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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some classical experiments proving the existence of a Tumoral Angiogenic Factor are reproduced. They show the presence of T.A.F. in a solid tumor (Walker 256) and its apparent absence in a leukemia (L 1210). We point out that the biological activity oversteps the barrier of zoological class.
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PMID:[Tumor angiogenic activity (introductory note)]. 16 Aug 26

The association between chronic lymphocytic leukemia and a solid tumor is well known. When the leukemia appears before the tumor a question may be asked : is the tumor a cancer or a localisation of the leukemia ? When the cancer is diagnosed before the leukemia, an other question may be asked : is it a true leukemia or is it a paraneoplasic leukemoid reaction ?
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PMID:[Chronic lymphocytic leukemia and cystadenocarcinoma of the kidney. A report of one case (author's transl)]. 22 27

The mouse plasmacytoma cell line, MOPC-460, produces both intracisternal and intracytoplasmic A-type particles when grown as a solid tumor. When these cells are grown either as an ascites tumor or in tissue culture, a third type of particle is produced extracellularly. This particle, the "myeloma-associated virus," is closely related to, and probably an alternate form of, the intracisternal A-type particle. The proteins present in these two types of particles were compared by tryptic peptide mapping. Both types of particles were found to contain essentially the same major proteins of 76,000 (p76), 68,000 to 70,000 (p68-70), and 45,000 (p45) daltons, in addition to varying amounts of smaller proteins. The relative proportions of all these proteins varied from preparation to preparation in an unpredictable way. The p45, p68, and p70 proteins all contained sequences found in p76, suggesting precursor-product relationships of p76 leads to p70 leads to p45 for solid tumor A-type particles and p76 leads to p68 leads to p45 for extracellular myeloma-associated virus. In addition, immune precipitation experiments have established that p76 contains at least some of the antigenic determinants characteristic of murine leukemia virus p30. This confirms earlier nucleic acid hybridization studies which indicated a moderate degree of relatedness between MOPC-460 A-type particles and several standard murine leukemia and sarcoma viruses. Taken together, our results provide evidence supporting the concept that MOPC-460 A-type particles may represent aberrant forms of C-type murine viruses.
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PMID:Characterization of the proteins of intracisternal type A and extracellular oncornavirus-like particles produced by MOPC-460 myeloma cells. 23 64

Thirteen consecutive stage II breast cancer patients were treated with long-term adjuvant chemotherapy using chlorambucil. At least three of these patients developed acute myelogenous leukemia (AML). All three patients (and possibly a fourth) who developed AML were postmenopausal, received continuous chlorambucil for greater than or equal to 4 years, had acute red cell anemia at the time of treatment, and had a wbc count in the range of 2700-7700/mm3. After the chlorambucil was discontinued, the wbc count began to slowly rise and the patient developed clinical AML. In all three patients, the diagnosis of AML was established by pathologists on the basis of bone marrow biopsy, aspirate, and peripheral smears. Each of these was subsequently reviewed by the hematologist who treated the patients for AML. Patients who have breast cancer (or any other solid tumor malignancy) are at risk to develop a second malignancy. However, an increasing number of reports are appearing suggesting more than just a casual relationship between leukemia and the use of alkylating agents. This may be related to the dose and duration of therapy with these agents.
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PMID:Acute myelogenous leukemia in patients receiving chlorambucil as long-term adjuvant chemotherapy for stage II breast cancer. 27 42

Tumor cells were isolated from malignant effusions of three patients with disseminated solid tumors of different origin. Intracellular accumulation of nondiffusible cytosine arabinoside (ara-C) nucleotides was used to measure phosphorylation. Mouse leukemia L 1210 and L 1210/CA, and ara-C-resistant subline, were used as reference cells. Phosphorylation activity was similar in the cells from all three solid tumors and showed a linear increase with drug concentrations of 0.1--100 micograms/ml. In contrast to activity in L 1210 cells, the in vitro activity was not saturable at drug levels up to 100 micrograms/ml. Ara-C inhibited the incorporation of thymidine into DNA 84%--90% in the solid tumor cells at a concentration of 10 micrograms/ml. Higher drug concentrations did not result in further inhibition. In one patient, DNA synthesis of tumor cells isolated before and after intraperitoneal instillation of 1,000 mg ara-C was measured. The in vivo inhibition was found to correspond to the in vitro data. Solid tumor cells isolated from malignant effusion have no greatly reduced capacity for cellular formation of ara-C/nucleotides, but higher drug levels than achieved with conventional therapy are necessary for sufficient ara-C nucleotide synthesis.
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PMID:Action of cytosine arabinoside on human tumor cells isolated from malignant effusions: in vitro phosphorylation and inhibition of DNA synthesis. 48 20

10-Chloro-5-(2-dimethylaminoethyl)-7H-indolo [2,3-c]-quinolin-6(5H)-one hydrochloride (CIQ) was shown to exert significant antitumor activity against the Ehrlich carcinoma and sarcoma 180 transplantable tumors in mice by the intraperitoneal (ip) or oral (po) routes and when incorporated into diet. A solid tumor induced in BALB/c mice by the subcutaneous (sc) implantation of nonproducer murine sarcoma virus-transformed BALB/3T3 cells was also inhibited by CIQ after ip or po treatment but there was no effect against leukemia L1210 ascites or a transplantable murine renal adenocarcinoma. When tested in rats, CIQ significantly reduced the growth of Flexner-Jobling carcinoma, Murphy-Sturm lymphosarcoma and Walker 256 carcinosarcoma when administered by the ip or po routes. Pretreatment, but not posttreatment, with CIQ slightly inhibited the humoral antibody response of mice to sheep red blood cells. CIQ therefore differs from immunosuppressive agents such as imuran, methotrexate, cytosine arabinoside, or 6-mercaptopurine which affect the antibody response of mice to sheep erythrocytes when administered after immunization.
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PMID:Activity of 10-chloro-5-(2-dimethylaminoethyl)-7H-indolo [2,3-c]-quinolin-6(5H)-one hydrochloride against experimental tumors in mice and rats. 57 26

