Table 3-1 Nonrandom Chromosomal Abnormalities in Malignant Myeloid Diseases

Diseasea

Chromosomal Abnormality

CML

t(9;22)(q34;q11)

CML blast phase

t(9;22)(q34;q11) with +8,

+Ph1, +19, or i(17q)

AML-M2

t(8;21)(q22;q22)

APL-M3, M3V

t(15;17)(q22;q11–12)

AMMoL-M4Eo

inv(16)(p13q22) or

t(16;16)(p13;q22)

AMMol-M4

Translocations or

deletions of 11q23

AMoL-M5

t(9; 11) (p22;q23),

t(11q13 or q23)

AML

+8

 

-7 or del(7q)

 

-5 or del(5q)

 

del(20q)

 

t(3;3)(q21;q26)

or inv(3)(q21q26)

 

t(6;9)(p23;q34)

Therapy-related AML

-7 or del(7q) and/or

-5 or del(5q)

 

der(I)t(1;7)(p11;p11)

 

t(9;11)(p22;q23)

a CML, chronic myelogenous leukemia; AML, acute myeloblastic leukemia; AML-M2, AML with maturation; AMMoL, acute myelomonocytic leukemia; AMMoL-M4Eo, acute myelomonocytic leukemia with abnormal eosinophils; AMoL, acute monoblastic leukemia; APL-M3, M3V, hypergranular (M3) and microgranular (M3V) acute promyelocytic leukemia.

follows a well-defined course. Most patients present with a high white blood cell count, mild constitutional complaints, and splenomegaly. Many are asymptomatic at this stage of their disease, which is referred to as the chronic phase. Inevitably and tragically, after a period of months to years, most untreated patients with CML develop blast crisis, a phase that resembles acute leukemia. In some patients, blast crisis is presaged by a prodromal phase of disease acceleration. The only curative therapy for CML is bone marrow transplant, which has a good outcome when performed during the stable phase, but a poor outcome in patients in blast crisis.



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