Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0025202 (melanoma)
69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malignant melanoma can produce diagnostic problems for the histopathologist because of its protean histologic patterns. The recently recognized signet cell pattern can be particularly confusing and must be distinguished from adenocarcinoma, tumors of vascular endothelium or adipose tissue, lymphoma, and epithelioid smooth muscle lesions. We report four new cases of signet cell melanoma and illustrate this pattern in primary as well as metastatic sites. In addition, we document the signet cell pattern in benign nevi for the first time, expanding the concept of this pattern to melanocytic cells in general. The differential diagnosis of signet cell melanoma and its mimics is discussed and the utility of immunohistochemical stains in this diagnosis is stressed.
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PMID:Signet cell melanocytic lesions. 134 15

Synergy, when it can be convincingly established, is an effective strategy for the development of novel drug combinations. We have evaluated the interaction between 2'-deoxy-5-azacytidine (DAC) and 9-dimethylaminomethyl-10-hydroxycamptothecin (topotecan) based on our hypothesis that DAC, through DNA hypomethylation, might increase the transcription of topoisomerase I (topo I) leading to increased sensitivity to topotecan. Five human tumor cell lines, A375 melanoma, DX-3 melanoma, DMS4C non-small cell lung carcinoma, UP-1 unknown primary adenocarcinoma, SN12C renal carcinoma, and the murine CT-26 tumor cell line, were studied. Drug interactions were assessed using the multiple drug effect analysis of Chou and Talalay (Chors, T-C, and Talalay, P. Adv. Enzyme Regul., 22:27-54, 1984.). A synergistic interaction was documented in four human cell lines and the murine CT-26 line. An antagonistic interaction was observed with the SN12C cell line. The toxicology and efficacy of this combination were analyzed using CT-26 in BALB/c mice. Various treatment schedules were studied, including: single doses of each agent; single sequential combination treatments where DAC was administered followed by topotecan 24 h later; and multiple sequential treatments where DAC and topotecan were administered on days 1, 2, 8, and 9. Efficacy studies showed that the single sequential combination of DAC (50 mg/kg) and topotecan (10 mg/kg) resulted in tumor growth delay as compared to single doses of DAC (50 mg/kg) or topotecan (10 mg/kg). When the multiple sequential combination schedule was used, the antitumor effect was more pronounced. In that experiment 50% of the control animals had tumors of 20 mm by day 28. For animals receiving a single sequential treatment with DAC and topotecan, the median time until the mean tumor size reached 20 mm was 38 days, and for the group with multiple sequential combination treatments the time was 51 days. Studies of the mechanism of the interaction showed that the activity of topotecan versus each cell line correlated with the topo I activity in nuclear extracts However, there was no correlation between topo I levels and synergy and no reproducible increase in topo I activity following exposure to DAC. Thus, while the exact mechanism of the interaction remains unclear, DAC can be effectively combined with topotecan to enhance antitumor activity.
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PMID:Synergistic cytotoxicity with 2'-deoxy-5-azacytidine and topotecan in vitro and in vivo. 137 5

Stereotaxic radiosurgery delivered from a modified 4 MV linear accelerator was used to treat 47 brain metastases in 27 patients at Stanford. Response was assessed in 41 lesions. Histopathologies included adenocarcinoma (24 lesions), renal cell carcinoma (9 lesions), melanoma (6 lesions), and squamous cell carcinoma (2 lesions). Follow-up ranged from 1.0-16.5 months, with a median of 5.0 months. Radiographic local control was achieved in 88% of the lesions. Three patients developed enlarging contrast-enhancing lesions in the radiosurgical field; one of these was biopsied and revealed necrosis with no viable tumor. Adjuvant whole brain irradiation (10 patients) was associated with regional intracranial control in 80% of patients. This was statistically superior (p = 0.0007) to the regional intracranial control rate achieved when radiosurgery alone was employed (6 patients). Most patients reported resolution of their neurologic symptoms, and were able to discontinue dexamethasone without impairment of neurologic function.
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PMID:Stereotaxic radiosurgery for brain metastases: the importance of adjuvant whole brain irradiation. 137 18

