Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Granulocytic sarcoma is an extramedullary tumor of malignant granulocytic progenitor cells that accompanies, heralds, or signals relapse of acute myelogenous leukemia (AML), or indicates blastic transformation of a chronic myeloproliferative disorder. We describe a case involving the uterine cervix of a 51-year-old woman that led to the diagnosis of AML. Granulocytic sarcoma can occur in the female genital tract and may be the first clinically significant manifestation of a hematologic malignancy. The salient findings in 28 reported cases from 12 different countries are reviewed. Awareness of this lesion is important for all medical personnel involved in the health care of women.
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PMID:Granulocytic sarcoma of the uterine cervix--literature review of granulocytic sarcoma of the female genital tract. 163 33

Thymidine kinase (TK) is a cellular enzyme which is involved in a "salvage pathway" of DNA synthesis. It is activated in the G1/S phase of the cell cycle, and its activity has been shown to correlate with the proliferative activity of tumor cells. Additionally, certain viruses are able to induce cellular TK production and activity. Clinical studies have reported elevated serum TK levels in a variety of neoplasias. The majority of these studies concerned hematologic malignancies. TK seems to be a useful marker in non-Hodgkin's lymphoma, where it correlates with clinical staging and provides significant prognostic information on (progression-free) survival. Preliminary results in acute myeloid leukemia indicate that pretreatment serum TK values may predict the response to the first induction chemotherapy. Moreover, serum TK appears to have some clinical value in such solid tumors as prostate cancer, breast cancer, and small-cell lung cancer, whereas it is not a reliable marker of non-small-cell lung cancer and brain tumors.
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PMID:Thymidine kinase: a tumor marker with prognostic value for non-Hodgkin's lymphoma and a broad range of potential clinical applications. 164 53

In this study we demonstrate that tumor necrosis factors (TNF alpha and TNF beta) are potent modulators of the in vitro proliferation of human AML cells. Blast cells from 11 cases of acute myeloblastic leukemia (AML) were incubated with recombinant TNF alpha or TNF beta in serum-free 3H-TdR uptake and colony culture systems in the presence or absence of recombinant interleukin-3 (IL-3), granulocyte macrophage colony-stimulating factor (GM-CSF), G-CSF, or M-CSF. Depending on the supplemented CSF, TNF could upregulate or suppress AML blast proliferation. Enhancement of AML growth by TNF was observed in the presence of IL-3 (in 9 of 11 cases in 3H-TdR assay; 6 of 9 cases in colony assay) and GM-CSF (in 8 of 11 cases in 3H-TdR assay; 4 of 9 cases in colony assay). In certain cases in which IL-3 or GM-CSF alone was unable to induce proliferative responses of AML cells, the simultaneous addition of TNF elicited colony growth and DNA synthesis suggesting a synergistic action between TNF and IL-3 or GM-CSF. In contrast, TNF suppressed G-CSF-induced growth (9 of 10 cases in 3H-TdR assay; 5 of 6 cases in colony assay). TNF could also stimulate DNA synthesis (in 2 of 11 cases) or colony formation (in 2 of 9 cases) in AML cultures without the addition of other growth factors. Experiments with neutralizing antibodies and specific radioimmunoassays for individual CSFs showed that the synergistic and antagonistic effects of TNF on AML growth could not be attributed to a release of one of these CSFs by the AML cells. The opposing consequence of exposure of AML blasts to TNF are of interest in view of our understanding of the pathophysiology of AML growth and the in vivo application of recombinant cytokines in AML patients.
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PMID:Modulation of colony stimulating factor-(CSF) dependent growth of acute myeloid leukemia by tumor necrosis factor. 168 38

Immunohistochemical investigations were performed on decalcified, paraffin-embedded iliac crest trephine biopsy specimens from 30 cases of acute myeloid leukemia (AML, as defined by the FAB classification) with antibodies against B cells (L26, 4KB5, MB1, Ki-B3), T cells (UCHL1, MT1), myeloid/histiocytic cells (anti-neutrophil elastase, MAC387, anti-S-100 protein, anti-alpha 1-antichymotrypsin, DAKO-M1), natural killer/killer cells (anti-Leu-7), and megakaryocytes (anti-factor VIII-related antigen). (1) The blast cells of all the cases reacted with from at least two to at most eight different antibodies. Each antibody reacted with blast cells in a minimum of two (maximum 30) cases. (2) MT1, Ki-B3, anti-alpha 1-antichymotrypsin anti-neutrophil elastase, anti-S-100 protein, and MAC387 stained blast cells in more than 50% of the cases; MB1, L26, UCHL1, 4KB5, and DAKO-M1 in 20% to 50% of the cases; and anti-Leu-7 and anti-factor VIII-related antigen in less than 20% of the cases. (3) In the majority of cases many T lymphocytes, a small-to-moderate number of B lymphocytes, and a few Leu-7-positive lymphoid cells were intermingled with the blast cells. In some cases, especially where only a minor proportion of the blast cells was immunostained, it was nearly impossible to distinguish the lymphocytes of the tumor's stromal reaction from small blast cells. Thus, AML exhibits a heterogeneous immunophenotype in trephine biopsy specimens. Immunohistologic diagnosis of this disease in such specimens may be extremely difficult. Since staining of the blast cells with one or more of the antibodies generally used to define B cells, T cells, or their neoplastic derivatives is not uncommon, misinterpretation as non-Hodgkin's lymphoma of high-grade malignancy could easily occur. These findings also suggest that mixed-type (hybrid) acute leukemias with coexpression of myeloid and lymphoid cell markers could be more common than generally realized.
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PMID:Acute myeloid leukemia: immunohistologic findings in paraffin-embedded bone marrow biopsy specimens. 169 93

