Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The tumor inhibitory properties of Corynebacterium parvum obtained from Burroughs Wellcome (CP-BW) or from Institut Merieux (CP-IM) were compared in four animal tumor models: the CaD2 mouse mammary carcinoma treated by intravenous (I.V.) or intratumoral (I.T.) injection of C. parvum; 13762A rat mammary adenocarcinoma treated by I.T. injection of C. parvum either alone or combined with excision of the primary tumor; LSTRA murine leukemia and line 10 cavian hepatoma, each treated with vaccines containing irradiated tumor cells and C. parvum. Both preparations were active against each tumor. In most comparisons the potency of the two materials was not different, but in a few cases the CP-BW was effective at a lower dose than was the CP-IM. These results demonstrate the versatility of C. parvum for use in a variety of immunotherapy procedures and show that the potencies of the two major types of C. parvum are very similar.
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PMID:Treatment of cancer using Corynebacterium parvum: similarity of two preparations in four animal tumor models. 739 33

The antitumor effects of biological response modifiers (BRM) in an experimental mouse model, the "double grafted tumor system," were analysed. Intratumoral administration of PSK (polysaccharide Kureha), a Coriolus preparation into primary tumor induced a cure of not only the primary solid tumor but also the metastatic, distant tumor. The effect of PSK on in vitro invasion by murine RL male-1 leukemia cells was studied using Biocoat Matrigel Invasion Chamber (Becton Dickinson Labware). We determined the ability of tumor cells to penetrate matrigel-coated filters in the presence or absence of PSK. PSK (100 micrograms/ml) reduced to half the number of invasive tumor cells for 3 hr incubation. PSK inhibited tumor cell invasion of matrigel-coated filters in a dose-dependent manner. Matrigel includes laminin, collagen, fibronectin and heparan sulfate proteoglycan. It is possible, therefore, that PSK may inhibit enzymes which digest the components of basement membranes, extra cellular matrices (ECM). This phenomenon suggests that PSK also inhibits metastatic activity of tumor cells in vivo.
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PMID:[Antitumor effect of intratumoral administration of a Coriolus preparation, PSK: inhibition of tumor invasion in vitro]. 794 50

Detection of disseminated leukemia within organ is often very difficult and might lead to underestimation of the metastatic load. Therefore, we transduced the mouse ESb T lymphoma with the bacterial lacZ gene, which allowed us to follow metastasis at the single cell level. Intradermal primary tumor growth of lacZ transduced ESbL cells (L-CI.5s) comprised three phases: an initial expansion phase (day 0 to 9, increase from 0 to 8 mm, tumor diameter), a plateau phase (day 9 to 20, constant diameter of 8 mm and necrosis), and a second expansion phase (day 20 to 30, increase from 8 to 15 mm). Liver metastasis could already be detected at day 3 and maintained at that level until day 23, where exponential expansion started. A distinct mosaic-like metastasis pattern developed, with preferential localization of tumor cells to the periportal areas of the liver in immunocompetent animals. In contrast, in immunocompromised mice, primary tumor growth and metastasis were progressive and metastasis appeared as diffuse or focal/clustered. Healthy animals surviving a tumor cell inoculum of a variant cell ESbL-CI.5) with a reduced metastatic potential carried low levels of possibly dormant tumor cells in the bone marrow. Thus, this study showed that host immunocompetence determines to a large extent kinetics and load of spontaneous liver metastases and even influences the pattern and localization of disseminated lymphoma cells.
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PMID:Pattern and load of spontaneous liver metastasis dependent on host immune status studied with a lacZ transduced lymphoma. 794 89

From 1976 to 1989 the authors treated 21 infants and children with malignant tumors of the chest wall. Fifteen were classified as Askin's tumors or Ewing's sarcoma, which we now consider as a single entity of primitive neuroectodermal origin. They are infrequent but highly aggressive tumors that involve the chest wall in children. Five patients presented with metastatic disease; despite chemotherapy and radiotherapy, all succumbed to progressive disease. Ten patients with localized disease received combined modality therapy including surgical resection (three after initial chemotherapy), radiotherapy, and chemotherapy. Surgery involved resection of the mass and up to three ribs, with prosthetic mesh reconstruction in one patient. Six of the 10 patients with localized disease are continuously disease-free 3.5 to 9 years (median, 5 years) following diagnosis. No patient had local recurrence. Of the four whose treatment failed, one died (free of disease) from complications after resection of an extensive primary tumor. In the second patient, acute monocytic leukemia developed shortly after relapse in a distant bone site. The patient died during induction for the leukemia. In the other two patients, hilar and carinal lymph node relapse occurred 68 and 80 months after initial treatment. One of the patients is considered in second remission (now 105 months later) after further chemotherapy (Adria-VAC) and radiation; the other succumbed to secondary relapse 17 months after second remission was achieved through chemotherapy, radiation, and surgery. Initial percutaneous needle biopsy of the large lesions has provided adequate material for histological, immunohistochemical, cytogenetic and ultrastructural diagnosis, and permitted initial chemotherapy before proceeding to surgical resection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malignant small round cell tumor (Ewing's-PNET) of the chest wall in children. 817 88

