Breast cancer and acute leukemia: Report of 24 cases and review of the literature

Rosner, Fred; Carey, Robert W.; Zarrabi, Mahboobeh

doi:10.1002/ajh.2830040207

Cited by 108 publications

(33 citation statements)

References 70 publications

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“…60,61 Furthermore, an increased incidence of t-MDS/AML in patients treated with surgery alone and in patients with a family history of breast cancer suggests a possible association between the two diseases. [61][62][63] More aggressive therapy could even increase the rate of t-MDS/AML. [64][65][66] Praga et al analyzed 19 randomized trials, including patients treated with epirubicin and cyclophosphamide.…”

Section: Non-hematologic Diseasesmentioning

confidence: 99%

Therapy-related leukemia and myelodysplasia: susceptibility and incidence

Leone¹,

Pagano²,

et al. 2007

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Therapy-related myelodysplastic syndrome/acute myeloid leukemia (t-MDS/AML) is an increasingly recognized treatment complication in patients treated with radiotherapy or chemotherapy for previous hematologic malignancies or solid tumors. Distinct clinical entities have been described according to the primary treatment, corresponding to defined genetic lesions. Chromosome 7 and/or 5 losses or deletions are typical of alkylating agent-induced AML, while development of t-AML with balanced translocations involving chromosome bands 11q23 and 21q22 has been related to previous therapy with drugs targeting DNA-topoisomerase II. In addition, anti-metabolites, and in particular the immunosuppressant azathioprine, have been shown to induce defective DNA-mismatch repair. This could promote survival of misrepaired cells giving rise to the leukemic clone. Individual predisposing factors, including polymorphisms in detoxification and DNA repair enzymes have been identified. Their combination may significantly increase the risk of t-MDS/AML. Among patients with hematologic malignancies, long-term survivors of Hodgkin's lymphoma are exposed to an increased risk of t-MDS/AML, particularly when receiving MOPP-based, and escalated BEACOPP regimens, and when alkylators are combined with radiotherapy. Patients with Hodgkin's and non-Hodgkin's lymphoma are at highest risk when total body irradiation followed by autologous stem cell transplantation is used as rescue or consolidation therapy. The addition of granulocyte-colony-stimulating factor and radiotherapy plays a significant role in t-AML following treatment of children with acute lymphoblastic leukemia. In non-hematologic malignancies, treatment for breast cancer and germcell tumors has been associated with a 1-5% lifetime risk of both lymphoid as well as myeloid leukemia. In all cases the risk of t-MDS/AML drops sharply by 10 years after treatment.Key words: susceptibility, therapy-related, AML, MDS. Established genetic factors alone explain approximately 5% of all cancers, the remainder can be attributed to environmental carcinogens, tobacco smoke, dietary costituents, pollutants, drugs, radiation, and infectious agents that act in conjunction with both genetic and acquired susceptibility.1 Yet, the role of exogenous factors is not always so evident. Apart from radiotherapy and chemotherapy, which are recognized as the most frequent causes of secondary malignant neoplasms, therapy-related acute myeloid leukemia (t-AML) and myelodysplastic syndromes (t-MDS) account for 10-20% of all cases of AML.2 In the GIMEMA registry, the incidence of AML occurring as a second malignancy was about 5%, but this registry includes only patients in whom treatment is feasible.3 The high incidence of t-AML has been attributed to the increasing use of cytotoxic drugs causing DNA damage, and to the longer survival of many treated patients. Yet, only a minimal proportion of subjects exposed present with a secondary leukemia, indicating that an important role is played by the susceptibility of hemato...

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Section: Non-hematologic Diseasesmentioning

confidence: 99%

Therapy-related leukemia and myelodysplasia: susceptibility and incidence

Leone¹,

Pagano²,

et al. 2007

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“…It is now apparent that patients receiving prolonged treatment with melphalan are at increased risk of developing ANLL. The association between melphalan treatment and ANLL comes from numerous case reports of patients developing leukemia after melphalan treatment for malignant disease (50)(51)(52)(53)(54)(55)(56)(57)(58)(59)(60)(61)(62), including at least 21 The incidence of ANLL in multiple myeloma patients was calculated for seven groups of patients in which the appropriate information as to sample size, observation period, and number of patients developing this complication was specified (Fig. 2).…”

Section: Melphalanmentioning

confidence: 99%

“…Thio-TEPA Although this drug is no longer in wide use as an antineoplastic agent, a number of case reports published between 1970 and 1978 linked exposure to thio-TEPA with the subsequent development of ANLL. Thio-TEPA was the only chemotherapeutic agent employed in the treatment of nine patients with tumors (three with breast cancer, three with ovarian carcinoma, two with lung cancer, and one with bladder cancer) who developed ANLL (58,62,(77)(78)(79)(80)(81)(82). In two other patients, thio-TEPA was used in combination with irradiation and chlorambucil or cyclophosphamide (83,84), and three women with ovarian carcinoma received a combination of drugs which included thio-TEPA prior to developing ANLL (85,86).…”

Section: Melphalanmentioning

confidence: 99%

Chemically induced leukemia in humans.

Adamson¹,

Seiber²

1981

Environ Health Perspect

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The human population may be exposed to potentially leukemogenic agents, either in the form of drugs and food additives or as environmental contaminants and pollutants. However, in spite of the large number and diversity of these chemicals, only a few have been implicated as human leukemogens. One such agent is benzene, a known bone marrow depressant. A number of case reports have associated chronic exposure to this agent with the development of acute leukemia, as have several epidemiologic surveys. Treatment with various antitumor agents, including procarbazine, melphalan, thio-TEPA, chlorambucil, and cyclophosphamide, has also been associated with the development of acute leukemia. In addition, chloramphenicol and phenylbutazone have been implicated as human leukemogens, but the association between exposure to these two agents and acute leukemia appears at present to be weaker than it is for benzene and antitumor agent exposure. Despite such associations between exposure to chemicals and acute leukemia, several important problems exist with regard to implicating specific agents in the development of this neoplasm in man, including the paucity of animal models for chemically induced leukemia, and the frequent necessity to rely on single case reports or clusters of cases in which chemical exposures are associated with acute leukemia. Future efforts should be directed at performing properly designed and well executed epidemiologic studies, and at developing new in vitro and in vivo models for the study of this neoplasm.

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“…In severe forms, more aggressive immunosuppression is recommended, including methotrexate, cyclophosphamide, azathioprine and mycophenolate. 106 Similar to other ADs, the association between systemic lupus erythematosus and myeloid malignancies was initially suggested from case reports 23,24,[107][108][109][110][111][112][113][114][115][116][117][118][119][120] and small case series which are summarized in Tables 5 and 6. On reviewing the literature, we identified 22 cases of AML developing in systemic lupus patients reported between 1967 and 2009.…”

mentioning

confidence: 99%