Increase therapy-related leukemia secondary to breast cancer

Carli, Paule‐Marie; Sgro, C; Parchin-Geneste, N; Isambert, Nicolás; Mugneret, Francine; Girodon, François; Maynadié, Marc

doi:10.1038/sj.leu.2401787

Cited by 56 publications

(33 citation statements)

References 19 publications

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“…Besides the balanced translocation 11q23, inv (16), and t(15;17) are found with a high frequency in topoisomerase II-induced sAML, especially after treatment with mitoxantrone. 7,8,26 In a French study, two out of 10 patients with sAML after mitoxantrone-based chemotherapy for breast cancer showed an inv (16), and one patient the translocation t(15;17). 7 Furthermore, Carli et al found in four out of nine patients (44%) with sAML after mitoxantrone-based chemotherapy for breast cancer, a FAB M3 subtype with classical translocation t(15;17).…”

Section: Discussionmentioning

confidence: 99%

“…7 Furthermore, Carli et al found in four out of nine patients (44%) with sAML after mitoxantrone-based chemotherapy for breast cancer, a FAB M3 subtype with classical translocation t(15;17). 26 After autologous transplantation for non-Hodgkin lymphoma, there is some concern about the high probability of secondary MDS or AML, which is 14-18% at 5 years. [27][28][29] There are only a few reports of MDS/AML following HDCT for breast cancer.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Secondary acute leukemia following mitoxantrone-based high-dose chemotherapy for primary breast cancer patients

Kröger

Damon

Zander

et al. 2003

Bone Marrow Transplant

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Summary:The incidence of secondary myelodysplasia/acute myeloid leukemia (AML) was retrospectively assessed in an international joint study in 305 node-positive breast cancer patients, who received mitoxantrone-based high-dose chemotherapy (HDCT) followed by autologous stem cell support as adjuvant therapy. The median age of the patients was 57 years (range 22-67). In all, 268 patients received peripheral blood stem cells, and 47 patients received autologous bone marrow. After a median followup of 57 months (range 10-125), three cases of secondary AML (sAML) were observed, resulting in a cumulative incidence of 0.94%. One case of sAML developed 18 months after HDCT (FAB M3) The karyotype was translocation 15;17 and, after induction therapy, the patient underwent autologous stem cell transplantation, and is in complete remission (CR) of both breast cancer and AML. The second patient developed AML (FAB M4eo with inversion 16) 5 months after HDCT. This patient achieved CR after induction therapy, but died of infectious complication. A third patient developed AML (FAB M4) 6 months after HDCT. She achieved CR after induction therapy, but relapsed and expired 28 months after diagnosis of AML. sAML after mitoxantrone-based HDCT is a possible, but rare complication in breast cancer patients. Bone Marrow Transplantation (2003) 32, 1153-1157. doi:10.1038/sj.bmt.1704291 Keywords: high-dose chemotherapy; adjuvant therapy; breast cancer; mitoxantrone; secondary AML Secondary myelodysplasia (MDS) or acute myeloid leukemia (AML) in breast cancer patients is a rare but wellknown long-term complication of prior chemotherapy or radiation therapy as adjuvant therapy. 1-3 Specific risk factors are the combinations of chemotherapy and radiation therapy, the cumulative dose of alkylating agents and the duration of therapy. 2 Two different types of treatmentrelated leukemia can be distinguished. The first type results from prior therapy with alkylating agents or radiation therapy, and occurs after a latency period of 5-7 years. This type of AML is often preceded by a preleukemic period of MDS. Nearly 90% of the patients with alkylating agentrelated MDS or AML show clonal chromosome aberrations including monosomy or deletions on chromosomes 5 and/or 7 or complex aberrations involving chromosomes 3, 12, 17, and 21. 4 The second type of therapy-related leukemia is induced by topoisomerase II-targeted drugs like etoposide, anthracyclines or, recently, anthracenediones. [5][6][7] This type of AML usually occurs after a median of 2 years and is not preceded by a myelodysplastic syndrome. According to the French-American-British (FAB) classification, more frequently, M4 or M5 subtype is observed and cytogenetic analysis showed a high frequency of rearrangements of the chromosome band as 11q23, translocation (t)(8;21), t(15;17), inversion 16 (inv(16)) or t(8;16), as in de novo AML. 5,8 Recently, several studies indicated that adjuvant chemotherapy consisting of the anthracenedione mitoxantrone, a topoisomerase II-targeted drug, may induce sec...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Secondary acute leukemia following mitoxantrone-based high-dose chemotherapy for primary breast cancer patients

