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secondary leukemia or de novo leukemia should be considered when a new leukemia develops after successful treatment of various malignancies .
secondary leukemia refers to the appearance of a new , biologically - unrelated leukemia different from the primary malignancy , following the treatment of the primary malignancy ; de novo leukemia refers to leukemia in patients without exposure to potentially leukemogenic therapies or agents . in patients that undergo allogeneic hematopoietic stem cell transplantation ( hsct ) , the possibility of the appearance of leukemia from allogeneic hematopoiesis ( donor cell leukemia ) as well as de novo or secondary leukemia , which originates in the recipient ,
it is not surprising that a large percentage of patients who develop secondary acute myeloid leukemia ( aml ) were previously treated for hematological disorders but not solid tumors , considering the responsiveness of hematologic malignancies to chemotherapy .
however , in most cases , prior treatment was not for leukemia but for lymphoma and myeloma . indeed , although malignancies after hsct has been well documented , secondary leukemia occurring after hsct for aml is rare .
in addition , most reports of secondary aml follow autologous transplantation , and it is rare following allogeneic transplantation regardless of the primary disease , primarily because the anti - leukemic effects of the allogeneic graft reduce the risk of a secondary clone developing .
we present a case initially diagnosed as a de novo aml without a cytogenetic abnormality .
the patient was successfully treated with a hla - matched sibling allogeneic hsct . however , more than six years later , a second aml developed that was associated with new complex cytogenetic abnormalities .
a 36-year - old man was diagnosed with aml - m1 by the fab classification in april 1998 ( fig .
his chromosome analysis showed a 46 , xy karyotype without any cytogenetic abnormalities ( fig .
he was treated with induction chemotherapy ( idarubicin 12 mg / m / d on days 1 to 3 , enocitabine 300
mg / m / d on days 1 to 7 , 6-thioguanine 100 mg / m , bid on days 1 to 7 ) and augmentation chemotherapy ( enocitabine 400 mg / m / d for 2 days ) .
he achieved a complete remission , and underwent consolidation chemotherapy with amsacrine 100 mg / m / d on days 1 to 3 and etoposide 100 mg / m / d on days 1 to 5 .
the patient had two hla - identical sisters out of his three siblings , and received an allogeneic bone marrow ( bm ) hsct from one of his fully matched sisters on december 1998 ; conditioning included fractionated total body irradiation ( tbi ) 1200 cgy for three days , followed by cyclophosphamide 120 mg / m for two days . on day 21 ,
the first hsct resulted in a continuous , complete remission that lasted seventy three months . on december 2004
, he presented with a hemoglobin of 9.1 g / dl , white blood cells 2.0  10/l and platelets 52  10/l .
a bm aspirate showed that a majority of the nucleated elements were blasts without dysplastic changes ( fig .
cytogenetic analysis showed a complex karyotype : 46,x , der(y)t(y;15)(q11.2;q11.2 ) , del(1)(q32 ) , t(1;3)(p36.1;q21),inv(3)(p21q25),add(4)(p16 ) , del(7)(q22),+8,inv(9)(p13p24),-15,add(16)(p13.3)/46,idem , del(13)(q12q22)/46,xx(fig .
2b ) . molecular analysis with a y - chromosome probe revealed that the abnormal chromosomes originated from the recipient .
the patient achieved morphological and cytogenetic remission again with reinduction chemotherapy ; he underwent a second allogeneic peripheral blood hsct from another human leukocyte antigen - identical sister on may 2005 .
the patient has been followed for over 12 months after the second hsct without serious complications .
this case is characterized by a longer latency period than in previous reports of secondary aml following hematologic and/or non hematologic malignancies   as well as rare cases of secondary aml following de novo aml , in the setting of an allograft . in our case
, the new complex cytogenetic aberrations , as well as the allograft setting , suggested that the origin of the second aml might be biologically unrelated to the first .
there are two possible origins for the second aml : a secondary aml , another de novo aml , or perhaps a donor cell leukemia .
secondary aml is primarily associated with therapy - related myelodysplasia and/or therapy - related aml ( t - aml ) as a late complication following cytotoxic therapy [ 1 - 3,5,6 ] .
t - aml consists of 2 different syndromes : one with a long latency ( 5 to 7 years or more ) observed following the administration of alkylating agents , which frequently show antecedent dysplastic changes and clonal abnormalities with loss of all or part of chromosome 5 or 7 , or both .
the other syndrome has a short latency period ( 1 to 3 years ) , with no antecedent dysplastic phase , abnormalities of chromosome 11 , specifically 11q23 , or abnormalities of chromosome 21q22 , and usually follows the use of topoisomerase ii inhibitors .
our patient received topoisomerase ii inhibitors for induction ( idarubicin ) and consolidation ( amsacrine and etoposide ) chemotherapy , and the alkylating agents , tbi / cyclophosphamide , for conditioning therapy . in our case
, the long latency period and cytogenetic abnormalities characterized by deletion of 7q would suggest that the newly developed aml might be a t - aml caused by cyclophosphamide and/or tbi , rather than by topoisomerase ii inhibitors .
however , the dose of cyclophosphamide was much lower than normally associated with t - aml , there were no antecedent dysplastic changes and relatively long latency period , and secondary aml is very rare in the allograft setting , making it difficult to verify this possibility . another possibility is the development of another primary aml , either de novo aml or donor cell leukemia .
however , donor cell leukemia was excluded by cytogenetic studies showing the aberrations associated with a y chromosome . then , is the second de novo aml of recipient origin ?
first , our case had a longer latent period and an allogeneic hsct . generally , in all grafted adult aml
, patients without a relapse or chronic graft - versus - host disease five years after allogeneic hsct are often considered " cured " .
second , deletion of 7q , which may be associated with alkylating agents , often occurs in de novo aml as well as secondary aml .
third , considering the possible graft - versus - leukemia effect of the allograft , our patient was probably cured and then developed a new aml later .
finally , the patient showed a good clinical course after the second allogeneic hsct ; secondary aml due to alkylating agents has a uniformly poor prognosis .
alternatively , the clones found in the second aml may have been undetected subclones at the time of the first aml that later gained proliferative potential after the hsct
. however , this is unlikely and would be difficult to prove even with molecular genetic analysis . in conclusion
, our patient may have had a second de novo aml following successful treatment of the first de novo aml , although we could not rule out other possibilities .
future studies of a patient 's intrinsic genetic makeup may help indicate a predisposition to the rare development of a secondary or de novo aml .
secondary leukemia occurring after hematopoietic stem cell transplantation ( hsct ) for acute myeloid leukemia ( aml ) is rare . 
 secondary aml usually follows autologous and not allogeneic transplants . when a new leukemia develops in a patient successfully treated with an allogeneic hsct , the possibility of a de novo or secondary leukemia from either the donor or recipient should be considered . 
 we present a case initially diagnosed as de novo aml without a cytogenetic abnormality . 
 the patient was successfully treated with an hla - matched sibling allogeneic hsct . however , 
 more than six years later , aml developed again and was associated with new complex cytogenetic abnormalities . after a second hsct , the patient has been followed without serious complications . 
 considering the allogeneic setting , the newly developed cytogenetic abnormalities , a relatively long latent period , and the good clinical course after the second allogeneic hsct , this case might represent a second de novo aml following successful treatment of the first aml .