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)

BCG has successfuly been applied in lymphoid and in myeloid leukemia but no positive results have been demonstrated in solid tumors except malignant melanoma after intratumoral injection. The authors' approach consists in applying BCG as an only antitumor treatment, much smaller doses and in much longer intervals between them than used by other investigators. The analysis of the treatment schemes of BCG, applied to 171 lung cancer patients showed that positive responses have been obtained only in patients without peripheral dissemination of the disease and that in doses from 0.0001 mg to 0.05 mg. The results obtained depended on the frequency of BCG application: the 5 years survival rate, the mean survival period and the rate of the marked X-ray regression have been found best in patients treated once, good in patients treated in intervals longer than 30 days between the applications of the mycobacteria and worse in patients treated in intervals shorter than 20 days. A direct inverse correlation has been discovered between the mean survival period of the treated patients and the number of the applications of BCG in the first 6 months of the treatment.
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PMID:Analysis of the results of treament of lung cancer patients with BCG according to the scheme of application of the bacillus. 32 24

Eighteen patients with surgically incurable metastatic malignant melanoma were treated with a mixture of irradiated (15,000 rads) autologous tumors cells (1-2 X 10(8)) and BCG (Glaxo, 2-4.5 X 10(6) organisms), which was injected intradermally (in five divided doses) every 2 weeks (X5). Four of 18 (22%) evaluable patients achieved objective remissions. It is concluded that this treatment regimen does not have general clinical application because the remissions were infrequent, of shor duration (median, 3 months) and occurred only in patients with minimal, nonvisceral tumor burdens.
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PMID:A Phase II study of autologous irradiated tumor cells plus BCG in patients with metastatic malignant melanoma. 33 81

23 "high risk" melanoma patients treated with BCG-AIT are compared with a non-randomized control group of 35 Stage II melanoma patients receiving other treatment. The results are discussed. It has been noted that patients with weak initial BCG reactions survived longer than patients with strongly positive first BCG reactions. This observation could be interesting for the choice of immunotherapy.
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PMID:Experience with BCG adjuvant immunotherapy in stage II malignant melanoma. 34 6

A preliminary analysis of a controlled trial of BCG immunotherapy as an adjunct to surgery in the treatment of primary malignant melanoma has been carried out. The length of follow-up varied from 5 years to 6 months. No obvious benefit from BCG immunotherapy has been found so far. On the other hand the treatment is painful with an appreciable morbidity. Skin tests for delayed hypersensitivity have shown no recognisable differences in patients treated with surgery and those who also had BCG, or in the pattern of responses in those who developed recurrences and those who did not. In view of these early findings trial entry has been closed.
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PMID:A clinical trial of BCG immunotherapy as an adjunct to surgery in the treatment of primary malignant melanoma. 36 Nov 32

The immune response of malignant melanoma bases on evident humoral and cellular defence mechanisms of the host against his tumor. Of special interest is a defective immune response, developing in the course of the disease. Hence, any immunotherapy aims at an immunostimulation and immunoregulation. Local and systemic nonspecific immunotherapy try to raise an immune response against the tumor by stimulating unspecifically the whole immune system. On the contrary, specific immunotherapy tries to stimulate directly the defence mechanisms against the tumor by transfusion of antisera (passive immunotherapy) and sensitized cells (adoptive immunotherapy) and by immunizing the patient with tumor tissue (active immunotherapy). One of the best ways in therapy of melanoma seems to be the combination of immunotherapy with chemotherapy, as yet employed in BCG and DTIC treatment.
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PMID:[Possibilities of immunotherapy in malignant melanoma]. 36 50

Xenografts of 3 human malignant cell lines in congenitally athymic nude mice have been examined for susceptibility to BCG. Growth of all 3 tumours, a bladder carcinoma, a melanoma and a colon carcinoma, was suppressed when cells were injected in admixture with BCG. Distant injection of BCG was ineffective. Mice with progressive growths had no detectable anti-human antibody, and rejection of cells and BCG failed to confer protection against subsequent tumour challenge. These studies indicate that human malignant cells are susceptible to local BCG-activated host responses, and that athymic mouse xenografts may be a useful model for assessing the response of human tumours to such agents.
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PMID:BCG treatment of human tumour xenografts in athymic nude mice. 36 88

