Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0278883 (metastatic melanoma)
 6,224 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Murine, antihuman melanoma cell monoclonal antibody (mAb) 16.C8 was generated by fusing the murine myeloma cell line P3X63/Ag8.653 with splenocytes from a nude mouse bearing a human melanoma xenograft, after reconstitution with splenocytes from syngeneic immunocompetent BALB/c mice. The antibody reacted strongly with fresh human melanoma cells and exhibited preferential reactivity with established human melanoma and neuroectodermal tumor cell lines. Electrophoresis and Western blotting experiments indicated that 16.C8 is directed against a sialoglycoprotein antigen with a molecular weight of 110-120 kDa. mAb 16.C8 mediated lysis of melanoma cells in vitro in antibody-dependent cellular cytotoxicity assays using human mononuclear effector cells isolated from normal volunteers or malignant melanoma patients. In addition, the administration of mAb 16.C8 to nude mice bearing established human melanoma lung and liver metastases resulted in significant inhibition of tumor growth as shown by gross and histologic examination. In contrast, animals treated with Hanks' balanced salt solution or nonspecific immunoglobulin exhibited a large tumor burden. These results suggest that mAb 16.C8 may be of value in treatment of metastatic melanoma in humans.
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PMID:Cell binding and tumor inhibiting functions of a new antihuman melanoma murine monoclonal antibody. 176 67

A panel of melanoma cell lines derived from 7 primary and 20 metastatic lesions was tested for the production of interleukin 1 (IL-1) in standard mouse thymocyte costimulation assays. Constitutively produced IL-1 activity was found in the conditioned media of 4 of 7 primary and 5 of 20 metastatic melanoma cell lines tested. Four of 9 cell lines secreting IL-1 were also shown to contain cell-associated activity in their lysates. Melanoma-conditioned media were, however, unable to support the growth of CTLL, an interleukin 2-dependent cell line. The secreted IL-1 activity was significantly inhibited by antibodies to recombinant IL-1 alpha (3 of 3 lines), but not antibody to recombinant IL-1 beta. When conditioned medium from one cell line was fractionated on a Superose 12 column by fast protein liquid chromatography, a major peak of activity eluted at Mr 22,500-27,500. The presence of 2.2-kilobase mRNA hybridizing a probe for IL-1 alpha and 1.6-kilobase mRNA hybridizing a probe for IL-1 beta was detected by Northern blot in 3 of 4 secreting cell lines but not in a nonsecreting line. Taken together, these results suggest that cultured melanoma cells produce the cytokine IL-1 alpha, although the relationship between melanoma IL-1 and monocyte IL-1 is unclear. The production of IL-1 by melanoma cells is of interest because of its potential roles in the biology of melanoma through direct effects on tumor growth or through indirect effects on adjacent stromal and endothelial cells and infiltrating lymphoid cells.
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PMID:Production of interleukin 1 activity by cultured human melanoma cells. 278 59

In an attempt to understand the mechanism by which estrogens stimulate cell proliferation and mammary carcinogenesis, metastatic human breast cancer cell lines (MCF7, ZR75-1) were found to secrete a 52,000 dalton (52K) protein under estrogen stimulation. Following its purification to homogeneity, the 52K protein was identified as a secreted procathepsin-D-like aspartyl protease bearing mannose-6-phosphate signals. This precursor displays an in vitro autocrine mitogenic activity on estrogen-deprived MCF7 cells and is able to degrade basement membrane and proteoglycans following its autoactivation. The total protease (52K + 48K and 34K) was detected and assayed by monoclonal antibodies and was found to be highly concentrated in proliferative and cystic mastopathies. In breast cancer, its cytosolic concentration appears to be correlated more to tumor invasiveness than to hormone responsiveness. The mRNA of the 52K protease accumulates rapidly following estradiol treatment, as was shown by Northern blot analysis with cloned cDNA. The 52K cathepsin-D-like protease is the first example of a lysosomal protease induced by estrogens in cancer cells. Results obtained using different approaches suggest that two cysteinyl cathepsins are also related to cell transformation and invasiveness. It has been proposed that cathepsin-B is involved in breast cancer and metastatic melanoma, and its regulation by estrogen has been shown in the rat uterus. Cathepsin-L corresponds to the major excreted protein (MEP) whose synthesis and secretion are markedly increased by transformation of NIH 3T3 cells with Ki ras and are regulated by several growth factors. In addition to secreted autocrine growth factors and to other proteases (plasminogen activator, collagenase), lysosomal cathepsins may therefore play an important role in the process of tumor growth and invasion as long as their precursor is secreted abundantly.
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PMID:Estrogen-induced lysosomal proteases secreted by breast cancer cells: a role in carcinogenesis? 331 45

