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

Plasma lipid-bound sialic acid (LSA) was assayed in normal volunteers, patients with non-malignant diseases, and a variety of cancer patients. Mean plasma LSA in 50 normal volunteers, 16 patients with non-malignant diseases, 54 breast cancer, 17 lung cancer, 15 colon cancer, 7 ovarian cancer, 5 prostate cancer, 4 leukemia, 4 gastrointestinal, 3 thyroid cancer, 3 pancreas cancer and 2 adrenal cancer patients were 17.7, 23.2, 58, 85, 56.7, 46.2, 56.7, 53.3, 31.1, 33.2 and 119.5 mg/dl, respectively. None of the normal volunteers had elevated plasma LSA values. Plasma LSA level was not significantly different in male and female volunteers. Two out of 114 different cancer patients had plasma LSA levels within normal range exhibiting 98.2% sensitivity of the assay. Plasma LSA, which is relatively simple to assay, may be used as a tumor marker in wide variety of neoplastic diseases.
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PMID:Plasma lipid-bound sialic acid alterations in neoplastic diseases. 229 88

The effective treatment of systemic cancer began in the 1950s on two fronts, i.e., childhood leukemia and choriocarcinoma. These two diseases were successfully treated as a direct result of the use of antifolate methotrexate. The demonstration of complete durable remissions in these diseases quickly led to development of other anticancer drugs, tested using the prospective clinical trials. In the 1960s as the number of active drugs increased, combination chemotherapy was introduced. Other systemic cancers, such as Hodgkin's, large cell lymphoma, and testicular cancer, became curable in the 1970s. For the common low-growth fraction solid tumors, the curability of systemic disease remained elusive until the introduction of adjuvant therapy to treat micrometastases. The past decade of the 1980s has seen improvement in the outcomes for breast cancer, osteosarcoma, and possible colon cancer utilizing adjunctive chemotherapy. The 1980s also saw the introduction of biologic therapies that have further improved the outcomes of several leukemias and produced consistent responses in patients with renal cell and melanoma. The 1990s will undoubtedly see more improvements as the effects of current drugs will be enhanced not only by improved integration of systemic and local therapies but also by utilizing cytokines and biologic response modifiers in concert with cytotoxics. Moreover, as we understand more about the process of cancer induction, promotion, and progression, more specific anti-cancer approaches will be developed to control cancer even before clinical cancer is diagnosed. Underlying and facilitating the improvement in cancer therapy have been not only the experimental results of many laboratory scientists but also the outcomes from many controlled clinical trials, the laboratory of clinical scientists.
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PMID:Progress in the systemic treatment of cancer. Concepts, trials, drugs, and biologics. 230 52

In HT29 cells 5-fluorouracil (5FU) cytotoxicity is enhanced by subsequent incubation of cells in medium containing 1% N-methylformamide (NMF). This enhancement does not appear to be related to differences in the repair of 5FU-induced DNA damage. It is proposed that the inhibition of DNA synthesis by NMF (that is reversible and does not result in any detectable toxicity) becomes a lethal event in a cell in which DNA synthesis has already been altered by 5FU exposure. The synergism is sequence dependent (i.e. it does not occur when NMF is given before 5FU) and specific for some cell types as shown by the fact that no synergism was found in L1210 mouse leukaemia cells. In nude mice transplanted s.c. with HT29 cells daily 5FU treatment (for 5 days) followed by daily NMF treatment (for 10 days) caused much greater inhibition of tumour growth than either drug alone or the same combination given in the opposite order (NMF then 5FU). These results, if confirmed on other human colon tumours, could be of clinical interest as a means of increasing the therapeutic efficacy of 5FU in patients with colon cancer.
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PMID:Synergism between 5-fluorouracil and N-methylformamide in HT29 human colon cancer line. 232 1

The biodistribution of the 202 monoclonal antibody against CEA labeled with 88Y by the bicyclic DTPA anhydride method was studied in normal Balb/c mice. The in vitro binding to 1 X 10(7) CO112, LS174T and WiDR colon cancer cells was 21.0, 27.3 and 18.8%, respectively. The binding to an equal number of KM-3 leukemia cells and normal human lymphocytes was 8.9 and 3.2%, respectively. Liver, spleen, kidney and blood were the tissues that showed the highest uptake of radiolabeled antibody in vivo.
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PMID:Radiolabeling of monoclonal antibody against carcinoembryonic antigen with 88Y and biodistribution studies. 241 85

