidence within 7 weeks). Untreated cells were poorly tumorigenic (0/4 mice had tumors within 7 weeks), though they also gave rise to neoplasms after a longer latency. Spontaneous metastasis incidence was low for both controls and treated cells; however, almost all animals (15/16) injected i.v. with B(a)P-transformed cells had pulmonary nodules in the experimental metastasis assay. A few nodules in some of the animals in the control group were detected (4/16). B(a)P-transformed cells were able to invade a thin coating of matrigel in the chemoinvasion assay and also grew in matrigel showing an invasive, branching morphology. Untreated cells did not grow or invade. Our data suggest that a single treatment with a chemical carcinogen can increase tumorigenicity as well as confer invasive and experimental metastasis potential in BALB/c 3T3 cells. This work provides evidence for a role of chemical carcinogens in tumor progression.
Invasion Metastasis 1992
PMID:Induction of invasive and experimental metastasis potential in BALB/c 3T3 cells by benzo(a)pyrene transformation. 151 33

A model has been proposed for the induction of cytochrome P450c in liver by polycyclic hydrocarbons such as benzo(a)pyrene (BaP) and 3-methylcholanthrene (3MC). The polycyclic hydrocarbon interacts in specific, saturable, and high-affinity fashion with a rat liver cytosolic 4s binding protein. The latter enters the nucleus, complexes to 5' upstream regions of the cytochrome P450c gene, and stimulates the transcription. The 4s binding protein has been purified from rat liver and its substrate specificity has been determined. The affinity for 3MC or BaP is 1-2 mM. The binding protein has been demonstrated to complex with specific 5'-upstream regions of the P450c gene by using a filtration assay as well as exonuclease footprinting. In addition, the binding protein stimulates in vitro transcription with upstream regions of the P450c gene as template; these data confirm the hypotheses.
Cancer Metastasis Rev 1988 Apr
PMID:The 4S binding protein acts as a trans-regulator of the polycyclic hydrocarbon-inducible cytochrome P450. 329 33

The incidence of metastasis was evaluated in female SENCAR mice after induction of squamous cell carcinomas by repetitive applications of either benzo [a] pyrene (B [a] P) or N-methyl-N'-nitro-N-nitrosogaunidine (MNNG). Between 41 and 50 weeks 50% of the animals with carcinomas in the B [a] P group had metastases, whereas 20% had metastases in the MNNG group. Very few metastases were observed before 40 weeks of treatment. The major site of metastasis was the lungs; however, metastatic tumors were also found in lymph nodes, adrenal glands and kidneys.
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PMID:Metastasis from squamous cell carcinomas of SENCAR mouse skin produced by complete carcinogenesis. 381 25

Two cell lines were established from liver cells (BALB/c mouse) exposed to benzo(a)pyrene: one was highly metastatic (G-5) and the other poorly metastatic (G-1) to the lung when subcutaneously implanted. However, there was no difference in lung colonization between G-1 and G-5 cells when they were intravenously injected. When G-1 cells were subcutaneously inoculated on one side of the back of mice followed by a challenge on the other side with G-5 cells 10 days later, the growth of the latter tumor was inhibited and the number of metastatic nodules in the lung was reduced. The functional vascular volume of G-1 tumor was less than the G-5 one. In mice bearing G-1 tumors, the neovascularization of intradermally inoculated G-5 cells was reduced. The conditioned medium from G-1 culture contained an inhibitory activity on the growth of endothelial cells from calf pulmonary artery. The inhibitory substance(s) was heat-stable, trichloroacetic acid-soluble, nondialyzable and resistant to various proteinases. The present results imply that G-1 cells produce an antiangiogenic substance(s), probably a polysaccharide(s), which inhibits the angiogenesis required for growth and metastasis of the G-5 tumor.
Invasion Metastasis 1995
PMID:Antiangiogenic substance(s) in a tumor cell line with low metastatic potential originating from the BALB/c mouse liver. 754 55

