Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The biological features specific to the tumor growth in acute leukemia are responsible for the disease prognosis and its response to polychemotherapy. Current molecular-biological, karyological, cytological, kinetic, and culture investigation techniques have contributed much to the understanding of the pathogenesis of acute leukemia and may be used as a guide to appropriate disease management.
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PMID:[Biological principles of the therapy of acute leukemia]. 226 81

Soluble transferrin receptor (sTfR) in serum of cancer patients was measured by a sandwich enzyme-linked immunosorbent assay, and the effect of sTfR for natural killer cytotoxicity was also studied. The statistical values of sTfR levels in sera were found to be 250 +/- 77 U (Mean +/- SD) in healthy individuals, while 288 +/- 162 U in chronic liver disease, 402 +/- 290 U in hepatocellular carcinoma, 429 +/- 261 U in gastric cancer, 347 +/- 207 U in acute leukemia and malignant lymphoma, and 251 +/- 100 U in other cancer. No significant difference in the sTfR levels among the patients was observed, although the difference between the healthy individuals and the patient groups was shown to be statistically significant at p less than 0.01 level. The effect of sTfR isolated from serum of a patient with iron-deficiency anemia by means of Sephadex G-200 column for natural killer activity was carried out. Cytotoxicity of natural killer cell in healthy individuals was inhibited by sTfR as the dose dependent manner, and the inhibitory rate was found to be 23.1 +/- 12.8% (Mean +/- SD) when the concentration of the sTfR was 1,250 U added in the cytotoxicity test. Furthermore, the inhibitory activity of serum in cancer patients was correlated with the sTfR level. These results suggest that sTfR is one of the inhibitory factors for the natural killer cell activity in vivo, and the factor could be facilitated for tumor growth and metastasis. Therefore, the measurement of sTfR in serum may be useful for monitoring immunological competency in cancer patients.
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PMID:[Elevation of soluble transferrin receptor substance in serum of cancer patients with suppressed natural killer activity]. 261 80

The susceptibility of human myeloid and lymphoid leukemic blasts to the lytic action of recombinant interleukin-2 (rIL-2)-generated lymphokine activated killer (LAK) cells was analyzed. With the exception of the K562 cell line, all 9 leukemic cell lines tested were resistant to the natural killer activity of freshly isolated peripheral blood lymphocytes (PBL) from healthy donors but were susceptible to the lytic action of PBL cultured for 3 days in the presence of rIL-2. Of the 32 primary myeloid and lymphoid acute leukemia samples investigated, the great majority were natural killer cell-resistant but were variably sensitive to LAK effectors. Variations in LAK activity were observed according to the donor of PBL, while little or no difference was documented in the capacity to elicit LAK activity of PBL cultured with 100 or 1,000 U of rIL-2/ml. Pretreatment of the leukemic target cells with neuraminidase did not increase substantially their sensitivity to LAK activity. LAK cells generated from the PBL of patients at the onset of the disease or in complete clinicohematological remission lysed Raji cells as efficiently as normal LAK effectors. Finally, LAK cells were capable of abrogating the tumor growth in nude mice of a human leukemic T cell line. These findings demonstrate the susceptibility in vitro and in vivo of human leukemic blasts to the lytic effect of LAK cells and point to a possible clinical exploitment of this new form of adoptive immunotherapy in the management of acute leukemia.
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PMID:In vitro and in vivo susceptibility of human leukemic cells to lymphokine activated killer activity. 325 39

Of 305 consecutive patients with symptomatic multiple myeloma treated between 1965 and 1974, a total of 4% survived ten years. Virtually all were less than 65 years old, presented with low or intermediate stage disease, and responded well to chemotherapy. Prolonged unmaintained remissions, slow tumor growth, and recontrol of relapsing disease were common. Acute leukemia caused the death of two of six long-term survivors. Patients treated since 1974 lived longer than those seen previously, a finding attributed to better control of complications and more effective combination chemotherapy.
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PMID:Ten-year survival in multiple myeloma. 406 60

Acute leukemia is a heterogeneous tumor with respect to cellular proliferation and is sensitive to positive and negative growth control factors. Tumor associated inhibitory activity (TAIA) and simultaneously present humoral stimulatory activity (HSA) in this disease may be modulated by timed sequential chemotherapy to increase tumor growth at a predictable time and make it more sensitive to accurately administered drug. Our in vivo studies of timed sequential chemotherapy in human leukemia demonstrate than an increase in tumor labeling index (LI) temporally coincides with the detection of HSA following drug administration. Maximal HSA occurs at a predictable time following initial administration of the aplasia-producing drug and is coincident with an increased LI of recovering normal marrow granulocytic elements and marrow tumor cells. These studies demonstrate the salutary effect of drugs given in high dose to reduce tumor mass and recruit tumor cells to further high-dose drug sensitivity.
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PMID:Recruitment of quiescent tumor by humoral stimulatory activity: requirements for successful chemotherapy. 715 63

