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

Several histologic patterns of squamous cell carcinomas (SCC) have been described, including classical, adenoid, verrucous, and clear cell. We report 2 cases of an unusual purely exophytic papillary growth pattern. Both tumors occurred on sun-exposed skin of elderly patients and exhibited rapid growth. The tumors were red-tan and fungating, raising the clinical differential diagnoses of pyogenic granuloma, SCC, metastatic carcinoma or amelanotic melanoma. Histologically there was a prominent papillary growth pattern with several layers of notably atypical squamous epithelium overlying a fibro-vascular core in both cases. Mitoses were frequent. The tumors lacked deep invasion, although focal invasion of the stalk was present. These tumors were histologically distinct from verrucous carcinoma, verrucous Bowen's disease, and previously described adnexal carcinomas. The lack of deep invasion and the absence of local recurrence or metastatic disease after 18 months follow-up suggest that this histologic variant is a low-grade malignancy, although study of more cases and longer follow-up will be necessary to accurately assess the biology of this papillary variant of SCC. We believe that this growth pattern has not yet been described and a pure papillary form must be included as one of the histological subtypes of cutaneous SCC.
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PMID:Cutaneous papillary squamous cell carcinoma. A report of two cases. 185 43

Our earlier studies indicated a role for polyamines (namely, putrescine, spermidine, and spermine) not only in tumor growth but also in tumor metastases. We have observed that administration of alpha-difluoromethylornithine (DFMO), an irreversible inhibitor of ornithine decarboxylase, resulted in significant inhibition of visually detectable pulmonary metastases in mice implanted with Lewis lung carcinoma. The objective of the present study is to investigate the effect of DFMO on other spontaneous and experimental metastatic models and also to determine which step(s) in the tumor metastatic cascade is sensitive to DFMO. The results presented in this study with malignant mouse B16 amelanotic melanoma (B16a) showed a dose-dependent effect of DFMO on the inhibition of both tumor growth and grossly detectable pulmonary metastases. DFMO, when administered as 0.5, 1, and 2% solution in drinking water, resulted in 0, 24.5, and 60% inhibition of tumor growth, respectively, whereas at the same doses an inhibition of 55, 83, and 96% of visible metastases was observed. At treatment levels of 1 and 2% DFMO, 30 and 65% of the animals were free of metastases. DFMO, at 0.5%, did not show any effect on tumor growth, while a significant 55% inhibition of visible pulmonary metastasis was observed, suggesting a specific role for polyamines in tumor metastasis. DFMO treatment also resulted in a significant reduction of putrescine and spermidine levels with a slight increase in spermine concentration in the tumor tissue. DFMO administration did not inhibit the experimental metastases induced as a result of i.v. injection of B16 melanoma (line F10) tumor and Lewis lung carcinoma cells into the tail vein. These results provide preliminary evidence to indicate that tumor cell polyamine depletion by DFMO might affect the first step in the metastatic cascade, intravasation (i.e., prevent the invasion of metastatic tumor cells into lymphatics or blood vessels), although the effect of DFMO on other steps in the metastatic cascade cannot be ruled out.
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PMID:Antimetastatic activity of DL-alpha-difluoromethylornithine, an inhibitor of polyamine biosynthesis, in mice. 310 31

A case with advanced diffuse pulmonary ossification is described. The patient underwent surgical treatment of a malignant nodular melanoma of the right shoulder followed by postoperative cytostatic therapy for 6 months. He developed renal insufficiency and pulmonary infiltrates 3 years after the operation. Two metastases into the lung were operated 4 years after extirpation of the melanoma. Histopathological findings revealed two major metastases of a malignant amelanotic melanoma and multiple tumour thromboses in lymphatic and venous vessels. Severe interstitial lung damage including diffuse pulmonary ossification and focal interstitial fibrosis was noted. Morphometric measurements of ossified nodules revealed increased ossification in fibrotic lung areas. Immunohistology for differentiating immunoglobulins and lymphocytic subpopulations was insuspicious. The findings suggest that diffuse intraalveolar ossification is probably not related to pulmonary congestion.
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PMID:Diffuse pulmonary ossification associated with metastatic melanoma of the lung. 312 69

Platelet-adhesive protein-tumor cell interaction was studied in vitro and in vivo. Monoclonal antibody 10E5, which inhibits binding of fibronectin and von Willebrand factor to the platelet membrane glycoprotein GPIIb-GPIIIa complex, inhibited the binding of mouse CT26 and human HCT8 colon carcinoma cells to platelets by 63-65%, whereas an irrelevant monoclonal antibody, 3B2, had no effect. Monoclonal antibody 6D1, which inhibits binding of von Willebrand factor to GPIb, also had no effect. RGDS, a tetrapeptide that represents the adhesive domain of fibronectin and von Willebrand factor inhibited binding of the tumors to platelets by 64-69%. Monospecific polyclonal antifibronectin antibody inhibited binding by 60-82%; anti-von Willebrand factor antibody inhibited binding by 75-81%. In vivo, polyclonal monospecific anti-mouse von Willebrand factor antibody inhibited pulmonary metastases induced by CT26 tumor cells by 53-64%, B16a amelanotic melanoma cells by 45% and T241 Lewis bladder cells by 46% without induction of thrombocytopenia. Pulmonary metastases with CT26 cells could be inhibited by induction of thrombocytopenia, and reconstituted by infusion of either murine or human platelets. Reconstitution of pulmonary metastases with human platelets could be inhibited 77% by preincubation of human platelets with monoclonal antibody 10E5 before infusion of platelets into mice. Thus, platelets appear to contribute to metastases by their adhesive interaction with tumor cells via the adhesive proteins fibronectin and von Willebrand factor.
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PMID:Role of adhesive proteins in platelet tumor interaction in vitro and metastasis formation in vivo. 328 May 98

