Cross Resistance and Collateral Sensitivity Studies in Cancer Chemotherapy

Hutchison, Dorris J.

doi:10.1016/s0065-230x(08)60984-7

Cited by 63 publications

(34 citation statements)

References 100 publications

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“…and different aspects concerning collateral sensitivity and cross-resistance in eukaryotic cells as [45). Since then, new data on the resistance problem have been published, and it seems desirable to put them into context with the older knowledge.…”

Section: Resistance Toward Pyrimidine Analoguesmentioning

confidence: 99%

“…It was observed that the cell population resistant to a drug was more susceptible to the inhibitory effects of the other drugs than was the parental wild-type line, and that it would be feasible to eliminate mutant cells by a suitable combination of chosen drugs [45]. Another approach was to circumvent the loss of nucleotide-forming capacity of drug-resistant cell sublines.…”

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confidence: 99%

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Resistance of Mammalian Tumour Cells toward Pyrimidine Analogues

Vesely¹,

Čihák²

1973

Oncology

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The development of resistance of animal tumour tissue in vivo toward pyrimidine and purine analogues is generally accounted for by a process of mutation and selection, although in some cases metabolic alterations leading to the emergence of resistant cells are epigenetic. Neoplastic cells may develop resistance in vitro toward a pyrimidine analogue while they carry a repressed oncogenic virus genome; upon withdrawal of the drug, the synthesis of virus particles appears. Following the administration of one analogue, resistance in various tumours develops in different patterns. The underlying biochemical lesions resulting in the emergence of resistance following 6-azauridine, 5-fluorouracil and 5-azacytidine is the deletion of uridine kinase which is the rate-limiting enzyme along the salvage pathway. There is an indication that at least in some cases the decreased activity of this enzyme is due to its structural and/or conformational changes. The development of resistance toward 5-iodo- and 5-bromo-2′-deoxyuridine is accompanied by the deletion of thymidine kinase activity; resistance towards cytosine arabinoside is associated with the deletion of deoxycytidine kinase. Different means of circumventing the emergence of resistance are surveyed.

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Section: Resistance Toward Pyrimidine Analoguesmentioning

confidence: 99%

mentioning

confidence: 99%

Resistance of Mammalian Tumour Cells toward Pyrimidine Analogues

Vesely¹,

Čihák²

1973

Oncology

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“…Most of the studies in immunochemotherapy have involved the utilization of nonspecific immunostimulants such as BCG or C. parvum plus antitumor agents [Fisher et al, 1970;Pearson et al, 1972;Bast et al, 19741. Chemotherapy plus adoptive immunotherapy has been utilized in preclinical systems. For example, cyclo phosphamide plus specifically sensitized allogeneic spleen cells has been employed in the treatment of Moloney LSTRA leukemia with resultant marked in creases in survival time [Glynn et al, 1969|. The immunogenicity of tumor cells may be altered by neuraminidase in vitro [Simmons and Rios, 1971] or in vivo by administration of DTIC [Bonmassar et al, 1970], The alteration of tumor cell antigenicity which frequently accompanies the origin of tumor cell resis tance may result in improved therapeutic response (collateral sensitivity) on treatment with a chemo therapeutic agent with a differing mechanism of action [Law et al, 1954;Hutchison, 1963;Venditti and Goldin, 1964;Millicit, 1969;Nicolin et al, 1972], Additional procedures involve attempts at active and passive immunization.…”

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confidence: 99%

Combined Chemotherapy

Goldin¹

1980

Oncology

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Comined chemotherapy approaches should take into account the complex interrelationships with the host and tumor. Principles of combination drug chemotherapy that may contribute to increased antitumor specificity in the treatment of clinical neoplasia are reviewed and examples provided under the following broad headings; (a) Increased antitumor effectiveness without a proportionate increase in limiting host toxicity. This includes the biochemical concepts of sequential and concurrent blockade, complementary inhibition and error amplification, (b) Decrease in host toxicity without a proportionate loss in antitumor effectiveness, (c) Delay in origin and treatment of resistant mutants, (d) Treatment of metastatic and sequestered tumor cells, (e) Identification of optimal dosages, ratios and schedules for drug combinations, (f) Kinetic considerations such as tumor cell synchronization, choice of drugs that act at different phases of the cell cycle or that stimulate G_o cells to divide, (g) Use of drugs that assist active compounds, (h) Employment of combined modalities including surgery, radiation or immunotherapy plus chemotherapy, (i) Loading dose chemotherapy of advanced disseminated tumor, (j) Identification of drugs that may prevent viral or carcinogenic tumor induction, (k) Development of methodology for determination of the effectiveness of polychemotherapy.

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“…Resistance to these folic acid antagonists (FAAs) is known-to develop readily (18,23). Although data consistent with a mutagenic role for these compounds have been reported, this development of FAA resistance has generally been ascribed to the selection of spontaneously occurring resistant organisms (25).…”

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Mutagenic Studies of Folic Acid Antagonists

Genther

Schoeny

Loper

et al. 1977

Antimicrob Agents Chemother

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Compounds that compete with folic acid (folic acid antagonists [FAAs]) become limited in their usefulness in the treatment of leukemia, malaria, and bacterial infections by the rapid development of resistance. Assays of the plasma levels of certain of these FAAs led to the observation, in about 25% of the determinations, that a higher density of growth of Streptococcus faecium var. durans (ATCC 8043) was obtained at an FAA concentration just below the completely inhibitory level than at one-half this concentration. This and other considerations suggested that FAAs may act not only as selective agents for resistant organisms but also as mutagens. Seven FAAs including amethopterin, pyrimethamine, trimethoprim, chlorguanide triazine, an experimental quinazoline, WR-158,122, and two experimental triazines, WR-99,210 and WR-38,839, were tested for mutagenicity in the Salmonella reversion assay developed by Ames et al. (1975). All were found to be negative for strains TA1535, TA1537, TA1538, TA98, and TA100, both with and without microsomal activation. These compounds were then tested as mutagens for three traits in the folic acid-requiring S. faecium . FAAs were shown to cause mutations to folic acid independence, rifampin resistance, and FAA resistance. It is postulated that the FAAs induce mutations by causing thymine deprivation in the folic acid-requiring host.

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Cross Resistance and Collateral Sensitivity Studies in Cancer Chemotherapy

Cited by 63 publications

References 100 publications

Resistance of Mammalian Tumour Cells toward Pyrimidine Analogues

Resistance of Mammalian Tumour Cells toward Pyrimidine Analogues

Combined Chemotherapy

Mutagenic Studies of Folic Acid Antagonists

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