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)

The expression of gamma/delta T cell antigen receptors (TcR) in T cell lines or clones derived from tumor-infiltrating lymphocytes (TIL) from patients with solid tumors was investigated. gamma/delta TcR T cell lines were derived from TIL from patients with Wilms tumor, sarcoma or metastatic melanoma by stimulation with autologous tumor cells alone and recombinant interleukin 2 and they exhibited nonspecific cytotoxicity against autologous and allogeneic tumor cells, or cells of the K562 or the MEL21 tumor cell lines. Two T cell lines were derived from a patient with Wilms tumor. One of them expressed a non-disulfide-linked gamma/delta TcR using the 60-kDa gamma chain, whereas, the other expressed a disulfide-linked gamma/delta TcR. A T cell line was derived from a patient with sarcoma and expressed a disulfide-linked gamma/delta TcR, whereas, a T cell line derived from a patient with melanoma expressed a non-disulfide-linked gamma chain of 62 kDa. Several T cell clones were developed from patients with metastatic melanoma or Wilms tumor and expressed either disulfide- or non-disulfide-linked gamma/delta TcR. Northern analysis of RNA from certain of these clones revealed a full-length gamma chain transcript, whereas, the alpha or beta chain transcripts were either absent or truncated. These T cell clones exhibited nonspecific cytotoxicity. Both disulfide- and non-disulfide-linked TIL T cell lines and clones expressed the delta TCS1 determinant. gamma/delta TcR+ cells in freshly prepared TIL from these patients were present in low proportions (less than 5%) and their delta TCS1/delta 1 ratios were within the range observed in the peripheral blood of normal donors. These results demonstrate that both disulfide- and non-disulfide-linked gamma/delta TcR are expressed on T cell lines and clones derived from TIL from solid tumors. Non-disulfide-linked gamma/delta TcR using the 56-66-kDa gamma chain are frequently found on TIL-derived T cell lines and clones. These 56-66-kDa gamma chains are rarely expressed on T cell lines or clones derived from peripheral blood lymphocytes of normal donors.
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PMID:Gamma/delta T cell antigen receptors expressed on tumor-infiltrating lymphocytes from patients with solid tumors. 131 72

Etoposide has proven to be an active agent in the treatment of a variety of neoplasms, particularly germ cell cancers and small cell lung cancer. Yet despite its widespread use, the optimal dose and schedule for etoposide remain unknown. The fact that its efficacy appears to be schedule dependent, along with the recent availability of an oral formulation, formed the basis for several trials at Indiana University and through the Hoosier Oncology Group. These trials evaluated chronic daily administration of the drug in several malignancies. In testicular cancer, etoposide was shown to have a possible role in adjuvant therapy for refractory disease or as part of combination chemotherapy. In small cell lung cancer, etoposide demonstrated activity in both previously treated and untreated patients. The drug, however, had little impact on patients with advanced non-small cell lung cancer, advanced melanoma, or advanced soft tissue sarcoma. Since etoposide appears to be most effective in refractory small cell lung cancer and germ cell tumors, we believe the drug should be explored in tumors with a known history of chemosensitivity to conventionally administered etoposide.
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PMID:Chronic oral etoposide: trials at Indiana University and with the Hoosier Oncology Group. 133

Intestinal localization of rhabdomyosarcoma is exceptional, this case is the first to be published in the world literature. A 35-year-old patient with abdominal pain, fever, was found to have an infiltrative white-grey tumour, involving 20 cm the jejunoileal wall and also the surrounding mesenterium up to the origin of upper mesenterical vessels and lymph nodes. Histologic examination showed an alveolar type of rhabdomyosarcoma intricated with solid undifferentiated tumoral cells. The presence of multinucleated giant cells and the positivity of protein S 100 reaction was important for differential diagnosis, given the alveolar soft part sarcoma, malignant mesothelioma, malignant melanoma or papillary carcinoma.
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PMID:Jejunoileal alveolar rhabdomyosarcoma. A case report. 134 1

