1. Discuss in detail various classifications of leukemia. Give an account of chronic myeloid leukemia. 2. Classify acute leukemia. Discuss blood and bone marrow findings in acute myeloblastic leukemia. 3. Describe pathophysiology, laboratory diagnosis, and prognostic markers in chronic lymphocytic leukemia 4. Discuss acute lymphoblastic leukemia.

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Leukemia: Classification and Detailed Accounts

QUESTION 1: Classifications of Leukemia & Chronic Myeloid Leukemia

A. Classifications of Leukemia

Leukemia is a clonal malignant proliferation of hematopoietic cells. It can be classified by several schemes:

I. Based on Clinical Course

Type	Characteristics
Acute	Rapid onset, blasts predominate (>20% of marrow cells), survival weeks to months if untreated
Chronic	Insidious onset, more differentiated cells, survival months to years without treatment

II. Based on Cell Line (Lineage)

Myeloid	Lymphoid
AML, CML	ALL, CLL

III. FAB (French-American-British) Classification of Acute Leukemia

Acute Myeloid Leukemia (AML) - FAB:

Subtype	Name
M0	AML, minimally differentiated
M1	AML without maturation
M2	AML with maturation
M3	Acute promyelocytic leukemia (APL)
M4	Acute myelomonocytic leukemia
M5	Acute monoblastic/monocytic leukemia
M6	Acute erythroid leukemia
M7	Acute megakaryoblastic leukemia

Acute Lymphoblastic Leukemia (ALL) - FAB:

Subtype	Features
L1	Small uniform blasts (common in children)
L2	Larger pleomorphic blasts (common in adults)
L3	Burkitt-type, deeply basophilic cytoplasm with vacuoles

IV. WHO 2017/2022 Classification

The current WHO classification supersedes FAB and uses cytogenetics, molecular markers, and immunophenotype:

AML - WHO categories:

AML with recurrent genetic abnormalities (e.g., t(8;21), inv(16), t(15;17)/PML-RARA, t(9;11)/KMT2A, inv(3), t(1;22), BCR-ABL1, mutated NPM1, biallelic CEBPA)
AML with myelodysplasia-related changes
Therapy-related myeloid neoplasms
AML, NOS (not otherwise specified) - when cytogenetic/molecular criteria unmet

Lymphoid neoplasms:

Precursor B-cell neoplasms: B-ALL/lymphoma
Precursor T-cell neoplasms: T-ALL/lymphoma
Mature B-cell neoplasms: CLL/SLL, Burkitt lymphoma, etc.
Mature T/NK-cell neoplasms

(Henry's Clinical Diagnosis and Management by Laboratory Methods; Robbins, Cotran & Kumar Pathologic Basis of Disease)

V. Immunophenotypic Classification

Based on surface markers detected by flow cytometry:

Myeloid markers: CD13, CD15, CD33, CD117, MPO
Monocytic markers: CD14, CD64, CD33 (bright)
B-cell markers: CD19, CD20, CD10, CD22, CD79a
T-cell markers: CD2, CD3, CD4, CD5, CD7, CD8

Mixed phenotype (MPAL) and undifferentiated leukemia are recognized when blasts co-express myeloid and lymphoid markers.

B. Chronic Myeloid Leukemia (CML)

Definition and Pathogenesis

CML is a myeloproliferative neoplasm distinguished from all others by the presence of a chimeric BCR::ABL fusion gene. In >90% of cases this results from the t(9;22)(q34;q11) translocation - the so-called Philadelphia chromosome (Ph). The remaining ~10% have cryptic or complex rearrangements detected only by FISH or PCR.

The BCR moiety contains a dimerization domain that causes the ABL tyrosine kinase to constitutively self-associate and become permanently active. The resulting 210 kDa BCR-ABL protein phosphorylates downstream substrates activating the RAS and JAK/STAT progrowth/prosurvival pathways. BCR-ABL preferentially drives proliferation of granulocytic and megakaryocytic progenitors and causes abnormal release of immature granulocytes into blood. The cell of origin is a pluripotent hematopoietic stem cell (HSC).