We have investigated the lung colonizing ability of four newly established human metastatic melanoma xenografts, designated CRML1, CRML2, CRML3, and CRML4 following i.v. tail vein inoculation into 3- to 4-week-old gnotobiotic CD-1 athymic mice. The experimental metastatic potential of the tumors was assessed from the primary tumor samples through eight progressively growing s.c. passages. CRML1 and 2 were investigated in detail; five sublines (two from CRML1 and three from CRML2) were established from these tumors with various growth rates and lung colonizing abilities. The histopathologies of the patients' biopsies and the s.c. passaged parental lines were compared with these i.v.-derived sublines as one measure of tumor heterogeneity, in conjunction with the kinetics of lung tumor formation. The frequency and distribution of extrapulmonary tumor growth was also investigated after i.v. inoculation. In general, it reflected the clinical distribution of metastases, although their frequency of appearance was reduced. While CRML3 was the most aggressive disease clinically, it did not demonstrate the reproducible experimental metastasis of the other lines. CRML4 produced lung colonies routinely, but with latency periods of 20 weeks or more. On the other hand, the most rapidly growing sublines of CRML1 and CRML2 essentially replaced the normal lung tissue within 4 to 6 weeks following inoculation of 10(5) cells. The two sublines of CRML1 with higher effective metastatic potential were maximally able to colonize the lungs within only two i.v. cycles in one case, while the other line required six i.v. to i.v. passages to reach its maximum ability. In CRML2, two sublines were identified that rapidly increased in their lung colonizing ability, while another line remained effectively equal to the parental s.c. line over four cycles of reinoculation i.v. These results demonstrated that the athymic mouse can serve as a model for experimental metastasis of human tumors, and that aspects of the metastatic heterogeneity of these tumors can be investigated by using this system.
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PMID:Metastatic potential of four human melanoma xenografts in young athymic mice following tail vein inoculation. 356 24

We have identified and studied twenty-seven patients with melanoma who also had vitiligo. Four patients had vitiligo before the diagnosis of melanoma, and twenty-three developed depigmentation after the diagnosis of malignancy. We also have reviewed published reports about twenty-four other patients with melanoma who developed vitiligo. The clinical course of the melanoma in the fifty-one patients was remarkably similar. Thirty-seven had a melanoma arising at a site which tends to carry a poor prognosis, for example, on the trunk, under the nail, or on the mucous membranes. Forty-nine patients had metastases in regional lymph nodes or at distal sites. Thirty-three patients survived 5 years, and twenty-five survived 10 years. These data suggest that the appearance of vitiligo in patients with metastatic melanoma portends a longer survival than expected. The patients with vitiligo are not necessarily cured and eventually may succumb to metastatic disease. We were unable to determine whether the vitiligo caused retardation of tumor growth or whether the melanoma caused vitiligo.
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PMID:Vitiligo in patients with metastatic melanoma: a good prognostic sign. 664 67

From studying cell kinetic parameters it is demonstrated that both males and females with metastatic melanoma respond favourably to various chemotherapy schedules. Male patients have a shorter doubling time (DT) of pulmonary secondaries prior to chemotherapy compared to females, which seems to give them a less favorable starting point. Also, the DT of lung metastases of males after chemotherapy is less favourable than that of females. However, a significant difference in DT is noticed between measurements prior to and after the institution of chemotherapy in both sexes. It is concluded that the alleged sex differences in response to chemotherapy may be an artifact due to differences in tumor growth kinetics between males and females.
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PMID:Malignant melanoma: sex differences in response to chemotherapy? 720 Aug 89

