Response kinetics of host and experimental solid tumour after adriamycin

Hopkins, Harold A.; Looney, William B.; Teja, Kuldeep; Hobson, A. S.; MacLeod, M. S.

doi:10.1038/bjc.1978.146

Cited by 11 publications

(2 citation statements)

References 9 publications

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“…Tumour growth after ADR treatment was measured for doses up to 10 mg/kg only (LD10/30, Hopkins et al, 1978), as drug toxicity was excessive at higher doses. Drug-induced reduction of animal longevity also narrowly restricted the choice of endpoint volume for the determination of delay.…”

Section: Resultsmentioning

confidence: 99%

In vivo tumour-cell proliferation after adriamycin treatment

Rowley¹,

Hopkins²,

Looney³

1982

Br J Cancer

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Summary.-Adriamycin (10 mg/kg) administered s.c. to male ACI rats bearing Hepatoma H-4-1I-E caused a 9-day delay in tumour growth but no changes in the clonogenic fraction of the tumour were detectable by in vitro assay at any time after treatment. There is no significant decrease in the yield of cells on enzymatic dissociation of the tumour nor a reduction in mg DNA/g tumour that might indicate a decrease in tumour cellularity. Mitotic and labelling indices and [3H]dT uptake into DNA remain essentially unchanged, relative to age-equivalent controls, but are slightly lower than in controls of equal weight. The reliability of the clonogenic assay and possible mechanisms by which Adriamycin delays tumour growth are discussed.

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Section: Resultsmentioning

confidence: 99%

In vivo tumour-cell proliferation after adriamycin treatment

Rowley¹,

Hopkins²,

Looney³

1982

Br J Cancer

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“…); rats killed ness and the extent of interference with the biochemical program of cancer cells that could be achieved with adriamycin, the action of this drug on the nucleotide patterns was examined in animals carrying the chemi cally induced, transplantable, solid hepatoma 3924A. In these preliminary experiments, the acute effect of adriamycin was studied by using a dose (10 mg/kg) that has been found to result in marked remission in hepatoma 3924A [2). When rats were killed 2.5 h after a single intraperitoneal injection, a trend was detected for a rise in the concentrations of the ribo-and deoxyribonucleoside triphosphates.…”

Section: Effect Of Adriamycin On Nucleotide Programs Of Hepatoma 3 924amentioning

confidence: 99%

Recent Advances in the Design of Anticancer Chemotherapy

Weber¹

1980

Oncology

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Recent advances in the rational design of anticancer chemotherapy in this laboratory have been based on strategic differences between normal and cancer cells. On the basis of our identification of quantitative biochemical markers and characteristic enzymic and metabolic programs of neoplastic cells, we have designed single and combination drug treatments. This chemotherapeutic approach aims at specific enzymic targets in cancer cells that are closely linked with transformation and progression. With the identification of markedly increased concentrations of CTP, dATP, dGTP, dCTP and dTTP in neoplasms, there should be an operational advantage in directing chemotherapy to depress the concentration of these metabolites elevated in cancer cells, because a drug-imposed curtailment of these metabolites might destroy cancer cells that depend more stringently on the increased concentrations of these nucleotides. Experiments in tissue culture and in solid tumors utilizing treatment schedules with pyrazofurin in combination with galactosamine, and the use of adriamycin, succeeded in achieving profound alterations in the nucleotide concentrations of cancer cells.

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Solid tumor models for the assessment of different treatment modalities. VIII. The scheduling of treatment for a chemotherapeutically resistant experimental solid tumor

Looney

Hopkins

MacLeod

1979

Cancer

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Single, large doses of adriamycin, cyclophosphamide and 5-fluorouracil(5-FU) have been compared to the same amount of drug given in divided doses daily over a 3 or 5 day period in a solid tumor model which metastasizes to the regional lymph nodes and lungs. No significant increase in life expectancy occurred following adriamycin or cyclophosphamide. However, a significant reduction in life expectancy occurred after 5 fractionated doses of 5-FU but not after the large single dose. The increase in mortality following fractionated doses of 5-FU is attributed to the prolongation of the onset of recovery of bone marrow. Tumor volume reduction following a single dose of each agent was equal to or greater than the fractionated doses. The results of these studies on this chemotherapeutically resistant solid tumor indicate that small daily fractionated doses of adriamycin, cyclophosphamide or 5-FU result in increased morbidity and mortality without therapeutic benefit in tumor control. The time sequence of recovery of the limiting organ of the host (i.e., bone marrow) is similar to the time sequence of recovery of the tumor. Large intermittent single doses of chemotherapeutic agents given following recovery of the host from a previous treatment would be expected to be less toxic to the host and equally effective in control of tumor growth. None of the 3 chemotherapeutic agents was successful in tumor eradication. Previous studies of this series have shown that the utilization of sequential chemotherapy combined with radiotherapy can be successfully used for eradication of another solid tumor which did not metastasize. A similar therapeutic strategy using sequential combined modality therapy should also be effective in the control of the primary H-4-11-E tumor as well as its metastatic dissemination. Information gained from these experimental studies should eventually provide information which should be helpful in the clinical management of chemotherapeutically resistant solid tumors in man.

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Response kinetics of host and experimental solid tumour after adriamycin

Cited by 11 publications

References 9 publications

In vivo tumour-cell proliferation after adriamycin treatment

In vivo tumour-cell proliferation after adriamycin treatment

Recent Advances in the Design of Anticancer Chemotherapy

Solid tumor models for the assessment of different treatment modalities. VIII. The scheduling of treatment for a chemotherapeutically resistant experimental solid tumor

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