1. LEUKEMIA

2. Leukemias ↑ leukocytes Acute leukemias
1. Acute Lymphoblastic Leukemia (ALL)
2. Acute Myelogenous Leukemia (AML)
Chronic leukemias
1.Chronic Lymphoblastic Leukemia (CLL)
2. Chronic Myelogenous Leukemia (CML)

3. Acute Leukemias Blast predominate Child or elder
Short & drastic course
ALL – Lymphoblasts (pre-B or pre-T)
AML – Myeloblasts

4. Chronic Leukemias More mature cells Middle age
Longer & less devastating course
CLL – Lymphocytes
CML – Myeloid stem cells

5. Acute Leukemias
accumulation of blasts in the marrow

6. Acute Lymphoblastic Leukemia (ALL)
Children
Lymphoblasts (pre-B or pre-T)
Neoplastic transformation of the
lymphoid stem cells
• Progressive accumulation of Lymphoblasts in the bone marrow
• Suppression of normal hemopoiesis

7. ALL

8. • Primarily a disease of children and young adults
• B-cell subtype (80%)
• T-cell subtype (20%)

9. ALL Abrupt onset Signs and symptoms related to:
• Suppression of normal hemopoiesis
bone pain and tenderness
• Tissue infiltration ( megaly)
(lymph nodes, spleen, liver, testicles, CNS)
• Mediastinal mass ( T-ALL ) thymus involvement
Headache, vomiting, nerve palsies from meningeal spread.

10. Signs &Symptoms Anemia Infection Bleeding Bone pain Arthritis
Splenomegaly
Lymphadenopathy
CNS involvement

11. ALL - PROGNOSIS Favorable: Unfavorable: Pre-B T or mature B
Age < 1, > 10
WBC < /uL > /uL
Female Male
Minimal organ Prominent organ
involvement involvement

12. ALL Prognosis: • Age 3-7, pre-B, > 90% - CR ( 2/3 - cure )
• Adults, mature B and T-ALL:
Less favorable
Therapy: Chemotherapy
supportive care, BMT

13. ACUTE MYELOGENOUS LEUKEMIA ( AML )
Adults
Myeloblasts
monoblasts, eosinoblasts, megakarioblasts, proerythroblasts, basophiloblasts
Auer rods in the cytoplasm of the cells
Very rapidly progressive malignancy

14. AML

15. Auer rods in AML

16. Differentiation from ALL may be made by microscopy – presence of Auer Rods.
Can also be made based on immunotyping and molecular methods.
Clinical features based on
Marrow failure –anemia, bleeding, DIC, infection…
Leukemic infiltration – bone pain, CNS signs, hepatosplenomegaly, lymphadenopathy…
Constitutional upset -- malaise, fever, weakness, polyarthritis.

17. Course:
• Rapidly fatal if untreated (< 2 mo )
• Median survival - 3 years after chem..
• Adverse prognostic factors:
Age > 60
Previous chemotherapy
Leukocytosis > 100,000 /ul
Therapy: Chemotherapy, supportive, BMT

18. ***Remember this*** For Acute leukemias
acute leukemias = too many blasts in the marrow
2 broad categories: AML vs. ALL
a hematologic urgency
prognosis is poor in adults; but good in kids with ALL.

19. CHRONIC LYMPHOCYTIC LEUKEMIA (CLL)
A monoclonal lymphoproliferative
disorder characterized by lymphocytosis(>4000/cu.mm),
lymphadenopathy and splenomegaly
B - CLL > 95%
T - CLL

20. CLL • Most common adult leukemia in
Western society (30% of all leukemias)
• Monoclonal proliferation of the small lymphocytes…
• Age > 40 M:F / 2:1

22. CLL - Pathology Blood: • Lymphocytosis Bone marrow:
( > 10,000 u/L - diagnostic )
• (+) Coombs test (20%)
• Hypogammaglobulinemia (50-70%)
• Anemia, thrombocytopenia, neutropenia
Bone marrow:
• nodular / interstitial infiltrates
• diffuse - obliteration of normal hemopoiesis
Lymphadenopathy, Hepatosplenomegaly (50-60%)

23. CLL - Clinical course Initially: asymptomatic Advanced disease:
• bacterial infections, hemorrhage
Prognostic factors:
• extent of tumor burden
• pattern of marrow infiltration
• chromosomal abnormalities
Median survival: ~ 6 years

24. CLL - Course • CONVERSION TO PROLYMPHOCYTIC LEUKEMIA (10%)
• RICHTER SYNDROME (5%)(AGGRESSIVE LYMPHOMA)
• DEATH OFTEN DUE TO INFECTIONS..

25. Smudge cells - CLL

26. CLL
One more peripheral blood findings in CLL is Presence of Smudge cells
( parachute cells).
Along with increased number of normal appearing lymphocytes.

27. mainly uncontrolled proliferation of myeloid cells.
Males more than females
Splenomegaly – sometimes massive..

29. **Philadelphia chromosome**
Hybrid chromosome with translocation between the long arm of chr. 9 and long arm of chr t(9:22).
May be present in granulocyte, RBC or platelet precursors in more than 95% of CML..
Absence of these chr. may have worse prognosis.

30. CML - Clinical Features
% of all leukemias; age 25-60
Symptoms:
- non-specific
- related to hypermetabolism (high cell turnover)
- related to splenomegaly
Course:
- chronic phase (mean survival, 3-4y)
- accelerated phase
- blast crisis / myeloid or lymphoid (survival, < 1y)
Therapy: chemotherapy; BMT

31. CML: Sustained granulocytosis with immature cells; low LAP score; bone marrow pathology;
Philadelphia chromosome
LAP – leukocyte alkaline phosphatase