Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

MR features of 153 proved primary liver tumors (95 malignant, 58 benign) in 55 patients with hepatocellular carcinoma (21), cholangiocarcinoma (seven), carcinosarcoma (one), hepatoblastoma (one), hemangioma (16), hepatic adenoma (four), focal nodular hyperplasia (three), leiomyoma (one), and hemangioendothelioma (one) were studied retrospectively to determine which techniques are most reliable for lesion detection and which criteria are most useful for differential diagnosis. MR data were correlated with histologic features such as fatty degeneration, fibrosis, and peritumoral edema. Unlike metastatic cancer, hepatocellular carcinoma was best detected (p less than .01) with T2-weighted pulse sequences. The mean tumor-liver T2 difference was 34.4%, while the mean T1 difference was only 21.8%. A tissue-specific diagnosis of hepatocellular carcinoma was possible in 14 of 21 patients by identification of fatty degeneration of the tumor (eight of 17), tumor capsule (five of 21), and/or vascular invasion (six of 21). MR features of peritumoral edema, present in six of 21 patients with hepatocellular carcinoma and in seven of 25 patients with metastases, were exclusively associated with malignant tumors. The large variation in tissue characteristics (relaxation times and proton density) seen in primary liver tumors necessitates the use of multiple pulse sequences to maximize lesion detection. However, the combined use of T1- and T2-weighted spin-echo and T2-weighted phase-contrast images had the advantage of distinguishing benign from malignant primary liver tumors in 48 of 55 patients in this series.
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PMID:Primary liver tumors: diagnosis by MR imaging. 253 70

Antitumor efficacy of cryosurgery and standard surgical procedures for Lewis carcinoma, melanoma B16, Guerin's carcinoma and Walker's carcinosarcoma was compared in the treatment of 846 experimental animals. The study established the superiority or, at least, similar efficacy of cryosurgery in terms of cure, survival and radicality of primary tumor treatment. Unlike standard surgery, cryosurgery was followed by distant metastases being inhibited in mice. Although there was no significant difference in the incidence of metastases to regional lymph nodes in rats, it was higher than in untreated animals in both treatment groups. Cryonecrosis of tumor tissue is a factor of distant and regional metastases development following cryosurgery.
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PMID:[A comparative study of the efficacy of cryosurgical and operative treatments in transplanted tumors]. 260 25

The clinical and pathologic features of 70 examples of carcinosarcoma (CS) of the breast are reported. Thirty-three neoplasms had infiltrating carcinoma, seven had in situ carcinoma, and 28 had both admixed or contiguous with the sarcomatous component. Squamous carcinoma, present in 15 neoplasms, was the exclusive epithelial component of two. The admixed carcinoma often appeared distinct from the sarcoma component; however, at high magnification transitional differentiation zones and more subtle merging of infiltrating carcinoma with sarcoma were present in most neoplasms. A total of 40 neoplasms were studied by immunohistochemistry for keratins, EMA, vimentin, S-100 protein, and actin. The sarcomatous component in 55% of CS was immunoreactive for keratin, and 98% were immunoreactive for vimentin. A majority were also immunoreactive for actin (77%), and S-100 protein (55%). Ultrastructural examination of the sarcoma in eight neoplasms yielded variable nonspecific findings compatible with sarcoma. These findings indicate biphasic differentiation by cells possessing epithelial and mesenchymal characteristics and suggest myoepithelial origin or differentiation. The cumulative 5-year survival rate for CS was 49%, worse than for other forms of metaplastic carcinoma. The respective 5-year survivals for TNM clinical Stages I, II, and III were 100%, 63%, and 35%. Of patients with axillary dissection, 26% had metastases to axillary lymph nodes with carcinoma as the most frequent component to metastasize. Metastasis was an ominous sign as 33 of 34 patients who developed metastases died from tumor. Local recurrence was not as ominous as 40% who had only local recurrence subsequently died from tumor. Size and microscopic circumscription were also significant prognostic factors.
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PMID:Metaplastic carcinomas of the breast. III. Carcinosarcoma. 277 8

