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)

Expression of intermediate filament (IF) isotypes was studied in six human and two murine melanoma cell lines. With one exception, these lines expressed IFs only of the vimentin type; neurofilament peptides, desmin and GFAP were not detected. However, the M5 human melanoma line also expressed extensive cytokeratin tonofilament arrays, as visualized by immunofluorescence with a panel of eleven monoclonal antibodies and hetero-antisera to cytokeratins; only the keratin 19-specific antibody BA16 did not react. By 2 D gel electrophoresis, five major keratin peptides were detected (keratins 7, 8, 13, 17 and 18), and an additional 57 kD peptide was detected on immunoblots with several antikeratin antibodies. Also observed in M5 cells was focal collapse of tonofilament arrays in mitotic cells. All the melanoma lines tested were positive for S100; M5 and two other cell lines were also positive for the 220-240 kD neuroectoderm-associated cell-surface differentiation antigen defined by monoclonal antibody UJ 127:11. In all the melanoma cell lines, secretion of extracellular matrix proteins (fibronectin, laminin and collagen type IV) was sparse or absent, and all were negative for the epithelial cell markers HMG-1 and HMG-2. Co-expression of keratin and vimentin by a melanoma cell line is discussed in the light of recent controversy concerning expression of cytokeratins by other neoplasms of putative neuroectodermal origins.
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PMID:Phenotypic analysis of cultured melanoma cells. Expression of cytokeratin-type intermediate filaments by the M5 human melanoma cell line. 242 48

Photodynamic therapy is a recently introduced treatment for surface malignancies. Since January 1987, 10 patients with endobronchial neoplasms have had bronchoscopic photodynamic therapy at similar dose rates (400 mW/cm) for total atelectasis (2), carinal narrowing with respiratory insufficiency (2), or partial obstruction without collapse (4). Two patients underwent photodynamic therapy as a preliminary to immunotherapy. Histologies included endobronchial metastases (colon, ovary, melanoma, and sarcoma, 1 each; and renal cell, 3) and primary lung cancer (3). The 2 patients with total atelectasis had complete reexpansion after photodynamic therapy, which permitted eventual sleeve lobectomy in 1. Carinal narrowing was ameliorated in the 2 patients seen with inspiratory stridor, thereby permitting hospital discharge. Endoscopically resected fragments after photodynamic therapy exhibited avascular necrosis. These data support further controlled studies of photodynamic therapy by thoracic surgical oncologists to define its limitations as well as to improve and expand its efficacy as a palliative or surgical adjuvant.
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PMID:Bronchoscopic phototherapy at comparable dose rates: early results. 252 11

Four cases of human intraocular malignant melanoma were treated with ultrasonically induced hyperthermia immediately before enucleation. Tumors were treated in two regimens: 30 minutes at 43 degrees to 45 degrees C and 5 minutes at greater than 50 degrees C. Temperatures were estimated from applied power levels, based on empirical data and mathematical models. Histopathologic changes observed in human tumors were compared with changes seen in malignant melanoma xenografts in athymic nude mice which were treated with ultrasonically induced hyperthermia for 30 minutes at 42 degrees to 46 degrees C. The effects of treatment were similar to changes seen in the animal model treated under analogous conditions: increased intercellular spacing, cytoplasmic vacuole formation, clumping of chromatin, breaks in cell membranes, and swelling and collapse of cells. Perivascular and peripheral zones sometimes showed decreased damage levels. The high temperature (greater than 50 degrees C) technique is presently being used as a means of "sterilizing" tumors before planned enucleation. The moderate temperature (43 degrees-45 degrees C) technique has been used in combination with radiotherapy to treat tumors when vision can be salvaged.
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PMID:Histopathologic effects of ultrasonically induced hyperthermia in intraocular malignant melanoma. 305 Jul 5

Proton beam irradiation resulted in clinical and/or histopathological regression of large ciliary body and choroidal melanomas in three eyes. Enucleations were performed 6 1/2 weeks, five months, and 11 months after irradiation for angle-closure glaucoma from total retinal detachment, increase in retinal detachment, and neovascular glaucoma, respectively. A direct relationship was found between the length of the interval from irradiation to enucleation and the degree of histologic changes. Vascular changes in the tumors included endothelial cell swelling and decreased lumen size, basement membrane thickening, collapse of sinusoidal vessels, and thrombosis of vessels. Although apparently unaltered tumor cells remained, degenerative changes occurred in some melanoma cells, including lipid vacuoles in cytoplasm, pyknotic nuclei, and balloon cell formation. Patchy areas of necrosis and proteinaceous exudate were present. Pigment-laden macrophages were found near tumor vessels and all had a substantial chronic inflammatory infiltrate. The effect of proton beam irradiation on tumor vessels probably plays an important role in uveal melanoma regression.
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PMID:Ciliary body and choroidal melanomas treated by proton beam irradiation. Histopathologic study of eyes. 631 Nov 46

