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)

Honn et al. [Science (Wash. DC), 212: 1270, 1981] have recently reported a 93% reduction in the development of metastases of B16 amelanotic tumor cells given i.v. following a single dose of prostacyclin (PGI2) (100 micrograms) and theophylline (100 micrograms) 30 min prior to the injection of tumor cells. We have been unable to reduce pulmonary metastases induced by the i.v. injection of CT26 colon adenocarcinoma, Lewis lung carcinoma, or B16 amelanotic melanoma cells with a similar regimen. Thus, PGI2 and theophylline given prior to injection of tumor cells and 2 hr postinjection had no effect on the number or volume of pulmonary tumor nodules for CT26 cells, using 15 experimental and 14 control animals; Lewis lung cells, using 14 experimental and 13 control animals; or B16 amelanotic cells, using 26 experimental and 12 control animals. The PGI2 used was shown to be active in vitro, inhibiting tumor-induced platelet aggregation by all three tumors at 10(-9)M; and in vivo by inhibition of Lewis lung-induced thrombocytopenia at 1 hr, using 100 micrograms PGI2 prior to the injection of tumor cells.
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PMID:Lack of effect of in vivo prostacyclin on the development of pulmonary metastases in mice following intravenous injection of CT26 colon carcinoma, Lewis lung carcinoma, or B16 amelanotic melanoma cells. 637 76

Nimodipine, a dihydropyridine calcium channel blocker, was evaluated in vitro for its ability to inhibit platelet aggregation induced by B16 amelanotic melanoma (B16a) and Walker 256 carcinosarcoma (W256) cells, and for its ability to inhibit platelet-enhanced B16a and W256 adhesion to rat microvascular endothelial cells. Nimodipine produced a dose-dependent inhibition of tumor-cell-induced platelet aggregation (TCIPA). Platelets enhanced tumor cell adhesion to endothelium both in the presence and absence of overt platelet aggregation. However, the greatest enhancement of adhesion occurred under aggregatory conditions. Nimodipine at a dose of 40 micrograms/ml inhibited platelet-enhanced adhesion to endothelium under aggregatory and nonaggregatory conditions. Nimodipine was tested in vivo for its ability to inhibit both "experimental' and spontaneous metastasis. Nimodipine produced a 46 per cent inhibition of lung colony formation at a dose of 5 mg/kg body-weight. Over a dose range of 0.1-80 mg/kg, nimodipine produced a significant dose-dependent inhibition in the formation of lung metastases from a subcutaneous tumor. The in vitro results demonstrate that a dihydropyridine calcium channel blocker can inhibit tumor cell-platelet-endothelial cell interactions. The in vivo results suggest that these compounds may be a new class of antimetastatic agent.
Clin Exp Metastasis
PMID:Inhibition of tumor cell-platelet interactions and tumor metastasis by the calcium channel blocker, nimodipine. 654 91

Three different murine tumors, CT26 colon adenocarcinoma, Lewis lung carcinoma, and B16 amelanotic melanoma, were injected into syngeneic mice (BALB/c and C57BL/6J) to test the effect of rabbit anti-mouse platelet antibody on the development of pulmonary metastases. Antiplatelet antibody, when injected i.p., decreased the platelet count from 1.5 x 10(6)/microliters to 0.12 x 10(6)/microliters at 6 hr, which remained at this level for 24 hr. Antiplatelet antibody given 6 hr pre- and 18 hr post-i.v. injection of tumor cells decreased the mean number of CT26 tumor nodules per lung by 57% (range, 47 to 65%) and decreased the mean nodule volume of tumor per lung by 37% (range, 0 to 71%) (124 experimental animals), when compared to the effect of nonimmune serum or irrelevant anti-immunoglobulin antibody in 136 control animals. With Lewis lung carcinoma, antiplatelet antibody decreased the mean number of tumor nodules by 62% (range, 57 to 78%) and decreased the mean nodule volume of tumors by 64% (range, 60 to 77%) using 48 experimental animals and 65 control animals. When tumor cells were given s.c., antiplatelet antibody given 6 hr pre-injection, 18 hr post-injection, and every 48 hr thereafter also decreased the mean number of metastases by 42% in 14 experimental and 15 control animals. With B16 amelanotic melanoma, antiplatelet antibody given 6 hr pre- and 18 hr post-injection decreased the mean number of tumor nodules by 85% and decreased the mean nodule volume of tumors by 66% using 9 experimental and 9 control animals. Similar results were obtained when all three tumors were injected 6 hr after the injection of antiplatelet antibody. However, negative results were obtained if antiplatelet antibody was injected 6 hr after the injection of tumor cells. Since antiplatelet antibody has its maximum effect at 6 hr, it is likely that platelets play their role in the development of pulmonary metastases during the first 12 hr of tumor inoculation.
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PMID:Effect of antiplatelet antibody on the development of pulmonary metastases following injection of CT26 colon adenocarcinoma, Lewis lung carcinoma, and B16 amelanotic melanoma tumor cells into mice. 674 4

We report a case of amelanotic malignant melanoma of the female urethra. The clinical course was unusually long and complicated by asynchronous resectable metastases to the lung and the brain. The patient died of generalized metastasis in spite of successful resection of the metastatic lesions and post-operative chemotherapy, two years and five months after the first presentation. To the best of our knowledge this is the second reported case of amelanotic melanoma in the female urethra.
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PMID:A case of amelanotic malignant melanoma of the female urethra. 688 60