(Robbins, Cotran & Kumar Pathologic Basis of Disease)

Phases of CML

Phase	Features
Chronic phase (3-5 years)	Indolent; leukocytosis with full maturation of granulocytes; <10% blasts in blood/marrow
Accelerated phase (~1 year)	Increasing anemia and thrombocytopenia; rising basophils; additional cytogenetic changes (trisomy 8, isochromosome 17q, duplication of Ph); 10-19% blasts
Blast crisis	>20% blasts; resembles acute leukemia; 70% myeloid type, ~30% lymphoid (pre-B) type; survival weeks-months without treatment

About 50% of patients enter accelerated phase before blast crisis; the other 50% go directly into blast crisis. Median survival without treatment ~3 years.

Morphology and Laboratory Findings

Peripheral blood:

Leukocytosis often exceeding 100,000 cells/µL
Predominantly neutrophils, band forms, metamyelocytes, myelocytes, plus eosinophilia and basophilia
Blasts usually <10% in chronic phase
Thrombocytosis (platelets often markedly elevated)

Bone marrow:

Markedly hypercellular due to massively increased maturing granulocytic precursors
Increased eosinophils and basophils
Increased and often dysplastic megakaryocytes
Scattered macrophages with wrinkled green-blue cytoplasm - "sea-blue histiocytes"
Increased reticulin deposition; overt fibrosis rare in chronic phase

Other findings:

Massive splenomegaly from extramedullary hematopoiesis; splenic infarcts common
Mild hepatomegaly and lymphadenopathy possible
Low leukocyte alkaline phosphatase (LAP) score - characteristic finding (distinguishes CML from leukemoid reaction which has high LAP)

(Robbins, Cotran & Kumar Pathologic Basis of Disease)

Clinical Features

Peak incidence: 5th-6th decades; occurs in children too; ~4800 new cases/year (USA)
Insidious onset: fatigue, weakness, weight loss, anorexia from hypermetabolism
Dragging sensation in abdomen from splenomegaly, or acute left upper quadrant pain from splenic infarction
Diagnosis confirmed by detection of BCR::ABL fusion gene via chromosomal analysis or PCR

Treatment

Tyrosine kinase inhibitors (TKIs) - imatinib (Gleevec) was the first; now second-generation TKIs (dasatinib, nilotinib) and third-generation (ponatinib) are available. TKIs have transformed CML from a fatal disease into a manageable chronic condition for most patients, with near-normal life expectancy in those achieving deep molecular remission.

QUESTION 2: Classification of Acute Leukemia & AML Blood/Bone Marrow Findings

A. Classification of Acute Leukemia

Diagnosis requirement: ≥20% blasts in peripheral blood or bone marrow (WHO criteria); or presence of specific recurrent cytogenetic abnormalities regardless of blast %.

WHO 2017/2022 Classification of AML

1. AML with Recurrent Genetic Abnormalities:

AML with t(8;21)(q22;q22.1); RUNX1-RUNX1T1 - Auer rods, M2 morphology
AML with inv(16)(p13.1q22) or t(16;16); CBFB-MYH11 - myelomonocytic with eosinophilia (M4Eo)
APL with t(15;17)(q22;q12); PML-RARA - abnormal promyelocytes, Auer rods, faggot cells
AML with t(9;11)(p21;q23); MLLT3-KMT2A - monocytic features
AML with t(6;9); DEK-NUP214 - basophilia
AML with inv(3)/t(3;3); GATA2, MECOM - multilineage dysplasia, atypical megakaryocytes
AML with t(1;22)(p13;q13); RBM15-MKL1 - megakaryoblastic in infants
AML with BCR-ABL1 (provisional)
AML with mutated NPM1 (most common genetic lesion ~30%)
AML with biallelic mutated CEBPA
AML with mutated RUNX1 (provisional)

2. AML with Myelodysplasia-Related Changes

3. Therapy-Related Myeloid Neoplasms

4. AML, Not Otherwise Specified (NOS) - based on FAB morphology:

M0: Minimally differentiated
M1: Without maturation
M2: With maturation
M3: Acute promyelocytic
M4: Acute myelomonocytic
M5a/5b: Monoblastic/monocytic
M6: Erythroid
M7: Megakaryoblastic

5. Myeloid Sarcoma

6. Myeloid Proliferations Associated with Down Syndrome

(Henry's Clinical Diagnosis and Management by Laboratory Methods)

ALL Classification (WHO):