The ability of a panel of monoclonal antibodies generated in this laboratory to identify "pagetoid" melanoma cells and distinguish them from true Paget's adenocarcinoma cells in a retrospective analysis of vulvar neoplasms was investigated. Paraffin blocks of formalin and Carnoy's fixed tissue from 15 cases of vulvar Paget's disease and 11 cases of primary vulvar melanoma were retrieved and sections were incubated with the following panel of monoclonal antibodies: HMB45, a melanoma-specific monoclonal antibody; and 35 beta H11 and 34 beta E12, two different anti-cytokeratin monoclonal antibodies, to low molecular and high molecular weight cytokeratins, respectively. The anti-melanoma monoclonal antibody (HMB45) positively identified the melanoma cells, distinguishing them from normal melanocytes, in all 11 cases of melanoma. In contrast, the HMB45 antibody failed to react with the intraepithelial neoplastic cells in all cases of Paget's disease. These latter malignant cells were strongly positive only with the monoclonal anti-low molecular weight cytokeratin antibody 35 beta H11. This latter antibody absolutely distinguished tumor cells from neighboring uninvolved squamous epithelium, which was positive only with the monoclonal antibody 34 beta E12. Using this panel of monoclonal antibodies, the surgical margins could also be better evaluated; in at least one case the surgical margin thought by histological evaluation to be free of tumor was demonstrated by immunocytochemistry to be positive for tumor. In the vulvectomy specimens obtained in both diseases, Paget's or melanoma cells were identified in sections histologically interpreted as free of tumor. Thus, a panel of monoclonal antibodies is able to identify, with high sensitivity and specificity, vulvar melanoma cells and absolutely distinguish them from vulvar Paget's cells and can help in evaluating surgical margins in a more accurate manner.
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PMID:Paget's disease and melanoma of the vulva. Use of a panel of monoclonal antibodies to identify cell type and to microscopically define adequacy of surgical margins. 137 62

A panel of monoclonal antibodies (mAbs) to bovine fibronectin (FN) is described which modulates either heparin binding or cell adhesion to FN, or both. A combination of competitive exclusion and binding to proteolytic fragments identified epitopes in the Hep II, Hep III/I and CBF (cell binding fragment) regions of FN. mAb A17, which bound to the CBF region, strongly inhibited the cell adhesion of BHK-21 fibroblasts, primary corneal fibroblasts and endothelial cells, and NM4 mammary adenocarcinoma cells, to FN at mAb concentrations as low as 1 microgram/ml. This mAb was not so effective at inhibiting the adhesion of B16 mouse melanoma cells. Adhesion of B16 cells to FN was more sensitive to inhibition by mAbs binding to Hep II (A2, A9, A32, A35). Of these, A32 and A35 significantly increased the binding of 35S-heparin to FN, whereas A2 and A9 did not affect it. mAbs A2, A9 and A32 showed good binding to HBF, the 40 kDa proteolytic fragment of human FN which contains both Hep II and IIICS (type III connecting segment). These mAbs inhibited B16 cell adhesion to the HBF (heparin binding fragment) by 30-50%, the greatest inhibition being shown by mAb A32. Two synthetic peptides from the HBF, CS1 (peptide 1) from the IIICS region and peptide I from the Hep II region, also inhibited B16 cell adhesion to HBF by approximately 70 and 30%, respectively. These results suggest that maximal cell adhesion to the HBF involves both CS1 and Hep II. The inhibitory effects of the two peptides were linearly additive in combination, whereas the inhibitory mAbs A2, A9 and A32 showed synergistic additive effects with each of the peptides. This points to the existence of an additional important cell binding site in Hep II, other than peptide I. Recent independent evidence for an additional cell binding site in Hep II supports this view. Melanoma cellular receptor(s) for the Hep II region may be cell surface proteoglycans but do not appear to bind to areas of Hep II with high affinity for soluble heparin, as the latter was not an inhibitor of B16 cell adhesion to the HBF. The increased effectiveness of A32 in inhibiting cell adhesion, compared to A2 and A9, may be due to conformational effects which increase the binding of soluble heparin, but reduce affinity for the cellular receptor. These results are discussed in context with other reports in the literature.
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PMID:Anti-fibronectin antibodies that modify heparin binding and cell adhesion: evidence for a new cell binding site in the heparin binding region. 138 58

3',5'-O-dipalmitoyl-5-fluoro-2'-deoxyuridine (FUdR-dipalmitate), a lipophilic prodrug of 5-fluoro-2'-deoxyuridine (FUdR), was incorporated in different types of liposomes. The in vivo distribution and intrahepatic deacylation of liposomal FUdR-dipalmitate was found to be strongly dependent on liposome composition and on drug to lipid ratio. The use of fluid-type liposomes (egg PC/PS/CHOL) rendered FUdR-dipalmitate more susceptible to enzymatic breakdown than solid-type liposomes (DSPC/DPPG/CHOL). A decrease of the retention of the drug in the body was also obtained when FUdR-dipalmitate was incorporated in solid-type liposomes with high drug to lipid ratio (1:10) than with low ratio (1:50). In spite of these substantial differences in the rates at which FUdR was liberated from liposomes with different fluidity, size, or drug to lipid ratio, only minor differences in therapeutic effect were observed in a number of murine tumour models (P388 leukaemia, Lewis Lung carcinoma, B16 melanoma and a C26 adenocarcinoma liver metastasis model). The lipophilic prodrug of FUdR exhibited antitumour activity at 100-600 times lower doses than the free drug. However, at these therapeutic doses FUdR-dipalmitate was also far more toxic. This prohibited the use of higher doses to increase antitumour activity.
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PMID:In vivo distribution and antitumour activity of liposomal 3',5'-O-dipalmitoyl-5-fluoro-2'-deoxyuridine. 140 84