Clear-cell sarcoma is a rare soft tissue sarcoma that displays certain similarities to malignant melanoma. In this paper we describe the karyotypic findings and in vitro growth characteristics of a short-term-cultured clear-cell sarcoma. The cultured tumor cells had preserved immunohistochemical characteristics and certain ultrastructural features of the primary tumour, including positivity for vimentin, S-100 protein, and a melanoma-associated antigen, supporting the authenticity of the cultured cells. Cytogenetic analysis revealed an abnormal stemline karyotype of 49,XY, -1, +8, +8, +12, +der(1)t(1;?)(p36.1-.3;?), t(12;22)(q13;q13). A similar or identical t(12;22) was recently reported in two of four clear-cell sarcomas. It is suggested that the t(12;22)(q13;q13) is a primary cytogenetic abnormality in clear-cell sarcoma and distinguishes this tumor type from malignant melanoma.
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PMID:Reciprocal translocation t(12;22)(q13;q13) in clear-cell sarcoma of tendons and aponeuroses. 137 11

When lymphocytes from the lymph nodes draining the site of a progressively growing MCA-105 sarcoma are stimulated in vitro with autologous tumor and low-dose interleukin-2 (IL-2), they will grow and develop the ability to lyse autologous tumor cells in vitro; these lymphocytes can also eradicate tumor metastases in vivo. Phorbol esters and calcium ionophores activate signal transduction pathways in T cells and mimic the events triggered by antigen binding. We therefore sought to determine whether large numbers of MCA-105 tumor-specific, therapeutically active T cells could be obtained from MCA-105 draining lymph nodes (DLNs) following a brief exposure to phorbol dibutyrate (PDBu) and ionomycin (Io). DLN cells primarily stimulated with autologous tumor, followed by a secondary stimulation with PDBu-Io and cultured in 20 U/ml IL-2, demonstrated marked expansion of cell numbers during 3 weeks in culture, had moderate cytolytic activity [37% at effector:target ratio (E:T) = 80:1], and were all CD8+ T cells. In contrast, DLN cells stimulated primarily with PDBu-Io and cultured in 20 U/ml IL-2 demonstrated at least 8-10-fold greater growth than antigen-stimulated DLN cells during 3 weeks, were moderately cytolytic (31% at E:T = 80:1), and were a mixed population of CD8+ and CD4+ T lymphocytes. DLN cells that were expanded by either protocol, like cells stimulated repeatedly in vitro with tumor cells, could eliminate MCA-105 pulmonary metastases when given with IL-2 in an adoptive immunotherapy model. DLN cells stimulated primarily with PDBu-Io completely eradicated MCA-105 metastases but had no in vivo antitumor activity against the syngeneic B16 melanoma or MCA-203 sarcoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activation of CD8+ murine T cells from tumor-draining lymph nodes by phorbol dibutyrate plus calcium ionophore. 138 51

This report describes the development and applicability of a tumor-associated-antigen-specific immune complex (IC) detection assay to denote the presence of tumor cells in a cancer host. This assay utilizes a murine monoclonal antibody, AD1-40F4, which was produced to a glycoprotein tumor-associated antigen (TAA). In Western blot, the murine monoclonal antibody recognized a 90-100 kD subunit of the antigen. This antigen is immunogenic in cancer patients and induces formation of endogenous antigen-antibody complexes. Analysis of 250 sera from normal individuals and 419 sera from cancer patients revealed that a significantly (P less than .0005) greater proportion (234/419; 55.9%) of cancer sera was positive for the marker than the normal sera (8/250; 3.2%). The incidence of the 90 kD-TAA-specific-IC was consistently and significantly higher in melanoma (58.5%; 38/65), sarcoma (52.9%; 83/157), and carcinoma of breast (50.9%; 58/114), lung (68.2%; 30/44), and colon (64.1%, 25/39) than in the normal group. The age of serum donors did not affect the incidence of the reactivity. Also, at least in the cancer group the gender of the serum donor did not affect the incidence of the 90 kD-TAA-specific-IC positivity. In a retrospective study where sequential serum samples obtained postoperatively from 105 patients with melanoma were analyzed, the 90 kD-TAA-specific-IC could be detected in 72 (69%) of patients several years before the appearance of clinically detectable disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Monoclonal antibody-based ELISA to detect glycoprotein tumor-associated-antigen-specific immune complexes in cancer patients. 140 55

Didemnin B is a depsipeptide derived from a Caribbean tunicate (sea squirt) that has demonstrated antineoplastic activity against a variety of murine tumor models, including the L1210 and P388 leukemia, the B16 melanoma, and M5076 sarcoma cell lines. Based on these data, we designed a phase II trial in which 15 patients with measurable, unresectable colorectal cancer were treated with Didemnin B at an initial dosage of 3.47 mg/m2 over 30 minutes administered by intravenous infusion every 28 days; the dosage was altered in accordance with the toxicity observed, with only one patient requiring a dosage reduction for pronounced nausea and vomiting. No hematologic or nonhematologic toxicity developed. No complete or partial responses were observed. These results do not compare favorably with results of treatments using other single agents or combinations that are currently available for the treatment of advanced colorectal cancers. However, because of the tolerable levels of toxicity experienced by in our patients, it is possible that an insufficient dose of the medication was delivered. We concluded that Didemnin B is not active against of colorectal cancers at the dosage and schedule at which it was administered in this study.
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PMID:Phase II study of didemnin B in advanced colorectal cancer. 142 30

