Abstract
ET is a chronic myeloproliferative disorder rarely evolving into AML, sometimes preceded by a myelodysplastic syndrome (MDS). Such transformations mostly occur in patients treated with radiophosphorous (32P) or alkylating agents, especially busulfan. Recently, concern has also arisen about the longterm safety of hydroxyurea (HU). Pipobroman (PI), a well tolerated and simple to use drug, constitutes a valid alternative to those cytoreductive treatments. The present study reports on 155 ET patients treated at our institution from 1985 to 1995, and monitored until December 2000. A good control of thrombocytosis was achieved with PI as the only treatment in 106 patients and With HU in 23 patients. Twenty-six patients received no treatment. After a median follow-up of 104 months, seven patients (four treated with HU, and three with PI) developed AML whereas one patient treated with PI developed MDS. A significant difference in progression-free survival was observed between HU- and PI-treated patients (P = 0.004). A short-arm deletion of chromosome 17 was most frequently detected in HU-treated patients, while a long-arm trisomy of chromosome 1 and a monosomy 7q were seen in PI-treated patients. No TP53 mutation was discovered in the six patients studied (two HU-treated and four PI-treated). We conclude that these cytogenetic abnormalities are not linked to the natural history of the disease, but rather that they might be induced by the cytoreductive treatment.
| Original language | English |
|---|---|
| Pages (from-to) | 2078-2083 |
| Number of pages | 6 |
| Journal | Leukemia |
| Volume | 16 |
| Issue number | 10 |
| DOIs | |
| Publication status | Published - Oct 1 2002 |
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Keywords
- 17p-
- Chromosome abnormalities
- Cytogenetics
- FISH
- TP53
ASJC Scopus subject areas
- Cancer Research
- Hematology
Cite this
Acute myeloid leukemia (AML) having evolved from essential thrombocythemia (ET) : Distinctive chromosome abnormalities in patients treated with pipobroman or hydroxyurea. / Bernasconi, P.; Boni, M.; Caviglianio, P. M.; Calatroni, S.; Brusamolino, E.; Passamonti, F.; Volpe, G.; Pistorio, A.; Giardini, I.; Rocca, B.; Caresana, M.; Lazzarino, M.; Bernasconi, C.
In: Leukemia, Vol. 16, No. 10, 01.10.2002, p. 2078-2083.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Acute myeloid leukemia (AML) having evolved from essential thrombocythemia (ET)
T2 - Distinctive chromosome abnormalities in patients treated with pipobroman or hydroxyurea
AU - Bernasconi, P.
AU - Boni, M.
AU - Caviglianio, P. M.
AU - Calatroni, S.
AU - Brusamolino, E.
AU - Passamonti, F.
AU - Volpe, G.
AU - Pistorio, A.
AU - Giardini, I.
AU - Rocca, B.
AU - Caresana, M.
AU - Lazzarino, M.
AU - Bernasconi, C.
PY - 2002/10/1
Y1 - 2002/10/1
N2 - ET is a chronic myeloproliferative disorder rarely evolving into AML, sometimes preceded by a myelodysplastic syndrome (MDS). Such transformations mostly occur in patients treated with radiophosphorous (32P) or alkylating agents, especially busulfan. Recently, concern has also arisen about the longterm safety of hydroxyurea (HU). Pipobroman (PI), a well tolerated and simple to use drug, constitutes a valid alternative to those cytoreductive treatments. The present study reports on 155 ET patients treated at our institution from 1985 to 1995, and monitored until December 2000. A good control of thrombocytosis was achieved with PI as the only treatment in 106 patients and With HU in 23 patients. Twenty-six patients received no treatment. After a median follow-up of 104 months, seven patients (four treated with HU, and three with PI) developed AML whereas one patient treated with PI developed MDS. A significant difference in progression-free survival was observed between HU- and PI-treated patients (P = 0.004). A short-arm deletion of chromosome 17 was most frequently detected in HU-treated patients, while a long-arm trisomy of chromosome 1 and a monosomy 7q were seen in PI-treated patients. No TP53 mutation was discovered in the six patients studied (two HU-treated and four PI-treated). We conclude that these cytogenetic abnormalities are not linked to the natural history of the disease, but rather that they might be induced by the cytoreductive treatment.
AB - ET is a chronic myeloproliferative disorder rarely evolving into AML, sometimes preceded by a myelodysplastic syndrome (MDS). Such transformations mostly occur in patients treated with radiophosphorous (32P) or alkylating agents, especially busulfan. Recently, concern has also arisen about the longterm safety of hydroxyurea (HU). Pipobroman (PI), a well tolerated and simple to use drug, constitutes a valid alternative to those cytoreductive treatments. The present study reports on 155 ET patients treated at our institution from 1985 to 1995, and monitored until December 2000. A good control of thrombocytosis was achieved with PI as the only treatment in 106 patients and With HU in 23 patients. Twenty-six patients received no treatment. After a median follow-up of 104 months, seven patients (four treated with HU, and three with PI) developed AML whereas one patient treated with PI developed MDS. A significant difference in progression-free survival was observed between HU- and PI-treated patients (P = 0.004). A short-arm deletion of chromosome 17 was most frequently detected in HU-treated patients, while a long-arm trisomy of chromosome 1 and a monosomy 7q were seen in PI-treated patients. No TP53 mutation was discovered in the six patients studied (two HU-treated and four PI-treated). We conclude that these cytogenetic abnormalities are not linked to the natural history of the disease, but rather that they might be induced by the cytoreductive treatment.
KW - 17p-
KW - Chromosome abnormalities
KW - Cytogenetics
KW - FISH
KW - TP53
UR - http://www.scopus.com/inward/record.url?scp=0036797010&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036797010&partnerID=8YFLogxK
U2 - 10.1038/sj.leu.2402638
DO - 10.1038/sj.leu.2402638
M3 - Article
C2 - 12357360
AN - SCOPUS:0036797010
VL - 16
SP - 2078
EP - 2083
JO - Leukemia
JF - Leukemia
SN - 0887-6924
IS - 10
ER -