Hematopathology — MCQs

A 50-year-old patient presents with fever, bleeding episodes, and a leukocyte count of 48 x 10^9 cells/L and platelet count of 50 x 10^9 cells/L. The differential count showed 76% neutrophils, 8% blast cells, 12% myelocytes and metamyelocytes, and 4% other cells. Bone marrow examination showed 14% blasts. Cytogenetics showed t(8;21). What is the most likely diagnosis?

Q116Easy

Pseudothrombocytopenia is due to platelet agglutination antibodies when the calcium content is decreased by blood EDTA. The antibody responsible for this effect is mainly:

Q117Medium

Overexpression of BCL-2 proteins occurs in which of the following conditions?

Q118Easy

Which syndrome is associated with an increased risk of leukemia?

Q119Medium

Which lymphoid malignancy arises from thymic cells?

Q120Medium

All of the following are good prognostic factors for acute lymphoblastic leukemia except?

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 111: All of the following acute myeloid leukemias are diagnosed regardless of blast count, except?

A. AML with t(8;21)
B. AML with t(15;17)
C. AML with t(16;16)
D. AML with t(1;9) (Correct Answer)

Explanation: **Explanation:** In the classification of Acute Myeloid Leukemia (AML), the standard diagnostic threshold is a blast count of **≥20%** in the bone marrow or peripheral blood. However, according to the WHO classification (and further emphasized in the ICC 2022 guidelines), certain genetic abnormalities are considered **"defining"** for AML regardless of the blast percentage [1]. **1. Why Option D is Correct:** **AML with t(1;9)** is not a recognized genetic entity that bypasses the 20% blast requirement. In fact, t(1;9) is not a standard recurrent cytogenetic translocation associated with AML. Therefore, a diagnosis of AML in this case would still require the conventional ≥20% blast threshold. **2. Why the Other Options are Incorrect:** The following three specific cytogenetic abnormalities are diagnostic of AML even if the blast count is **less than 20%** [1]: * **AML with t(8;21)(q22;q22.1); RUNX1-RUNX1T1 (Option A):** Commonly associated with Auer rods and a favorable prognosis [1]. * **AML with t(15;17)(q24.1;q21.2); PML-RARA (Option B):** Also known as Acute Promyelocytic Leukemia (APL). It is a medical emergency due to the risk of DIC [1]. * **AML with inv(16)(p13.1q22) or t(16;16)(p13.1;q22); CBFB-MYH11 (Option C):** Typically shows monocytic differentiation and abnormal eosinophils in the marrow [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Core Binding Factor (CBF) Leukemias:** This group includes t(8;21) and inv(16). They generally have a **favorable prognosis** [1]. * **The "20% Rule" Exceptions:** Remember the mnemonic **"8, 15, 16"**—translocations involving these chromosomes allow for an AML diagnosis even with low blast counts. * **Recent Update:** The WHO 5th Edition and ICC guidelines have expanded this list to include other rearrangements (like *KMT2A*, *DEK-NUP214*), but the "Big Three" listed in options A, B, and C remain the most high-yield for exams. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 620-622.

Question 112: Which of the following is associated with an adverse prognosis in Acute Myeloid Leukemia (AML)?

A. t(8;21)
B. t(15;17)
C. Normal cytogenetics
D. Del 7q (Correct Answer)

Explanation: **Explanation:** In Acute Myeloid Leukemia (AML), cytogenetic abnormalities are the most important independent prognostic factors used to determine treatment intensity and predict survival outcomes [1]. **1. Why Del 7q is the Correct Answer:** Deletions of the long arm of chromosome 7 (**del 7q**) or monosomy 7 (-7) are classified under **adverse (poor) risk** cytogenetics. These abnormalities are frequently associated with therapy-related AML (t-AML) or AML arising from myelodysplastic syndrome (MDS). They are characterized by poor response to standard induction chemotherapy and a high rate of relapse. **2. Analysis of Incorrect Options:** * **t(8;21):** This translocation involves the *RUNX1-RUNX1T1* genes (AML1-ETO). It is a hallmark of AML-M2 and is associated with a **favorable prognosis**, often showing a good response to high-dose cytarabine [1]. * **t(15;17):** This is diagnostic of Acute Promyelocytic Leukemia (APL/AML-M3) [1]. Due to the high sensitivity to All-Trans Retinoic Acid (ATRA) and Arsenic Trioxide, it carries a **favorable prognosis** if early coagulopathy is managed [2]. * **Normal Cytogenetics:** This is classified as **Intermediate-I risk**. While not as good as the favorable group, it carries a significantly better prognosis than del 7q. **3. High-Yield Clinical Pearls for NEET-PG:** * **Favorable Risk:** t(8;21), inv(16), t(16;16), and t(15;17) [1]. * **Adverse Risk:** Monosomy 5 (-5), del 5q, Monosomy 7 (-7), del 7q, inv(3), and complex karyotypes (≥3 abnormalities). * **Molecular Markers:** *NPM1* and *CEBPA* mutations (without FLT3-ITD) improve prognosis [1], whereas ***FLT3-ITD*** mutations signify a poor prognosis [2]. * **Auer Rods:** Most commonly seen in t(15;17) and t(8;21) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 620. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 620-621.

