Control of Malignant Metastases by ICRF 159

Hellmann, K.; Burrage, Karen

doi:10.1038/224273a0

Cited by 103 publications

(35 citation statements)

References 9 publications

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“…1, R = H), the bis cyclic imide derivative of EDTA was first synthesized at the Imperial Cancer Research Fund Laboratories in 1969 in art attempt to prepare intracellularly activated chelating agents as potential antitumour drugs [2]. This compound, and some closely related analogues, were shown to be potent inhibitors of transplanted tumours in mice and rats [3][4][5]. Subsequently, one of them, the homologue ICRF 159 (Fig.…”

Section: Introductionmentioning

confidence: 99%

Metal binding by pharmaceuticals. part 2. interactions of Ca(II), Cu(II), Fe(II), Mg(II), Mn(II) and Zn(II) with the intracellular hydrolysis products of the antitumour agent ICRF 159 and its inactive homologue ICRF 192

et al. 1982

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Formation constants for the calcium(II), copper(II), iron(II), magnesium(II), manganese(II) and zinc(II) complexes of dl-NN'-dicarboxamidomethyl-NN'-dicarboxymethyl-1,2-diaminopropane (ICRF 198) and the 1,2-diamino-butane homologue (ICRF 226) have been measured potentiometrically at 37 degrees C and I=150 mmol dm-3 [NaCl]. The constants are used in computer simulation models to assess the relative avidity of these compounds for biologically essential metal ions in vivo. It is shown that the agents interact similarly with all of the ions studied except those of zinc(II), which are particularly strongly chelated by the hydrolysis product of ICRF 192. This effect could be responsible for the difference in cytotoxicity exhibited by the antitumour agent ICRF 159 (Razoxane) and its inactive homologue ICRF 192. However, the mechanism through which this might occur remains unclear.

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Section: Introductionmentioning

confidence: 99%

Metal binding by pharmaceuticals. part 2. interactions of Ca(II), Cu(II), Fe(II), Mg(II), Mn(II) and Zn(II) with the intracellular hydrolysis products of the antitumour agent ICRF 159 and its inactive homologue ICRF 192

et al. 1982

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“…Several reports have suggested that multiple treatments with ICRF-159 inhibited the growth of the LL, although the degree of inhibition ranged from negligible to highly effective (Hellmann & Burrage, 1969;Salsbury, 1970;James & Salsbury, 1974). The results in our present studies (Figs.…”

Section: Discussionmentioning

confidence: 99%

ICRF-159 enhancement of radiation response in combined modality therapies. I. Time/dose relationships for tumour response

Kovacs¹,

Evans²,

Schenken³

et al. 1979

Br J Cancer

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Summary-The combined effect of the chemotherapeutic agent ICRF-159 and irradiation were evaluated using the Lewis lung tumour (LL). At a daily dose of 25 mg/kg, ICOF given alone prevented the progressive growth of LL. Daily pretreatment also potentiated the effects of radiation (600 rad) on tumour growth, provided the pretreatment kinetics of the tumour permitted a response to radiation alone. Single acute doses of the drug failed to alter the growth of LL, and when combined with radiation failed to enhance the radiation effect. Fractionation of the drug (25 mg/kg; 4 doses at 3h intervals) before irradiation, however, results in immediate effects on tumour growth which are more than additive. The results suggest that a low dose of ICRF-159 for extended periods is more effective in enhancing radiotherapy than a high dose provided acutely.

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“…The presence in ICRF 159 treated animals of a well formed vasculature between tumour cells and blood has been interpreted as the main factor in preventing haematogenous tumour spread (Salsbury et al, 1970;Hellmann et al, 1973). The clinical application of ICRF 159 to the treatment of acute leukaemia and lymphosarcoma has been described (Hellmann et al, 1969), although the beneficial effects reported in these cases were interpreted as due to the drug's anti-mitotic action.…”

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confidence: 99%

Influence of ICRF 159 and triton WR 1339 on metastases of a rat epithelioma

Pimm¹,

Baldwin²

1975

Br J Cancer

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Summary.-ICRF 159 and Triton WR 1339 have been examined for their ability to suppress subcutaneous growth and pulmonary metastases from a transplanted rat epithelioma. Neither compound influenced subcutaneous tumour development or reduced the propensity to metastasize when administered in regimens reported to suppress pulmonary, lymph node or intracerebral metastases in other experimental systems.

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Control of Malignant Metastases by ICRF 159

Cited by 103 publications

References 9 publications

Metal binding by pharmaceuticals. part 2. interactions of Ca(II), Cu(II), Fe(II), Mg(II), Mn(II) and Zn(II) with the intracellular hydrolysis products of the antitumour agent ICRF 159 and its inactive homologue ICRF 192

Metal binding by pharmaceuticals. part 2. interactions of Ca(II), Cu(II), Fe(II), Mg(II), Mn(II) and Zn(II) with the intracellular hydrolysis products of the antitumour agent ICRF 159 and its inactive homologue ICRF 192

ICRF-159 enhancement of radiation response in combined modality therapies. I. Time/dose relationships for tumour response

Influence of ICRF 159 and triton WR 1339 on metastases of a rat epithelioma

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