Top 10 anemias to know for Boards

7/26/2019 Top 10 anemias to know for Boards

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The Top Ten Anemias toKnow for Boards A Quick Review of High-Yield Anemias

Kristine Krafts, M.D.2nd Edition



Introduction 3 ............................................................................

Important basic stuff 4 ...............................................................Iron-Deficiency Anemia 9 ..........................................................

Megaloblastic Anemia 10 ...........................................................

Hereditary Spherocytosis 11 ......................................................

G6PD Deficiency 12 ..................................................................

Sickle-Cell Anemia 13 ................................................................

Thalassemia 14 ...........................................................................

Autoimmune Hemolytic Anemia 15 ..........................................

Microangiopathic Hemolytic Anemia 17 ...................................

Anemia of Chronic Disease 18 ..................................................

Aplastic Anemia 19 ...................................................................

Preview: The Complete Hematopathology Guide 20 ...............

Table of Contents



Introduction

Thanks for downloading The Top Ten Anemias to Know for Boards. This short study guide

covers the anemias most often covered on board exams (and on pathology course exams). It

quickly summarizes the most high-yield points about pathogenesis, morphology and treatment

for each anemia, and gives you a nice image of each type. We'll also take a quick look at some

important clinical features of anemias, and we'll discuss the meaning of CBC indices as well as

how to look at a blood smear.

Getting Started

You can click on any of the anemia titles in the table of contents to go straight to that anemia.

Or just read the whole thing straight through - it should only take 15 - 20 minutes.

If you like this book…You might find some of our other guides useful. Here's a summary of Pathology Student stuff:

The Complete (But Not Obsessive) Hematopathology Guide

A concise but thorough review of benign and malignant hematopathology.

Clot or Bleed: A Painless Guide for People Who Hate Coag

Coag made understandable! Covers basic mechanisms and bleeding and thrombotic diseases.

Path Bites Anthology: A Collection of Short, Easy and Strangely Fun Pathology

LessonsOver 500 quick, high-yield essays that cover all major areas in general and systemic pathology.

Anatomic Pathology Compendium

A collection of our best Pathology Student essays on difficult anatomic pathology topics.

Hematopathology Compendium

A collection of our best Pathology Student essays on hematopathology.

General Pathology Compendium

A collection of our best Pathology Student essays on general pathology topics.

Neuropathology Mini-Course

A 4-week course that covers 12 high-yield neuropath topics, with memory strategies you can put

to use right away.

www.PathologyStudent.com Top 10 Anemias page 3

http://www.pathologystudent.com/?page_id=7150



















Important basic stuff

Clinical Information

Anemia (from an-, without, and -emia, blood) is a reduction below normal in

hemoglobin or red blood cell number. Patients with anemia can present in different

ways, depending on what kind of anemia they have and how severe it is. The

general signs and symptoms of anemia relate to the underlying lack of oxygen-

carrying capacity: fatigue, weakness, dizziness, tachycardia, pallor of skin and

mucous membranes. It’s important to remember that if an anemia is fairly mild,

symptoms will not be present. Also, if the anemia is chronic and slowly progressive,

the cardiovascular system adjusts to the new diminished level of oxygen, and

symptoms will only appear when the anemia becomes quite severe.

In addition to the general symptoms of anemia, some specific findings may be

present. If the anemia is hemolytic, the patient may be jaundiced. Patients with

iron-deficiency anemia may show spoon-shaped nails (koilonychia), a smooth

tongue, or pica (a craving to eat dirt and other non-food items). And patients with

megaloblastic anemia may develop a big, beefy tongue.




The Complete Blood Count

The CBC is comprised of a bunch of different indices. You get all of these on

every report, whether you ask for them specifically or not (that’s just the way the

machine does it!). Some of these indices are really useful (like the hemoglobin,

MCV and RDW), and some of them are rarely if ever used (like the mean platelet

volume). You should know what each one measures, and be able to recognize the

normal range.

Red blood cell count (RBC)

• Total number of red blood cells in blood

• Normal ranges: male 4.5-6.0 x 1012/L, female 3.8-5.2 x 1012/L

Hemoglobin (Hgb)

• Concentration of hemoglobin in blood

• Normal ranges: male 13-18 g/dL; female 12-16 g/dL

• Hgb below normal = anemia

Hematocrit (Hct)

• Volume of “packed” red blood cells.