CD7 has been used as a valuable marker for normal and malignant T cells and also for a proportion of acute nonlymphocytic leukemia (ANLL) cells. Difference in reactivity was noticed among CD7 antibodies, however, when tested against ANLL cells and myeloid/monocytoid cell lines; Tp40 antibody produced in our laboratories was not reactive with the HL-60 promyelocytic line, whereas 4A antibody was reactive, even though both detected a quite similar or an identical epitope on CD7 molecule. Preincubation of HL-60 cells with human immunoglobulin preparation clearly negated the reactivity by 4A, suggesting that 4A antibody is not reactive to CD7 itself, but it probably binds with immunoglobulin G Fc receptors expressed on HL-60 cells. Five cases of ANLL which were positive with 4A antibody were selected and tested with Tp40 antibody, and only two were found to be positive. Expression of CD7 mRNA in these two cases (but not in other cases) was also demonstrated by Northern blotting with a cDNA probe for CD7 recently cloned in our laboratories, indicating that CD7 is expressed on a certain fraction of ANLL, although the positive cases may be smaller than the reports so far appeared. A Northern blot study was also conducted with two acute lymphocytic leukemia cases and one lymphoblastic lymphoma case with CD7+, CD2-/+/-, CD5-/+/- phenotype and germline T cell receptor beta genes. CD7 mRNA is expressed in all three cases and CD3 mRNA is also observed in two cases, suggesting that these tumor cells are of T precursor origin.
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PMID:Genuine CD7 expression in acute leukemia and lymphoblastic lymphoma. 170 41

The 9-year-old boy was admitted to Shizuoka Children's Hospital because of cervical lymphoadenopathy. Complete blood count showed normal RBC and platelet counts. WBC was 2700/microliters with no tumor cells. Bone marrow aspirate showed normocellularity with 34% tumor cells. Lymph node biopsy from his right neck was performed and the patient was diagnosed as non-Hodgkin's lymphoma (lymphoblastic type). Surface marker analysis disclosed that the tumor cells were positive for CD5, CD7, CD19, CD38, CD71, and Ia antigen. Chromosomal analysis of the cervical lymph node revealed 46, XY, t(7;14) (p15;q32). Molecular investigation with appropriate probe showed germ-line configurations of IgH gene, TcR beta gene, and TcR gamma gene, and one rearranged band of TcR delta gene. Monoclonality of tumor cells was demonstrated from chromosomal analysis and molecular study. CD7 and CD19 are not lineage specific antigens because CD7 is expressed on immature AML cells and CD19 is expressed on T ALL cells or AML cells. Moreover, TcR delta rearrangement is considered to occur at early phase of hematolymphoid cells. Based on these data, tumor cells of this patient is considered to originate from immature lymphoid cell, so-called lymphoid stem cell.
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PMID:[CD5+, CD7+, and CD19+ non-Hodgkin's lymphoma in a child]. 170 16

High-dose recombinant interleukin-2 (rIL-2) therapy can induce long-term remission in patients with melanoma and renal and colon cancer. More recently, in vivo IL-2 therapy was shown to induce complete or partial remission in some cases of relapsed chemotherapy-resistant acute myeloid leukemia. We have investigated the phenotypic modifications of bone marrow cells obtained from five patients with acute myeloid leukemia in relapse receiving high-dose i.v. rIL-2. We found that, in three of five patients, IL-2 could induce, in vivo, an increase in the expression of CD54/ICAM-1 and to a lesser extent of CD58/LFA-3 on bone marrow leukemic blasts. This demonstrates that rIL-2 modifies directly or indirectly the expression of the cell surface molecules of the tumor cells themselves. Upregulation of such adhesion molecules could account for the enhancement of cell interactions between the tumor and effector cells such as T, natural killer, and phagocytic cells as well as being indicators of differentiation signaling.
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PMID:Cell surface expression of ICAM-1 (CD54) and LFA-3 (CD58), two adhesion molecules, is up-regulated on bone marrow leukemic blasts after in vivo administration of high-dose recombinant interleukin-2. 172 5