B-ALL/lymphoma
- B-ALL with t(9;22)/BCR-ABL1 (Philadelphia positive - poor prognosis)
- B-ALL with t(v;11q23)/KMT2A
- B-ALL with t(12;21)/ETV6-RUNX1 (favorable prognosis)
- B-ALL with hyperdiploidy (favorable)
- B-ALL with hypodiploidy (poor prognosis)
- B-ALL with t(5;14)/IL3-IGH
- B-ALL with t(1;19)/TCF3-PBX1
T-ALL/lymphoma

B. Blood and Bone Marrow Findings in Acute Myeloblastic Leukemia (AML)

Peripheral Blood

Leukocytosis - WBC may range from very low to markedly elevated; ~20% present with WBC >100,000/µL (hyperleukocytosis)
Circulating blasts (myeloblasts): Large cells with high N:C ratio, fine chromatin, prominent nucleoli, scant cytoplasm
Auer rods: Pathognomonic pink-red rod-shaped cytoplasmic inclusions in myeloblasts (crystallized azurophilic granules); most prominent in M3 (APL) where they form bundles called "faggot cells"
Anemia - normochromic, normocytic (from marrow replacement)
Thrombocytopenia - often severe; petechiae and purpura in patients
Neutropenia - despite high WBC, mature neutrophils are reduced (susceptibility to infection)
Blasts positive for MPO (myeloperoxidase) and Sudan Black B (≥3% positivity defines myeloid lineage)

Bone Marrow

Hypercellular with replacement of normal hematopoietic elements by blasts
≥20% blasts of all nucleated marrow cells (WHO criterion)
Morphology varies by subtype:

Subtype (FAB)	Marrow Findings
M0 (Minimally differentiated)	Blasts show <3% MPO/SBB positivity; myeloid antigens (CD13, CD33, CD117) on ≥20% blasts by flow cytometry; TdT and CD34 often expressed
M1 (Without maturation)	≥90% of non-erythroid cells are myeloblasts; ≥3% MPO or SBB positive; CD13, CD33, CD117 expressed
M2 (With maturation)	Myeloblasts 20%-89% of marrow cells; granulocytes >10%; monocytes <20%; most blasts MPO/SBB/CAE positive; Auer rods common
M3 (APL)	Predominantly abnormal hypergranular promyelocytes; abundant coarse granules; faggot cells (multiple Auer rods); t(15;17)/PML-RARA; associated with DIC
M4 (Myelomonocytic)	Myeloblasts >20%; sum of monocytic cells 20-80%; granulocytic cells 20-80%; both MPO/SBB and non-specific esterase (NSE/ANA) positive
M5 (Monoblastic)	≥80% non-erythroid cells are monocytic; monoblasts large with abundant cytoplasm; intensely ANA/ANB positive; lysozyme elevated in serum/urine
M6 (Erythroid)	Previously: ≥50% erythroid precursors + ≥20% myeloblasts; now reclassified per WHO
M7 (Megakaryoblastic)	Blasts express platelet markers CD41, CD61; reticulin fibrosis common; dry tap on aspiration

(Henry's Clinical Diagnosis and Management by Laboratory Methods)

Cytochemistry Summary

Stain	Myeloid (MPO+, SBB+, CAE+)	Monocytic (NSE+)	Lymphoid (PAS+)
MPO	Positive	Negative/weak	Negative
Sudan Black B	Positive	Negative	Negative
NSE (non-specific esterase)	Negative	Strongly positive	Negative
PAS	Variable	Variable	Positive (block)

Immunophenotype

Myeloid blast gate by CD45 vs side scatter (SSC)
Confirm immaturity: CD34, TdT, CD117
Myeloid antigens: CD13, CD33, CD117, MPO
Monocytic: CD14, CD64, CD11b, CD11c, CD68, lysozyme

QUESTION 3: Pathophysiology, Laboratory Diagnosis, and Prognostic Markers in CLL

A. Pathophysiology of CLL

CLL is a mature B-cell malignancy - the most common leukemia in the Western world (>20,000 new cases/year in USA; median age at diagnosis 70 years; 2:1 male predominance).

Cell of Origin

Lymphoid-primed hematopoietic stem cells give rise to mature B cells that expand clonally. Whether the cell of origin is a post-germinal center memory B cell (hypermutated IGHV) or a naive B cell (unmutated IGHV) appears to determine disease behavior.

Key Molecular Mechanisms

1. BCL-2 overexpression (anti-apoptosis)

Chromosomal deletions at 13q14.3 remove microRNAs miR-15a and miR-16-1 - these normally suppress BCL-2 mRNA. Their loss leads to uniform BCL-2 overexpression, prolonging tumor cell survival.