• In the old days, was performed by spinning a tube of blood and estimating

the amount of total blood volume taken up by the red cells (not a greatmethod – because if the cells are of unusual shape, they may not pack aswell as normal red cells, producing an artificially elevated Hct)

• Now calculated by machine (MCV x RBC)

• Normal ranges: male 40-52%, female 35-47%

Mean red blood cell volume (MCV)

• Average size of red blood cells

• Normal range: 80-100 fL (1 fL = 10-15

L)• Differentiates between microcytic (MCV < 80), normocytic (MCV 80-100)

and macrocytic (MCV > 100) anemias




Mean cell hemoglobin (MCH)

• Weight of Hgb in the average red blood cell

• Normal range: 26-34 pg (1 pg = 10-12 g)

• Not a frequently used parameter

Mean cell Hgb concentration (MCHC)

• Concentration of Hgb in the average red blood cell

• Normal range: 32-36 g/dL

• Calculated by machine (Hgb/Hct)

• Differentiates between hypochromic (MCHC < 32) and normochromic(MCHC 32-36) anemias

• There is no such thing as a hyper chromic red cell (you can’t put excesshemoglobin into a cell, or it would burst!)

• You can see this nicely on a blood smear: normochromic cells have a “zoneof central pallor” (that white dot in the middle of the cell) that is no morethan 1/3 the diameter of the red cell. Hypochromic red cells have just a thinrim of hemoglobin.

Red cell distribution width (RDW)

• Standard deviation of the MCV

• Tells you how much the red blood cells differ from each other in size . If theyare all pretty similar in size, the RDW is low. If some cells are little and someare big, the RDW is high.

• Normal range = 12-13.5%

• Differentiates between anemias with minimal anisocytosis (difference in cellsize) (RDW = 12-13.5%) and those with increased anisocytosis (RDW >13.5%).

White blood cell count (WBC)

• Total number of leukocytes in blood

• Normal ranges: adult: 4.5-11 x 109/L, newborn: 9-30, child over 1: 5.0-17.0

• A high WBC is seen in many conditions. Some are benign, such as infectionand inflammation. Others are malignant, such as leukemia.




Differential (“diff ”)

• Amounts of each white blood cell type in blood

• Normal ranges:

Platelet count (Plt)

• Total number of platelets in blood

• Normal range = 150-450 x 109/L

• Causes of a low platelet count are numerous and include splenomegaly,idiopathic thrombocytopenic purpura, disseminated intravascularcoagulation, and bone marrow failure.

• Causes of a high platelet count are also numerous, and include reactivethrombocytosis (as seen in iron-deficiency anemia) and essentialthrombocythemia.

MPV (mean platelet volume)

• Average size of platelets

• Normal range depends on the platelet count! (Normally, if the platelet countfalls, the body compensates a little by trying to make bigger platelets.)

• Not used all that often.




The Blood Smear

There are three main things you need to look at when you’re faced with a blood

smear: the red cells, the white cells, and the platelets. It helps if you have a plan

that you follow every time, kind of like radiologists do when they look at imaging

studies. That way you’re not tempted to just start looking at the exciting stuff and

forget about all the other stuff. Here’s your plan for the red cells.

1. Estimate number (just eyeball it; make sure there aren’t a lot of “holes” between

the cells).

2. Look for variation in size (anisocytosis).

• Oval macrocytes (B12/folate deficiency)

• Microcytes (iron deficiency anemia, thalassemia)

• The size range can often help you narrow down which type of anemia ispresent (for example, in iron-deficiency anemia, there is usually a big rangeof sizes)

3. Look for variation in shape (poikilocytosis).

• Schistocytes (microangiopathic hemolytic anemia)

• Spherocytes (hemolytic anemia, hereditary spherocytosis)

• Teardrop cells or dacryocytes (myelofibrosis or myelophthisic processes)

• Target cells or codocytes (hemoglobinopathies, thalassemias, liver disease)• Sickle cells (sickle cell anemia)

• Echinocytes and acanthocytes (liver disease)

4. Estimate the average amount of hemoglobin in each cell (chromasia).

• Normochromic (zone of central pallor = 1/3 of the cell diameter)

• Hypochromic (zone of central pallor >1/3 of the cell diameter)

5. Estimate number of reticulocytes (polychromatophilic cells).

• Normal: one or two polychromatophilic cells per field.

• The lower the Hgb, the higher the reticulocyte count should be.