Question 113: Which of the following is NOT a classical feature of primary myelofibrosis?

A. Tear drop RBCs
B. Leucoerythroblastosis
C. Abnormal megakaryocytes
D. Biconcave RBCs (Correct Answer)

Explanation: **Explanation:** Primary Myelofibrosis (PMF) is a chronic myeloproliferative neoplasm characterized by clonal proliferation of megakaryocytes and granulocytes, leading to reactive bone marrow fibrosis [1]. **Why "Biconcave RBCs" is the correct answer:** Normal, healthy red blood cells are biconcave discs. In PMF, the bone marrow is replaced by dense collagen (fibrosis). As RBCs attempt to squeeze through the narrowed, fibrotic marrow spaces and the distorted vasculature of the spleen (extramedullary hematopoiesis), they undergo mechanical trauma. This results in the formation of **Dacrocytes (Tear-drop RBCs)**, not the maintenance of normal biconcave morphology [1]. **Analysis of Incorrect Options:** * **Tear drop RBCs (Dacrocytes):** These are the hallmark peripheral smear finding in PMF [1]. They occur due to the "stretching" of RBCs as they exit the fibrotic marrow. * **Leucoerythroblastosis:** This refers to the presence of immature white cells (myelocytes, metamyelocytes) and nucleated red cells in the peripheral blood [1]. It occurs because the fibrotic marrow cannot hold onto developing cells, and extramedullary sites (liver/spleen) lack the "blood-marrow barrier." * **Abnormal Megakaryocytes:** PMF is characterized by "cloud-like" or "balloon-like" clusters of atypical megakaryocytes with bulbous, hyperchromatic nuclei. **High-Yield Clinical Pearls for NEET-PG:** * **Mutation:** JAK2 V617F (approx. 50%), CALR, or MPL mutations. * **Clinical Sign:** Massive splenomegaly (due to extramedullary hematopoiesis) [1]. * **Bone Marrow:** Often results in a **"Dry Tap"** on aspiration; diagnosis requires a trephine biopsy showing silver-stained reticulin fibers. * **Laboratory:** Increased serum uric acid and LDH are common. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 628-629.

Question 114: Prothrombin time is useful for which of the following?

A. Detection of clot retraction
B. Platelet count
C. Diagnosis of hemophilia
D. Evaluation of a patient taking anticoagulant drugs (Correct Answer)

Explanation: **Explanation:** **1. Why Option D is Correct:** Prothrombin Time (PT) measures the integrity of the **Extrinsic** and **Common pathways** of the coagulation cascade (Factors VII, X, V, II, and I). It is the primary test used to monitor patients on **Oral Anticoagulant Therapy (Warfarin/Coumadin)**. Warfarin inhibits Vitamin K Epoxide Reductase, affecting Vitamin K-dependent factors (II, VII, IX, X) [1]. Since Factor VII has the shortest half-life, PT is the first to be prolonged, making it an ideal monitoring tool. For standardization, PT results are reported as the **International Normalized Ratio (INR)**. **2. Why Other Options are Incorrect:** * **Option A (Clot Retraction):** This is primarily a function of **platelet number and quality** (specifically Thrombosthenin/Actomyosin). PT does not assess the mechanical contraction of a clot. * **Option B (Platelet Count):** PT is a test of secondary hemostasis (clotting factors). Platelet count is a quantitative measure of primary hemostasis and is measured via automated cell counters or peripheral smears. * **Option C (Hemophilia):** Hemophilia A (Factor VIII deficiency) and Hemophilia B (Factor IX deficiency) involve the **Intrinsic pathway** [1]. These are screened using **Activated Partial Thromboplastin Time (aPTT)**, not PT. **3. NEET-PG High-Yield Pearls:** * **PT:** Monitors Warfarin; reflects Extrinsic pathway (Factor VII). * **aPTT:** Monitors Unfractionated Heparin; reflects Intrinsic pathway (XII, XI, IX, VIII). * **Mixing Studies:** If PT/aPTT corrects after mixing with normal plasma, it indicates a **factor deficiency**. If it does not correct, it indicates the presence of an **inhibitor** (e.g., Lupus anticoagulant). * **Vitamin K Deficiency:** Prolongs both PT and aPTT (but PT is affected earlier) [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-626.