2. B-cell receptor (BCR) signaling

Tumor cells in proliferation centers receive survival signals via BCR
Downstream signaling involves Bruton tyrosine kinase (BTK)
Unmutated IGHV shows stronger BCR activation - drives proliferation and clonal evolution
This explains why BTK inhibitors (ibrutinib, acalabrutinib, zanubrutinib) are highly effective

3. NF-κB and MYC activation

Stromal cells in proliferation centers express factors activating NF-κB (promotes survival) and MYC (promotes growth)

4. Chromosomal Abnormalities (detected by interphase FISH)

Del(13q14): ~55% - only favorable FISH abnormality when sole abnormality
Del(11q22): deletes ATM - unfavorable; associated with bulky lymphadenopathy
Del(17p13): ~5-10% - deletes TP53 - worst prognosis; resistance to chemotherapy
Trisomy 12: ~10-15% - intermediate prognosis
Balanced translocations are rare (unlike other B-cell malignancies)

5. Somatic Mutations (by next-generation sequencing)

NOTCH1 gain-of-function mutations: 10-18% - worse prognosis
BIRC3 mutations (related to ATM/del11q)
SF3B1 (RNA splicing) mutations - adverse
TP53 mutations - very high risk
ATM mutations
DNMT3A, ASXL1

6. IGHV Mutational Status

Mutated IGHV (>2% from germline): Indolent course; sometimes no therapy needed; memory B-cell origin
Unmutated IGHV (≤2% from germline): Aggressive course; more clonal evolution; active BCR signaling; naive B-cell origin

7. Richter Transformation About 5% of CLL patients develop transformation to diffuse large B-cell lymphoma (DLBCL) - called Richter syndrome. Presents with rapidly enlarging lymph node, B symptoms, elevated LDH.

(Goldman-Cecil Medicine; Robbins, Cotran & Kumar)

B. Laboratory Diagnosis of CLL

Diagnostic criteria (iwCLL 2018):

≥5,000 clonal B-lymphocytes/µL in peripheral blood (sustained)
Confirmed by flow cytometry showing characteristic immunophenotype

1. Peripheral Blood Smear

Predominant small, mature-appearing lymphocytes with scant cytoplasm, round nucleus, condensed chromatin
Smudge cells (basket cells) - fragile CLL lymphocytes that rupture during smear preparation; pathognomonic finding; higher smudge cell count correlates with more indolent disease
Variable lymphocytosis (5,000 to >300,000/µL)

2. Flow Cytometry (most useful diagnostic test)

Classic CLL immunophenotype:

CD19+ (B-cell marker)
CD20 dim (weak expression - distinguishes from normal B cells)
CD23+
CD5+ (T-cell marker aberrantly expressed - key for CLL diagnosis)
Surface immunoglobulin (sIg) dim (weak expression)
FMC7 negative, CD10 negative

This CD5+/CD23+/dim CD20 pattern distinguishes CLL from:

Mantle cell lymphoma (CD5+, CD23-, cyclin D1+)
Marginal zone lymphoma (CD5-, CD23-)
Follicular lymphoma (CD10+, CD5-)

3. Bone Marrow Biopsy

Not required for diagnosis
May show: diffuse, nodular, interstitial, or mixed patterns of infiltration
Diffuse pattern = worst prognosis
Used to evaluate cytopenias before therapy

4. Lymph Node Biopsy (if done)

Diffuse effacement by small lymphocytes
Proliferation centers (pale areas with larger cells) - pathognomonic for CLL/SLL

5. Other Blood Tests

CBC: lymphocytosis + anemia + thrombocytopenia (if advanced)
Serum immunoglobulin: hypogammaglobulinemia (infection risk)
Direct Coombs test: positive in autoimmune hemolytic anemia (~10-15% of CLL)
Elevated LDH and beta-2 microglobulin: correlate with tumor burden/prognosis
Serum protein electrophoresis: paraprotein in ~5%

C. Prognostic Markers in CLL

Staging Systems

Rai Staging System (USA):

Stage	Features	Risk
0	Lymphocytosis only	Low
I	Lymphocytosis + lymphadenopathy	Intermediate
II	Lymphocytosis + hepatomegaly or splenomegaly	Intermediate
III	Anemia (Hb <11 g/dL)	High
IV	Thrombocytopenia (platelets <100,000/µL)	High

