Bladder damage in mice after combined treatment with cyclophosphamide and X-rays. The influence of timing and sequence

Edrees, G.M.; Luts, A.; Stewart, Fiona

doi:10.1016/0167-8140(88)90206-x

Cited by 23 publications

(5 citation statements)

References 17 publications

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“…It is interesting that the combination of cyclo-phosphamide and radiotherapy did not further increase the risk of developing bladder cancer significantly, compared to either alone. These results did not substantiate a prior report that cyclophosphamide-induced urothelial proliferation contributes to an early expression of radiation injury [24]. Rather, it appears that cyclophosphamide by itself is carcinogenic.…”

Section: Treatment-related Carcinogenesiscontrasting

confidence: 99%

Epidemiology and etiology of bladder cancer

Johansson

Cohen

1997

Semin. Surg. Oncol.

246

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The incidence of bladder cancer continues to increase, with an estimated 53,000 new cases diagnosed in the United States in 1996—90% of which are transitional cell carcinomas. The male‐to‐female ratio is 3:1. A number of etiological factors are associated with the development of bladder cancer, but in industrialized countries, cigarette smoking is the most important. Specific chemicals have also been identified as causing bladder cancer, as have a number of occupational exposures to less well‐defined specific agents. Treatment with cytostatic drugs, especially cyclophosphamide, is associated with increased risk of bladder cancer, as is treatment with radiotherapy for uterine cancer. In developing countries, especially in the Middle East and parts of Africa, infections with members of the genus Schistosoma are responsible for a high incidence of bladder cancer—75% of which are squamous cell carcinomas. Arsenic has been indicated as a bladder carcinogen in Argentina, Chile, and Taiwan. The reason for the high incidence of urinary tract cancer in individuals suffering from Balkan nephropathy has yet to be determined. A careful history of patients with bladder cancer is an important and useful process in helping to identify causal factor and, in more than one‐half the cases, a known relationship is found. Bladder cancer is a potentially preventable disease, with a significant morbidity and mortality in many parts of the world. Semin. Surg. Oncol. 13:291‐298, 1997. © 1997 Wiley‐Liss, Inc.

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Section: Treatment-related Carcinogenesiscontrasting

confidence: 99%

Epidemiology and etiology of bladder cancer

Johansson

Cohen

1997

Semin. Surg. Oncol.

246

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“…Part of this effect is probably due to stimulated urothelial proliferation after cyclophosphamide and precipitation of latent radiation injury. Increased late damage was also seen for combined irradiation and cyclophosphamide, although this seems to be largely due to additive toxicity from the two agents rather than increased radiosensitivity (Edrees et al, 1988;Lundbeck et al, 1993). Cisplatinum is not specifically toxic to the bladder when used alone, but does significantly increase both early and late radiation damage (Lundbeck and Overgaard, 1992;Lundbeck et al, 1993).…”

Section: Bladdermentioning

confidence: 94%

ICRP PUBLICATION 118: ICRP Statement on Tissue Reactions and Early and Late Effects of Radiation in Normal Tissues and Organs — Threshold Doses for Tissue Reactions in a Radiation Protection Context