Two morphologically distinct types of polarization and locomotion are found in Walker carcinosarcoma cells. Spontaneously polarized cells are characterized by formation of ruffles and spikes, cells polarized in the presence of microtubule-disassembling drugs by blebbing at the leading edge. Polarization and locomotion are closely correlated. Both can be stimulated by the microtubule-disassembling agents colchicine, nocodazole and vinblastine and suppressed by taxol or cytochalasin B. The results suggest that both microfilaments and microtubules may be involved in regulating polarization and chemokinesis, and that shape changes elicited by microtubule-disassembling agents depend on microfilaments.
Invasion Metastasis 1986
PMID:Shape changes and chemokinesis of Walker 256 carcinosarcoma cells in response to colchicine, vinblastine, nocodazole and taxol. 286 63

Prostacyclin and its synthetic analog carbacyclin were compared as to their abilities to inhibit tumor cell-platelet interactions. Aggregation of rat platelets was induced in vitro by homologous rat Walker 256 carcinosarcoma cells. The extent of cellular interactions was examined ultrastructurally. The ultrastructural data presented here indicate that the tumor cell-platelet interactions began with individual platelets which initiated platelet chain formation in focal association with tumor cell surfaces. By mid-phase aggregation large homotypic platelet aggregates had formed with tumor cells positioned on the external surfaces of the emboli. Tumor cell-platelet interactions became progressively more extensive as tumor cells became enmeshed with growing platelet aggregates. Prostacyclin and carbacyclin inhibited tumor cell platelet interactions in a dose-dependent manner. Carbacyclin inhibition of tumor cell induced platelet aggregation was longer in duration but carbacyclin was 10-fold less effective than was prostacyclin. We report here that prostacyclin and carbacyclin inhibit both aggregation and the ultrastructural changes associated with tumor cell-platelet interactions.
Invasion Metastasis 1987
PMID:Inhibition of tumor cell induced platelet aggregation by prostacyclin and carbacyclin: an ultrastructural study. 329 27

A patient who was 61 years of age had obstruction of the thoracic duct by metastases from an adenocarcinoma of the endometrium together with a carcinosarcoma of the tube. She developed chylous ascite. The diagnostic approach and the treatment has been reviewed by the authors.
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PMID:[Chylous ascites: apropos of a case of endometrial adenocarcinoma associated with homologous carcinosarcoma of a fallopian tube]. 338 56

The lung, a frequent site of cancer metastases, is also a susceptible target in several models of endothelial injury. In previous studies we have demonstrated that such injury, induced by bleomycin or by exposure to high concentrations of atmospheric oxygen, can facilitate the localization and metastasis of circulating tumor cells. Here we have tested the hypothesis that neutrophil-mediated injury to pulmonary endothelium has a similar effect. In Sprague-Dawley rats, intravenous injection of cobra venom factor resulted in complement activation, rapid sequestration of neutrophils in the lung, and endothelial damage, demonstrated by morphology, and by increased protein content and leakage of intravenous 125I-albumin into bronchoalveolar lavage fluids. When 125I-iododeoxyuridine-labeled Walker carcinosarcoma cells were injected intravenously during the period of endothelial injury, the pulmonary capillaries contained aggregates of neutrophils and tumor cells 2 h later, and there was a 3-fold increase in pulmonary tumor cell localization after 24 h in treated animals, compared to controls. Enhancement of tumor cell localization was prevented by pretreatment of the rats with catalase or by antineutrophil antisera. When animals were examined 2 weeks after cell injection, treatment groups had significantly more metastatic tumor nodules and a greater area of lung tissue involved by metastatic tumors. We conclude that neutrophil-mediated damage to the pulmonary endothelium can significantly increase the trapping of circulating tumor cells, and is likely to be clinically important since the large vascular bed of the lung is susceptible to host-mediated injury.
Invasion Metastasis 1987
PMID:Effects of neutrophil-mediated pulmonary endothelial injury on the localization and metastasis of circulating Walker carcinosarcoma cells. 359 84