Pinealectomy (PX) increased MM1 (melanotic melanoma no. 1) hamster melanoma growth in animals held under a 14-h light, 10-h dark (14:10) photoperiod without altering tumor latency. Hamsters maintained under a 6-h light, 18-h dark (6:18) photoperiod exhibited gonadal collapse, a longer tumor latency, and slower tumor growth rate than animals held under 14:10. PX produced a further increase in tumor latency and a decrease in growth in these animals. In contrast, acute morning injection of low doses (50 micrograms/day) of melatonin or delivery by Silastic capsule (35 micrograms/day) implanted at the time of tumor cell inoculation increased MM1 melanoma growth in hamsters held under 14:10 photocycle, without affecting testicular or adrenal function. Treatment of hamsters 11 weeks before tumor cell inoculation with 14 micrograms/day melatonin via Silastic capsule produced a decrease in serum PRL but no change in tumor growth or testicular or adrenal weights in animals held under 14:10. Treatment of hamsters with 17.7 micrograms/day melatonin (Silastic capsule) 11 weeks before tumor cell inoculation increased testes and adrenal weights as well as serum PRL and androgen levels, but significantly decreased tumor growth in hamsters held under a short daily photoperiod. These results suggest that the photoperiod under which hamsters are maintained dictates the growth rate of MM1 tumors and the effect of PX on tumor behavior. When photoperiod significantly alters gonadal and adrenal function, the quantity, time, and duration of melatonin presentation are all important variables in the effect of melatonin on tumor growth.
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PMID:Photoperiodic control of melanoma growth in hamsters: influence of pinealectomy and melatonin. 687 38

Adjuvant chemo- and immuno-therapy with dacarbazine (1st to 5th day 250 mg/m2 daily) and BCG (6th day 0.01 ml intracutaneously)was administered to a 50-year-old male patient in a three-week cycle after surgical removal of a superficially spreading malignant melanoma. Metoclopramide was used as an antiemetic. During the second therapy cycle sudden severe vascular collapse with increasing hepatomegaly and signs of acute hepatic failure occurred leading to death after two days. At necropsy a Budd-Chiari syndrome with thombosed hepatic veins and congestive liver parenchyma necroses was found. The cause was hyperergic endophlebitis combined with severe infiltration of the vascular walls by eosinophilic granulocytes. In association with 5 more similar cases from other clinics (personal communications) this picture must be assumed to be a complication of dacarbazine treatment.
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PMID:[Budd-Chiari syndrome during treatment with dacarbazine (DTIC) (author's transl)]. 698 51

Esophagectomies have a high morbidity rate, mainly related to pulmonary complications. The aim of this work was to assess whether the thoracoscopic approach could reduce this morbidity. We have made a prospective study of the results of 29 attempts of esophagectomy using a right thoracoscopic approach. There were 20 males and 9 females having an average age of 47. The indication was a squamous cell carcinoma in 22 patients, an adenocarcinoma in 1 patient, a melanoma in 1 patient, and a caustic stenosis in 5. The whole esophagus was mobilized thoracoscopically and the esophagectomy was completed through the abdomen. The reconstruction was achieved using a gastric pull-through and a cervical anastomosis. There were five failures for the following reasons: unresectable carcinoma (one case), large tumor making a thoracoscopic dissection unsafe (two cases), and incomplete lung collapse making the exposure of the posterior mediastinum difficult (two cases). The average time of the thoracoscopic procedure was 135 min. The postoperative course was uneventful in all but five patients who had a pulmonary complication: atelectasis (three cases), right purulent pleural effusion (one case), acute respiratory disease syndrome (one case). The latter complication was lethal. Four out of five respiratory complications occurred in patients for whom the dissection was considered difficult. Among the other complications, there were five anastomotic leakages and three cases of laryngeal nerve palsy. The mortality rate was 3.8%. These initial results do not show a real benefit of the thoracoscopic approach for esophageal dissection, especially with respect to difficult esophagectomies. Further evaluation of the technique is needed.
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PMID:Can the morbidity of esophagectomy be reduced by the thoracoscopic approach? 855 14