This study was conducted to assess the enhanced antitumor effects of natural human tumor necrosis factor alpha (nHuTNF-alpha) and natural human interferon alpha or gamma (nHuIFN-alpha or -gamma), in combination, on ten human cancer cell lines. The cell lines tested were colon cancer (RPMI4788), lung cancer (PC10), gastric cancer (MKN-1 and MKN-28), nasopharyngeal cancer (KB), leukemia (K562), lymphoma (Daudi), Liver cancer (H-7) and breast cancer (ZR-75-30 and ZR-75-1). A mixture of nHuTNF-alpha and nHuIFN-alpha (1:1, by unit) showed cytotoxic effects on nHuTNF-alpha resistant cell lines such as RPMI4788, KB and Daudi or nHuIFN-alpha resistant cell lines such as KB, and ZR-75-1, as well as on nHuTNF-alpha or nHuIFN-alpha sensitive cells. A synergistic antitumor effect occurred in four cell lines (RPMI4788, PC10, Daudi and ZR-75-1) treated with a combination of nHuTNF-alpha and nHuIFN-alpha. Also, a combined treatment with nHuTNF-alpha and nHuIFN-gamma (1:1/100, by unit) showed cytotoxic effects on nHuTNF-alpha or nHuIFN-gamma resistant cell lines such as MKN-1, MKN-28, Daudi, H-7 and ZR-75-1. A synergistic antitumor effect occurred in eight cell lines (RPMI4788, PC10, MKN-1, MKN-28, KB, Daudi, H-7 and ZR-75-1). Thus, the combined treatment with nHuTNF-alpha and nHuIFN-alpha or -gamma expanded the spectrum of sensitive cells. These results indicate that the combined use of nHuTNF and nHuIFN may provide a certain approach to cancer treatment.
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PMID:Synergistic antitumor effects of natural human tumor necrosis factor-alpha and natural human interferon-alpha or -gamma on human cancer cell lines. 250 39

Control mechanisms of normal differentiation are disrupted in cancer cells but can be restored by treatment with site-selective cAMP analogs. The cellular events associated with such changes entail compartmental redistribution of the cAMP-dependent protein kinase type II regulatory subunit, RII beta. The results of this study indicate that the molecular mechanisms of action involve changes in specific DNA-binding activity of putative transcription factors. Gel retardation analyses revealed that nuclear extracts from cells of various human cancer cell lines [colon cancer (LS-174T), gastric cancer (TMK-1), and leukemia (K-562)] and rodent pheochromocytoma (PC12) show a concentration-dependent increase in binding activity to a synthetic DNA that contained the cAMP-responsive element 5'-TGACGTCA-3' after treatment with 8-Cl-cAMP. Such an increase in cAMP-responsive element binding activity was not observed in the 8-C1-cAMP-unresponsive MKN-1 gastric cancer cells. These findings indicate that the antitumor activity of site-selective cAMP analogs may reside in the induction of transcription factors that restore normal gene regulation in cancer cells.
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PMID:Site-selective 8-Cl-cAMP which causes growth inhibition and differentiation increases DNA (CRE)-binding activity in cancer cells. 252 74

Correlation between sensitivity to two cross-linking agents, 1-(4-amino-2-methylpyridine-5-yl)-methyl-3-(2-chloroethyl)-3-nitrosourea (ACNU) and cisplatin (DDP), and intracellular glutathione (GSH) level was investigated for two naturally drug-resistant human colon cancer cell lines in comparison with two drug-sensitive human leukemia cell lines. As a result, no appreciable correlation was observed between them. We also studied the possibility that DL-buthionine-S,R-sulfoximine (BSO), an inhibitor of GSH biosynthesis, can sensitize the cancer cells to these anticancer agents via depletion of intracellular GSH. It was found that BSO potentiated ACNU cytotoxicity against human leukemia K562 cells and DDP cytotoxicity against K562 and human colon cancer WiDr cells. It indicates that cancer cells with higher GSH level are more effectively sensitized by BSO regardless of degree of their intrinsic sensitivity to these anticancer agents. These results suggest that intracellular GSH level is not a common mechanism for natural resistance to cross-linking agents in human colon cancer cells but one of the determinants of sensitivity to these anticancer agents of GSH-rich cells.
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PMID:Intracellular glutathione levels in human colon cancer cells naturally resistant to cross-linking agents. 259 79