The therapeutic value of interspersing cyclophosphamide (CPM) chemotherapy and BCG immunotherapy was investigated in two tumor models: L1210 leukemia and Lewis solid tumor (LLT). In the case of L1210 leukemia, the antileukemic effect of CPM was enhanced by subsequent BCG administration where a single cycle of combined treatment was applied; treatment by repeated doses of CPM interspersed with BCG was no more effective than CPM chemotherapy alone. In the case of LLT tumor, the effect of one cycle of combined CPM-BCG treatment was not different from CPM administered alone but treatment by repeated doses of CPM interspersed with BCG immunotherapy was less effective than CPM chemotherapy alone. These results indicate that, while the effect of BCG immunotherapy may be favorable or nil when BCG is applied after cell-reducing chemotherapy, it may be nil or unfavorable when applied repeatedly in interspersed chemoimmunotherapy treatments.
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PMID:Interspersion of cyclophosphamide and BCG in the treatment of L1210 leukemia and Lewis Tumor. 60 38

During a 14 month period there were 364 episodes of bacteremia and fungemia at Memorial Sloan-Kettering Cancer Center. The first nine months of the study were retrospective, and the next five prospective. In patients with leukemia or lymphoma (group 1), Escherichia coli, Pseudomonas aeruginosa, Klebsiella pneumoniae and Staphylococcus aureus were the most frequently isolated organisms. The mortality in this group was 40.5 per cent. In the patients with solid tumor (group 2), Esch. coli, Staph. aureus, Bacteroides sp. and Candida sp. were most frequent. Mortality was 27.8 per cent. The source of infection in both groups was often indeterminate. High mortality was associated with pulmonary and intraabdominal infection and with Ps. aeruginosa, K. pneumoniae or polymicrobic sepsis. Factors of prognostic significance were the causative microorganism, source of infection and shock. Although mortality was higher in patients with leukopenia than in those with normal leukocyte counts, the differences were not significant. The mortality in this series was low considering the severity of the underlying diseases and the immunosuppressed state of many of the patients. In a prospective, randomly controlled study, mortality was further diminished by infectious disease consultation at the time the positive blood culture was reported. Severe fungal superinfection, predominantly aspergillosis and candidiasis, was found in 52 per cent of the autopsy patients with leukemia or lymphoma (group 1), but in only 8 per cent of those with solid tumors (group 2).
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PMID:Bacteremia and fungemia complicating neoplastic disease. A study of 364 cases. 87 Nov 28

Triazinate (TZT), a triazine folate antagonist, is a potent inhibitor of dihydrofolate reductase from mammalian cells. Because antitumor activity of triazinate in experimental tumors correlated closely with the in vitro inhibition of DNA synthesis in tumor cells derived from these tumors, we studied cells from patients with leukemia, solid tumor effusions, and cells from normal marrow to determine their in vitro sensitivity to TZT. DNA synthesis in cells from patients with acute leukemia was less sensitive to TZT than it was to methotrexate (MTX) at 2 X 10(-6) M concentration of the inhibitor, whereas the sensitivity was similar at 10(-5) M. This could be accounted for by the known greater sensitivity of dihydrofolate reductase to MTX than to TZT, and the observation that, whereas intracellular drug levels were similar at low (2 X 10(-6) M) extracellular concentrations of TZT or MTX, at the higher (10(-5) M) extracellular drug concentration intracellular TZT was greater than 3 times intracellular MTX. In vitro inhibition of DNA synthesis in cells obtained after patients were treated with TZT was correlated with drug serum concentration and with leukemia cell kill. The sensitivity of cells from solid tumor effusions to TZT was similar to the sensitivity to MTX. Since patients can tolerate doses of TZT five times higher than MTX with less toxicity, there may be advantage to the clinical use of TZT in some tumor cell types.
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PMID:Inhibition of DNA synthesis in normal and malignant human cells by triazinate (Baker's antifol) and methotrexate. 95 90

Murine sarcoma virus (Moloney strain) (MSV-M)-induced tumors are unusual in that they regularly appear less than 2 weeks after virus inoculation, progress for 1 to 2 weeks, and are rejected by normal adult BALB/c mice. Rejectio leaves the animals immune to tumor induction. In the present study, presensitization of normal adult BALB/c mice with attenuated MSV-M resulted in an altered pattern of tumor immunity. Injection of active MSV-M into the presensitized animals resulted in tumor induction and rejection similar to that observed in normal animals, but rejection failed to produce protection against the secondary inoculation with MSV-M. After the second inoculation with active MSV-M, tumors appeared and progressed but ultimately were rejected. Over 80% of the mice died, 25% after the primary challenge and the remainder after the secondary challenge. At death, all mice had histological evidence of leukemia which was the probable cause of death. The animals that died following the secondary challenge also had evidence of disseminated MSV-M. Solid tumor nodules were found in skeletal muscle distant from the original site of inoculation, and active MSV-M was isolated from spleen and lungs. The possibility that the results were produced by specific suppression of MSV-Moloney leukemia virus immunity is discussed.
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PMID:Suppression of Moloney sarcoma virus immunity following sensitization with attenuated virus. 100 May


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