6. Look for anything else weird.

• Nucleated red blood cells

• Inclusions (Howell-Jolly bodies, Pappenheimer bodies, bugs)




Iron-Deficiency Anemia

Pathogenesis

Blood loss (e.g., GI bleed or heavy menses) or really bad diet (rare).

Morphology

The red cells are hypochromic and microcytic. There is increased anisocytosis

(each successive wave of new red cells is smaller, because there's less and less iron

around!) and poikilocytosis (elliptocytes are often present). Reticulocytes are

decreased, because the lack of iron leads to decreased red cell production. The

platelet count is often increased, for some reason.

Iron studies

• ! serum iron

• " TIBC (total iron binding capacity)

• ! ferritin

Treatment

Figure out why patient is iron deficient (don't just treat the anemia, or you might miss

something really important, like a GI bleed due to colon cancer). Then give oral iron

supplements.

IDA: hypochromic red cells and anisocytosis




Megaloblastic Anemia

Pathogenesis

Vitamin B12 and/or folate deficiency (from bad diet, absorption problems, folate-

antagonist drugs) makes it hard to make DNA (you need both B12 and folate to

make DNA). RNA production runs smoothly though. So the nucleus (full of DNA)

lags behind the cytoplasm (full of RNA) in development, and the cell divides more

slowly (because it’s waiting for signals from the slow-moving nucleus).

Morphology

Blood

The red cells are macrocytic, and you often see great big oval macrocytes.

Hypersegmented neutrophils (with more than 6 nuclear lobes) are also present.

Bone marrow

The bone marrow shows "megaloblastic" cells: giant red cell or neutrophil

precursors with nuclear-cytoplasmic asynchrony (mature cytoplasm, immature

nucleus).

Treatment

Treatment depends on the cause of the anemia. You can’t (or shouldn’t) just replace

the B12 and/or folate without knowing what’s wrong with the patient.

Megaloblastic anemia: hypersegmented neutrophil




Hereditary Spherocytosis

Pathogenesis

Patients with HS have defects in the membrane cytoskeleton (in spectrin, ankyrin,

band 3, or band 4.2). The red cell membrane is unstable, leading to increased

fragility and the formation of spherocytes, which get eaten by macrophages.

Morphology

The red cells are normochromic and normocytic, and depending on the patient's

particular genetic defect, there may be a ton of spherocytes (which look smaller

than normal red cells, and lack central pallor) or just a few.

Treatment

If the disease is mild, patients don’t need treatment. In severe cases, splenectomy

can be useful (because that’s where the red cells get destroyed).

HS: moderate amount of spherocytes




G6PD Deficiency

Pathogenesis

Glucose-6-phosphate dehydrogenase (G6PD) helps reduce nasty free radicals made

during cell metabolism. Patients who have a deficiency of G6PD are usually okay

until they encounter some sort of oxidizing substance (like a drug, or fava beans).

Without enough G6PD around, free radicals attack the molecular bonds between

heme and globin, and globin becomes denatured, forming a little blob called a

Heinz body. The spleen bites out these Heinz bodies, leaving what look like actual

bite marks in the cell.

MorphologyWithout exposure to offending agents, most patients have no anemia. After

exposure, though, patients get an acute hemolytic episode, with cell fragments,

microspherocytes, and bite cells (caused by recent pitting of Heinz bodies).

Supravital staining reveals Heinz bodies (these decrease in number as Hgb bottoms

out, because younger cells have greater G6PD activity).

Treatment

Avoid exposure to known oxidants. Usually the hemolysis is self-limiting, with

spontaneous resolution in a week or so.

G6PD deficiency: bite cell




Sickle-Cell Anemia

Pathogenesis

Sickle cell anemia is a type of hemoglobinopathy (a group of diseases of

hemoglobin characterized by point mutations in a globin chain gene). The

abnormal hemoglobin in sickle cell anemia changes shape when it releases oxygen,

causing it to polymerize, which distorts the red cell into a sickle shape.

Sickle cells are fragile, and they stick together in small vessels, leading to ischemia.

Tiny, repeated infarcts in the spleen lead to fibrosis and eventual "autosplenectomy"

(the spleen becomes a small, fibrotic lump that doesn't work well at all).