Chemical carcinogenesis in the regenerating rat liver is cell-cycle-dependent. Proliferating hepatocytes were maximally susceptible to initiation by a single dose of benzo[a]pyrene diolepoxide I when at the G1/S border. Hepatocytes in early G1 or late S/G2/M were less susceptible and non-proliferating G0 hepatocytes were resistant to initiation. Radiation clastogenesis in proliferating human fibroblasts also is cell-cycle-dependent. Ultraviolet radiation (UV) induced maximal frequencies of chromosomal aberrations in synchronized cells that were at the G1/S border. Cells in early G1 or G2 were significantly less sensitive. For both initiation of chemical carcinogenesis and UV-clastogenesis, it appears that replication of damaged DNA is required and DNA repair before replication reduces cellular risk. If DNA repair is protective, cell cycle checkpoints which delay DNA replication and mitosis should augment this protective influence by providing more time for repair. The contribution of cell cycle checkpoint function to DNA repair during cell cycle-dependent clastogenesis was studied using ataxia telangiectasia (AT) fibroblasts. The AT cells displayed a defect in the coupling of DNA damage to checkpoints which control the G1/S and G2/M transitions and the rate of replicon initiation in S phase cells. UV-clastogenesis in AT cells was cell-cycle-dependent with irradiation at the G1/S boundary inducing 3-times more aberrations than treatment in G0 at the time of release into the cell cycle. Thus, DNA excision repair during the pre-replicative G1 phase was protective even in cells with defective checkpoint function. However, following irradiation at the G1/S border, AT cells displayed about 6-fold increased levels of UV-induced chromosome aberrations in comparison to normal human fibroblasts that were treated at this time. These observations indicate that secondary and tertiary DNA lesions that are produced during replication of UV-damaged DNA (replicative gaps and double-strand breaks) also depend on checkpoint function for repair. The replicon initiation and G2-delay checkpoints that operate after initiation of S phase appear to play a major role in protection against UV-clastogenesis.
Cancer Metastasis Rev 1995 Mar
PMID:Cell cycle checkpoints and DNA repair preserve the stability of the human genome. 760 19

Expression of the intermediate filament protein vimentin, and loss of the cellular adhesion protein uvomorulin (E-cadherin) have been associated with increased invasiveness of established human breast cancer cell lines in vitro and in vivo. In the current study, we have further examined these relationships in oncogenically transformed human mammary epithelial cells. A normal human mammary epithelial strain, termed 184, was previously immortalized with benzo[a]pyrene, and two distinct sublines were derived (A1N4 and 184B5). These sublines were infected with retroviral vectors containing a single or two oncogenes of the nuclear, cytoplasmic, and plasma membrane-associated type (v-rasH, v-rasKi, v-mos, SV40T and c-myc). All infectants have been previously shown to exhibit some aspects of phenotypic transformation. In the current study, cellular invasiveness was determined in vitro using Matrigel, a reconstituted basement membrane extract. Lineage-specific differences were observed with respect to low constitutive invasiveness and invasive changes after infection with ras, despite similar ras-induced transformation of each line. Major effects on cellular invasiveness were observed after infection of the cells with two different oncogenes (v-rasH + SV40T and v-rasH + v-mos). In contrast, the effects of single oncogenes were only modest or negligible. All oncogenic infectants demonstrated increased attachment to laminin, but altered secretion of the 72 kDa and 92 kDa gelatinases was not associated with any aspect of malignant progression. Each of the two highly invasive double oncogene transformants were vimentin-positive and uvomorulin-negative, a phenotype indicative of the epithelial-mesenchymal transition (EMT) previously associated with invasiveness of established human breast cancer cell lines. Weakly invasive untransformed mammary epithelial cells in this study were positive for both vimentin and uvomorulin, suggesting that uvomorulin may over-ride the otherwise vimentin-associated invasiveness.
Clin Exp Metastasis 1994 May
PMID:Oncogene-induced basement membrane invasiveness in human mammary epithelial cells. 819 93

Cyclins and cyclin-dependent kinases (Cdks) are central to regulation of the cell cycle. Their abnormal expression may cause loss of cell-cycle control and result in autonomous cell growth, a critical feature of neoplasias. In this study, using immunoblotting, we analyzed the protein levels of several G1/S cyclins (cyclins D1, D2, D3, A, and E) and their respective Cdks (Cdk 2, 4, and 6) in 17 mouse squamous cell carcinomas (SCCs) and 18 mouse skin tumor cell lines. Overexpression of these cell cycle-related genes was frequent in tumors and cell lines. Of special interest was the fact that a group of cell lines that became more aggressive after animal passaging expressed more cyclins D2 and D3 than their respective parental lines did. In addition, SCCs had higher cyclin D3 expression levels than papillomas, and metastases had higher levels than the respective primary tumors, indicating that overexpression of cyclin D3 may be associated with increased aggressiveness of mouse SCC. Interestingly, overexpression of cyclin E was seen in most SCCs induced by a complete carcinogenesis protocol with benzo[a]pyrene (B(a)P) and only in a few SCCs induced by a two-stage carcinogenesis protocol using 7,12-dimethylbenz[a]anthracene as initiator. In contrast, more of the latter tumors overexpressed cyclin D1 and D2 than those induced by B(a)P. Thus, it is possible that different components of the cell-cycle machinery are involved in proliferative dysfunctions that take place during tumor development with different carcinogenesis protocols. Taken together, these results indicate that overexpression of G1 cyclins and their related Cdks is a significant molecular abnormality that could be involved in the process of tumor progression.
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PMID:Increased expression of G1 cyclins and cyclin-dependent kinases during tumor progression of chemically induced mouse skin neoplasms. 911 84


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