Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peripheral blood mononuclear cells (PBM) from normal donors and patients with recurrent glioma were activated initially for 48-72 h with phytohemagglutinin-P (PHA) and recombinant human interleukin-2 (IL-2), and then proliferated in vitro for up to 5 months with IL-2. These cells are termed mitogen-stimulated lymphokine-activated T killer (T-LAK) cells. We measured patterns of T-LAK cell growth, in vitro cytolytic activity on a panel of continuous and primary tumor cells, and the phenotypes of the cells in these cultures. Lymphocyte viability declined dramatically over the first 3-5 days; and then the remaining cells in these cultures began to divide and maintained a constant 30-36 h doubling time for long periods in vitro. Phenotyping revealed that cells in the initial few days of culture were heterogeneous, but became almost totally CD3 T cells after 7-10 days in culture. The T-LAK cells from individual normal donors and cancer patients demonstrated a non-genetically restricted cytolytic ability against a panel of both continuous cell lines and primary autologous and allogeneic glioblastoma cells in vitro. This technique provides a method of generating large numbers of autologous cytolytic T cells with non-restricted anti-tumor activity that can be derived from peripheral blood mononuclear cells.
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PMID:Generation of stimulated, lymphokine activated T killer (T-LAK) cells from the peripheral blood of normal donors and adult patients with recurrent glioblastoma. 201 99

We have investigated the therapeutic effects of a combination of cyclophosphamide (CY, 150 mg/kg, iv) and human recombinant interleukin 2 (IL-2, 5 x 10(4) JU/day, ip for 5 days) on autochthonous tumors induced in mice by 3-methylcholanthrene. The initial treatment was carried out when the tumor had reached 8 to 10 mm in diameter. Twenty-eight out of 35 mice (80%) died of local recurrence and pulmonary metastasis of tumor cells within 53 +/- 40 days (mean survival time, MST +/- SD) after the surgical removal of the primary tumor. When these mice were treated with both CY and IL-2 following the operation (Op), only 10 out of 20 mice (50%) died of recurrence and metastasis. The survival rate, however, was not improved by CY chemotherapy alone or IL-2 immunotherapy alone, although each provided a prolongation of the MST. Natural killer cell and LAK precursor cell activities in the spleen cells from the treated mice were found to be restored by IL-2 alone or CY + IL-2, whereas they were suppressed by CY alone. These findings reveal that the restoration of the antitumor activity of spleen cells does not provide an improved therapeutic effect by itself and that IL-2 immunotherapy requires the associated effect of CY chemotherapy to achieve an improved therapeutic effect.
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PMID:Effects of a combination of cyclophosphamide and human recombinant interleukin 2 on pulmonary metastasis after the surgical removal of a 3-methylcholanthrene-induced primary tumor in autochthonous mice. 314 3

Antigenic differences between primary tumors and their cervical lymph node metastases of 12 patients with head and neck cancers were examined by measuring their sensitivity to cytotoxic lymphocytes (CL). Cytotoxicity was induced by autologous mixed lymphocyte (CL). Cytotoxicity was induced by autologous mixed lymphocyte tumor cell culture (MLTC), and further cultivation with recombinant interleukin-2 (rIL-2). The effector cells which were used in this study consisted of OKT3+8+ and OKT3+4+ subpopulations. Their cytotoxic nature was different from lymphokine activated killer cell (LAK cell) activity. Cytotoxicity of CLs stimulated by autologous primary tumor cells (CLP) was observed in 7 out of 12 patients (58.3%). In contrast, cytotoxicity of CLs stimulated by metastatic tumor cells (CLM) was observed in 4 out of 12 patients (33.3%). In the cases in which both CLP and CLM were successfully induced, cross-reactivity tests and cold target inhibition tests were performed. These results suggested that a reduction in immunogenicity had occurred at the metastatic site, and sensitivity against autologous CL was different between primary and metastatic tumor cells.
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PMID:Differences of sensitivity to autologous cytotoxic lymphocytes between primary tumor and its cervical lymph node metastases. 350 23

In the clinical evolution of malign tumors, prognosis depends on whether metastasis develops or not. Biologically speaking, the formation of metastasis implies the existence of tumor cells capable of successfully performing all the steps in the metastatic process: local invasion, lymphatic or hematogenous dissemination, arrest in the microvascular bed of an organ, extravasation and growth of a secondary colony. Clinical observations have demonstrated that for each primary tumor there is a colonization pattern determined by the characteristics of the microvascular endothelium and the functional environment of the target organ. Moreover, the formation of metastasis depends on at least two additional factors: a) tumor cell-tumor cell and tumor cell-host cell relations modulated by intercellular contact and/or soluble paracrine or autocrine growth factors; b) the antitumor efficiency of the immune system, mediated primarily by the action of NK/LAK cells, macrophages and cytolytic T-lymphocytes, whose activity is in turn regulated by a complex of cytokines, including interferons, tumor necrosis factors and interleukins. In this work, we first review certain aspects of tumor biology that are specifically involved in tumor cell-host cell interactions determining non-random metastatic pattern distribution, and then review the implication of certain cytokines in the regulation of tumor proliferation.
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PMID:Tumor-host interaction in non-random metastatic pattern distribution. 867 53