Morphology

During times of decreased oxygenation ("crises"), sickle cells are present in the

blood. Also, after autosplenectomy occurs, you can see a "post-splenectomy blood

picture," which includes things the spleen normally removes, like nucleated red

blood cells, Howell-Jolly bodies, and Pappenheimer bodies.

Treatment

It’s important to prevent triggers (things that makes the red cells want to give up

oxygen, like infection). Vaccination against encapsulated bugs is given in patients

who have undergone autosplenectomy.

Sickle cell anemia: lots of sickle cells




Thalassemia

Pathogenesis

The thalassemias are quantitative diseases of hemoglobin. They are characterized

by a decrease in amount of one of the hemoglobin chains. In "-thalassemia, there

is a decreased amount of α chains. In #-thalassemia, there is a decreased amount of

β chains. You end up with a two-fold problem:

1. Decreased hemoglobin production (due to decreased globin chains)

2. Excess unpaired " chains (in # thal) or #, $, and % chains (in " thal), which

form tetramers and lead to premature red cell destruction.

Morphology

In mild thalassemia, patients have a mild microcytic, hypochromic anemia.

Sometimes there are target cells, or cells with basophilic stippling. Patients with

severe thalassemia have a whopping anemia marked anisocytosis and poikilocytosis.

Treatment

Patients with mild thalassemia don’t require treatment. Patients with severe anemia

may need repeated red cell transfusions or even bone marrow transplantation.

Moderate thalassemia: target cells, anisocytosis and poikilocytosis




Autoimmune Hemolytic Anemia

Pathogenesis

There are two flavors of autoimmune hemolytic anemia, warm and cold. In warm

autoimmune hemolytic anemia (WAIHA), the patient makes IgG anti-red-cell

antibodies which bind best at 37º C (“warm”). Splenic macrophages think these

antibody-coated red cells are yummy, and they nibble on them (or gobble them up

entirely).

In cold autoimmune hemolytic anemia (CAIHA), the patient makes IgM anti-red-

cell antibodies that bind best at temperatures <37º C (“cold”). This means they

bind in distal body parts but fall off in warm body parts. Because the antibodies areIgM in nature, they bind a bunch of red cells together, forming clumps. In

addition, complement binds to the red cells, causing intravascular hemolysis.

Morphology

In WAIHA, the blood smear shows prominent spherocytosis. In CAIHA, if you

make the blood smear at a cool temperature, you can see nice big red blood cell

agglutinates (clumps).

CAIHA: red cell agglutinates




Important lab test

Direct antiglobulin test (DAT)

Also called the Coombs test. Mix patient's red cells with anti-human globulin (an

antibody against human immunoglobulins). If the red cells are coated withantibodies (as they are in some immune processes), the anti-human globulin will

attach to those antibodies, bridging the red cells and making them clump together.

So if you see red cell clumping, that means the patient's red cells are coated with

antibodies, and the patient's hemolysis is probably immune-related.

Treatment

Treat underlying cause, if there is one. In WAIHA, steroids can be useful, and if all

else fails, splenectomy might be necessary. In CAIHA, it’s helpful to keep thepatient warm.




Microangiopathic Hemolytic Anemia

Pathogenesis

Red cells are ripped apart by physical trauma (fibrin strands snag them or

mechanical devices bash them). There are a ton of possible causes, including

disseminated intravascular coagulation, hemolytic-uremic syndrome, thrombotic

thrombocytopenic purpura, malignancies (especially adenocarcinoma), sepsis,

trauma, and artificial heart valves.

Morphology

The blood smear shows schistocytes, which are small, pointy red cell fragments.

Treatment

The important thing is to figure out what’s causing the MAHA and then treat that.

Schistocytes are never normal - so if you see them, you have to seek out an

underlying cause!

MAHA: schistocyte




Anemia of Chronic Disease

Pathogenesis

Anemia of chronic disease happens in a ton of different diseases, from infections to

inflammatory conditions to malignancies. There is a complex disturbance in iron

metabolism which prevents iron from making it into normoblasts.

Morphology

The blood shows a normochromic, normocytic anemia with minimal anisocytosis

and poikilocytosis (it’s a “bland-looking” anemia). Some cases (about 25%) are

microcytic, but the MCV rarely gets below 72 fL.

Iron studies

• ! serum iron

• ! TIBC

• ! ferritin (ferritin is an acute phase reactant - so it goes up in the types of

conditions that cause ACD)

Treatment

ACD is usually so mild that no treatment of the anemia is required. The

underlying disease is the focus of the patient’s treatment.