A number of anti-cancer agents have been implicated in vascular toxicity. The effects have been attributed to direct drug toxicity towards endothelium. Little attention has been focussed on the interaction between anticancer drugs, endothelial cells and tumour secreted factors. It is well known that tumours can secrete factors such as vascular permeability factor which do affect endothelial cells and could alter their response to the vascular effects of anticancer drugs. In the present study, we have examined, in vitro, the direct effects of vinblastine (VBL), 5-fluorouracil (5-FU), melphalan (L-PAM) and the novel tubulin inhibitor combretastatin A-1 (CBS) on endothelial permeability under normal and tumour simulated conditions. Monolayers of human umbilical vein endothelial cells (HUVEC) grown on membrane filters were incubated in drug in normal growth medium or medium conditioned by the human melanoma cell line, RPMI-7951 (TCM). VBL caused a rapid increase in permeability during the first 20 minutes, which was maintained for the duration of the experiment (120 minutes). The effect was not altered by TCM or restored to control levels when VBL was replaced by drug-free medium. Similarly, CBS caused a rapid increase in permeability; however, in contrast to VBL, this increase was enhanced by TCM. The changes induced by VBL and CBS were accompanied by contraction of the endothelial F-actin cytoskeleton. Neither L-PAM nor 5-FU altered the permeability of HUVEC monolayers. This study demonstrates that certain anti-cancer agents have a direct effect on endothelial cells, leading to an increase in the permeability of endothelial monolayers. Both VBL and CBS have vascular components in their mode of action which may lead to vascular collapse and tumour necrosis.
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PMID:Effects of novel and conventional anti-cancer agents on human endothelial permeability: influence of tumour secreted factors. 906 32

Flavone acetic acid, an agent which has been implicated in both tumor vasculature collapse and NK cell activations, has been tested recently as a potential anti-cancer chemotherapeutic agent. We have tested this agent in combination with adoptive immunotherapy using IL-2 activated natural killer (A-NK) cells in a metastatic B16 melanoma model in C57BL/6 mice. By using rhodamine-labeled A-NK cells we have been able to quantitate both the number of A-NK cells that localize within each tumor section and the percentage of the tumor area occupied by A-NK cells. This has been accomplished using an image analysis system. Flavone acetic acid (200 mg/kg, i.p.) given one day prior to the injection of A-NK cells increased the area of the tumor occupied by A-NK cells and the area of individual A-NK cells approximately 2-fold; however, it did not appear to increase the number of A-NK cells per tumor cross-section. Nevertheless, this increase did not lead to any significant change in the therapeutic efficacy of A-NK cell adoptive immunotherapy. Our studies therefore suggest that mere enhancement of A-NK cell recruitment into tumor metastases does not necessarily translate into enhanced metastatic therapeutic efficacy. Moreover, this method may be a useful tool for pre-screening of compounds which enhance the accumulation of adoptively transferred cells into tumor metastases prior to in vivo screening for therapeutic efficacy.
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PMID:Flavone acetic acid enhances accumulation of IL-2 activated NK cells within established metastases. 989 Dec 22

The selective induction of tumor vascular collapse represents an exciting approach to cancer treatment. However, clinical evaluation of tumor necrosis factor-alpha (TNF), an agent that accomplishes this goal, has been limited by systemic toxicity, and clinical approaches using bacterial components to induce TNF production have also been disappointing. Our laboratory has developed synthetic low molecular weight inducers of TNF, including 5,6-dimethylxanthenone-4-acetic acid (DMXAA), as an alternative strategy. DMXAA induces rapid vascular collapse in transplantable murine tumors and induces TNF synthesis in vitro in both murine and human systems. We show here that the extent of DMXAA-induced TNF synthesis is greater in tumors than that in the spleen, liver, or serum. As shown by in situ hybridization studies of the murine Colon 38 tumor, DMXAA induced tumor as well as host cells to express TNF mRNA. The distribution of cells containing TNF mRNA in tumor tissues after DMXAA administration contrasted significantly with that obtained after lipopolysaccharide (LPS) treatment, although splenic and hepatic tissues showed a similar distribution of TNF mRNA-positive cells. In the Colon 38 tumor, the action of LPS was limited to host cells in the periphery of the vessels. DMXAA treatment induced 7-fold higher peak TNF levels in tumor than in serum. In contrast, LPS treatment induced 9-fold higher TNF levels in serum than in tumor. DMXAA induced 35-fold higher TNF activity in the Colon 38 tissue than did LPS. One ovarian, one squamous, and three melanoma human tumor xenografts implanted in athymic nude mice expressed TNF mRNA of human and murine origin in response to DMXAA, confirming that DMXAA can activate both host and tumor cells. The use of low molecular weight agents to induce TNF synthesis in situ in the tumor represents a novel approach to TNF-mediated therapy of cancers.
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PMID:Stimulation of tumors to synthesize tumor necrosis factor-alpha in situ using 5,6-dimethylxanthenone-4-acetic acid: a novel approach to cancer therapy. 997 11


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