Types of Leukemia

Leukemia is classifed by how quickly it progresses. Acute leukemia is fast-growing

and can overrun the body within a few weeks or months. By contrast, chronic
leukemia is slow-growing and progressively worsens over years.
Acute versus Chronic Leukemia
he blood-forming !hematopoietic" cells of acute leukemia remain in an immature
state, so they reproduce and accumulate very rapidly. herefore, acute leukemia
needs to be treated immediately, otherwise the disease may be fatal within a few
months. #ortunately, some subtypes of acute leukemia respond very well to
available therapies and they are curable. $hildren often develop acute forms of
leukemia, which are managed di%erently from leukemia in adults.
&n chronic leukemia, the blood-forming cells eventually mature, or di%erentiate, but
they are not 'normal.' hey remain in the bloodstream much longer than normal
white blood cells, and they are unable to combat infection well.
Myelogenous versus Lymphocytic Leukemia
Leukemia also is classifed according to the type of white blood cell that is
multiplying(that is, lymphocytes !immune system cells", granulocytes !bacteria-
destroying cells", or monocytes !macrophage-forming cells". &f the abnormal white
blood cells are primarily granulocytes or monocytes, the leukemia is categori)ed as
myelogenous, or myeloid, leukemia. *n the other hand, if the abnormal blood cells
arise from bone marrow lymphocytes, the cancer is called lymphocytic leukemia.
*ther cancers, known as lymphomas, develop from lymphocytes within the lymph
nodes, spleen, and other organs. +uch cancers do not originate in the bone marrow
and have a biological behavior that is di%erent from lymphocytic leukemia.
here are over a do)en di%erent types of leukemia, but four types occur most
frequently. hese classifcations are based upon whether the leukemia is acute
versus chronic and myelogenous versus lymphocytic, that is,
Acute -yelogenous !granulocytic" Leukemia !A-L"
$hronic -yelogenous !granulocytic" Leukemia !$-L"
Acute Lymphocytic !lymphoblastic" Leukemia !ALL"
$hronic Lymphocytic Leukemia !$LL"
Acute Myelogenous Leukemia (AML)
Acute myelogenous leukemia !A-L".also known as acute nonlymphocytic leukemia
!A/LL".is the most common form of adult leukemia. -ost patients are of retirement
age !average age at diagnosis is 01 years", and more men are a%ected than
women. #ortunately, because of recent advances in treatment, A-L can be kept in
remission !lessening of the disease" in appro2imately 034 to 534 of adults who
undergo appropriate therapy. &nitial response rates are appro2imately 01-514 but
the overall cure rates are more on the order of 63-134.
A-L begins with abnormalities in the bone marrow blast cells that develop to form
granulocytes, the white blood cells that contain small particles, or granules. he
A-L blasts do not mature, and they become too numerous in the blood and bone
marrow. As the cells build up, they hamper the body7s ability to fght infection and
prevent bleeding. herefore, it is necessary to treat this disease within a short time
after making a diagnosis. A-L, particularly in the monocytic -1 form, may spread to
the gums and cause them to swell, bleed, and become painful. A-L also may
metastasi)e !spread" to the skin, causing small colored spots that mimic a rash.
Acute leukemia, such as A-L, is categori)ed according to a system known as
#rench-American-British !#AB" classifcation. #AB divides A-L into eight subtypes,
undiferentiated AML (M0).&n this form of leukemia, the bone marrow
cells show no signifcant signs of di%erentiation !maturation to obtain
distinguishing cell characteristics".
myeloblastic leukemia (M8 with9without minimal cell maturation".he
bone marrow cells show some signs of granulocytic di%erentiation.
myeloblastic leukemia (M!8 with cell maturation".he maturation of bone
marrow cells is at or beyond the promyelocyte !early granulocyte" stage8
varying amounts of maturing granulocytes may be seen. his subtype often is
associated with a specifc genetic change involving translocation of
chromosomes : and ;<.
promyelocytic leukemia (M" or M" variant #M"$%".-ost cells are
abnormal early granulocytes that are between myeloblasts and myelocytes in
their stage of development and contain many small particles. he cell
nucleus may vary in si)e and shape. Bleeding and blood clotting problems,
such as disseminated intravascular coagulation !=&$", are commonly seen
with this form of leukemia. >ood responses are observed after treatment with
retinoids, which are drugs chemically related to vitamin A.