Anemia of chronic disease: pretty normal-looking blood smear




Aplastic Anemia

Pathogenesis

In aplastic anemia, there are very few hematopoietic precursor cells in the bone

marrow (and therefore, decreased numbers of red cells, white cells, and platelets in

the blood). The potential causes are numerous (like drugs, viruses, or hereditary

conditions), but in many cases, no specific cause can be identified.

Morphology

The blood is pancytopenic, meaning that the red cells, white cells, and platelets are

all decreased. The bone marrow is markedly hypocellular, or "empty".

Treatment

Treatment includes transfusion of blood components as needed, drug therapy to

stimulate hematopoiesis and suppress the immune system, and if necessary, bone

marrow transplant.

Aplastic anemia: "empty" bone marrow




Preview: The CompleteHematopathology Guide

Everything you need to know about hematopathology,illustrated with tons of nice photos and easy ways toremember what you learn.

“The only reason I did well in hemepath in medicalschool is because of you."Richard, Medical Student

Chronic Leukemias

Chronic leukemias are very different from acute leukemias. Chronic leukemias are

for the most part diseases of older adults (acute leukemias occur in both children

and adults). They appear in an insidious fashion and have a relatively good

prognosis (as opposed to acute leukemias, which have a stormy onset and poor

prognosis). In addition, chronic leukemias are composed of fairly mature-appearing

hematopoietic cells (as opposed to acute leukemias, which are composed of blasts).

There are two kinds of chronic leukemias: myeloid and lymphoid. Instead of being

reasonable, and calling them “chronic myeloid leukemias” and “chronic lymphoid

leukemias,” the powers that be dubbed the two divisions “chronic

myeloproliferative disorders” and “chronic lymphoproliferative disorders.” These

names are not so great, in my opinion, since these are not just “disorders” – they

are real leukemias!

PathophysiologyChronic leukemias are malignant, monoclonal proliferations of mostly mature

myeloid or lymphoid cells in the bone marrow (and blood). These leukemias

progress more slowly than acute leukemias. So early on, the marrow is involved –

but not totally replaced – by malignant cells. Still, it is hard for the normal white

cells to function properly. The lymphoid cells, in particular, have a hard time

making normal immunoglobulin in certain chronic lymphoproliferative disorders.




One of the major causes of mortality in these patients is infection. As chronic

leukemias evolve, more and more of the marrow is replaced by tumor, and

eventually there is little room for normal white cells to grow.

Clinical Features Chronic leukemias present in over a period of weeks or months. Patients might

have splenomegaly (which shows up as a dragging sensation or fullness in the left

upper quadrant of the abdomen), lymphadenopathy, or a general feeling of

malaise and fatigue. Some patients are asymptomatic at diagnosis, and the disease

is picked up on a routine blood smear or CBC. Likewise, the clinical course is

different in chronic leukemia. In many cases of chronic leukemia, patients can live

for years without treatment at all.

Chronic Myeloproliferative Disorders

Chronic myeloproliferative disorders are malignant clonal proliferations of a

pluripotent stem cell that lead to excessive proliferation of myeloid cells in the

blood and bone marrow. What that means in plain English is that a stem cell

somewhere way back (before it’s even committed to the neutrophil line, or red cell

line) goes bad and starts proliferating like crazy – so you wind up with a marrow

packed with cells from all the myeloid lineages (the official name is

“panhyperplasia”).

Usually, one particular myeloid lineage predominates in this growth fest – so you’ll

see a ton of all the myeloid cells, but the majority are neutrophils, or red cells, or

megakaryocytes. So the chronic myeloproliferative disorders have been divided into

four types according to what is proliferating most:

• Chronic myeloid leukemia (tons of neutrophils and precursors)

• Polycythemia vera (tons of red cells and precursors)

• Essential thrombocythemia (tons of platelets and megakaryocytes)

• Chronic myelofibrosis (tons of everything…then nothing! See below.)

We’ll consider each of these separately because they are very different clinically

and morphologically. But they do have some common features: all of them have a

high white count with a left shift, a hypercellular marrow, and splenomegaly.




Chronic Myeloid Leukemia

Chronic myeloid leukemia (CML) is a chronic myeloproliferative disorder

characterized by a marked proliferation of neutrophils (and precursors) in the bone

marrow and blood. All cases have a t(9;22), also known as the Philadelphia

chromosome (it’s the 22 that’s officially the Philadelphia chromosome).