Fifty percent of patients with the myelodysplastic syndrome, frequently following treatment by radiation or chemotherapy, have prognostically unfavorable deletions of the long arms of chromosomes 5 and 7, or trisomy 8, as have the 25% of patients with acute myeloblastic leukemia where remissions last 6-12 months, and where relapse cannot be prevented. In contrast, patients with prognostically favorable cytogenetics (translocation 15; 17 or 8; 21 or inversion 16) maintenance chemotherapy may prevent relapses. Of chronic myelocytic leukemia patients, 85% can achieve hematological remission with interferon alpha, and 40% a partial cytogenetic remission, which probably delays relapse.
Med Oncol Tumor Pharmacother 1991
PMID:Prevention of chemotherapy-induced leukemia and of leukemia relapses. 172 55

We analyzed the cytotoxicity and characterized the phenotype of oncolytic bone marrow (BM) lymphocyte subsets generated in vitro by interleukin-2 (IL-2) and stimulator cells (SC). Two irradiated B-lymphoblastoid cell lines (Daudi and EBV-transformed BSM) and fresh human acute myelogenous leukemia (AML) were used as SC. Stimulation with Daudi and IL-2 resulted in a substantial increase in cytotoxic activity (100- to 1000-fold) against a broad range of tumor targets, and total cellular expansion was higher compared to stimulation with IL-2 alone. The most prominent increase was observed in the CD16+ and CD56+/CD3- natural killer (NK) cell subset; however, a significant increase was also observed in CD56+/CD3+ T cells. Functional analysis of Daudi- and IL-2-generated subsets using fluorescence-activated cell sorting (FACS) revealed that most of the lytic activity was mediated by NK cells. Significant potentiation of oncolytic activity and cell growth was also seen in the cultures stimulated with BSM or fresh AML and IL-2. The highest oncolytic activity in the latter cultures was mediated primarily by CD8+, CD3+, and CD56- T cells, although NK cells also participated in cytotoxic activity. The T cell-mediated cytotoxicity was restricted by the major histocompatibility complex (MHC), since most cytotoxicity could be blocked by HLA I antibodies. Additionally, we observed that optimum stimulation of cytotoxicity required effector cell-stimulator cell contact. These data indicate that depending on the tumor used for stimulation, different lymphocyte subsets may be generated in IL-2 cultures. These different approaches may be useful in both specific and nonspecific immunotherapy.
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PMID:Generation of MHC-nonrestricted and restricted oncolytic subsets from human bone marrow. 172 69

The hemolymphopoietic growth factors, including the colony-stimulating factors (CSF) and interleukins (IL), are described and categorized on the basis of their biological features in laboratory systems. Although these agents are varied and exceptions exist, in general they lack lineage specificity although they may express lineage-predominant activity. They act at multiple levels of hemolymphopoietic cell differentiation, demonstrate additive or synergistic effects when combined in vitro, require surface receptors on target cells to directly express their activity, and may be produced by a variety of cells. This framework of behavioral generalizations, completed by the specifics of each factor's activity, despite the artifactual and simplified nature of in vivo systems, forms the basis for concepts of in vitro activity and for clinical applications. Hemolymphopoietic growth factors studied in the clinic have demonstrated impressive and important activity, validating much of the in vitro data. Granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) have clearly reduced neutropenia and infection rates when administered following conventional chemotherapy and high-dose chemotherapy followed by autologous bone marrow transplantation. To a varying degree, similar results with G-CSF and/or GM-CSF have been described in other diseases including acute myelogenous leukemia (AML) treated following induction chemotherapy, myelodysplastic syndrome, hairy cell leukemia, aplastic anemia, and chronic neutropenias. In preliminary studies IL-3 has been shown to have similar qualitative activities. However, these agents have not demonstrated a reproducible salutary impact on platelet or red cell lineages. Adverse effects on platelet counts and/or platelet recovery have been noted. Additionally, hemolymphopoietic growth factor receptors have been identified on malignant cells, suggesting that these factors could stimulate neoplastic growth. Studies with GM-CSF and IL-3 have demonstrated blast proliferation in some cases of AML and myelodysplasia, underscoring the capacity of these agents to stimulate the growth of myeloid leukemia. No clinically evident impact of these factors upon the growth of solid tumors has been identified but this issue has not been adequately studied. The toxicity of these agents has been surprisingly limited and appears to be related to their biologic activities. Hemolymphopoietic growth factors as single agents have broad clinical applications in cytopenias. Several methods for enhancing the clinical activity of these agents are under study, including the use of combinations of growth factors synergistic in vitro.
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PMID:Recombinant human hematopoietic growth factors in the treatment of cytopenias. 172 85


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