We have characterized a family of transplantable melanomas in Syrian (golden) hamsters, which originated in 1959 as a spontaneous melanoma of hamster skin, and which has been maintained since then by serial passage. Emphasis has been placed on using the same method of transplantation, keeping strict records on all passages, and applying the same investigative techniques, in order to trace tumor behavior over long periods of time. This tumor family consists of five variants linked by common origin, but which differ with respect to differentiation level, malignancy, intermediary metabolism, chromosome number, and cell surface properties. Once established, these melanomas possessed a considerable degree of phenotypic stability over decades of passaging. One tumor line in this family is emphasized. The Ab amelanotic melanoma lost its differentiated functions (the ability to synthetize melanin) a quarter of a century ago, and since then has remained dedifferentiated in serial passage in hamsters. After transfer to primary cell culture, the Ab melanoma cells differentiate readily and lose much of their proliferative potential. This process is reversible by reimplantation of the cells into a hamster. Inasmuch as this hamster melanoma system meets many of the conditions required for an experimental tumor model, five melanoma variants are characterized concisely and compared to other melanomas in humans and animals. Mechanisms by which new melanoma variants arise are discussed and compared to some phenomena in the evolution of the species.
Cancer Metastasis Rev 1988 Jun
PMID:The natural history of a family of transplantable melanomas in hamsters. 329 37

A case of a primary amelanotic melanoma of the vagina is reported. The patient was a 58-year-old Japanese female. A polypoid tumor was found on the lateral wall of the vagina and a cytologic examination of a scraping showed a few large atypical cells with cleaved nuclei and intranuclear vacuoles. A lateral junctional spread was histologically observed and stage II melanosomes were found in the cytoplasm. Two years after a radical operation, the patient died of a widespread melanotic metastases. The authors survey the number of incidences of malignant melanoma in the female genital organ. In Japanese women, melanoma is seen more frequently in the vagina than in the vulva, which is quite the opposite in cases of malignant melanomas of the genital organs in women of the United States and Europe.
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PMID:[Primary amelanotic malignant melanoma of the vagina--a case report]. 331 36

Ten patients with intracerebral metastases from malignant melanoma were evaluated with magnetic resonance (MR) imaging performed at 1.5 T using spin-echo techniques. On the basis of histopathologic findings in three of 10 cases and CT appearances in all 10 cases, three patterns were identified on analysis of MR signal intensities in both short repetition time/echo time (TR/TE) and long TR/TE spin-echo scans. In comparison to normal cortex, nonhemorrhagic melanotic melanoma appeared markedly hyperintense on short TR/TE images and isointense, mildly hypointense on long TR/TE images. Nonhemorrhagic, amelanotic melanoma appeared isointense or mildly hypointense on short TR/TE and isointense or mildly hyperintense on long TR/TE images. Hemorrhagic melanoma varied in appearance, depending on the stage of hemorrhage. Melanotic, nonhemorrhagic melanoma can be distinguished from early and late subacute hemorrhage by its signal intensity on long TR/TE images. Spin-echo MR appears to be the method of choice for diagnosing melanotic metastases.
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PMID:MR imaging of intracranial metastatic melanoma. 359 77

A 15-year old boy was admitted to hospital with an acute left hemiparesis because of a 3.5 cm-diameter-tumor in the right frontoparietal region. In CCT 4 other tumors were to be seen in both hemispheres after giving contrast medium. Upon a diagnostic operation, a hemorrhage into a metastasis of an amelanotic melanoma was found. The boy survived 2.5 months. In the pathological examination the primary tumor was not found, but there were 12 other intracerebral metastases and two metastases in the left lung and the thyroid gland. Histologically it was an amelanotic melanoma.
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PMID:Brain metastases of an amelanotic melanoma as the primary manifestation in a 15-year old boy. 363 99

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

The interaction between metastasizing tumor cells and the hemostatic system of the host has been implicated in successful tumor cell dissemination. Prostacyclin (PGI2) decreases metastasis from tail vein injected B16 amelanotic melanoma (B16a) cells when administered 15 min prior to tumor cells. This effect is potentiated by a phosphodiesterase inhibitor. Initial trapping of 125I Udr labelled tumor cells in pulmonary vascular beds is unaltered by PGI2 but retention time is decreased. PGI2 decreases retention time even when administered 60 min post tumor cells. Structurally unrelated thromboxane (TX) synthetase inhibitors and a TXA2 receptor antagonist also reduce metastasis from tail vein injected B16a cells. Furthermore, one inhibitor, 1-(7-carboxyheptyl)imidazole, when injected intraperitoneally reduced spontaneous metastasis from subcutaneous B16a and Lewis lung carcinoma tumors. These results suggest that selective manipulation of PGI2 and TXA2 can reduce the hematogenous spread of tumor cells.
Clin Exp Metastasis
PMID:Inhibition of tumor cell metastasis by modulation of the vascular prostacyclin/thromboxane A2 system. 624 6


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