Clinical FeaturesCML frequently occurs in patients who are around 40 or 50. It does not occur in

children (though there is a separate disease similar to CML, called juvenile CML,

that does occur in kids). Usually, the onset is slow, with a long asymptomatic period,

followed by fevers, fatigue, night sweats and abdominal fullness. On physical exam,

patients usually have an enlarged spleen. Hepatomegaly and lymphadenopathy

may also be present.

There are three clinical stages, or phases, of CML: chronic phase, accelerated

phase and blast crisis. Patients generally present in chronic phase and then progress

to one or both of the other phases.

Chronic phase

• High but stable number of neutrophils and precursors.

• Stable hemoglobin and platelet count.

• Easily controlled by therapy.

• With traditional treatment (not imatinib, see below), usually lasts 3-4 years; isthen followed by accelerated phase and/or blast crisis.

Accelerated phase

• Characterized by a change in the patient's previously stable state.

• Usually see increasing leukocytosis, decreasing hemoglobin and plateletcount.

• May terminate in this stage, or may progress to blast crisis.

• Usually fatal within several months.

Blast crisis

• Characterized by a marked increase in blasts (myeloblasts or lymphoblasts).

• Usually fatal within a few weeks or months.




Morphology

Blood

The blood smear shows a marked neutrophilia with a left shift. The left shift is a

little weird in that it is not evenly distributed between all the neutrophil stages.There are tons of neutrophils at all stages of development, but there are relatively

more myelocytes and segmented neutrophils (and relatively less of the other stages).

There are a few myeloblasts around (which you don’t see in normal blood, of

course) but they don’t number more than 2 or 3%.

Here’s an interesting thing: patients with CML almost always have a basophilia.

That’s actually one of the first things that happens in the development of the

disease! There are few if any other reasons for a basophilia. So if you see this in apatient, even if they don’t have the typical findings of CML (big white count with

lots of neutrophils and precursors), you should rule out CML!

The platelet count may be increased (because of all the megakaryocytes around in

the bone marrow).

CML, blood: leukoc tosis with le t shi t




Bone marrow

The bone marrow is hypercellular, with a pan-myeloid hyperplasia (all the myeloid

cells are increased – neutrophils and precursors, red cell precursors, and

megakaryocytes). However, if you look closely, you’ll see that the neutrophils and

precursors make up the bulk of the cells. Later in the course of the disease, the

marrow may become fibrotic. You can detect this using a reticulin stain. This is not

a good sign.

PathophysiologyAll cases of CML have a translocation between chromosomes 9 and 22, resulting in

what’s commonly known as the Philadelphia chromosome (Ph). This designation

refers to the new chromosome 22 that results from the translocation. Nobody talks

about poor chromosome 9. The translocation places the c-abl proto-oncogene on

chromosome 9 next to the bcr gene on chromosome 22. A new, fusion gene is

created: the bcr-abl gene. The bcr-abl gene encodes a protein called p210, which is a

super-powerful tyrosine kinase that drives the cells to grow like crazy.

CML, bone marrow: hypercellular




Here’s a weird fact: the Philadelphia chromosome is found not only in the myeloid

cells in CML, but also in some B lymphocytes! That’s weird, considering that this is

a myeloid lesion with no morphologic changes in the lymphoid cells. This probably

means that the initial bad cell (the one that became malignant) was a very early stem

cell, one that hadn’t even committed itself to myeloid or lymphoid lineage yet - so

the Philadelphia chromosome is present in all the descendants of that cell. Further

supporting this idea is the fact that when patients enter blast crisis, the blasts are

sometimes lymphoid!

Treatment and PrognosisIn the old days, CML was treated with myelosuppressive agents like hydroxyurea,

and then if the patient had a match and could tolerate it, allogeneic bone marrow

transplant was performed. That was the only hope for a cure.

Not long ago, a new drug called imatinib (or Gleevec) was developed. This drug

targets the bcr-abl gene product, preventing it from exerting its massive tyrosine-

kinase-mediated growth stimulation. It has been like a miracle for many patients –

even patients in the later stages of the disease. In fact, we don’t even know what the

typical prognosis of CML is anymore, because these patients are still living with the

disease. This drug has turned CML into a chronic but treatable disease, like

diabetes, for many patients. It’s one of the happiest leukemia research stories ever.

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