Binet Staging System (Europe):

Stage	Features
A	<3 involved areas; no anemia/thrombocytopenia
B	≥3 involved areas; no anemia/thrombocytopenia
C	Anemia (Hb <10 g/dL) or thrombocytopenia (Plt <100,000)

Molecular/Biologic Prognostic Markers

Marker	Favorable	Unfavorable
IGHV mutation status	Mutated (>2% from germline)	Unmutated (≤2% from germline)
Del(17p13) / TP53 mutation	Absent	Present (worst prognosis; resistance to chemotherapy)
Del(11q22) / ATM	Absent	Present
Del(13q14)	Present (sole abnormality)	Multiple FISH abnormalities
Trisomy 12	Intermediate	-
NOTCH1 mutation	Absent	Present
ZAP-70	Negative	Positive (surrogate for unmutated IGHV)
CD38	Negative (<30%)	Positive (≥30%)
Beta-2 microglobulin	Low	High
Smudge cell count	High (>30%)	Low
Stimulated karyotype	Simple	Complex (≥3 abnormalities)

Key point: Del(17p)/TP53 mutation must be checked before every new line of therapy as it evolves over time and predicts resistance to chemoimmunotherapy - these patients require targeted therapy (BTK inhibitors or venetoclax).

(Goldman-Cecil Medicine; Robbins, Cotran & Kumar)

QUESTION 4: Acute Lymphoblastic Leukemia (ALL)

Definition and Epidemiology

ALL is a malignant neoplasm of immature B (pre-B) or T (pre-T) lymphoid precursors called lymphoblasts. It is the most common cancer of children (~2500 new cases/year in USA; peak incidence at ~3 years for B-ALL; adolescent males for T-ALL). Hispanic/Latino children have the highest incidence.

B-ALL: ~85% of ALL cases; typically childhood leukemia
T-ALL: ~15%; tends to present in adolescent males as thymic lymphomas; overlap with leukemic presentation

(Robbins, Cotran & Kumar Pathologic Basis of Disease)

Pathogenesis

ALL arises through mutations that block lymphoid differentiation and promote abnormal self-renewal, creating a stem cell-like phenotype.

Key molecular mechanisms:

Transcription factor mutations - disrupt B- or T-cell development:
- B-ALL: PAX5, TCF3, ETV6, RUNX1, BCR::ABL1, KMT2A, PBX1
- T-ALL: NOTCH1 mutations (50-70%) - NOTCH1 is essential for T-cell development
Chromosomal abnormalities (~90% of ALL cases):
- Hyperploidy (>50 chromosomes) - most common; seen only in B-ALL; better prognosis
- Hypoploidy - seen in B-ALL; worse prognosis
- Balanced translocations (different sets for B-ALL vs T-ALL)
Key translocations:
- t(12;21)/ETV6::RUNX1 - 25% of pediatric B-ALL; most favorable prognosis
- t(9;22)/BCR::ABL1 (Philadelphia chromosome) - creates 190 kDa BCR-ABL (stronger kinase than 210 kDa in CML); poor prognosis but responds to TKIs + chemotherapy
- t(v;11q23)/KMT2A (MLL rearrangements) - infant ALL; poor prognosis
- t(1;19)/TCF3-PBX1
- t(5;14)/IL3-IGH
Complementary driver mutations promoting growth (RAS pathway, tyrosine kinase activating mutations) - fewer than 10 total mutations typically sufficient for full-blown ALL

Classification

Immunophenotypic classification of ALL:

Type	Markers	Comments
Pre-pre-B (Pro-B)	TdT+, CD19+, CD34+, HLA-DR+; sIg-, cIg-	Most primitive; KMT2A rearrangements common
Common B-ALL	CD10+ (CALLA), CD19+, TdT+	Most common in children; peak age 3 yrs
Pre-B ALL	CD19+, CD10+, cytoplasmic IgM (cIgM+)
Mature B-ALL (Burkitt)	Surface IgM+, CD20+, CD10+; TdT-	FAB L3; MYC translocations
T-ALL	CD2, CD3, CD5, CD7+; TdT+	Mediastinal mass common; older boys

Morphology

Peripheral blood:

Elevated or very low WBC; lymphocytosis with circulating lymphoblasts
Lymphoblasts are smaller than myeloblasts; high N:C ratio; condensed chromatin; 1-2 indistinct nucleoli; scant cytoplasm; no Auer rods
Anemia (normochromic, normocytic)
Thrombocytopenia (risk of bleeding)