Therapy-related acute myeloid leukemia (t-AML), often presenting as myelodysplasia (t-MDS), has become the most serious long-term complication of cancer therapy and offers a unique opportunity to study chemical leukemogenesis. Seven cohorts of patients treated for six different types of primary tumor have been followed closely for leukemic complications, and 115 consecutive patients with t-MDS or t-AML, including 45 cases from the cohorts, have been investigated cytogenetically at our institutions during the past 16 years. In patients primarily treated with alkylating agents, the risk of t-MDS and t-AML increased by approximately 1% per year from 2 to at least 8 years after start of treatment. In most cases, the disease presented as t-MDS with loss of a whole chromosome 5 or 7, or various parts of their long arms, and the leukemias were of FAB-subtypes M1, M2, or M4. In patients treated with drugs targeting at DNA-topoisomerase II, such as etoposide, doxorubicin, 4-epidoxorubicin, or mitoxantrone combined with drugs reacting directly with DNA, such as cisplatin or alkylating agents, the risk of leukemia increased much more steeply from only one year after start of therapy. These early onset cases often presented as overt leukemia of FAB-subtypes M4 or M5 with balanced translocations to chromosome bands 11q23 and 21q22, whereas later onset cases often shared characteristics with cases observed after therapy with alkylating agents alone. Both alkylation of DNA and poisoning of DNA-topoisomerase II may result in development of t-AML with different clinical and cytogenetic characteristics. There may be a synergistic leukemogenic effect between the two types of drug, and in patients with germ cell tumors treated with etoposide, cisplatin and bleomycin, reassessment suggested the risk of leukemia to increase exponentially with increasing doses of cisplatin and etoposide.
Leukemia 1993 Dec
PMID:Therapy-related myelodysplasia and acute myeloid leukemia. Cytogenetic characteristics of 115 consecutive cases and risk in seven cohorts of patients treated intensively for malignant diseases in the Copenhagen series. 825 96

The ELM erythroleukemia is novel in that long-term survival of leukemic cells in culture (ELM-D cells) is dependent on contact with a bone marrow-derived stromal feeder cell layer. However, a number of stroma-independent (ELM-I) mutants that vary in their ability to differentiate in vitro in response to erythropoietin and interleukin-3 have been derived. We have attempted to define the genetic changes responsible for these different phenotypes. At the p53 locus in the primary leukemic cells, one copy of the gene has been lost whereas the other contains an 18-bp depletion, implicating its mutation as an early step in the development of the leukemia. Changes in ets gene expression have also been found. The Fli-1 gene region is rearranged in the primary tumor because of the insertion of a retrovirus inserted upstream of one Fli-1 allele, but this does not result in Fli-1 gene activation in any of the ELM-D or ELM-I cell lines except one. It seems significant that this line is the only one to have lost the ability to differentiate in response to erythropoietin. In addition, up-regulation of erg is associated with stromal cell-independent growth, since all ELM-I mutants have moderate levels of erg mRNA, whereas only low or undetectable levels are found in primary leukemic cells in vivo or in ELM-D cells in vitro. This up-regulation of erg mRNA seems to be important for stromal cell-independent growth, since ELM-D cells show elevated expression of the erg gene after separation from stromal cells. This seems to be made permanent in ELM-I mutants, since they do not down-regulate erg mRNA when grown in contact with stromal cells. We therefore propose that ets family members regulate both the survival and differentiation of erythroid cells.
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PMID:Differentiation arrest and stromal cell-independent growth of murine erythroleukemia cells are associated with elevated expression of ets-related genes but not with mutation of p53. 835 1

Three cases of secondary (therapy-related) hematologic malignant conditions were identified among 95 children as old as 18 years of age; the cases were diagnosed between 1984 and 1990 and consisted of acute lymphoblastic leukemia, acute myeloid leukemia (AML), and myelodysplastic syndrome (MDSs). They constituted 10% of all new cases of AML and MDS seen at the University Hospitals of Cleveland during this time and were not related to congenital factors. The primary malignant conditions were malignant thoracopulmonary tumor (Askin tumor), neuroblastoma, and Burkitt's lymphoma. The secondary hematologic disorders all showed a prominent monocytic component: acute monocytic leukemia, MDSs evolving to acute myelomonocytic leukemia, and chronic myelomonocytic leukemia. The mean interval between treatment for the primary malignant condition and the onset of secondary disease was 36 months. All had received cyclophosphamide and an epipodophyllotoxin for the primary tumor; two were treated with radiation therapy. Cytogenetic abnormalities included del(5), del(13), t(1;6), and t(9;11)(p22[symbol:see text]3). The survival time after the onset of secondary disease was short.
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PMID:Myelodysplastic syndrome and acute myeloid leukemia after treatment for solid tumors of childhood. 837 35

