Search PubMed⌕ Search

Biomedical subjects

T L Loo

Publications and source records attributed to T L Loo.

At least 109 records · Page 6Linked to original sources
PubMed1976

Biological active peptides in human urine: III. Inhibitors of the growth of human leukemia, osteosarcoma, and HeLa cells.

Medium-sized peptides isolated from normal humans urine were tested for their effect on DNA, RNA, and protein synthesis, and mitosis, in tissue culture of human myeloblastic leukemia, osteosarcoma, and HeLa cells. Two types of antineoplastic peptides were found. One type consists of strongly acidic peptides (probably sulfated glycopeptides) which act specifically on different kinds of neoplasma. The other type comprises slightly acidic and neutral peptides, and has broad specificity. The active peptides produce up to 97% inhibition of DNA synthesis and mitosis in the neoplastic cells in tissue culture. The peptide fraction which has broad specificity was tested in different concentrations and gave good dose-response relationship.

Antineoplastic Agents↗
PubMed1976

A comparison of the lethal effects of three nitrosourea derivatives on cultured human lymphoma cells.

The cellular effects of three nitrosourea derivatives were investigated on a human lymphoma cell line. The three drugs show similar threshold-type dose-response survival curves on asynchronous cells treated for 1 hr. Longer incubation periods result in rapid biological degradation for 1,3-bis(2-chloroethyl)-1-nitrosourea and 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea, whereas, 1-(2-chloroethyl)-3-trans-4-methylcyclohexyl)-1-nitrosourea, remains cytotoxic after about 24 hr. Important differences were noted with respect to cell cycle dependency. The 1,3-bis(2-chloroethyl)-1-nitrosourea was more effective in early S and in G2 phase, whereas both 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea and 1-(2-chloroethyl)-3-trans-4-methylcyclohexyl)-1-nitrosourea were more effective in early S. 1,3-bis(2-chlrorethyl)-1-nitrosourea exerted a considerable degree of killing in G1. Cells were unable to recover from priming damage induced by all 3 nitrosourea derivatives. No synergistic effects were observed in combination with vitamin A.

Amphotericin B↗
PubMed1976

Combination chemotherapy in vitro with adriamycin. Observations of additive, antagonistic, and synergistic effects when used in two-drug combinations on cultured human lymphoma cells.

Adriamycin was paired with 12 other chemotherapeutic drugs in a search for possible synergistic pairs. Cell lethality was investigated by the colony-formation method utilizing a long-term human lymphoma cell line. Addative effects were noted with CCNU, ara-C, prednisolone, DDP, VP-16, and Yoshi, and mild synergistic effects with BLEO and CS. Adriamycin reduced the killing ability of BCNU and MeCCNU when applied simultaneously. This antagonistic effect was canceled by sequential incubation with each drug. It appears that no significant synergism can be expected by simultaneous pairing of adriamycin with some currently available chemotherapeutic agents.

Antineoplastic Agents↗
PubMed1975

Clincal pharmacology of O2,2'-cyclocytidine.

Two metabolites of 2-14C-cyclocytidine (cyclo-C) were found in the plasma and urine and a hydrolytic product, arabinosylcytosine (ara-C), and its deaminated product, arabinosyluracil (ara-U), were found in patients with cancer; 80% of the dose was found in urine in 24 hr, 70% as cyclo-C and 10% as ara-C and ara-U. The plasma disappearance curve of ara-C curvilinear; the half-life of ara-C estimated from the terminal phase is 8 hr. By 6 hr, the ara-C level is 0.35 mug/ml and falls exponentially to 0.006 mug/ml by 24 hr. Plasma concentration ratios of ara-U to ara-C are 0.1 to 0.3, 0.3 to 0.4, and 1.1 to 1.3 at 10 min, 1 hr, and 4 hr following intravenous injection of cyclo-C at 200 mg/m2. Five min after an equal dose of ara-C, this ratio is approximately 2, and by 4 hr, plasma ara-C levels are immeasurable. After intramuscular and subcutaneous administration, cyclo-C is rapidly absorbed. The plasma disappearance curves of the cyclo-C hydrolytic product, ara-C, are similar to those of the intravenous route. Intramuscularly, subcutaneously, and intravenously cyclo-C should be equally effective. Intrathecal injections of cyclo-C (50 mg/m2) result in an effective ara-C level (0.1 mug/ml) in cerebrospinal fluid (CSF) at 24 hr. When cyclo-C is given orally to fasting patients, less than 15% of the dose is excreted in urine in 24 hr and none can be detected in the plasma.

Administration, Oral↗
PubMed1975

Schedule-dependent synergistic cytotoxicity of arabinofuranosylcytosine with adriamycin or 3,6-bis(5-chloro-2-piperidinyl)-2,5-piperazinedione in cultured cells.

The purpose of this study was to demonstrate that in vitro cell culture systems could serve a useful purpose in providing some guidelines in formulating drug schedules for combination cancer chemotherapy in the clinic. Using monolayer cultures of Chinese hamster ovary cells as the test system, we screened the combinations of 1-beta-D-arabinofuranosylcytosine (ara-C) + adriamycin, ara-C + 3,6 - BIS(5 - CHloro - 2 - piperidinyl) - 2,5 - piperazinedione, melphalan + 5-fluorouracil, and melphalan + ara-C as to the effect of drug sequence on the plating efficiency of these cells. Schedule-dependent therapeutic synergism was observed only when ara-C treatment was followed by either adriamycin or 3,6-bis(5-chloro-2-piperidinyl)2,5-piperazinedione but not vice versa. No synergistic effects were observed in the combination of melphalan with 5-fluorouracil or ara-C. The basis for this synergism appeared to be that ara-C was primarily acting as a synchronizing agent to set up the cells in S phase so that subsequent treatment with an S-phase-specific drug, such as adriamycin or 3,6-bis(5-chloro-2-piperidinyl)-2,5-piperazinedione, would produce the maximum cell kill. On the other hand, the lack of synergism in the combinations of melphalan with 5-fluorouracil or ara-C was due to the lack of S-phase specificity for melphalan. On the basis of these data, we postulate that schedule-dependent synergism could be expected if the first agent renders the cells more sensitive (for example, by selectively blocking cells in one of the phases of the cell cycle) to the action of the second drug.

Cell Division↗