Multiple primary cancer risk after therapy for Hodgkin's disease

Brody, Robert S.; Schottenfeld, David; Reid, Ann

doi:10.1002/1097-0142(197710)40:4+<1917::aid-cncr2820400824>3.0.co;2-w

Cited by 103 publications

(14 citation statements)

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“…Although an increase in the risk of acute non-lymphocytic leukaemia (ANLL) following Hodgkin's disease has been appreciated for some time (Brody et al, 1977) it has not been possible to implicate directly cyclophosphamide, even though it has been widely used in Hodgkin's disease therapy (Boivin & Hutchison, 1984). Acute leukaemia also occurs in excess in patients with nonHodgkin's lymphoma who have undergone chemotherapy including cyclophosphamide (Pedersen-Bjergaard et al, 1985).…”

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Risk of leukaemia in ovarian tumour and breast cancer patients following treatment by cyclophosphamide

Haas¹,

B²,

Wh³

et al. 1987

Br J Cancer

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Summary A case-control study was conducted to determine whether the development of leukaemia was associated with chemotherapy for neoplasms of the ovary or breast, in a population where most such chemotherapy consisted of cyclophosphamide alone. Cases and controls were identified from the National Cancer Registry of the German Democratic Republic. Cases were women who had developed leukaemia as a second primary after an initial diagnosis, at least one year before, of an ovarian or breast tumour. Controls were patients with an ovarian tumour or breast cancer who had survived to the year when the case developed a leukaemia but who had not themselves developed a second malignancy. Controls were matched to cases by the site of the first primary and its year of diagnosis, as well as year of birth. The relative risk for acute leukaemia following treatment with cyclophosphamide alone was significantly elevated (P<0.05), at 14.6 for ovarian tumour patients and 2.7 for breast cancer patients. Among breast cancer patients the increased risk of leukaemia associated with chemotherapy was confined to women who had been under 50 years of age at the time of diagnosis of the breast cancer (for whom the relative risk was 13.1). No excess risk of leukaemia was observed in association with radiotherapy for either ovarian or breast cancer patients. The present findings strongly suggest that cyclophosphamide as a single chemotherapeutic agent is capable of inducing leukaemia in humans.Cyclophosphamide is carcinogenic by several routes of administration in rats and mice (Schmahl & Habs, 1979; IARC, 1981). In humans there is also strong evidence that it is a carcinogen (Plotz et al., 1979;Elliot et al., 1982), producing tumours of the bladder and possibly other sites.There are a number of case reports of acute leukaemia following treatment with cyclophosphamide of nonmalignant diseases including rheumatoid arthritis, Wegener's granulomatosis, chronic glomerulonephritis, idiopathic thrombocytopaenia purpura, and Sj6gren's syndrome (Grunwald & Rosner, 1979). While cyclophosphamide is suspected to be a leukaemogen, it is widely believed to be less potent than many other nitrogen mustard-derived alkylating agents, and it is recommended as a component of adjuvant therapy following surgery for breast cancer (National Institutes of Health, 1986).Studies of leukaemia in cancer patients treated with cyclophosphamide have been difficult to interpret, because it is often given in combination with other agents known to be leukaemogenic. Although an increase in the risk of acute non-lymphocytic leukaemia (ANLL) following Hodgkin's disease has been appreciated for some time (Brody et al., 1977) it has not been possible to implicate directly cyclophosphamide, even though it has been widely used in Hodgkin's disease therapy (Boivin & Hutchison, 1984). Acute leukaemia also occurs in excess in patients with nonHodgkin's lymphoma who have undergone chemotherapy including cyclophosphamide (Pedersen-Bjergaard et al., 1985). In a study of multiple myeloma...

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Risk of leukaemia in ovarian tumour and breast cancer patients following treatment by cyclophosphamide

Haas¹,

B²,

Wh³

et al. 1987

Br J Cancer

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“…Thus, delayed cutanAlong with the successful treatment with eous hypersensitivity to recall antigens intensive radio-and chemotherapy, have (Chase, 1966;Young et al, 1972; Holm come reports of late complications. and to sensitizing agents increased risk of acute myelocytic leu-such as dinitrochlorobenzene (Aisenberg, kaemia (Bonadonna et al, 1973;Canellos 1962;Brown et al, 1967;Eltringham & et al, 1975;Brody & Schottenfeld, 1980) Kaplan, 1973 allograft survival is prolonged (Green & Corso, 1958;Kelly et al, 1958;Miller et al, 1961). It is also generally agreed that the in vitro T-lymphocyte proliferative response to phyto-hemagglutinin (PHA), concanavalin A (ConA), pokeweed mitogen (PWM) and allogeneic lymphocytes, is low both in untreated patients and in patients during remission (Aisenberg, 1965;Hersh & Oppenheim, 1965;Holm et al, 1967;Bjorkholm, 1978).…”

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Lymphocyte function in untreated Hodgkin's disease: An important predictor of prognosis

Wedelin¹,

Björkholm²,

Holm³

et al. 1982

Br J Cancer

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“…While a second neoplasm after treatment of childhood malignancy is a well recognised occurrence, studies showing a 1±17´6% cumulative risk (Boivin et al, 1984 ;Kusher et al, 1988 ;T ucker et al, 1988;Sont et al, 1992) the developm ent of two or more subsequent tumours is rare (Brody et al, 1977).…”

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confidence: 99%