Lymphoma represents a major source of morbidity and mortality among AIDS patients. AIDS-associated non-Hodgkin lymphomas (AIDS-NHL) are almost invariably B-cell derived, are classified as high or intermediate grade lymphomas, and display three main histologic types: namely, small non-cleaved cell lymphoma (SNCCL), large cell immunoblastic plasmacytoid lymphoma (LC-IBPL), and large cell lymphoma (LCL). Here we report the in vitro establishment of three new AIDS-NHL cell lines (termed HBL-1, HBL-2, and HBL-3) derived from three AIDS-SNCCL patients differing in primary tumor sites and risk factors for HIV infection. The derivation of the cell lines from the original tumor clones was established by immunophenotypic and molecular genetic analysis. These cell lines display clonal immunoglobulin gene rearrangement, express surface immunoglobulin and B-cell restricted markers, and exhibit a phenotype consistent with SNCCL. Monoclonal Epstein-Barr virus infection was found in only one of the cell lines (HBL-1). Cytogenetic analysis demonstrated the presence of a chromosomal translocation involving the c-myc proto-oncogene and an immunoglobulin locus in all three cell lines. The pattern of genetic lesions detected in HBL-1, HBL-2, and HBL-3 reflects that found in primary AIDS-SNCCL and includes activation of the c-myc oncogene as well as inactivation of the p53 tumor suppressor gene. These cell lines should prove useful in studies of the biological, immunological, and viral factors involved in AIDS-associated lymphomagenesis.
Leukemia 1993 Oct
PMID:In vitro establishment of AIDS-related lymphoma cell lines: phenotypic characterization, oncogene and tumor suppressor gene lesions, and heterogeneity in Epstein-Barr virus infection. 841 24

Eleven therapy related leukemias (TRL) who were hospitalized in the Department of Hematology and Chemotherapy, Kanagawa Cancer Center between October 1983 and December 1993 were identified. Six of the patients were males and five were females. Their median age was 62 years (range from 14 to 75). Three patients had previously received treatment for breast cancer and two patients for malignant lymphoma. The other patients had received treatment for lung cancer, urinary bladder cancer, gastric cancer, brain tumor, maxillary sinus cancer and macroglobulinemia, respectively. Seven patients had been treated with chemotherapy and four patients had been treated with chemotherapy and irradiation for the primary tumor. The TRL cases consisted of 8 acute non-lymphoid leukemias, two acute lymphoid leukemias and one hypoplastic leukemia, respectively. The status of primary tumors at the development of TRL was complete remission in ten patients and partial remission in one patient. Three of the 10 patients who received anti-leukemic therapy entered complete remission and the median survival time was 36 days (from 7 days to 489 days). One patient expired of pneumonia before he received anti-leukemic therapy. TRL patients showed poor response to chemotherapy and had poor prognosis. These data suggest that the use of reduced doses of carcinogenic drugs for primary tumors might be required to prevent the development of TRL.
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PMID:[Therapy related leukemia]. 853 25

We examined autonomous and interleukin-2 (IL-2)-responsive growth activities of leukemic cells derived from peripheral blood, as well as several clinical manifestations, including serum lactate dehydrogenase (LDH) level, of 35 patients with adult T-cell leukemia (ATL) to determine whether these properties were related to prognosis. Growth activities were measured by [3H]-thymidine incorporation of the cells after 24 hours' culture with or without exogenous IL-2. Both autonomous and IL-2-responsive growth activities were higher in the patients than in healthy controls and were significantly correlated with each other (P < .0001, r = .956). Both higher growth activities were significantly associated with shorter survival times (P = .0042, r = .472 and P = .0117, r = .421, respectively). An increased serum LDH value was also significantly associated with shorter survival times (P = .0011, r = .530), but corrected calcium level, sex, white blood cell count, or age were not. These results strongly suggest that both growth activities of primary tumor cells, in addition to the serum LDH value, are prognostic determinants in ATL. We propose a new prognostic classification combining LDH values and autonomous growth activity into three groups: (1) high growth activity and high LDH; (2) high growth activity and low LDH, or low growth activity and high LDH; and (3) low growth activity and low LDH, which showed a significant relationship to survival time (P = .0014; the median survival time for each group was 39, 94, and 340 days, respectively).
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PMID:Relation of autonomous and interleukin-2-responsive growth of leukemic cells to survival in adult T-cell leukemia. 863 10


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