Only transient engraftment of infused fetal liver cells has been demonstrated in a small proportion of patients with hypoplastic bone marrow or patients undergoing treatment for acute leukemia. This presumably reflects the ability of the recipient to reject the infused cells, the infusion of too few viable stem cells or the availability of too few accessory cells; it is clear from the successful engraftment of infused fetal liver cells in a high proportion of infants and fetuses with severe immunodeficiency diseases that, under favorable circumstances, cells derived from human fetal liver are capable of establishing effective grafts and making a substantial contribution to hematopoiesis comparable to that of transplanted cells derived from the liver of the fetal mouse, rat, rabbit or dog. Significant clinical and hematological improvements have been described following infusions of fetal liver cells without evidence of engraftment. These improvements have been attributed to the ability of the infused cells to promote regeneration of autologous hematopoiesis and to inhibit the growth of tumor cells. These possibilities are worthy of evaluation in relation to the production of putative regulators of cellular proliferation in the liver. Meanwhile a suppressor of tumor growth is being used to purge bone marrow prior to autologous transplantation. The generation in vitro of cells which possess the properties of hematopoietic stem cells generated in the liver--from cells which can be maintained as permanent cell lines--would transform hematopoietic cell replacement therapy, and the possibility may not be too unrealistic to contemplate.
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PMID:The infusion of human fetal liver cells. 831 22

Hematopoietic stem cell transplants (SCT) are used in the treatment of neoplastic diseases, in addition to congenital, autoimmune, and inflammatory disorders. Both autologous and allogeneic SCT are used, depending on donor availability and the type of disease being treated, resulting in different morbidity and outcomes. In both types of SCT, immune regulation via graft manipulation is being studied, although with highly different targeted outcomes. In general, autologous SCT have lower treatment-related morbidity and mortality, but a higher incidence of tumor relapse, and graft manipulation targets immune augmentation and/or the reduction of immune tolerance. In contrast, allogeneic SCT have a higher incidence of treatment-related morbidity and mortality and a significantly longer time of disease progression, and the targeted outcomes or graft manipulation focus on a reduction in graft versus host disease (GVHD). One source of the increased relapse rate and shorter overall survival (OS) following high dose chemotherapy (HDT) and autologous SCT is the immune tolerance that limits host response, both innate and antigen (Ag) specific, against the tumor. The immune tolerance that is observed is due in part to the tumor burden and prior cytotoxic therapy. Therefore, graft manipulation, as an adjuvant therapeutic approach in autologous SCT, is primarily focused on non-specific or specific immune augmentation using cytokines and vaccines. Recently, manipulation of the infused product as a form of cellular therapy has begun to also focus on approaches to reduce immune tolerance found in transplant patients, both prior to and following HDT and SCT. To this end, graft manipulation to reduce the presence of Fas Ligand (FasL)-expressing cells or interleukin (IL)10 and tumor growth factor (TGF)beta production has been proposed. In contrast to autologous transplantation, graft manipulation during allogeneic transplantation is used extensively. This includes limiting the infusion of T cells within the product or as a donor leukocyte infusion (DLI), resulting in a reduction in GVHD and the induction of long-term survivors. Indeed, allogeneic SCT provide the only curative therapy for patients with chronic myelogenous leukemia (CML), refractory acute leukemia, and myelodysplasia. The curative potential of allogeneic SCT is reduced, however, by the development of GVHD, a potentially lethal T-cell-mediated immune response targeting host tissues [Int. Arch. Allergy Immunol. 102 (1993) 309, J. Exp. Med. 183 (1996) 589]. The morbidity and mortality associated with GVHD limit this technology, resulting focus on those patients who have no alternative therapeutic options or who have advanced disease. Thus, allogeneic SCT provide one of the few statistically supported demonstrations of therapeutic efficacy by T cells (comparison of allogeneic to autologous transplantation). In contrast to autologous transplantation, control of GVHD following allogeneic SCT focuses on immune suppression and the induction of tolerance. Here too, graft manipulation is appropriate, and there are numerous studies of T-cell depletion to reduce GVHD, with or without the isolation and infusion of T cells as DLI. Additional strategies are examining the isolation and infusion of T cells with graft versus leukemia (GVL) activity to reduce GVHD and/or the infusion of genetically manipulated and/or selected cellular populations (monocytes or dendritic cells (DC)) to induce tolerance. Therefore, depending upon the type of transplant, the goals associated with graft manipulation can be radically different. In this review, we emphasize using graft manipulation to regulate immune tolerance and anergy in association with SCT. Although this paper focuses on hematopoietic SCT, it should be noted that these strategies are relevant to conditions other than neoplastic and congenital diseases, including solid organ transplants, and autoimmune and inflammatory diseases.
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PMID:Hematopoietic stem cell graft manipulation as a mechanism of immunotherapy. 1286 Jan 68