Metastasis is the principal cause of failures to cure human cancers. Prostacyclin is a powerful antimetastatic agent against B16 amelanotic melanoma cells. This effect, which may result from the platelet antiaggregatory action of prostacyclin, is potentiated by a phosphodiesterase inhibitor. Inhibitors of prostacyclin synthesis increase metastasis. Prostacyclin and agents that may increase endogenous prostacyclin production or prolong its activity are suggested as new antimetastatic agents.
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PMID:Prostacyclin: a potent antimetastatic agent. 701 12

The ability of tumor cells to metastasize may be related to their ability to promote aggregation of host platelets. The use of inhibitors of cysteine proteinases resulted in parallel inhibition of B16 amelanotic melanoma-induced platelet aggregation and of a cathepsin B activity. The antimetastatic agent prostacyclin inhibited platelet aggregation induced by the tumor cells and by papain, a cathepsin B-mimicking agent.
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PMID:Tumor cell-platelet aggregation: induced by cathepsin B-like proteinase and inhibited by prostacyclin. 704 53

Synthetic antioxidants: EPO (p-ethoxyphenol), PHP (p-hydroxypropiophenone), and DPPD (N,N'-diphenyl-p-phenylenediamine) dissolved in dimethylsulfoxide were administered subcutaneously to mice after subcutaneous implantation of Lewis lung carcinoma or amelanotic B16 melanoma into the tails. The doses of antioxidants used were: 50 mg/kg, 100 mg/kg, and 200 mg/kg per day, respectively. The animals received five injections a week during two weeks. The tails with Lewis lung carcinoma were amputated after 16 days and with amelanotic melanoma after 20 days; tumors weight was measured. 25 days after Lewis lung carcinoma and 42 days after B16 melanoma implantation mice were sacrificed, lungs weighed and incidence of pulmonary and extrapulmonary metastases were estimated. There was a significant increase of weight of amelanotic melanoma in animals treated with EOP or PHP (p less than or equal to 0.05). No influence of antioxidants on the metastases incidence of B16 melanoma was found. Antioxidants used did not influence the Lewis lung carcinoma weight, whereas EOP or PHP increased the incidence of extrapulmonary metastases (p = 0.05, and p = 0.1, respectively).
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PMID:Influence of some synthetic antioxidants on the growth and metastases formation of Lewis lung carcinoma and amelanotic B16 melanoma in C57BL mice. 730 12

There were 487 patients treated for malignant melanoma of the upper extremities at the Pack Medical Group in New York City between 1939 and 1967 inclusive, fourth in frequency (14.7%) of total malignant melanomas treated here, being exceeded by malignant melanoma of the trunk (34%), head and neck (23%), and the lower extremities (20%). A 10-year survival rate of 342 determinate patients was 63%. Fourteen percent of the patients who died of melanoma died between the fifth and tenth years, indicating the need to report survival at the 10-year span. Survival was equal for the sexes (61% male and 64% female). The majority of the patients had infiltrating melanomas (Clark's Level 4 and 5) with a survival rate of 62%. Ten patients with superficial spreading melanomas (Clark's Level 2 and 3) and juvenile melanomas enjoyed a 100% 10-year survival. The worst prognosis was for six patients with amelanotic melanoma in that only two of ten survived ten years or longer. The question of elective axillary dissection remains elusive. In 106 patients classified as clinical Stage I, elective axillary dissection was performed in 55 instances, and 26 patients had microscopic evidence of metastases. Their 10-year survival rate was 65%, slightly higher than 16 patients in whom no elective axillary dissection was performed, among whom six later developed evidence of metastases, underwent therapeutic node dissections, and had a 10-year survival of 56%. Radical amputation is occasionally indicated with great palliation and often prolongation of life.
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PMID:Malignant melanoma of the upper extremities. 746 52

The ability of the human amelanotic melanoma cell line MM-RU to produce experimental metastases and to grow tumors at subcutaneous inoculation sites in 4-week-old nude mice was examined. After i.v. inoculation of 10(6) cells, all injected mice (n = 21) developed consistent numbers of metastatic pulmonary colonies within 32 days. The coefficients of variation for the number of colonies were between 17%-23% in three independent experiments. Survival time after i.v. inoculation was 63 +/- 7 days (mean +/- SD) (n = 20). Within 20 days, subcutaneous inoculation of 5 x 10(6) cells resulted in tumor growths of 13 +/- 3 mm (mean +/- SD) at the inoculation sites in all nude mice (n = 12). The MM-RU cell line seems to be a simple, fast vehicle for testing the effect of melanoma growth modulators on experimental pulmonary metastases as well as on subcutaneously growing melanoma.
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PMID:Metastatic behavior and tumorigenicity of a human melanoma cell line (MM-RU) after injection into nude mice. 827 38

A case of amelanotic melanoma arising in the upper molar region, which was difficult to diagnose histologically, is reported. The patient was a 79-year-old woman, who complained of a painful swelling in the gingiva of the left upper molar region. Routine histological examination showed that the lesion was composed of diffusely scattered atypical cells with round, spindle-shaped and irregular nuclei and scanty fibrous connective tissue. A fascicular arrangement was often found in the lesion, and no cancer nests were observed. Immunohistochemical study demonstrated positive staining for S-100 protein in both the nuclei and cytoplasm of the tumor cells. Electron microscopic examination revealed that cell organelles were abundant, and an interrupted basal lamina was often found along the cell membrane. The preliminary diagnosis was a non-epithelial malignant tumor. After surgery, histological examination of metastases in lymph nodes from the submandibular region revealed that the tumor cells contained melanin pigment in the cytoplasm, as confirmed by Masson's melanin stain. The final pathological diagnosis was therefore amelanotic melanoma. Immunohistochemical staining for S-100 protein may be useful for differential diagnosis of amelanotic melanoma in conjunction with electron microscopic examination.
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PMID:Amelanotic melanoma of the oral cavity. 841 Feb 6


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