Bone marrow:

Hypercellular; >20% lymphoblasts (often >80-90%)
Lymphoblasts replace normal hematopoietic cells
Fine chromatin, inconspicuous nucleoli in L1; larger nucleoli in L2
L3 (Burkitt): deeply basophilic cytoplasm with vacuoles ("starry sky" pattern with macrophages)

Cytochemistry:

MPO negative (distinguishes from AML - crucial)
TdT (terminal deoxynucleotidyl transferase) - positive in >90% (absent in mature B-ALL/Burkitt)
PAS - positive in coarse blocks (especially B-ALL)
NSE - negative

Immunophenotype:

B-ALL: CD19, CD10 (CALLA), CD20, CD22, CD79a, TdT, HLA-DR
T-ALL: CD2, CD3, CD5, CD7, TdT; CD4/CD8 variable
Lineage-specific markers cCD3, cCD20, cCD79a used for definitive lineage assignment

Clinical Features

Symptoms of bone marrow failure: Fatigue (anemia), infections (neutropenia), bleeding/petechiae (thrombocytopenia)
Bone pain (marrow expansion)
Lymphadenopathy, hepatosplenomegaly (tumor infiltration)
CNS involvement: Headache, cranial nerve palsies, meningism; especially common in T-ALL and Burkitt-type
Mediastinal (thymic) mass - T-ALL; can cause SVC syndrome and respiratory distress
Testicular infiltration - males; sanctuary site

Prognostic Factors in ALL

Favorable:

Age 1-10 years (children)
WBC <50,000/µL at presentation
Hyperdiploidy (>50 chromosomes)
Trisomy 4, 7, 10
t(12;21)/ETV6::RUNX1
Early response to induction chemotherapy
Negative minimal residual disease (MRD) after induction

Unfavorable:

Age <1 year (infants) or >10 years (especially adults)
High WBC at presentation
Hypodiploidy (<44 chromosomes)
t(9;22)/BCR-ABL1 (Ph+ ALL) - now better with TKIs
t(v;11q23)/KMT2A rearrangements (especially infant ALL)
T-ALL with ETP (early T-cell precursor) phenotype
Positive MRD after induction

Key: Molecular detection of minimal residual disease (MRD) after therapy is now the strongest predictor of outcome in both B-ALL and T-ALL and guides treatment intensification decisions.

Treatment Principles

Induction: Multi-agent chemotherapy (vincristine, dexamethasone/prednisone, L-asparaginase, anthracycline) - aim for complete remission in 95% of children
CNS prophylaxis: Intrathecal chemotherapy (methotrexate ± cytarabine ± hydrocortisone); cranial irradiation now largely replaced
Consolidation/Maintenance: 2-3 years total; includes 6-mercaptopurine + methotrexate
Ph+ ALL: Add TKI (imatinib, dasatinib) to chemotherapy - dramatically improved outcomes
Relapsed/Refractory B-ALL: CAR-T cell therapy targeting CD19 (tisagenlecleucel) - high response rates but can be costly with serious toxicities
Allogeneic stem cell transplant for high-risk or relapsed disease

Summary Comparison Table

Feature	AML	CML	ALL	CLL
Age	Adults (any age)	5th-6th decade	Children (peak 3 yr)	Elderly (median 70 yr)
Key marker	MPO+, Auer rods	BCR::ABL (Ph+)	TdT+, MPO-	CD5+/CD19+/CD23+
Key mutation	FLT3, NPM1, CEBPA	t(9;22)	t(12;21), hyperdiploidy, NOTCH1	Del(17p), del(13q), IGHV status
Smear	Myeloblasts	Leukocytosis, all stages of granulopoiesis	Lymphoblasts	Small lymphocytes + smudge cells
Auer rods	Yes (myeloid)	No	No	No
Course	Acute, aggressive	Chronic → blast crisis	Acute, aggressive (good pediatric prognosis)	Chronic, indolent
Splenomegaly	Variable	Massive	Variable	Moderate

References:

Robbins, Cotran & Kumar - Pathologic Basis of Disease, Chapters 13 (Hematopoietic and Lymphoid Systems)
Goldman-Cecil Medicine, Chapters 168, 169 (AML, CLL)
Henry's Clinical Diagnosis and Management by Laboratory Methods, Chapters 34-35 (Hematology)

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