Stewart¹,

Akleyev²,

et al. 2012

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This report provides a review of early and late effects of radiation in normal tissues and organs with respect to radiation protection. It was instigated following a recommendation in Publication 103 (ICRP, 2007), and it provides updated estimates of 'practical' threshold doses for tissue injury defined at the level of 1% incidence. Estimates are given for morbidity and mortality endpoints in all organ systems following acute, fractionated, or chronic exposure. The organ systems comprise the haematopoietic, immune, reproductive, circulatory, respiratory, musculoskeletal, endocrine, and nervous systems; the digestive and urinary tracts; the skin; and the eye. Particular attention is paid to circulatory disease and cataracts because of recent evidence of higher incidences of injury than expected after lower doses; hence, threshold doses appear to be lower than previously considered. This is largely because of the increasing incidences with increasing times after exposure. In the context of protection, it is the threshold doses for very long follow-up times that are the most relevant for workers and the public; for example, the atomic bomb survivors with 40-50years of follow-up. Radiotherapy data generally apply for shorter follow-up times because of competing causes of death in cancer patients, and hence the risks of radiation-induced circulatory disease at those earlier times are lower. A variety of biological response modifiers have been used to help reduce late reactions in many tissues. These include antioxidants, radical scavengers, inhibitors of apoptosis, anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, growth factors, and cytokines. In many cases, these give dose modification factors of 1.1-1.2, and in a few cases 1.5-2, indicating the potential for increasing threshold doses in known exposure cases. In contrast, there are agents that enhance radiation responses, notably other cytotoxic agents such as antimetabolites, alkylating agents, anti-angiogenic drugs, and antibiotics, as well as genetic and comorbidity factors. Most tissues show a sparing effect of dose fractionation, so that total doses for a given endpoint are higher if the dose is fractionated rather than when given as a single dose. However, for reactions manifesting very late after low total doses, particularly for cataracts and circulatory disease, it appears that the rate of dose delivery does not modify the low incidence. This implies that the injury in these cases and at these low dose levels is caused by single-hit irreparable-type events. For these two tissues, a threshold dose of 0.5Gy is proposed herein for practical purposes, irrespective of the rate of dose delivery, and future studies may elucidate this judgement further.

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“…Urination frequency tests were carried out over a 24h period during which the mice were placed in individual cages with wire bar floors (with free access to food and water). Absorbent paper was drawn beneath the cages and at the end of the test period the number of discrete urination events was counted as previously described (Stewart et al, 1978;Edrees et al, 1988). The volume of urine produced by each mouse was also estimated by comparing the area of each urine spot with a calibration curve for known volumes of urine.…”

Section: Methodsmentioning

confidence: 99%

Functional and histological bladder damage in mice after photodynamic therapy: the influence of sensitiser dose and time of administration

Stewart

Oussoren²

1993

Br J Cancer

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Summary The bladders of anaesthetised mice were illuminated with red laser light (630 nm) at intervals of I day to 4 weeks after i.p. administration of Photofrin. Light was delivered intravesically by inserting a fibre optic, with a diffusing bulb tip, into the centre of fluid filled bladders. A single light dose of 11.3 J cm-2 applied 1 day after 10 mg kg-' Photofrin caused a severe acute response, with increased urination frequency (five to seven times control) and haematuria. Recovery was good, however, and by 10 weeks only a mild (approximately two-fold) increase in frequency remained. There was no reduction in the amount of acute bladder damage or in the rate of healing when the interval between Photofrin and light was increased from 1 to 7 days but a 2 to 3 week interval lead to a significant reduction in damage. For an interval of 4 weeks there was only a mild (less than two-fold) increase in urination frequency during the first week. A drug dose of 2.5 mg kg-I given I day before illumination caused transient haematuria but no increase in urination frequency. Doses of 5, 7.5 or 10 mg kg-' all caused photosensitisation and the amount of bladder damage was drug dose dependent. The bladder seems to be well able to recover from severe acute damage induced by PDT. Occasional incidences of pyelonephritis were seen, however, suggesting that urinary tract infection during the acute period may lead to permanent renal damage.

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Bladder damage in mice after combined treatment with cyclophosphamide and X-rays. The influence of timing and sequence

Cited by 23 publications

References 17 publications

Epidemiology and etiology of bladder cancer

Epidemiology and etiology of bladder cancer

ICRP PUBLICATION 118: ICRP Statement on Tissue Reactions and Early and Late Effects of Radiation in Normal Tissues and Organs — Threshold Doses for Tissue Reactions in a Radiation Protection Context

Functional and histological bladder damage in mice after photodynamic therapy: the influence of sensitiser dose and time of administration

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