Rhizoxin is a 16-membered antifungal macrocyclic lactone isolated from the plant pathogenic fungus Rhizopus chinensis. The compound binds to tubulin, preventing microtubule formation, and inhibiting mitosis. It possesses antitumour activity in vivo against various preclinical murine models, both leukaemias and solid tumours model, as well as in vincristine- and doxorubicin-resistant leukaemia lines. In the present study, cytotoxic activity was observed in human tumour cell lines in vitro at very low concentrations (+/- 10(-10) M) particularly against melanoma, colon, renal, non-small cell and small cell lung cancer. In vivo antitumour activity was demonstrated in murine P388 and L1210 murine leukaemias, solid tumour models B16 melanoma and M5076 sarcoma, and in 5 out of 9 human solid tumour xenografts: LOX melanoma, MX-1 breast cancer, non-small cell lung cancer A549, and small cell lung cancers LXFS 605 and LXFS 650. The absence of cross-resistance to vinca alkaloids was confirmed in vivo against the vincristine-resistant P388 leukaemia subline and the vincristine-resistant human small cell lung cancer LXFS 650. In addition, the antitumour activity of rhizoxin was improved by prolonged or repeated drug administration indicating a schedule dependency. In animal toxicology studies, transient changes in erythrocyte and leukocyte numbers, local phlebitis, diarrhea, and spermatogenic arrest were observed. The LD10 value of rhizoxin after a single intravenous injection was 2.8 mg/kg (8.4 mg/m2). One-tenth of the mouse equivalent LD10 (0.84 mg/m2), the starting dose for clinical phase I studies, was considered to be safe in rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Preclinical antitumour activity and animal toxicology studies of rhizoxin, a novel tubulin-interacting agent. 145 59

The production of tumor-binding antibodies was studied in a group of cancer patients undergoing active specific immunotherapy with irradiated, cholesterol-treated, cell culture-derived autologous tumor cells injected by the intralymphatic route. Fifteen patients were analyzed: nine patients (four melanoma, one breast, one sarcoma, one colon, and one undifferentiated cancer) received three injections of 10 to 15 x 10(6) tumor cells, spaced 2 weeks apart, and six patients (two melanoma, two renal, one breast, and one colon cancer) received tumor cells admixed with 3 x 10(6) U recombinant interleukin-2 (IL-2) (Proleukin, Cetus, Emeryville, CA, USA) plus a 10-day intravenous infusion of 15 x 10(6) U/kg/day IL-2 after each immunization. Serum antibody binding to autologous tumor cells was measured at 2 and 4 weeks after initiation of therapy using an enzyme-linked immunosorbent assay with patient serum being added to adherent tumor cells bound to 96-well microtiter plates. After 4 weeks, we found a significant difference (0.02 less than P less than 0.04) in serum titer in the group receiving IL-2 (33% mean increase) compared with the non-IL-2 group (8% mean increase). Although neither group showed clinical improvement in response to the therapy, the results clearly demonstrated the efficacy of IL-2 in augmenting patient antibody response to autologous intralymphatic tumor cell immunization.
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PMID:Interleukin-2 increases the antibody response in patients receiving autologous intralymphatic tumor cell vaccine immunotherapy. 151 96

Up until the last several decades, surgeons have of necessity focused on survival as the first priority of cancer treatment, and quality of life has been a secondary issue. Now, very radical surgical procedures are less often necessary, because early diagnosis and smaller tumors are more common, and because radiotherapy and chemotherapy have been shown to be as or more effective than extensive surgical resections for many large cancers. Therefore, surgeons can select treatment options that maximize quality of life without increasing the risk of treatment failure. Older patients respond to surgical cancer treatment in much the same way as younger adults, and can benefit greatly from this flexible therapeutic approach. Solid tumors for which treatment options are discussed in this paper include cancer of the breast, rectum, prostate, oral cavity, melanoma, and soft tissue sarcoma.
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PMID:Surgical interventions that can improve quality of life for older cancer patients. 153 42


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