Question 115: A 50-year-old patient presents with fever, bleeding episodes, and a leukocyte count of 48 x 10^9 cells/L and platelet count of 50 x 10^9 cells/L. The differential count showed 76% neutrophils, 8% blast cells, 12% myelocytes and metamyelocytes, and 4% other cells. Bone marrow examination showed 14% blasts. Cytogenetics showed t(8;21). What is the most likely diagnosis?

A. Acute myeloid leukemia (Correct Answer)
B. Chronic myeloid leukemia
C. Chronic lymphoid leukemia
D. Myelodysplastic syndrome

Explanation: ### Explanation The correct diagnosis is **Acute Myeloid Leukemia (AML)**. **1. Why the correct answer is right:** According to the **WHO classification of myeloid neoplasms**, the standard threshold for diagnosing AML is a blast count of **≥20%** in the blood or bone marrow. However, there is a critical exception: the presence of specific recurrent genetic abnormalities—namely **t(8;21)**, **inv(16)**, or **t(15;17)**—defines AML **regardless of the blast percentage** [1]. In this case, although the blasts are only 8% in the peripheral blood and 14% in the marrow, the cytogenetic finding of **t(8;21)** (which involves the *RUNX1-RUNX1T1* fusion) is pathognomonic for AML (specifically AML-M2 in the FAB classification) [1]. **2. Why the incorrect options are wrong:** * **Chronic Myeloid Leukemia (CML):** While CML presents with a high leukocyte count and a **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 620-622. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614.

Question 116: Pseudothrombocytopenia is due to platelet agglutination antibodies when the calcium content is decreased by blood EDTA. The antibody responsible for this effect is mainly:

A. IgG (Correct Answer)
B. IgA
C. IgM
D. IgD

Explanation: **Explanation:** **Pseudothrombocytopenia (PTCP)** is an *in vitro* laboratory artifact where the automated platelet count is falsely low. This occurs due to platelet clumping (agglutination) in blood samples collected in **EDTA-anticoagulated tubes**. **1. Why IgG is the correct answer:** The phenomenon is mediated by **naturally occurring autoantibodies**, which are almost always of the **IgG class** (though IgM is rarely implicated). These antibodies are "cryptic," meaning they only recognize and bind to the **GP IIb/IIIa receptor** on the platelet surface when its conformation is altered. EDTA acts as a chelating agent that decreases ionized calcium; this reduction in calcium causes a structural change in the GP IIb/IIIa complex, exposing the hidden epitopes. The IgG antibodies then bind to these sites, causing platelets to agglutinate, which the automated counter misidentifies as single large particles or leukocytes. **2. Why other options are incorrect:** * **IgA and IgD:** These immunoglobulins are not associated with the cold-reacting autoantibody mechanism involved in EDTA-induced clumping. * **IgM:** While IgM can occasionally be involved in cold agglutinin diseases, the specific EDTA-dependent mechanism that targets the GP IIb/IIIa complex is predominantly mediated by IgG. **Clinical Pearls for NEET-PG:** * **Diagnosis:** Suspect PTCP if the patient has a low platelet count but **no clinical signs of bleeding** (petechiae/purpura). * **Confirmation:** Examine a **peripheral blood smear** to visualize platelet clumps. * **Management:** Repeat the test using a different anticoagulant, such as **Sodium Citrate (blue top)** or Heparin, or perform a manual count immediately after collection. * **Key Association:** It is a purely *in vitro* phenomenon with no clinical significance for the patient's actual hemostatic status.

Question 117: Overexpression of BCL-2 proteins occurs in which of the following conditions?