Intraperitoneal injections of 2 X 10(7) SH-Me cells (human metastatic melanoma cells)( to 20 Balb/c nu/nu mice (Group A) and 1 X 10(7) cells to 20 mice (Group B) were performed. All animals were studied clinicopathologically. Five animals in Group A were sacrificed serially, revealing marked tumor growth of the melanoma within the peritoneal cavity. These tumors grew in multiple nodular configurations and tumor ascites was present by the third week. The remaining 15 animals in Group A were allowed to progress and seven subsequently died with mouse viral hepatitis (MVH). These animals had suppressed tumor growth. The remaining eight animals died of peritoneal carcinomatosis with survival time of 24.1 +/- 5.0 days. Eight of the animals in Group B died of mouse viral hepatitis while the remainder died of peritoneal tumor without distant metastasis. Survival time in these animals was 23.8 +/- 2.6 days. Both 2 X 10(7) and 1 X 10(7) tumor cells injected intraperitoneally will constantly produce tumor nodules in non-MHV-infected nude mice with similar survival. This experimental model has proven useful for in vivo study to assess the immunoreactivity of melanoma patient cells reactive against target tumor cells.
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PMID:Human melanoma growth in the peritoneal cavity of the athymic mouse--a model for in vivo study of cell-mediated immunity. 726 71

One hundred and sixteen patients with suspected malignant melanoma of the choroid and ciliary body were observed for evidence of tumor growth prior to enucleation. All patients were followed for a minimum of five years after tumor detection. The tumor failed to grow in 69 patients, and none developed evidence of metastatic melanoma. The tumor grew in 47 patients, and 35 patients had enucleation. Five patients (4 having enucleation) died of metastatic melanoma. Deaths caused by other primary malignancies (9 patients) and other causes (11 patients) outnumbered those caused by melanomas. The clinical accuracy of predicting growth of small and medium suspected melanomas was approximately 75%. Five patients died because of metastatic melanoma. This study demonstrated no evidence of increased mortality caused by observation of small tumors for evidence of growth prior to enucleation.
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PMID:Observation of suspected choroidal and ciliary body melanomas for evidence of growth prior to enucleation. 741 41

We screened a panel of 8 primary and 21 metastatic melanoma cell lines for constitutive secretion of cytokines. Melanomas expressed bioactivity for TGF-beta (8/25 lines) and IFN (7/12), but not IL-2. Immunoassays detected IL-1 alpha (4/25), IL-1 beta (12/25), IL-6 (13/29), IL-8 (29/29), TGF-beta 2 (5/12) and GM-CSF (11/29), but not IL-3, IL-4, TNF-alpha, or IFN-gamma. There was no preferential association of cytokine production with cells cultured from primary versus metastatic disease, and only IL-8 was produced by all lines tested. These data demonstrate that cultured melanomas produce a variety of cytokines which are potentially capable of influencing tumor growth in vivo.
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PMID:Production of multiple cytokines by cultured human melanomas. 751 80

Metastatic melanoma cell lines were derived from a lymph node of a laboratory opossum, Monodelphis domestica, which had been exposed to mid-wavelength ultraviolet radiation (UVB) initially as a suckling young, and subsequently as a shaved juvenile and adult. The melanoma cell lines were dendritic and pigmented in vitro and contained a t(6;8)(p13;q13) as the only cytogenetic abnormality. The translocation was detected in 15% of primary cultures (passage 2) from the affected lymph node and in 100% of two ring-clone-derived lines, L1 and L2. The breakpoint or resulting partial trisomy of chromosomes 8 may have played a functional role in the tumorigenesis or metastasis of the tumor. The t(6;8) served as a convenient cytogenetic marker for allogeneic grafting studies in Monodelphis. The L2 cells were allografted subcutaneously (s.c.) into genetically diverse suckling young at 3 weeks of age and resulted in the growth of invasive, pigmented, primary and metastatic lesions affecting lymph nodes, lung, and other tissues. Metastatic variant cell lines, M1 and M3, were derived from the affected lungs of two animals and both lines demonstrated the same t(6;8), without additional numerical or structural chromosomal abnormalities. The maintenance of karyotypic stability with a single translocation during in vivo tumor growth and dissemination in this new allografting model is quiet remarkable, as most human metastatic melanomas exhibit multiple structural and numerical cytogenetic abnormalities.
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PMID:UV-induced melanoma. A karyotype with a single translocation is stable after allografting and metastasis. 755 87


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