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.