A. Burkitt's lymphoma
B. Follicular lymphoma (Correct Answer)
C. Diffuse large B-cell lymphoma
D. AML

Explanation: **Explanation:** **1. Why Follicular Lymphoma (FL) is correct:** The hallmark of Follicular Lymphoma is the chromosomal translocation **t(14;18)(q32;q21)** [1]. This translocation moves the *BCL-2* gene from chromosome 18 to the Immunoglobulin Heavy chain (IgH) locus on chromosome 14 [2]. Because the IgH promoter is highly active in B-cells, this results in the **overexpression of BCL-2 protein** [3]. BCL-2 is an **anti-apoptotic** protein that stabilizes the mitochondrial membrane; its overexpression prevents programmed cell death, leading to the accumulation of long-lived neoplastic B-cells [1]. **2. Why other options are incorrect:** * **Burkitt’s Lymphoma:** Characterized by **t(8;14)** involving the ***c-MYC*** oncogene [1]. This leads to increased cellular proliferation rather than anti-apoptotic signaling. * **Diffuse Large B-cell Lymphoma (DLBCL):** While some cases may show BCL-2 expression, it is not the defining pathognomonic feature [4]. DLBCL is more commonly associated with *BCL-6* mutations or *c-MYC* rearrangements. * **AML:** Acute Myeloid Leukemia is driven by mutations affecting hematopoietic differentiation (e.g., *FLT3*, *NPM1*, or *t(8;21)*), not primarily by the t(14;18) BCL-2 mechanism. **3. High-Yield NEET-PG Pearls:** * **BCL-2 Staining:** In a normal lymph node, germinal centers are **BCL-2 negative**. In Follicular Lymphoma, the neoplastic follicles are **BCL-2 positive**—this is a crucial diagnostic differentiator [2]. * **Grading:** FL is graded based on the number of **centroblasts** per high-power field (Mann and Berard system) [3]. * **Transformation:** FL can transform into a more aggressive DLBCL (Richter’s-like transformation). * **Buttock Cells:** Look for **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 602-604. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 561-562. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 563-564.

Question 118: Which syndrome is associated with an increased risk of leukemia?

A. Plummer Vinson syndrome
B. Klinefelter syndrome (Correct Answer)
C. Sturge Weber syndrome
D. Multiple hamartoma syndrome

Explanation: **Explanation:** **Correct Option: B. Klinefelter Syndrome (47, XXY)** Klinefelter syndrome is associated with an increased risk of several malignancies, most notably **germ cell tumors** (specifically mediastinal extragonadal germ cell tumors) and **breast cancer**. However, it is also linked to an increased risk of **hematologic malignancies**, including Acute Myeloid Leukemia (AML), Acute Lymphoblastic Leukemia (ALL), and Non-Hodgkin Lymphoma. The underlying mechanism is thought to involve gene dosage effects from the extra X chromosome and hormonal imbalances [2]. **Incorrect Options:** * **A. Plummer-Vinson Syndrome:** Characterized by the triad of iron deficiency anemia, esophageal webs, and glossitis. It is a precursor to **Squamous Cell Carcinoma of the esophagus** and pharynx, not leukemia. * **C. Sturge-Weber Syndrome:** A neurocutaneous disorder (phakomatosis) characterized by port-wine stains (trigeminal distribution) and leptomeningeal angiomas. It is not associated with an increased risk of malignancy. * **D. Multiple Hamartoma Syndrome (Cowden Syndrome):** Caused by a mutation in the *PTEN* gene. It increases the risk of **breast, thyroid (follicular), and endometrial cancers**, but is not typically linked to leukemia. **High-Yield Clinical Pearls for NEET-PG:** * **Down Syndrome (Trisomy 21):** The most common chromosomal disorder associated with leukemia [1]. Risk of **AMKL (M7)** is high before age 3; risk of **ALL** is high after age 3. * **Fanconi Anemia:** An autosomal recessive DNA repair defect; carries a very high risk of AML and MDS. * **Wiskott-Aldrich Syndrome & Bloom Syndrome:** Other genetic conditions with a predisposition to leukemia/lymphoma. * **Klinefelter Fact:** It is the most common cause of primary hypogonadism in males. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 92-93. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 173-174.

Question 119: Which lymphoid malignancy arises from thymic cells?