Kröger

Damon

Zander

et al. 2003

Bone Marrow Transplant

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“…Therapy-related promyelocytic leukemia is reported increasingly these years particularly in patients treated with doxorubicin or mitoxantrone for breast cancer. [37][38][39] Most patients in this pathway present with overt t-AML, and like their counterpart of patients with de novo AML and t(15;17) they often respond favorably to therapy with retinoic acid. One of our only two patients in this pathway presented an FLT3 internal tandem duplication ( Figure 2).…”

Section: Pathway Vmentioning

confidence: 99%

Alternative genetic pathways and cooperating genetic abnormalities in the pathogenesis of therapy-related myelodysplasia and acute myeloid leukemia

Pedersen‐Bjergaard¹,

Christiansen²,

Desta³

et al. 2006

Leukemia

133

100

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Alternative genetic pathways were previously outlined in the pathogenesis of therapy-related myelodysplasia (t-MDS) and acute myeloid leukemia (t-AML) based on cytogenetic characteristics. Some of the chromosome aberrations, the recurrent balanced translocations or inversions, directly result in chimeric rearrangement of genes for hematopoietic transcription factors (class II mutations) which disturb cellular differentiation. Other genetic abnormalities in t-MDS and t-AML comprise activating point mutations or internal tandem duplications of genes involved in signal transduction as tyrosine kinase receptors or genes more downstream in the RAS-BRAF pathway (class I mutations). The alternative genetic pathways of t-MDS and t-AML can now be further characterized by a different clustering of six individual class I mutations and mutations of AML1 and p53 in the various pathways. In addition, there is a significant association between class I and class II mutations possibly indicating cooperation in leukemogenesis, and between mutations of AML1 and RAS related to subsequent progression from t-MDS to t-AML. Therapy-related and de novo myelodysplasia and acute myeloid leukemia seem to share genetic pathways, and surprisingly gene mutations were in general not more frequent in patients with t-MDS or t-AML as compared to similar cases of de novo MDS and AML studied previously.

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“…25 Similarly, anticancer drugs, especially topoisomerase inhibitors, cause secondary cancers. [26][27][28][29] To complicate matters further, chemopreventive agents may promote cancer in some conditions. 30 In certain mice, sulindac, a nonsteroidal anti-inflammatory drug, prevents tumors in the small intestine but increases the incidence of tumors in the large intestine.…”

Section: Introductionmentioning

confidence: 99%

Carcinogenesis, cancer therapy and chemoprevention

Blagosklonny

2005

Cell Death Differ

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Carcinogenesis and cancer therapy are two sides of the same coin, such that the same cytotoxic agent can cause cancer and be used to treat cancer. This review links carcinogenesis, chemoprevention and cancer therapy in one process driven by cytotoxic agents (carcinoagents) that select either for or against cells with oncogenic alterations. By unifying therapy and cancer promotion and by distinguishing nononcogenic and oncogenic mechanisms of resistance, I discuss anticancer-and chemopreventive agent-induced carcinogenesis and tumor progression and, vice versa, carcinogens as anticancer drugs, anticancer drugs as chemopreventive agents and exploiting oncogene-addiction and drug resistance for chemoprevention and cancer therapy.

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Increase therapy-related leukemia secondary to breast cancer

Cited by 56 publications

References 19 publications

Secondary acute leukemia following mitoxantrone-based high-dose chemotherapy for primary breast cancer patients

Secondary acute leukemia following mitoxantrone-based high-dose chemotherapy for primary breast cancer patients

Alternative genetic pathways and cooperating genetic abnormalities in the pathogenesis of therapy-related myelodysplasia and acute myeloid leukemia

Carcinogenesis, cancer therapy and chemoprevention

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