There is a strong graft-versus-leukemia (GVL) effect of allogeneic stem cell transplantation (SCT) due to elimination of tumor cells by alloimmune effector lymphocytes. When leukemia relapses after allogeneic SCT, donor lymphocyte transfusions (DLTs) can induce sustained remissions in some patients. This review summarizes the current status on clinical use of DLT, the basis of GVL reactions, problems associated with this therapy, and new strategies to improve DLT. Several multicenter surveys demonstrated that the GVL effect of DLT is most effective in chronic myelogenous leukemia (CML), whereas it is less pronounced in acute leukemia and myeloma. Cytokine stimulation to induce differentiation of myeloid progenitor cells or to up-regulate costimulatory molecules on tumor cells may improve the efficacy of DLT. Infections and graft-versus-host disease (GVHD) are major complications of DLT. Control of GVHD may be improved using suicide gene-modified T cells for DLT, allowing T-cell elimination if severe GVHD develops. Hopefully, in the future, GVL effect can be separated from GVHD through adoptive transfer of selected T cells that recognize leukemia-specific antigens or minor histocompatibility antigens, which are expressed predominantly on hematopoietic cells, thereby precluding attack of normal tissues. In patients with leukemia and lymphomas with fast progression, tumor growth may outpace development of effector T cells. Here it may be preferable to select stem cell transplant donors with HLA-mismatches that allow alloreactive natural killer cells, which appear early after transplantation, to retain their cytolytic function. New approaches for adoptive immune therapy of leukemia, which promise a better prognosis for these patients, are being developed.
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PMID:Graft-versus-leukemia reactions in allogeneic chimeras. 1295 64

In the past decades, a lot of effort has been put in identifying the role of matrix metalloproteinases (MMPs) in cancer. The main role of MMPs in angiogenesis, tumor growth and metastasis is degradation of extracellular matrix (ECM) and release and/or activation of growth factors through their degradative activity. The degradative activity finally results in cancer progression. MMP-inhibitors (MMPIs) have already been designed and tested, based on the degradative role of MMPs in cancer progression. First clinical trials with MMPIs have been performed with disappointing results, showing that in order to use MMP-inhibition the mechanisms underlying MMP-expression in cancer have to be further elucidated. This paper reviews the mechanisms of MMPs on molecular and cellular level and discusses the role for MMPs and MMP-inhibition in cancer with special focus on acute leukemia.
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PMID:The possible role of matrix metalloproteinase (MMP)-2 and MMP-9 in cancer, e.g. acute leukemia. 1515 58

B7-H1 (B7 homologue 1, PD-L1), expressed on the surface of tumor cells or antigen-presenting cells in the tumor microenvironment, can suppress antitumor immune reaction, promote tumor growth and help tumor cells to escape the immune response. To investigate the correlations between B7-H1 expression and acute leukemia patients' immunotherapeutic efficacies and prognoses, we detected the expression of B7-H1 by immunohistochemistry and Real-time quantitative PCR and monitored the immunotherapeutic efficacies and prognosis in 60 acute leukemia patients, in which 14 cases of acute monocyte leukemia(M5) patients received active immunotherapy. The levels of mRNA and protein expression of B7-H1 changed synchronously.B7-H1 was expressed in human acute leukemia cells, especially in M5. The expressions of B7-H1 were significantly higher in the relapse patients than in the de novo patients and after immunotherapy than before immunotherapy. Significant correlations existed between the expressions of B7-H1 and the M5 patients' immunological reactions and immunotherapeutic efficacies.B7-H1 negative patients had better immunotherapeutic efficacies than the positive patients who were prone to have a severe complication of pulmonary infection. Multivariate analysis indicated that B7-H1 status was an independent prognostic factor for M5 patients. In conclusion, B7-H1 is highly expressed on leukemia cells of M5 patients, can significantly affect the immunotherapeutic efficacies of M5 patients and is a novel prognostic marker for M5.
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PMID:Clinical significance of B7-H1 (PD-L1) expression in human acute leukemia. 1875 22


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