Squamous cell carcinoma was the most common neoplasm found in a review of case records of 21 cats with histopathologically confirmed orbital neoplasms. Other neoplasms found were lymphosarcoma, undifferentiated carcinoma, malignant melanoma, adenocarcinoma, fibrosarcoma, chondroma, and hemangiosarcoma. Three (14%) neoplasms were primary, 15 (71%) were secondary, invading the orbit from adjacent tissues, and 3 (14%) were a manifestation of multicentric disease. The most common clinical sign was exophthalmia, followed by chronic epiphora, enophthalmia, and strabismus. Mean survival time after diagnosis was 1.9 months. Ten cats were euthanatized at the time of diagnosis because of extensive disease. Mean survival time of the other 11 cats was 4.3 months. Skull radiography was helpful in diagnosing orbital neoplasms in 8 of 11 cats that had invasion of the orbit by adjacent neoplasms.
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PMID:Orbital neoplasms in cats: 21 cases (1974-1990). 142 40

Fifty-seven tannins and related compounds, including gallotannins, ellagitannins, and condensed and complex tannins, were evaluated for their cytotoxicities against human tumor cell lines, including malignant melanoma, lung carcinoma, ileocecal adenocarcinoma, epidermoid carcinoma, malignant melanoma, and medulloblastoma cell lines. Among them, chebulagic acid [1], geraniin [2], sanguiin H-11 [3], 4,5-di-O-galloylquinic acid [12], 1,3,4,5-tetra-O-galloylquinic acid [15], 1(beta)-O-galloylpedunculagin [24], furosin [29], castalagin [38], sanguiin H-2 [34], vescalagin [39], grandinin [40], phyllyraeoidin A [42], (-)-epicatechin 3-O-gallate [50], cinnamtannin B2 [55], and acutissimin A [56] exhibited moderate selective cytotoxicity against PRMI-7951 melanoma cells with ED50 values in the range of 0.1-0.8 microgram/ml. Selective cytotoxicities against the melanoma cells were also observed for strictinin [22], pedunculagin [23], eugeniin [25], elaeocarpusin [28], punicacortein C [37], casuarinin [41], sanguiin H-6 [43], procyanidin B-2 3,3'-di-O-gallate [51], procyanidin C-1 3,3',3"-tri-O-gallate [52], and cinnamtannin B1 [54] with ED50 values of 1-4 micrograms/ml. All of the tannins were found to be inactive (greater than 10 micrograms/ml) against lung carcinoma (A-549), ileocecal adenocarcinoma (HCT-8), epidermoid carcinoma of nasopharnyx (KB), and medulloblastoma (TE-671) tumor cells.
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PMID:Antitumor agents, 129. Tannins and related compounds as selective cytotoxic agents. 143 32

Between 1982 and 1990, 2388 bronchoscopic examinations were carried out in patients with cancer in our hospital. A diagnosis of endobronchial metastasis was established in 30 patients (2.09%), with the following primary tumors in descending order of frequency: breast, large bowel, melanoma, neuroblastoma, leiomyosarcoma and endometrial. Despite the rarity of endobronchial metastases secondary to colon adenocarcinoma, we were able to study 3 cases from our Center. In one case the diagnosis of endobronchial metastasis was simultaneous with that of the primary tumor, and in the other 2 this metastatic complication occurred 16 and 42 months, after the original diagnosis. When this complication occurred, the stage of the disease was advanced in all 3 cases: 2 were Dukes' stage C and one stage D. Although this metastatic location usually implies a very negative prognosis as regards life expectancy, it did not seem to significantly reduce the latter in our patients.
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PMID:Endobronchial metastases in colorectal adenocarcinoma. 146 85

Endoscopic examination of the oesophagus accompanied by histological examination of biopsies or cytological examination of smears enables a confident diagnosis of carcinoma to be established within a period of 24-48 h and in the case of cytology within 15-60 min. Squamous cell carcinoma and adenocarcinoma are easily identified in biopsies or smears taken directly from the lesion. The histopathologist should be alerted to the possible diagnosis of Barrett's adenocarcinoma provided adequate information is given regarding the level of the squamo-columnar junction and the level of the targeted lesion. Unusual tumours are encountered rarely and they include carcinosarcoma, mucoepidermoid carcinoma, adenocystic carcinoma, carcinoid, malignant melanoma, oat cell carcinoma, spindle cell sarcoma, malignant lymphoma, Kaposi's sarcoma, etc. Special stains and multiple levels from the biopsies will be required for accurate identification of these tumours. Dysplasia constitutes a difficult diagnostic problem with reference to its significance regarding surveillance and treatment. Low grade dysplasia represents a recommendation for surveillance provided that the patient is regarded as a good surgical risk if cancer should develop at a later stage. High grade dysplasia is associated with a high risk of invasive cancer and close surveillance is required for the detection and treatment of invasive cancer provided also that the patient is a good surgical risk.
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PMID:Histological and cytological diagnosis of carcinoma of the oesophagus. 146 81


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