Risk of Therapy-Related Leukaemia and Preleukaemia After Hodgkin's Disease

Pedersen‐Bjergaard, Jens; Larsen, Severin Olesen; Struck, J.; Hansen, H. S.; Specht, Lena; Ersbøll, Jens; Hansen, M; Nissen, N I

doi:10.1016/s0140-6736(87)92744-9

Cited by 200 publications

(22 citation statements)

References 37 publications

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“…It is noteworthy that earlier studies on second malignancy after Hodgkin disease had suggested that the leukemia risk after Hodgkin disease appears to be limited to the first 10 years after treatment. 4,5,7,9,10,18,51,52 However, in the current study, 2 cases were observed beyond 20 years. Nevertheless, it is clear that the increased excess risk of second malignancy in the later years is predominantly driven by solid tumors, in particular, breast cancer.…”

Section: Discussioncontrasting

confidence: 66%

Second malignancy after Hodgkin disease treated with radiation therapy with or without chemotherapy: long-term risks and risk factors

Bernardo

Weller

et al. 2002

Blood

409

294

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The excess risk of second malignancy after Hodgkin disease is an increasing problem. In light of the long-term data, guidelines for follow-up of survivors of Hodgkin disease need to be redefined. In this study we attempt to analyze the longterm risks and temporal trends, identify patient-and treatment-related risk factors, and determine the prognosis of patients who develop a second malignancy after radiation treatment with or without chemotherapy for Hodgkin disease. Among 1319 patients with clinical stage I-IV Hodgkin disease, 181 second malignancies and 18 third malignancies were observed. With a median follow-up of 12 years, the relative risk (RR) and absolute excess risk of second malignancy were 4.6 and 89.3/10 000 person-years. The RR was significantly higher with combined chemotherapy and radiation therapy (6.1) than with radiation therapy alone (4.0, P ‫؍‬ .015). The risk increased with increasing radiation field size (P ‫؍‬ .03) in patients who received combined modality therapy, and with time after Hodgkin disease. After 15 and 20 years, there was a 2.3% and 4.0% excess risk of second malignancy per person per year. The 5-year survival after development of a second malignancy was 38.1%, with the worst prognosis seen after acute leukemia and lung cancer. The excess risk of second malignancy after Hodgkin disease continues to be increased after 15 to 20 years, and there does not appear to be a plateau. Our analysis suggests that the risk may be reduced with smaller radiation fields, as are used in current trials of abbreviated chemotherapy and limitedfield radiation therapy.

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Section: Discussioncontrasting

confidence: 66%

Second malignancy after Hodgkin disease treated with radiation therapy with or without chemotherapy: long-term risks and risk factors

Bernardo

Weller

et al. 2002

Blood

409

294

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“…6,[12][13][14] Many of these studies showed that the risk of t-MDS and t-AML increases with the cumulative dose of drug 4,5,7,9,10,13,14 and with patient age. 3,6,13,14 After the first reports of t-AML it was realized that in most of these patients the disease presents in a preleukemic stage as t-MDS with abrupt thrombocytopenia 2-5 years after start of therapy with alkylating agents. Characteristically, the karyotypes, even early in the course of the disease, show loss of whole chromosomes 5 or 7 or loss of various parts of the long arms of these two chromosomes, often with many additional chromosome abnormalities.…”

Section: The 'Alkylator Types' Of Mds and Amlmentioning

confidence: 99%

Causality of myelodysplasia and acute myeloid leukemia and their genetic abnormalities

et al. 2002

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New insights into causative factors for the development of myelodysplasia (MDS) and acute myeloid leukemia (AML), with associations to specific cytogenetic and genetic abnormalities have been obtained primarily from studies of patients with the therapy-related subsets of the two diseases. Current knowledge now makes it possible to distinguish between at least seven major genetic subgroups of MDS and AML, and has directed research towards more specific causative factors also for de novo MDS and AML.

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“…For example, the permanent immune deficiency in patients cured of Hodgkin's disease is considered to bc inherent to this particular disease (Fisher et al, 1980). Similarly, a higher incidence of late myelodysplastic syndrome and acute leukemia may occur more frequently in chemotherapy-treatcd patients with certain types of primary malignancy such as Hodgkin's disease or multiplc myeloma (Koeffler and Rowley, 1985;Pedersen-Bjergaar et al, 1987;Kaldor et al, 1990), than in patients with other malignancies treated with the same chemotherapeutic modality. The delineation between tumor/host effects versus therapeutic effects can be addressed adequately by comparing chemotherapy-treated animals which previously carried a tumor with age-and sex-matched normal mice treated similarly with the same Chemotherapy.…”

Section: Myeloproliferation In Long-term Plasmacytoma-regressor Micementioning

confidence: 99%

Myeloproliferation in long‐term plasmacytoma‐regressor mice

Sagi‐Assif

Douer

Shaked

et al. 1994

Intl Journal of Cancer

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MOPC-315 plasmacytoma-bearing BALB/c mice were treated with high doses of melphalan, causing a permanent and complete regression of the tumor. In the present study we analyzed plasmacytoma-regressor mice (PRM) 3-6 months after plasmacytoma regression. A second group of otherwise untreated normal mice was treated with melphalan (M--control group). A third group of mice remained untreated and served as an age- and sex-matched control group. PRM were cachectic and had an increased mortality rate compared to the M and the C control groups. Histopathological examination indicated that the spleen of PRM showed pronounced abnormalities, primarily in the red pulp. These abnormalities consisted of extramedullary hematopoiesis and myeloid-granulocytic hyperplasia. Spleens of M mice showed similar abnormalities but to a much lesser extent. Flow cytometric analysis of cellular surface markers of PRM splenocytes indicated a high number of large MAC-I- and GR-I-positive cells compared to splenocytes of M or C controls. These large cells also expressed Fc tau receptors (Fc tau RII), stained positively with non-specific esterase and adhered to plastic dishes; a certain percentage expressed MAC-2 and MAC-3 antigens. A quantitative suppression of CD4+ T cells and of B cells was also shown. Circulating levels of TNF were higher in PRM than in M or C mice. The capacity of splenocytes from PRM to secrete factors that stimulated CFU-GM colony formation in soft agar by bone-marrow cells from normal mice was significantly up-regulated compared to that of splenocytes from M or C mice.(ABSTRACT TRUNCATED AT 250 WORDS)

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Risk of Therapy-Related Leukaemia and Preleukaemia After Hodgkin's Disease

Cited by 200 publications

References 37 publications

Second malignancy after Hodgkin disease treated with radiation therapy with or without chemotherapy: long-term risks and risk factors

Second malignancy after Hodgkin disease treated with radiation therapy with or without chemotherapy: long-term risks and risk factors

Causality of myelodysplasia and acute myeloid leukemia and their genetic abnormalities

Myeloproliferation in long‐term plasmacytoma‐regressor mice

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