Objectives:
•	What's the normal size of the spleen - Are you supposed to feel it or not?

An average human spleen is 10 cm long and weighs 150 grams.[2] Abnormal enlargement of the spleen, splenomegaly, is usually determined by physical examination. It may be difficult to palpate an enlarged spleen in the settings of obesity, a muscular abdominal wall, or the inability to sufficiently relax the abdominal musculature. In these cases, spleen size may need to be determined by radiographical tests. It is not uncommon for a radiologist interpreting a chest x-ray to comment that the spleen seems enlarged (usually considered an incidental finding). If splenomegaly is suspected, an ultrasound of the left upper quadrant can be helpful, with the advantage of lack of exposure to radiation. Computed tomography and nuclear imaging (liver-spleen scan) may be complementary; the former may confirm an enlarged spleen, whereas a liver-spleen scan may contribute valuable information about the presence of colloid shift, signifying portal hypertension.

•	Why do we have splenomegaly in thalassemia?

Unpaired alpha chains form insoluble aggregates in RBC. Precipitates in RBC. Membrane damage. Extravascular hemolysis occurs when RBCs are phagocytized by macrophages in the spleen.

•	Why are platelets high in this case?
•	Why is lymphoma not the diagnosis?
•	Peripheral film interpretation.
•	Chronic myeloid leukemia and ALL. Clinical features, pathogenesis, phases, prognosis, ...

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•	Pharmacological agents: Imatinib, nilotinib and chemotherapeutic agents - Side effect, MOA, and success rate of imatinib as primary medication for CML.

Philadelphia (Ph) chromosome, which encodes the BCR-ABL1 fusion oncoprotein [Figure 1]. 2-4 This protein has constitutive tyrosine kinase activity, which stimulates hematopoietic transformation and myeloproliferation.

The goals of treatment are to achieve complete cytogenetic response (CCyR), complete haematological remission, and major molecular response (MMR). Treatment may not achieve all of these goals; aiming for at least a CCyR is considered the main goal.

Standard initial treatment is with the with the first-generation TKI imatinib.[12][15] There is no clear evidence that higher doses are superior to the standard dose of imatinib.[36][37]

Imatinib is well tolerated, and approximately 87% of patients achieve complete haematological response. Overall survival rates with 8-year follow-up are about 85% to 90%.[19] There is a 7% risk of disease progression to accelerated or blast phase in the first 5 years, a significant improvement on the pre-imatinib era.[3][19]

Resistance to imatinib therapy can develop due to mutations in the BCR-ABL tyrosine kinase, BCR-ABL amplification, or other reasons. Patients with resistant disease may fail to respond to primary therapy, have a suboptimal response, or lose their initial response. If available, mutation analysis should be performed to help guide treatment.[21]

•	How does CML transform into AML and discuss how to differentiate between them. + ALL management
•	What are CD10 CD19 and CD22 specific for?
•	Cytochemistry and immunophenotyping findings (PAS stain and CD10 CD19 CD22)