We reported a rare case of triple cancers with acute lymphoblastic leukemia (ALL) associated with disseminated intravascular coagulopathy (DIC) after the operations of colon cancer and primary lung cancer. A 78-year-old Japanese male, who had been operated upon for colon cancer (adenocarcinoma) on March 1981, metastatic brain tumor (adenocarcinoma) on December 1986, and primary lung cancer (squamous cell carcinoma) on February 1987, was admitted to our hospital because of severe general malaise on December 6 1987. On admission, he had mild hepatosplenomegaly and hemorrhage diathesis such as purpura. Serum LDH increased to 2,515 mU/ml. The white blood cell count was 6,210/microliters with 53% leukemia cells, and the platelet count was 12,000/microliters. A bone marrow was infiltrated with 96.0% leukemia cells. The leukemia cells stained positively for PAS and negatively for peroxidase. Immunological examination of leukemia cells showed that HLA-DR, TdT, B1 and J5 were positive and cytoplasmic Igmu and surface Ig were negative, indicating common ALL. The coagulation studies revealed that the activated partial thromboplastin time was prolonged to 42.0 seconds, FDP increased to 79.9 micrograms/ml, and antithrombin-III decreased to 62%. Chromosome analysis showed a 48, XY, +2, +21q-, t(9;22) karyotype. He was diagnosed as having Ph1 positive ALL associated with DIC. He was treated with vindesine, prednisolone, L-asparaginase, and adriamycin and complete remission (CR) was achieved after two months. But on August 1988, 8 months after CR, ALL and brain tumor relapsed and he died of pneumonia on September 19, 1988.
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PMID:[Ph1 positive acute lymphoblastic leukemia with DIC after operation of colon and lung cancer]. 281 Jul 93

A monoclonal antibody specific for a modified nucleoside, 1-methyladenosine, was prepared and characterized. This antibody, termed AMA-2, reacts with 1-methyladenosine and 1-methyladenine but not with other nucleosides, particularly methylated adenosines other than 1-methyladenosine and methylated guanosines, tested in this investigation. In our experiments, AMA-2 was used in an enzyme-linked immunosorbent assay (ELISA) system for the quantitation of the levels of 1-methyladenosine in urine. Sensitivity was in the picomole range and accuracy was nearly equal to that of the high-performance liquid chromatography (HPLC) assay system. Urinary levels of 1-methyladenosine in healthy donors and patients with various advanced cancers were determined by the inhibition ELISA. The amount of 1-methyladenosine in urine of 33 healthy donors was 1.91 +/- 0.66 nmol/mumol creatinine. In 54% (51/94) of patients, urinary 1-methyladenosine was elevated above the mean plus 2 standard deviations for the healthy donors (3.23 nmol/mumol creatinine). In patients with leukemia, esophageal cancer, stomach cancer, colon cancer, and bladder cancer, urinary levels of 1-methyladenosine were significantly elevated. In patients with leukemia, urinary 1-methyladenosine levels changed almost in parallel with the change in the clinical response during chemotherapy. These results suggest that urinary 1-methyladenosine might be useful in monitoring the effectiveness of therapy.
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PMID:Preparation of a monoclonal antibody specific for 1-methyladenosine and its application for the detection of elevated levels of 1-methyladenosine in urines from cancer patients. 314 1

We tested the antiproliferative effect induced by the natural human tumor necrosis factors alpha and beta (nHuTNF-alpha, -beta) or a combination of these in the clonogenic assay. The antiproliferative effects were evaluated by examining the inhibition of clonogenic growth of RPMI-4788 cells, which had been established from a human colon cancer. TNF-alpha and -beta were natural human types produced by a B cell leukemia line (BALL-1 cells) and were both over 99% pure. The antiproliferative effect in combination of nHuTNF-alpha and -beta was analysed by using the median effect plot and the combination index. The results indicate a synergism between two factors.
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PMID:Synergistic effect of natural human tumor necrosis factors alpha and beta in the clonogenic assay. 322 48


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