A. Hairy cell leukemia
B. Burkitt lymphoma
C. Pre-B cell ALL
D. Pre-T cell ALL (Correct Answer)

Explanation: **Explanation:** The correct answer is **Pre-T cell ALL (T-Acute Lymphoblastic Leukemia/Lymphoma)**. **1. Why the correct answer is right:** Pre-T cell ALL arises from immature T-cell precursors (lymphoblasts) [1]. In the normal physiological process of hematopoiesis, T-cell progenitors migrate from the bone marrow to the **thymus** to undergo maturation and "education." Because these malignant cells are derived from thymic residents, Pre-T cell ALL characteristically presents as a **mediastinal (thymic) mass** in adolescent males [3]. This can lead to emergency complications like Superior Vena Cava (SVC) syndrome or pleural effusions. **2. Why the incorrect options are wrong:** * **Hairy cell leukemia:** This is a mature **B-cell** neoplasm characterized by "hairy" cytoplasmic projections. It typically involves the bone marrow and spleen (causing massive splenomegaly) but has no association with the thymus [2]. * **Burkitt lymphoma:** This is a highly aggressive mature **B-cell** lymphoma associated with c-MYC translocation [t(8;14)]. It typically presents in the jaw (Endemic/African type) or abdomen (Sporadic type). * **Pre-B cell ALL:** While this is the most common subtype of ALL, it arises from B-cell precursors in the **bone marrow**, not the thymus [3]. It typically presents with bone marrow failure (anemia, thrombocytopenia) rather than a mediastinal mass. **3. NEET-PG High-Yield Pearls:** * **Immunophenotype:** Pre-T ALL cells are typically positive for **TdT** (marker of immaturity) and T-cell markers like **CD3 and CD7** [2]. * **Clinical Presentation:** Always suspect T-ALL in a teenage male presenting with a rapidly enlarging anterior mediastinal mass and respiratory distress [3]. * **Genetics:** Often associated with mutations in the **NOTCH1** gene (essential for T-cell development). * **Prognosis:** Historically worse than B-ALL, but modern intensive chemotherapy has significantly improved outcomes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 596-598. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 598. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 599-600.

Question 120: All of the following are good prognostic factors for acute lymphoblastic leukemia except?

A. Age of onset between 2-8 years
B. Hyperdiploidy, trisomy of chromosomes 4, 7 and 10 and + (12;21)
C. Initial WBC count less than 50000
D. + (9;22), + (8;14) (Correct Answer)

Explanation: In Acute Lymphoblastic Leukemia (ALL), prognosis is determined by a combination of clinical features and cytogenetic abnormalities [1]. **Why Option D is the correct answer:** Translocations **t(9;22)** (Philadelphia chromosome) and **t(8;14)** (Burkitt-type ALL) are classic **poor prognostic markers** [1][2]. * **t(9;22):** More common in adults, it involves the *BCR-ABL1* fusion gene, leading to constitutive tyrosine kinase activity and resistance to standard chemotherapy [1]. * **t(8;14):** Involves the *MYC* oncogene and is associated with a very aggressive clinical course [2]. Other poor prognostic factors include t(4;11) and hypodiploidy [1][3]. **Analysis of Incorrect Options (Good Prognostic Factors):** * **Option A (Age 2–8 years):** This is the "optimal age window." Children younger than 1 year (infantile ALL) or older than 10 years have a significantly worse prognosis [1]. * **Option B (Hyperdiploidy & t(12;21)):** **Hyperdiploidy** (>50 chromosomes) and specific trisomies (4, 10, 17) are associated with excellent responses to therapy [1][3]. **t(12;21)** involving the *ETV6-RUNX1* fusion is the most common pediatric translocation and carries an excellent prognosis [1]. * **Option C (WBC < 50,000/µL):** A low initial white cell count is one of the strongest predictors of a favorable outcome [1]. A count >50,000/µL is considered high-risk. **High-Yield Clinical Pearls for NEET-PG:** * **Most common childhood malignancy:** ALL. * **Best Prognosis:** Age 2–10, WBC <50k, Hyperdiploidy, t(12;21) [1]. * **Worst Prognosis:** Age <1 or >10, WBC >50k, Hypodiploidy, t(9;22) [1]. * **Immunophenotype:** Early B-cell ALL has a better prognosis than T-cell ALL. * **CNS/Testis:** These are common "sanctuary sites" for relapse. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 600-602. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 599-600.

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Anemias: Classification and Approach

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Chronic Leukemias

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Lymphomas and Lymphoid Neoplasms

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