5. In tumors manifesting as leukemias ,blast
accumulating in the marrow suppress the growth
of normal hemopoietic cells by physical
displacement and by other poorly understood
mechanisms.Eventully this suppresion
manifested as bone marrow failure. Which
account for the major clinical presentation.
6. Pathogenesis
The principle pathogenic defect in acute leukemia
is a block in differentiation.
This mutation arrest stems from acquired
mutations in specific transcription factors that
regulate the differentiation of immature
lymphoid or myeloid progenitors.
Normal B cell , T cell,and myeloid differentiation
are regulated by different lineage -specific
transcription factors, accordingly, the mutated
transcription factor genes found in acute
leukemias derived from each of these lineages
7. Clinical features
-Abrupt,stormy onsent
-Clinical signs and symptoms related to suppressed
marrow function , including fatigue due to anemia
-Bone pain and tenderness resulting from marrow
expansion and infiltration of subperiosteum.
_Generalized lymphadenopathy, splenomegaly and
Hepatomegaly ,thymic mass in ALL.
-CNS manifestation from meningeal spread. More
common in chidren than adult and ALL than AML.
10. Leukaemia: Neoplastic disease of WBC forming
tissue.
Classification (FAB)
I. Acute lymphoblastic leuk. ALL
Morphological
L1 – Monomorphic type . . . . Good risk
L2 – Heterogenous type
L 3 – Burkitt’s type
Immunological
1) Non T, Non B ALL (common)
good risk ALL
2) T- ALL
3) B- ALL
11. II. Acute Myeloid Leukaemia (AML)
[ FAB]
M0 AML . . . Poorly differentiated
M1 AML . . . Without Maturation
M2 AML . . . With Maturation
M3 AproL . . . Promyelocytic
M4 AMML . . . MyeloMonocytic
M5 AMOL . . . Monocytic
M6 A. ErythroLeukaemia
M7 A. Megakaryoblastic L
Age groups : ALL – mostly in children
AML – mostly in Adults