Mononuclear cell-mediated cytotoxicity (MCMC) against cultured tumor target cells was studied sequentially in melanoma and breast cancer patients before and during BGC administration. MCMC showed temporary fluctuations. In patients with locally advanced melanoma and carcinoma of the breast after tumor load reduction, the administration of BCG may increase the MCMC. This did not always correlate with a favorable clinical course. Potentiating serum factors appeared in 50% of these patients during BCG therapy, while blocking factors were rare. Neither correlated with prognosis. In patients with disseminated melanoma receiving chemoimmunotherapy, increases in MCMC may be related to clinical course. Blocking serum factors frequently developed in this group of patients and potentiating factors were rare. Neither correlated with the clinical course. Significant MCMC among normal donors and the apparent lack of specificity suggest a common nonspecific (? natural) cellular reactivity against cultured tumor target cells.
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PMID:In vitro antitumor reactivity of mononuclear leukocytes from cancer patients receiving immunotherapy with BCG. 37 May 32

Tumour-necrosis factor (TNF) is growth-inhibitory or cytotoxic to certain tumour cell lines, and is present in the serum of rabbits injected i.v. with BCG and endotoxin 2 weeks apart (TNF serum). TNF serum also has interferon activity, and as TNF and interferons have a number of properties in common their relationship has been investigated further. TNF was assayed by cytotoxicity in vitro against L cells and interferon by a CPE-inhibition assay with Semliki Forest virus.TNF appears not to be an interferon, on the following bases:1. TNF activity could be separated from the Type I interferon of TNF serum by passage through a Cibacron blue-agarose column or by sequential salt precipitation, ion-exchange chromatography and gel filtration.2. Preparations of Type I interferon induced by poly I, poly C or virus lacked TNF activity.3. Though it was not possible to compare TNF with rabbit Type II interferon (as methods used to induce Type II interferon in other species were unsuccessful in the rabbit) rabbit TNF has a number of properties which distinguish it from the Type II interferons of other species.4. Rabbit TNF inhibited the growth of a human melanoma cell line, and also had effects on certain mouse and rabbit cell lines, whereas the anti-cellular effects of interferons are reported to be species-specific.
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PMID:Tumour-necrosis factor from the rabbit. III. Relationship to interferons. 38 59

BCG immunotherapy often has severe complications in cancer patients despite lack of toxicity in the immunocompetent individual. MER, a cell wall fraction of BCG, has been reported to cause immunopotentiation similar to that of BCG without equivalent toxicity. Recently, animal models have been reported to develop MER complications, especially disseminated granuloma formation, like those of BCG. For the past several years, MER has been used as adjuvant immunotherapy for treatment of malignant tumors with minimal systemic toxicity reported. A patient with malignant melanoma was treated with intralesional MER at the site of local metastases. He developed military pulmonary granulomatosis and a severe cutaneous eruption in association with MER therapy. The toxicities of BCG and MER therapy were compared with the pathogenesis of granuloma formation reviewed. This patient's complications were consistent with a hypersensitivity reaction to MER. Pulmonary granulomatosis and rash must be added to the list of known MER toxicities.
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PMID:Systemic complications of MER immunotherapy of cancer: pulmonary granulomatosis and rash. 42 Nov 77

From a series of 712 patients with melanoma, 38 patients (5.3%) had more than one primary melanoma. Twenty-four patients had two primaries, 11 patients had three, 2 patients had four, and 1 patient had eight. Twelve patients (32%) had one or more synchronous primaries. Forty-five percent of all multiple primaries were diagnosed within the first year. Microstaging by level and depth was determined prior to treatment and in patients with nonsynchronous primaries, 83% had a subsequent melanoma equal or less advanced than the original. Twenty-six patients with Stage I primaries were skin-tested with DNCB prior to therapy. No significant differences in delayed cutaneous hypersensitivity reactions were found between multiple primary and matched controls with only a single melanoma. Four of 10 patients with multiple primaries treated with adjuvant BCG or BCG-tumor cell vaccine developed subsequent melanomas suggesting that immunotherapy with BCG will not prevent the development of a new primary melanoma. Survival in patients with Stage I and II multiple primary melanomas was improved compared to Stage I and Stage II patients with a single primary. This study suggests that prognosis in multiple primary melanomas is better reflected by the most advanced primary based on microstaging and the presence or absence of regional lymph node metastases than by multiplicity.
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PMID:Multiple primary melanoma. 42 33


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