The association of specific “favorable” cytogenetic abnormalities with secondary leukemia

Kantarjian, Hagop M.; Keating, Michael J.; Walters, Ronald S.; Beran, Miloslav; McLaughlin, Peter; McCredie, Kenneth B.; Freireich, And Emil J.

doi:10.1002/1097-0142(19860815)58:4<924::aid-cncr2820580420>3.0.co;2-y

Cited by 71 publications

(13 citation statements)

References 17 publications

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“…Of these, 11 were excluded from analysis for the following reasons: insufficient details available in two, 17,18 no anti-leukemic treatment administered in three (including current case 2), 19,20 prior radiation therapy only in three, 13,21,22 aberrant breakpoints in one 23 unacknowledged multiple publication in one, 19,24 and finally, one case included in an earlier review (patient number 5 from Quesnel et al 12 ) could not be verified from the primary reference cited. 25 Thus, 25 cases with treatment and follow-up data were available for analysis 6,[12][13][14]19,[26][27][28][29] (Table 1). Follow-up information on the six cases from the MD Anderson Cancer Centre was updated to May 1999.…”

Section: Previously Reported Cases Of S-aml With Inv(16)mentioning

confidence: 99%

“…[1][2][3] Subsequently, the strong association between abnormalities of chromosome 11q23 at the site of the MLL gene, 4 and prior exposure to the epipodophyllotoxins was clearly delineated. 3,5 Throughout this period, with some notable exceptions, 6,7 it was generally held that the prognostically favorable balanced translocations, particularly inv(16), were not within the spectrum of chromosomal abnormalities caused by prior cytotoxic therapies. 8,9 However, in the last 5 years there has been an increasing recognition of the occurrence, albeit uncommon, of inv (16) in patients with secondary AML (s-AML).…”

Section: Introductionmentioning

confidence: 99%

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Secondary acute myeloid leukemia with inv(16): report of two cases following paclitaxel-containing chemotherapy and review of the role of intensified ara-C therapy

et al. 1999

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Acute myeloid leukemia developing secondary to prior cytotoxic chemotherapy (s-AML) encompasses a range of distinct entities. We report two cases of s-AML with inv(16)(p13q22) who had prior exposure to paclitaxel. Additionally, two previously reported cases of s-AML with inv(16) had prior paclitaxel exposure raising the possibility that the taxanes may predispose to this specific syndrome of s-AML. One of our patients received escalated-dose ara-C chemotherapy, achieving a complete remission (12+ months). We therefore examined the prognosis of previously reported cases of s-AML with inv(16) and analyzed the influence of escalated-dose ara-C (у400 mg/m 2 /day). A total of 25 evaluable cases were identified, with 96% attaining CR independent of ara-C dose. The estimated median remission duration was 40 months and the median survival has not been reached (actuarial 5-year survival 52 ± 18%). Although not achieving statistical significance, patients treated with escalated dose ara-C (n = 15) had longer remission duration and overall survival than those treated with standard dose ara-C (n = 10) (P = 0.063 and 0.20, respectively). In univariate analysis, younger age, male gender, and the presence of additional cytogenetic abnormalities were associated with a tendency towards adverse outcomes (P Ͻ 0.1). Age and gender were equally distributed between ara-C dose cohorts, but more patients treated with standard-dose ara-C had additional cytogenetic abnormalities (P = 0.048). Within the limitations of this retrospective study, this analysis suggests that, similar to de novo AML with inv(16), secondary cases may also potentially benefit from treatment with escalated-dose ara-C. This is consistent with the premise that the underlying molecular defect, rather than the presence of prior cytotoxic drug exposure, may be the most important determinant of disease behavior and chemotherapy responsiveness in AML.

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Section: Previously Reported Cases Of S-aml With Inv(16)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Secondary acute myeloid leukemia with inv(16): report of two cases following paclitaxel-containing chemotherapy and review of the role of intensified ara-C therapy

et al. 1999

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“…Numerous studies have reported an increased risk of acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) after treatment of BC [4,5]. Support for this association has been strengthened by the description of signature chromosomal aberrations found in bone marrow specimens from patients with secondary AML and MDS [8][9][10][11][12]. Although several studies describe the increased risk of leukemia for up to 10-15 years after BC diagnosis [5,13,14], data beyond 15 years are not as readily available.…”

Section: Introductionmentioning

confidence: 99%

Secondary hematological malignancies following breast cancer treatment

Bayraktar

Escalón

2010

Oncol Rev

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Breast cancer (BC) incidence has increased among women in most Western countries. Concurrently, the survival time of BC patients has increased with 5-year survival rates reaching 80-90%. Secondary hematological malignancies (SHM) following BC treatment are an issue of concern to clinicians and also to patients and their families. However, therapy-induced leukemia after BC is an underemphasized clinical problem. In this review, we will focus on the incidences and patterns of occurrence of SHM in patients with BC. We will address risk factors for the development of SHM and we will explore how secondary hematological malignancies impact the survival of BC patients.

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“…Another subtype, which is induced by topoisomerase II inhibitors including etoposide or anthracyclines, has no preleukemic phase, often demonstrates balanced translocations such as t(9;11), t(8;21), t (15;17), and, like de novo AML with the same karyotypes, responds well to conventional chemotherapies (2)(3)(4)(5).…”

Section: Introductionmentioning

confidence: 99%

Therapy-related Myelodysplastic Syndrome with Trisomy 1q due to der(1;7) and Megakaryoblastic Proliferation Developing during Complete Remission of Therapy-related Acute Myeloid Leukemia with t(8;21)

et al. 2004

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Therapy-related acute myeloid leukemia (t-AML) with t(8;21) and therapy-related myelodysplastic syndrome (t-MDS) with trisomy 1q due to der(1;7) developed in the same patient with T-cell lymphoma at intervals of six years. After the development of t-MDS with trisomy 1q, during complete remission of t-AML, the number of megakaryoblasts increased to maximally 74% of leukocytes in the blood. This is a very rare case of two separate therapy-related myeloid malignancies (early t-AML and late t-MDS) and is also a notable case of t-MDS with trisomy 1q due to der(1;7) accompanied by megakaryoblastic proliferation.

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The association of specific “favorable” cytogenetic abnormalities with secondary leukemia

Cited by 71 publications

References 17 publications

Secondary acute myeloid leukemia with inv(16): report of two cases following paclitaxel-containing chemotherapy and review of the role of intensified ara-C therapy

Secondary acute myeloid leukemia with inv(16): report of two cases following paclitaxel-containing chemotherapy and review of the role of intensified ara-C therapy

Secondary hematological malignancies following breast cancer treatment

Therapy-related Myelodysplastic Syndrome with Trisomy 1q due to der(1;7) and Megakaryoblastic Proliferation Developing during Complete Remission of Therapy-related Acute Myeloid Leukemia with t(8;21)

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