Walker 256 carcinosarcoma cells produce subpleural pulmonary metastases when given intravenously to the Sprague-Dawley rat. The number of metastases increases when the rat is given morphine subsequent to the tumor load. The increase in the number of metastases can be blocked be pretreatment with the opiate antagonist naloxone. Naloxone itself does not influence the number of metastases. Pentazocine is an opiate that is agonistic to the endorphin kappa-type opiate receptor and partially antagonistic to the mu-type receptor, where morphine acts primarily. While pentazocine alone has no influence on metastases and may decrease the number when given early, pentazocine partially blocks the metastatic inducing effect of morphine.
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PMID:Morphine increases metastatic tumor growth. 370 90

Aggregation of rat platelets was induced in vitro by homologous rat Walker 256 carcinosarcoma cells and the extent of tumor cell-platelet interactions examined ultrastructurally. By 30s there was surface contact between unstimulated platelets and tumor cell microvilli. By midphase aggregation (2-3 min) tumor cells became enmeshed within expanding platelet aggregates. Tumor cell microvilli and platelet pseudopodia interdigitated as aggregation progressed. During the later stages of aggregation (6-10 min) tumor cells formed large processes which penetrated deep into the aggregate. Platelet activation (i.e. degranulation) occurred in gradient fashion and was concentrated near tumor cell membrane sites involved in process formation. At these later stages tumor cells near the aggregate periphery were found to have engulfed platelets or platelet fragments. Tumor cell-platelet interactions in the pulmonary microvasculature were also studied in vivo following injection of murine Lewis lung carcinoma, 16C mammary adenocarcinoma, and B16 amelanotic melanoma tumor cells into the tail vein. Platelets demonstrated a biphasic association with arrested tumor cells with peak interactions occurring at 10-30 min and 4-24 h. Ultrastructurally, tumor cells exhibited newly formed processes which interdigitated with the platelet aggregate. Such processes formed only in areas of contact with platelets and not in areas of contact with endothelial cells or other blood elements (i.e. erythrocytes, polymorphonuclear leukocytes). Numerous tumor cell mitochondria were concentrated in the areas of greatest platelet-tumor cell process activity. At early time intervals (2-10 min), intravascular platelet degranulation was observed primarily in platelets associated with tumor cell processes. Tumor cells also were found to have engulfed platelet fragments in vivo.
Clin Exp Metastasis
PMID:Tumor cell-platelet interactions in vitro and their relationship to in vivo arrest of hematogenously circulating tumor cells. 382 98

Cells from the Walker 256 carcinosarcoma, a rat breast tumor with a propensity to metastasize to bone, were labeled with [131I]5-iodo-2'-deoxyuridine and then added to 96-hour organ cultures of fetal Sprague-Dawley rat calvaria that had been prelabeled with 45Ca and incubated with various stimulators or inhibitors of resorption. In conditioned media from resorbing bone cultures, the number of cells that attached to the bone surfaces correlated with the degree of bone resorption (r = 0.65; P less than .005). The attachment response was maximal after 180 minutes of cocultivation and was inhibited by preincubation of the tumor cells with 10(-5) M cytochalasin B. Cellular attachment appeared to be promoted by a trypsin-sensitive factor released into the organ culture medium from resorbing bones. Enhanced tumor cell attachment did not appear to be related to a change in the surface properties of the resorbing bone, since it was not observed when the conditioned media were replaced with fresh medium. Furthermore, tumor cells placed in conditioned medium demonstrated increased attachment to plastic surfaces and formed aggregates. While there was a direct correlation between the ability of conditioned medium to promote cellular adhesion and chemotactic migration (r = 0.85; P less than .05), the factors responsible for chemotaxis and adhesion could be separated by gel filtration. The release of such factors from resorbing bones may promote the formation of secondary bone tumors, since in this system attachment of unlabeled cells was followed by proliferation of tumor cells and evidence of bone invasion.
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PMID:Adhesion, chemotaxis, and aggregation of Walker carcinosarcoma cells in response to products of resorbing bone. 385 80


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