myelomonocytic leukemia (M& or M& variant 'ith eosinophilia #M&(%"
.he bone marrow and circulating blood have variable amounts of
di%erentiated granulocytes and monocytes. he proportion of monocytes and
promonocytes !early monocyte form" in the bone marrow is greater than ;34
of all nucleated !nucleus-containing" cells. he -6? variant also contains a
number of abnormal eosinophils !granular leukocyte with a two-lobed
nucleus" in the bone marrow.
monocytic leukemia (M)).here are two forms of this subtype. he frst
form is characteri)ed by poorly di%erentiated monoblasts !immature
monocytes" with lacy-appearing genetic material. he second, di%erentiated
form is characteri)ed by a large population of monoblasts, promonocytes, and
monocytes. he proportion of monocytes in the bloodstream may be higher
than that in the bone marrow. -1 leukemia may infltrate the skin and gums,
and it has a worse prognosis than other subtypes.
erythroleukemia (M*).his form of leukemia is characteri)ed by abnormal
red blood cell-forming cells, which make up over half of the nucleated cells in
the bone marrow.
megakaryoblastic leukemia (M+).he blast cells in this form of leukemia
look like immature megakaryocytes !giant cells of the bone marrow" or
lymphoblasts !lymphocyte-forming cells". -5 leukemia may be distinguished
by e2tensive fbrous tissue deposits !fbrosis" in the bone marrow.
&n addition, patients sometimes develop isolated tumors of the myeloblasts !early
granulocytes". An e2ample of this is isolated granulocytic sarcoma, or chloroma.a
malignant tumor of the connective tissue. &ndividuals with chloroma frequently
develop A-L, so they usually are treated with an aggressive, A-L-specifc
chemotherapy program.
Chronic Myelogenous Leukemia (CML)
$hronic myelogenous leukemia !$-L" is known as a myeloproliferative disorder.
that is, it is a disease in which bone marrow cells proliferate !multiply" outside of the
bone marrow tissue.
$-L is easy to diagnose, since it has a genetic peculiarity, or marker, that is readily
identifable under a microscope. About @14 of $-L patients have a genetic
translocation between chromosomes @ and ;; in their leukemic cells. his
abnormality, which is known as the Ahiladelphia chromosome !Ah<", is named after
the city in which it was discovered. he Ahiladelphia chromosome causes
uncontrolled reproduction and proliferation of all types of white blood cells and
platelets !blood clotting factors". +adly, $-L is not yet curable by standard methods
of chemotherapy or immunotherapy.
$-L tends to occur in middle- and retirement-aged people !the median age is 05
years". &t occasionally a%ects people in their ;3s, but it is rare in the very young8
only ;4 to B4 of childhood leukemias are $-L. ?arly disease often is without
symptoms !asymptomatic" and is discovered accidentally. &ndividuals with more
advanced cases of $-L may appear sickly and e2perience fevers, easy bruising, and
bone pain. Laboratory and physical fndings include enlarged spleen
!splenomegaly", a high white blood cell count, and absent or low amounts of the
white blood cell en)yme alkaline phosphatase.
Like other forms of leukemia, $-L is not 'staged'. Cather, this unstable disease is
categori)ed according to the three phases of its development, chronic, accelerated,
and blast.
Chronic phase.Aatients in this initial phase have fewer than 14 blast cells
and promyelocytes !immature granulocytes" in their blood and bone marrow.
his phase is marked by increasing overproduction of granulocytes.
&ndividuals generally e2perience only mild symptoms, and they respond well
to conventional treatment.
Accelerated phase.Aatients in this progressive phase have more than 14,
but fewer than B34 blast cells. heir leukemic cells e2hibit more
chromosomal abnormalities besides the Ahiladelphia chromosome, and so
more abnormal cells are produced. /oticeable symptoms such as fever, poor
appetite, weight loss occur, and patients may not respond as well to therapy.
,last phase !acute phase, blast crisis".Aatients in this fnal phase have
more than B34 blast cells in their blood and bone marrow samples. he blast
cells frequently invade other tissues and organs outside of the bone marrow.
=uring this phase, the disease transforms into an aggressive, acute leukemia
!534 acute myelogenous leukemia, B34 acute lymphocytic leukemia". &f
untreated, $-L is fatal in roughly ;34 of all patients each year.